title: Development of miRNA expression signatures for induction of histone deacetylase inhibitor (part 2)

summary: To clarify the relationship between histone acetylation and miRNA expression, we performed miRNA arrays to detect histone deacetylase inhibitor (OBP-801) induced miRNA regulating AR expression in 22Rv1.

overall_design: Agilent-031181 Unrestricted Human miRNA Microarray (Agilent Technologies, Santa Clara, California) was used according to the manufacturer’s protocols.

first: Shinya

last: Sato

first: Keiko

last: Shinjo

first: Akira

last: Hatanaka

first: Fumiharu

last: Ohka

first: Satoru

last: Takahashi

first: Yutaka

last: Kondo


title: Expression data from melanosis coli (MC)

status: Public on May 30 2016

city: Hangzhou

first: Shiyi

last: Wang

state: Zhejiang Province

address: No. 54, Youdian Road

department: Department of Gastroenterology

country: China

institute: The First Affiliated Hospital of Zhejiang Chinese Medical University

summary:
There is still a big debate about the correlation between melanosis coli (MC) and carcinoma. We used HTA2.0 to investigate the expression changes of lncRNAs and mRNAs in human colonic mucosa with or without MC and try to investigate MC from gene aspect, eventually to demonstrate whether there’s a certain correlation between MC and carcinoma.
GeneChip® Human Transcriptome Array 2.0 (HTA 2.0) microarrays were adopted. The expression profile of lncRNAs and mRNA were tested in five colon tissue biopsy specimen of MC patients and five demographically-matched controls.

overall_design: This study recruited a total of five MC patients and five coupled matched controls. All specimens were obtained from colonoscopy. The fresh specimens of colon tissues form MC patients and control patients were washed with RNAase free water and put into RNAlater (Qiagen) immediately and frozen in -80°C. Gene Ontology (GO) and KEGG Pathway analyses of aberrantly expressed mRNAs were performed to identify the related biological functions and pathologic pathways.

first: Shi-Yi

first: Yi-Hong

last: Fan

first: Bin

last: Lv


title: Transcriptome data of multiple sclerosis patients receiving fingolimod therapy [HTA-2_0, CD14+ cells, gene level]

status: Public on May 20 2016

city: Rostock

first: Michael

last: Hecker

address: Gehlsheimer Str. 20

department: Department of Neurology

country: Germany

institute: University of Rostock

summary:
We analyzed the gene expression patterns of different blood cell types before and during fingolimod treatment in a group of patients with relapsing-remitting multiple sclerosis (RRMS).
Affymetrix Human Transcriptome Arrays (HTA) 2.0 were used to obtain gene expression profiles of immune cell populations from 10 RRMS patients within the first 3 months of fingolimod treatment.
This GEO entry provides the Affymetrix HTA 2.0 microarray data of peripheral blood CD14+ cells, preprocessed according to the gene level workflow.

overall_design:
EDTA blood samples were taken from all patients immediately before first and second fingolimod administration as well as after 3 months of therapy.
Total RNA of CD14+ cells positively selected from each blood sample was extracted, labeled and hybridized to high-density Affymetrix HTA 2.0 microarrays to quantify the transcript levels.

first: Dirk

last: Koczan

first: Uwe

middle: K

last: Zettl


title: Cordycepin induces apoptosis by caveolin-1 mediated JNK’s regulation of Foxo3a in lung cancer A549 cells

status: Public on May 24 2016

city: Seoul

first: Jung Min

last: Kim

address: Gangnam-gu Teheran-ro 216

department: Department of Health Genomics

country: South Korea

institute: NAR Center, Inc. & Genoplan, Inc.

summary: c-Jun N-terminal kinase (JNK) plays a pivotal role in the regulation of cancer cell apoptosis. Previous studies have revealed that forkhead transcription factor (Foxo3a) is a critical effector of JNK-mediated tumor suppression. However, it is not clear whether caveolin-1 (CAV1) mediated JNK/Foxo3a pathway is involved in cancer cell apoptosis. We found that cordycepin upregulates CAV1 expression, which was accompanied by JNK phosphorylation (p-JNK), which induced Foxo3a translocation into the nucleus, resulting in the upregulation of levels of Bax protein. Furthermore, we found that CAV1 overexpression upregulated p-JNK, whereas siRNA mediated inhibition of CAV1 downregulated p-JNK, and that JNK inhibition by SP600125, a specific JNK inhibitor, significantly increased Foxo3a phosphorylation (p-Foxo3a), which attenuated Foxo3a translocation into the nucleus, indicating caveolin-1 mediated JNK’s regulation of Foxo3a. siRNA mediated inhibition of Foxo3a downregulated levels of Bax protein, attenuated A549 cell apoptosis, indicating that CAV1 mediated JNK/Foxo3a pathway induce the apoptosis of A549 lung cancer cells. Taken, together, these results indicate that cordycepin promotes CAV1 upregulation to enhance JNK/Foxo3a signaling pathway activation to induce apoptosis in lung cancer cells and support the potential of cordycepin as a therapeutic agent for lung cancer.

overall_design: A549 lung cancer cells were treated with 0.1% DMSO, cordycepin 60 ug/mL, and cordyceps 100 ug/mL for 48hrs.

first: Jung

middle: M

first: Ik-Soon

last: Jang


title: A Novel role for GSK3B as a modulator of Drosha Microprocessor activity and microRNA biogenesis

city: London

first: Charlotte

last: Bevan

address: South Kensington Campus

department: Department of Surgery & Cancer

country: United Kingdom

institute: Imperial College London

summary: Regulation of microRNA (miR) biogenesis is complex and stringently controlled.  Here we identify the kinase GSK3B as an important modulator of global miR biogenesis at microprocessor level. Repression of GSK3B activity reduces Drosha activity towards pri-miRs, leading to accumulation of unprocessed pri-miRs and reduction of pre-miRs and mature miRs without altering levels or cellular localisationof miR biogenesisproteins.  Conversly, GSK3B activation increases Drosha activityand mature miR accumulation.  GSK3B achieves this through promoting Drosha:cofactor and Drosha:pri-miR interactions: it binds to DGCR8 and p72 in the Microprocessor, an effect dependent of RNA.  Indeed GSK3B itself can immunoprecipitate pri-miRs, suggesting possible RNA binding capacity.   Kinase assays identify the mechanism for GSK3B-enhansed Drosha activity, which requires GSK3B nuclear localisation, as phosphorylation of Drosha at s300 and/or s302 confirmed by enhanced Drosha activity and association with cofactors, and increased abundance of mature microRNAs in the presence of phospho-mimetic Drosha.  Functional implicatons of GSK3B-enhanced miR biogenesis are illustrated by increased levels of GSK3B-upregulatd miR targets following GSK3B inhibition.  These data, the first link GSK3B with the miR cascade in humans, hilight a novel pro-biogenesis role for GSK3B in increasing miR biogenesis as a component of the Microprocessor complex with wide ranging consiquences.

overall_design: A total of 6 samples were analysed using one colour microarrays.  3 samples were treated with an inhibitor (99021) and the remaining 3 were treated with a vehicle control.

first: Claire

last: Fletcher

first: Jack

last: Godfrey

first: Akifumi

last: Shibakawa

first: Martin

last: Bushell


title: Transcriptome data of multiple sclerosis patients receiving fingolimod therapy [HTA-2_0, CD56+ cells, gene level]

summary:
We analyzed the gene expression patterns of different blood cell types before and during fingolimod treatment in a group of patients with relapsing-remitting multiple sclerosis (RRMS).
Affymetrix Human Transcriptome Arrays (HTA) 2.0 were used to obtain gene expression profiles of immune cell populations from 10 RRMS patients within the first 3 months of fingolimod treatment.
This GEO entry provides the Affymetrix HTA 2.0 microarray data of peripheral blood CD56+ cells, preprocessed according to the gene level workflow.

overall_design:
EDTA blood samples were taken from all patients immediately before first and second fingolimod administration as well as after 3 months of therapy.
Total RNA of CD56+ cells positively selected from each blood sample was extracted, labeled and hybridized to high-density Affymetrix HTA 2.0 microarrays to quantify the transcript levels.


title: Transcriptome data of multiple sclerosis patients receiving fingolimod therapy [HTA-2_0, CD19+ cells, gene level]

summary:
We analyzed the gene expression patterns of different blood cell types before and during fingolimod treatment in a group of patients with relapsing-remitting multiple sclerosis (RRMS).
Affymetrix Human Transcriptome Arrays (HTA) 2.0 were used to obtain gene expression profiles of immune cell populations from 10 RRMS patients within the first 3 months of fingolimod treatment.
This GEO entry provides the Affymetrix HTA 2.0 microarray data of peripheral blood CD19+ cells, preprocessed according to the gene level workflow.

overall_design:
EDTA blood samples were taken from all patients immediately before first and second fingolimod administration as well as after 3 months of therapy.
Total RNA of CD19+ cells positively selected from each blood sample was extracted, labeled and hybridized to high-density Affymetrix HTA 2.0 microarrays to quantify the transcript levels.


title: 6-acetoxy-anopterine: A novel structure class of mitotic inhibitor disrupting microtubule dynamics in prostate cancer cells

status: Public on May 11 2016

city: Brisbane

first: Colleen

last: Nelson

state: Queensland

address: 199 Ipswich Road

department: Institute of Health and Biomedical Innovation; Vancouver Prostate Centre

country: Australia

institute: Queensland University of Technology; University of British Columbia

summary: The lack of a cure for metastatic prostate cancer (PCa) highlights the urgent need for more efficient drugs to fight this disease. Here, we report the molecular mechanism of action of the natural product 6-acetoxy-anopterine (6-AA) in malignant cells of the prostate. This potent cytotoxic alkaloid from the endemic Australian tree Anopterus macleayanus induced at low nanomolar doses a strong accumulation of LNCaP and PC3 PCa cells in mitosis, severe mitotic spindle defects and asymmetric cell divisions, ultimately leading to mitotic catastrophe accompanied by cell death through apoptosis. DNA microarray of 6-AA treated LNCaP cells combined with pathway analysis identified very similar transcriptional changes when compared to vinblastine, highlighting pathways involved in mitosis, microtubule spindle organisation and microtubule binding. Like vinblastine, 6-AA inhibited microtubule polymerization in a cell-free system and reduced microtubule polymer mass in vitro. Yet, microtubule alterations that are associated with resistance to microtubule-destabilizing drugs like vinca alkaloids or 2-methoxyestradiol did not confer cross-resistance to 6-AA, suggesting a different mechanism of microtubule interaction. Finally, 6-AA is the first-in-class microtubule inhibitor that features the unique anopterine scaffold. Altogether, this study provides a strong rationale to further develop this novel structure class of microtubule inhibitor for the treatment of malignant disease.

overall_design: The dataset was derived from three biological repeats of each of the treatment groups DMSO and vinblastine and four repeats of the treatment group 6-AA.

last: Levrier

middle: C

last: Sadowski

first: Brian

last: Gabrielli

first: Anja

last: Rockstroh

first: Maria

last: Kavallaris

first: Melanie

middle: L

last: Lehman

first: Rohan

middle: A

last: Davis


title: Protracted p53-independent stimulation of p21WAF1/Cip1 fuels genomic instability by deregulating the replication licensing machinery

status: Public on May 15 2016

city: New York

first: Prokopios Alexandros

last: Polyzos

address: 413 E 69th St

country: USA

institute: Weill Cornell Medicine

summary: The cyclin-dependent kinase inhibitor p21WAF1/Cip1 is the prototype downstream effector of the tumor suppressor protein p53. Yet, evidence from human cancer and mice models, imply that p21WAF1/Cip1, under certain conditions, can exercise oncogenic activity. The mechanism behind this behavior is still obscure. Within this context we unexpectedly noticed, predominantly in p53 mutant human cancers, that a subset of highly atypical cancerous cells expressing strongly p21WAF1/Cip1 demonstrated also signs of proliferation. This finding suggests either tolerance to high p21WAF1/Cip1 levels or that p21WAF1/Cip1 per se guided a selective process that led to more aggressive off-springs. To address the latter scenario we employed p21WAF1/Cip1-inducible p53-null cellular models and monitored them over a prolonged time period, using high-throughput screening means. After an initial phase characterized by stalled growth, mainly due to senescence, a subpopulation of p21WAF1/Cip1 cells emerged, demonstrating increased genomic instability, aggressiveness and chemo-resistance. At the mechanistic level unremitted p21WAF1/Cip1 production “saturates” the CRL4CDT2 and SCFSkp2 ubiquitin ligase complexes reducing the turn-over of the replication licensing machinery. Deregulation of replication licensing triggered replication stress fuelling genomic instability. Conceptually, the above notion should be considered when anti-tumor strategies are designed, since p21WAF1/Cip1 responds also to p53-independent signals, including various chemotherapeutic compounds.

overall_design:
We used microarrays to compare the non-induced and “escaped” Saos2-p21WAF1/Cip1 Tet-ON cells gene expression profile
Multiple arrays for non-induced and “escaped” Saos2-p21WAF1/Cip1 Tet-ON cells

first: Alexander

first: Konstantinos

last: Vougas

first: Vasilios

last: Gorgoulis


title: A microfluidics-based in vitro model of the gastrointestinal human-microbe interface

status: Public on May 05 2016

city: Belvaux

first: Enrico

last: Glaab

state: Capellen

address: 6, avenue du Swing

country: Luxembourg

institute: University of Luxembourg

type:
Expression profiling by array
Non-coding RNA profiling by array

summary:
We have developed a microfluidics-based in vitro model of the human gut allowing co-culture of human and microbial cells and subsequent multi-omic assessment of the effect of the co-culture on the host transcriptome.
We compare the transcriptional changes induced in the human epithelial cell line, Caco-2 after co-culture with Lactobacillus rhamnosus GG or a consortium of Lactobacillus rhamnosus GG and Bacteroides caccae.

platform_organism:
Homo sapiens
synthetic construct

overall_design: Caco-2 cells were monocultured, co-cultured with LGG and a consortium of LGG & B.caccae and the RNA was analyzed for evaluating the transcriptional changes induced in Caco-2 cells following HuMiX-based co-culture. Both for mRNA and miRNA expression profiling, 9 microarray samples were analyzed, covering 3 biological replicates for 3 conditions (control, co-culture with the commensal Lactobacillus rhamnosus GG (LGG), and co-culture with the obligate anaerobe Bacteroides caccae and LGG).

first: Pranjul

last: Shah

first: Joëlle

middle: V

last: Fritz

first: Mahesh

middle: S

last: Desai

first: Kacy

last: Greenhalgh

first: Audrey

last: Frachet

first: Magdalena

last: Niegowska

first: Matthew

last: Estes

first: Christian

last: Jäger

first: Carole

last: Seguin-Devaux

first: Frederic

last: Zenhausern

first: Paul

last: Wilmes


title: Gene expression profiling of Caco2 cells treated with Cudraflavone C

status: Public on Mar 08 2016

city: Bukit Jalil

first: Chee-Onn

last: Leong

country: Malaysia

institute: International Medical University

summary: A total of 26 genes were up-regulated and 63 genes were down-regulated > 2-fold following Cudraflavone C treatment

overall_design: Microarray experiments were performed in duplicate as follows: Caco2 cells were treated with 10 uM of Cudraflavone C or control vehicle (0.1% DMSO) for 48 h. Total RNA from cells was extracted using Qiagen RNA isolation kit (Qiagen, Valencia, CA, USA) according to the manufacturers’ protocol. RNA purity was examined by spectrophotometric determination at 260/280 nm. The microarray hybridizations were carried out using the GeneChip® Human Transcriptome Array 2.0 arrays.


title: Medullary Carcinoma of the colon

status: Public on Apr 01 2016

city: PROVIDENCE

last: Brodsky

state: RI

address: 593 Eddy St.

department: MCB

institute: Rhode Island Hospital/Brown University

summary: This study examined the expression profile of medullary carcioma of the colon compared to adjacent histologically normal colonic mucosa.

overall_design: Medullary carcinomas of the colon were selected from Rhode Island Hosptial and The Miriam Hospital to identify new molecular markers of this disease. Medullary carcinoma was defined by applying strict morphologic criteria and demonstration of mismatch repair protein deficiency (MMRd) by IHC.

first: Murray

middle: B

last: Resnick

first: Kenneth

last: Friedman


title: Aberrantly expressed long noncoding RNAs in the eutopic endometrium of women with adenomyosis

status: Public on May 01 2016

city: Beijing

first: fa

middle: jian

last: jiang

address: Dongcheng District, Shuaifuyuan NO.1

department: Obstetrics and Gynecology

institute: Peking Union Medical College Hospital

summary: Objective: To identify differentially expressed long noncoding RNA in the eutopic endometrium tissue of adenomyosis on a genome-wide scale.  Patient(s): Seventeen women with adenomyosis and fifteen patients without adenomyosis or endometriosis receiving surgical treatment.   Intervention(s): Total RNAs containing long nocoding RNAs was extracted from endometrial tissue obtained during surgery.  Main Outcome Measure(s): Differentially expressed lncRNAs and mRNAs were detected by human lncRNA microarray. Result(s): We identified 165 lncRNAs and 612 mRNAs abnormally expressed (P<0.05) in the eutopic endometrium of adenomyosis.  Conclusion(s): This study showed for the first time that the lncRNA expression profile was altered in women with adenomyosis.

overall_design: Total 8 samples was analyzed, including 4 samples in the experiment group and 4 in the control group.

first: Fa

middle: J

last: Jiang

first: Jun

last: Sun


title: Gene expression data from H1299 cells

status: Public on May 06 2016

first: Jie

last: Li

state: HaiDian Qu

address: Taiping Road 27

department: Biochemistry and Molecular Biology

institute: Institute of Basic Medical Sciences

summary: MiR-138 has a variety of biological functions because of its capacity to act on different target genes in various cells and tissues; however, the targets of miR-138 in human non-small cell lung cancer cell line H1299 cannot be determined by bioinformatics alone. Thus, H1299 cells overexpressing miR-138 in H1299 cells were subjected to microarray analysis to analyse the differences of gene expression.

overall_design: Total RNAs were extracted from H1299 cells transfected with miR-138 or NC mimics for 48h. Their gene expression profiles were investigated using the Affymetrix GeneChip Human Transcriptome Array 2.0 platform.

first: J

first: W

last: Xia

first: N

last: Shao


title: Transcriptomic Effects of SSX2 on a Prostate Cancer Cell Line

status: Public on Feb 11 2016

city: Madison

first: Jordan

middle: Edmund

last: Bloom

state: WI

address: 1111 Highland Ave.

department: Medicine

institute: University of Wisconsin-Madison

summary: Prostate cancer is the most commonly diagnosed malignancy in the United States. While the majority of cases are cured with radiation or surgery, about 1/3 of patients will develop metastatic disease which there is no cure, and has a life expectancy of less than 5 years. Identification of antigens associated with this transition to metastatic disease is crucial for future therapies. One such antigen of interest is the SSX gene family, which are cancer/testis antigens that are associated with the epithelial to mesenchymal transition in other cancer types. Prior work has shown that, in prostate cancer, SSX expression was restricted to metastatic tissue and not primary tumor tissue which may indicate a role in disease progression.  Some work has been done into the function of the SSX family, which revealed transcriptional regulator activity. But neither the targets of this activity or the function of SSX are known. Through a transcriptomics approach, we are seeking a better understanding of the different genes and pathways SSX regulates in the context of prostate cancer, and to determine if these pathways may contribute to disease progression.

overall_design: We analyzed the 22Rv1 prostate cancer cell under three different conditions with 3 technical replicates each (9 total samples) They are as follow: KD the 22Rv1 cell line tranfected with shRNA targetted against the gene SSX2, SCR the 22Rv1 cell line transfected with a scrambled control shRNA, WT the wildtype 22Rv1 cell line

middle: E

first: Douglas

middle: G

last: McNeel


title: Gene expression in colorectal liver metastasis tissues from EPA-treated patients

status: Public on Mar 16 2016

city: LEEDS

first: Milene

last: Volpato

address: St James University Hospital

department: LIRM

institute: University of Leeds

summary:
Eicosapentaenoic acid in its free fatty acid form (EPA-FFA), 2g daily, is safe and well-tolerated in patients undergoing liver resection surgery for colorectal liver metastasis.Oral EPA incorporates into colorectal liver metastasis tissue. EPA-FFA treatment is associated with reduced vascularity of liver metastases in ω-3 PUFA-naïve patients. Preoperative (median 30 days) EPA-FFA treatment may have prolonged benefit on postoperative overall and disease-free survival.
We used whole genome expression array to study whether systemic CCL2 level changes were linked to a specific tumour gene expression profile in colorectal liver metastasis patients treated with EPA-FFA.

overall_design: 15 tumour RNA samples from colorectal liver metastasis patients treated with EPA-FFA during the EMT study (ClinicalTrials.gov NCT01070355) were extracted from formalin-fixed paraffin-wax embedded tissue blocks.  The RNA samples were used for whole genome expression microarray experiments.  We then performed a differential gene expression analysis to compare the tumour expression profile of patients with increased or decreased plasma CCL2 levels after intervention.

first: Sarah

last: Perry

first: Gemma

last: Marston

first: Nicola

last: Ingram

first: Andrew

last: Cockbain

first: Heather

last: Burghel

first: Jake

last: Mann

first: David

last: Lowes

first: Erica

last: Wilson

first: Alastair

last: Droop

first: Juliette

last: Randerson-Moor

first: P

last: Coletta

first: Mark

last: Hull


title: Downregulation of microRNA-132 is associated with liver metastasis of colorectal cancer by targeting Anoctamin 1.

status: Public on Feb 14 2016

city: Suita

first: Daisuke

last: Okuzaki

state: Osaka

address: Yamadaoka 3-1

department: Immunology Frontier Research Center

country: Japan

institute: Osaka univ.

summary: In this study, we conducted a microarray-based analysis to identify differentially expressed miRNAs in CRC by comparing miRNA profiles among primary CRC tissues from patients with liver metastases, primary tissues without liver metastases, and liver metastatic lesions. microRNAs (miRNAs) have been shown to have a potential for cancer diagnosis lately. The main objective of this study is to identify a novel biomarker serum miRNA from the patients with colorectal cancer (CRC). Microarray analysis of miRNA expression was performed using paired pre- and post- operative serum from 10 CRC patients. Two miRNAs (let-7a, miR-199a-3p) decreased significantly in the post-operative serum when compared to pre-operative serum (P=0.015 and 0.029, respectively).

overall_design: Microarrays were performed for the testing cohort of primary CRC lesions (n=28) and liver metastatic lesions (n=8).

first: Yukako

last: Mokutani

first: Hirofumi

last: Yamamoto


title: Large genomic alteration of 7q in two patients with multiple primary cancers, including triple negative breast cancer, and family history of malignant neoplasms

status: Public on Feb 15 2016

city: Brasília

first: Rolando

middle: Andre Rios

last: Villacis

state: DF

address: Asa Norte

department: Genetics and Morphology

country: Brazil

institute: University of Brasília - UnB

type: Genome binding/occupancy profiling by genome tiling array

summary: A great percentage of patients with multiple primary cancers (MPCs) and family history of cancer are suspected to have a hereditary cancer predisposition syndrome. However, only a small proportion of these cases are explained by mutations in high-penetrance genes, suggesting the involvement of undiscovered genes in cancer predisposition. In this study, we report the molecular and clinical characterization of two unrelated patients with MPCs, a positive family history of cancer, no germline pathogenic mutations in BRCA1, BRCA2 and TP53 genes and large genomic rearrangements mapped on chromosome 7q.

overall_design: Genomic rearrangements were assessed with Affymetrix CytoScan HD Array platform in two unrelated patients (Patient 1 and Patient 2) with multiple primary cancers. The mother of Patient 2 and five children (two of Patient 1 and three of Patient 2) were also evaluated. In addition, we performed the transcriptome analysis of the triple negative BC from Patient 2 using the Affymetrix HTA 2.0 platform.


title: Gene expression and alternative splicing data from human cartilage endplate-derived stem cells

status: Public on Dec 21 2015

city: Chongqing

first: Jin

last: Shang

address: No. 183, Xinqiao Main Street

institute: Third Military Medical University

summary:
Low back pain (LBP) is one of the most prevalent conditions which need medical advice and result in chronic disabilities. Degenerative disc disease (DDD) is a common reason for LBP. A lot of researchers think that CEP degeneration play critical roles in the initiation and development of DDD. In recent years, researchers have put interests on cell-based therapies for regenerating disc structure and function. Our research team has isolated cartilage endplate-derived stem cells (CESCs) and validated their chondrogenic and osteogenic differentiation ability. Enhanced chondrogenic differentiation and inhibited osteogenic differentiation of CESCs may retard CEP calcification and restore the nutrition supply, possibly regenerating the degenerated discs.
We used Affymetrix Human Transcriptome Array 2.0 to study the global gene expression profilling and alternative splicing events during the chondrogenic and osteogenic differentiation of cartilage endplate-derived stem cells.

overall_design: The cartilage endplate-derived stem cells(CESCs) were induced to undergo chondrogenic(CD) and osteogenic differentiation(OD). Both undifferentiated and differentiated CESCs were sent for RNA extraction and hybridization on Affymetrix microarrays. A comparative analysis was done between the undifferentiated and differentiated samples.

first: Yue

last: Zhou

first: Huan

last: Liu


title: Environmental enteric dysfunction includes a broad spectrum of inflammatory responses and epithelial repair processes.

status: Public on Mar 01 2016

city: St. Louis

first: Jinsheng

last: Yu

state: MO

address: 660 S. Euclid Ave.

department: Genetics

institute: Washington University School of Medicine

summary: Environmental enteric dysfunction (EED), a chronic diffuse inflammation of the small intestine, is associated with stunting in children in the developing world. The pathobiology of EED is poorly understood because of the lack of a method to elucidate the host response. This study utilized a novel microarray method to interrogate the host transcriptome in feces in Malawian children with EED.  Our data showed that the children studied had a range of %L values, consistent a spectrum of EED from normal to severe. We identified 12 transcripts associated with the severity of EED, including chemokines that stimulate T-cell proliferation, Fc fragments of multiple immunoglobulin families, interferon-induced proteins, activators of neutrophils and B-cells, and mediators that dampen cellular responses to hormones. EED associated transcripts mapped to pathways related to cell adhesion, and responses to a broad spectrum of viral, bacterial and parasitic microbes and enhanced phagocytosis. Several mucins, regulatory factors and protein kinases associated with the maintenance of the mucous layer were expressed less in children with EED than normal children.  In conclusion, EED represents the focused activation of elements of the immune system and is associated with widespread intestinal barrier disruption. The differentially expressed transcripts may be explored as potential biomarkers.

overall_design: In 259 children, EED was measured by lactulose permeability (%L) in the small intestine. After isolating low copy numbers of mRNA, the transcriptome was reliably and reproducibly profiled. mRNA copy number was correlated with %L using analyses of covariance. The transcripts identified were mapped to biological pathways and processes.

first: Isabel

last: Ordiz

first: Jennifer

last: Stauber

first: Nurmohammad

last: Shaikh

last: Manary


title: Analysis of differentially expressed genes in MDA-MB-453 after treatment with the compound sulforaphene

status: Public on Feb 05 2016

city: Beijing,China

first: Wendi

last: Teng

address: North three ring,East road,15

institute: Beijing University of Chemical Technology

summary: This study aimed to identify differential expressed genes before and after treatment with the compound sulforaphene, using the MDA-MB-453 breast cancer cell line as a model.

overall_design: There were a total of 2 samples examined.

first: Qipeng

last: Yuan


title: Expression data fom human capillary network-derived cells before and after adipogenic differentation, and after chronic  adenylate cyclase activation of differentiated cells

status: Public on Jan 01 2016

city: Worcester

first: Silvia

last: Corvera

state: MA

address: 373 Platantion Street

department: Molecular Medicine

institute: UMASS Medical School

summary:
Progenitors in human vasculature expanded in-vitro were differentiated with adipogenic cocktail for 12 days, following which they were stimulated with forskolin for 7 days
Microarrays were used to detail the program of differentiation of thermogenic human adipose cells

overall_design: Adipose tissue from three individuals was cultured in hydrogel under pro-angiogenic conditions. Capillary networks emerging from the explants were subcultured on plastic, grown to confluence, subjected to adipogenic differentiation and after 12 days treated with vehicle or forskolin for 7 days

first: So

middle: Y

last: Min


title: Genome-wide profiling of histone H3 lysine 27 and lysine 4 trimethylation in multiple myeloma reveals the importance of Polycomb gene targeting and highlights EZH2 as a potential therapeutic target [Affymetrix]

status: Public on Dec 31 2015

city: Uppsala

first: Prasoon

last: Agarwal

state: Sweden

address: Dag Hammarshkojlds vag 20

department: IGP

country: Sweden

institute: Rudbeck Laboratory, Uppsala University

summary: in this study we define an epigenomic profile of PRC2 (H3K27me3 and bivalent) tragets in four newly diagnosed MM patients. Using Oncomine database we demonstarte that PRC2 targets are underexpressed with advanced ISS stages and correlated to poor outcome. Pharmacological inhibition of UNC1999 showed anti-myeloma potential in vitro by activating the expression genes related to apoptosis and cell differenatiation.

overall_design: In this array the differences between the gene expression profiles of samll molecule inhibitor (UNC1999) of EZH2 and the control (UNC2400) have been tested. So multiple myeloma cell line INA-6 was treated with 2μM of UNC1999 and UNC2400. This design contains three biological replicates.

first: Mohammad

last: Alzrigat

first: Helena

last: Wiklund


title: Combination of multiomics approach and BCR-ABL based molecular testing: A better way to monitor treatment regimen and  disease progression in Chronic Myeloid Leukemia

city: Lucknow

first: Neetu

last: Singh

address: Chowk

department: Center for Advance Research

country: India

institute: King George's Medical University

type:
Expression profiling by array
Genome variation profiling by SNP array

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Combination of multiomics approach and BCR-ABL based molecular testing: A better way to monitor treatment regimen and  disease progression in Chronic Myeloid Leukemia [HTA-2_0]

status: Public on Jan 26 2016

summary:
We screened TKI-treated-CML-samples in different-phases  based on < or >10% copies of BCR-ABL, undetected and control-samples for generating transcriptomics-profile.
Transcriptionally, three clusters were identified which showed correlation with BCR-ABL transcript-levels i.e. <10% copies (I-cluster) , undetectable (II-cluster) and >10% copies (III-cluster).

overall_design: CML-new cases as well as Tyrosine kinase treated-different phases of CML

first: Anil

last: Kumar Tripathi

first: Dinesh

last: Kumar Sahu

first: Archana

last: Mishra

first: Rebecca

last: Chowdhry

first: Ravi

last: Kant


title: Expression data from U937 cells infected by hsa-miR-608 inhibitor virus

status: Public on Dec 12 2015

city: chongqing

first: Wei

last: Gu

address: 10th, Changjiangzhilu

department: the institue of surgery research

institute: the third military medical university

summary:
The expression level of miR-608 was found to be down regulated in several types of cancer. In our previous study, a single SNP in miR-608 (rs4919510)  was found to be strongly associated with a higher risk of developing sepsis and multiple organ dysfunctions in all 3 independent study cohorts. However, the clinicopathological impact and the exact roles of miR-608 and its underlying molecular mechanisms in inflammation remain to be identified.
In order to identify the exact terget gene of miR-608 in monocytes, we constructed lentiviral vectors with has-miR-608 inhibitor sequences and transfected U937 cells.We used microarrays to identified distinct classes of up-regulated genes during this process and look for possible target genes.

overall_design: U937 cells transfected by has-miR-608 inhibitor lentiviral vectors or negative control virus were analyzed. There are three samples in each group.


title: The YY1/MMP2 axis promotes trophoblast invasion at the maternal-fetal interface

status: Public on Jan 21 2016

city: shanghai

first: Fu-Ju

last: Tian

state: shangahi

address: room 602, number145 guangyuan Road, xuhui

institute: Institute of Embryo-Fetal Original Adult Disease Affiliated to Shanghai Jiao Tong University School of Medicine

summary: YY1 is a sequence-specific DNA-binding transcription factor that has many important biological roles. However, its function in trophoblasts at the maternal-foetal interface remains to be elucidated. In this study, we used an mRNA microarray and quantitative reverse transcription-PCR and compared the YY1 mRNA expression level in trophoblasts between patients with recurrent miscarriage (RM) and healthy control subjects. Our results revealed that YY1 mRNA expression was significantly lower in the trophoblasts of the RM group compared with the healthy control group. Furthermore, immunofluorescence and immunohistochemical data showed that YY1 was highly expressed in human placental villi during early pregnancy, especially in cytotrophoblast cells and invasive extravillous trophoblasts, and it was expressed at a much lower level in the placental villi of term pregnancy. YY1 overexpression enhanced the invasion and proliferation of trophoblasts, while knockdown of YY1 repressed these effects. Antibody array screening revealed that YY1 significantly promoted MMP2 expression in trophoblasts. Bioinformatics analysis identified three YY1-binding sites in the MMP2 promoter region, and chromatin immunoprecipitation analysis verified that YY1 binds directly to its promoter region. Importantly, inhibition of YY1 by siRNA clearly decreased trophoblast invasion in an ex vivo explant culture model. Overall, our findings revealed a new regulatory pathway of YY1/MMP2 in trophoblast cells invasion during early pregnancy, and indicated that YY1 may be involved in the pathogenesis of RM.

overall_design: Total RNA was isolated using Trizol from trophoblast cells from three healthy controls (HC) and three recurrent miscarriage (RM) patients.  Total RNA were extracted and used for hybridizing Affymetrix chips (GeneChip® Human Transcriptome Array 2.0(HTA2.0)). Data were normalised by gcRMA method and raw p-values adjusted by Bonferroni procedure (1%).

first: Yan-Xiang

last: Cheng

first: Xiao-Cui

last: Li

first: Chuan-Mei

last: Qin

first: Fa

last: Wang

first: Xiao-Ling

last: Ma

first: Jing

last: Yang

first: Yi

last: Lin


title: Insights on cryoprotectant toxicity from gene expression profiling of endothelial cells exposed to ethylene glycol

status: Public on Nov 30 2015

city: Liverpool

first: Rui

middle: Augusto

last: Martins Cordeiro

state: Merseyside

address: Crown Street

department: Integrative Biology

institute: University of Liverpool

summary: Cryopreservation consists of preserving living cells or tissues at <-100˚C and has many applications in, for instance, stem cell and organ banking. Cryoprotectant agents, like ethylene glycol, are required for successful cryopreservation but have toxic side effects due to largely unknown mechanisms. In this work, we studied the toxicity of ethylene glycol in Human Umbilical Vein Endothelial Cells (HUVECs). Exposing cells to 60% ethylene glycol for two hours at 4˚C resulted in a slight decrease in cell growth, suggesting a modest toxicity of ethylene glycol and that HUVECs do not exhibit particular sensitivity to it. Gene expression analysis with whole genome micro-arrays revealed signatures indicative of a generalized stress response at 24 hours after stress and recovery at 72 hours, involving signaling pathways, glycoproteins, and genes involved in extracellular and transmembrane functions. These results reveal a new paradigm and signatures for future experiments in elucidating the toxicity effects of ethylene glycol in vascular endothelial cells.

overall_design: 18 samples; 2 timepoints (24h and 72h), 6 controls per timepoint - 3 non treaded samples and 3 cold controls; other 3 were treated with increasing concentrations of EG.

last: Cordeiro

first: Soren

last: Stirling

first: Gregory

last: Fahy

first: Joao

last: Pedro de Magalhaes


title: Expression data in histone-depleted cells [gene-level]

status: Public on Dec 30 2015

city: Sevilla

first: Jose

middle: C.

last: Reyes

address: Av. Américo Vespucio

department: Genome biology

country: Spain

institute: CABIMER

summary:
How chromatin controls transcription elongation and splicing is an open question. Here we determine the transcriptomic changes of cells partially depleted of core histones. For that we construct a cell line with Doxycycline-controlled levels of the histone regulatory protein SLBP (HCT-shSLBP). HCT-shSLBP is derived from the human colon cancer cell line HCT116.
Exon level and gene level transcriptomic data of Doxycycline-treated cells is compared with that non-treated cells. The final goal is to determine how chromatin depletion affects transcription and splicing.

overall_design: HCT-shSLBP cells from three independent Doxycycline-treated or nontreated cultures were recovered and processed for RNA extraction and hybridization on Affymetrix microarrays

first: Silvia

last: Jimeno-Gonzalez


title: MLL5 Orchestrates a Cancer Self-Renewal State by Repressing the Histone Variant H3.3 and Globally Reorganizing Chromatin [expression]

status: Public on Nov 11 2015

city: Houston

first: Marco

last: Gallo

state: TX

address: 1102 Bates Avenue

department: Pediatrics

institute: Baylor College of Medicine

summary: Mutations in the histone 3 variant H3.3 have been identified in one-third of pediatric glioblastomas (GBMs), but not in adult tumors. Here we show that H3.3 is a dynamic determinant of functional properties in adult GBM. H3.3 is repressed by mixed lineage leukemia 5 (MLL5) in self-renewing GBM cells. MLL5 is a global epigenetic repressor that orchestrates reorganization of chromatin structure by punctuating chromosomes with foci of compacted chromatin, favoring tumorigenic and self-renewing properties. Conversely, H3.3 antagonizes self-renewal and promotes differentiation. We exploited these epigenetic states to rationally identify two small molecules that effectively curb cancer stem cell properties in a preclinical model. Our work uncovers a role for MLL5 and H3.3 in maintaining self-renewal hierarchies in adult GBM.

overall_design:
MLL5 was over-expressed in the GBM primary culture G514NS. EGFP was expressed from the same vector backbone as a control. N = 3 biological replicates for each of EGFP- and MLL5-overexpressing cells.

Please note that complete data output (with 74,342 data rows) from Partek analysis contains several identifiers which are not represented in the GPL17586, and therefore is linked as Series supplementary file.

first: Peter

last: Dirks


title: Changes in global gene expression profiles induced by HPV 16 E6 oncoprotein  variants in cervical carcinoma C33-A cells

status: Public on Nov 20 2015

city: Mexico

first: Sandra

middle: Lorena

last: Romero-Cordoba

state: Mexico

address: Periférico Sur No. 4809, Col. Arenal Tepepan, Delegación Tlalpan. México, D.F.

department: Cancer Genomics

country: Mexico

institute: National Instute of Genomic Medicine

summary: We analyzed the effects of the expression of HPV 16 E6 oncoprotein variants (AA-a, AA-c,  E-A176/G350, E-C188/G350, E-G350), and the E- Prototype in global gene expression  profiles in an in vitro model. E6 gene was cloned into an expression vector fused to GFP  and was transfected in C33-A cells. Affymetrix GeneChip Human Transcriptome Array 2.0  platform was used to analyze the expression of over 245,000 coding transcripts. We found  that HPV16 E6 variants altered the expression of 431 genes in comparison with EPrototype.  The altered genes are involved in cellular processes related to the development  of cervical carcinoma, such as adhesion, angiogenesis, apoptosis, differentiation, cell cycle,  proliferation, transcription and protein translation. Our results show that polymorphic  changes in HPV16 E6 natural variants are sufficient to alter the overall gene expression  profile in C33-A cells, explaining in part the observed differences in oncogenic potential of  HPV16 variants.

overall_design: We analyzed RNA from 16 cell cultures from the cell line C33-A, with the following experimental conditions: C33-A Non-transfected (WT) and C33-A transfected with: 1) mock, 2) HPV16 E-prototype and 3) HPV16 variants: E-G350, E-A176/G350, E-C188/G350, AAa and AAc, performed by duplicate (biological replicates processed independently N=8x2); using the Affymetrix Gene Chip Human Transcriptome Array (HTA) 2.0 platform. Array signal intensities were analyzed with the Affymetrix expression console and normalized data were analyzed by Affymetrix Transcriptome Analysis Console (TAC).

first: Ana

last: Zacapala-Gómez

first: Oscar

last: Del Moral-Hernández

first: Nicolás

last: Villegas-Sepúlveda

first: Alfredo

last: Hidalgo-Miranda

last: Romero-Córdoba

first: Fredy

middle: O

last: Beltrán-Anaya

last: Leyva-Vázquez

first: Luz

last: del Carmen Alarcón-Romero

first: Berenice

last: Illades-Aguiar


title: transCONFIRM gene expression analysis

status: Public on Dec 16 2015

city: Boston

first: Rinath

last: Jeselsohn

state: MD

address: 450 Brookline Ave, D728

department: Medical Oncology

institute: DFCI

summary: gene expression analysis ussing microarray analysis of a subset of primary tumors collected from patients that participated in the CONFIRM phase III study, which randomized post menopausal patients with ER+ metastatic breast cancer to fulvestrant 500mg and fulvestrant 250mg.

overall_design: Primary tumor samples were collected from patients participating in the CONFIRM study.

first: Luca

last: Malorni


title: Functional investigation of miRNAs by characterization of SH-SY5Y cells overexpressing wild type or mutant miRNA genes

status: Public on Nov 24 2015

city: Antwerp

first: Sophia

last: Cammaerts

address: Universiteitsplein 1

department: Department of Molecular Genetics

country: Belgium

institute: VIB, University of Antwerp

summary:
Genome wide mRNA and miRNA profiling was performed in SH-SY5Y cells stably overexpressing wild type or mutant MIR204 or MIR618. Mutants came from a large scale genetic screening of brain expressed miRNA genes in patients with schizophrenia or idiopathic generalized epilepsy and in control individuals. Based on enrichment of the variants with the schizophrenic or epileptic phenotype and based on impact prediction, two variants, one near MIR204 (rs7861254) and one in MIR618 (rs2682818) were selected for functional validation. Genome wide profiling of mRNA (micro-array) and mature miRNAs (small RNA sequencing, submitted to SRA) was performed in the created stable cells to assess the effect of the variants and to investigate the function of these miRNA genes.
Micro-array analysis on HTA2.0 array was performed at AROS Applied Biotechnology, Denmark.

overall_design: SH-SY5Y cells (purchased from Sigma-Aldrich, catalog number: 94030304-1VL) were transduced with MIR204 or MIR618 wild type or mutant constructs. The stable cells were then split to obtain biological replicates and were cultured separately prior to total RNA extraction and micro-array analysis on the HTA2.0 array. For MIR204 analysis: 2 wt cells versus 3 mutant cells; for MIR618 analysis: 3 wt cells versus 3 mutant cells were used.

first: Jurgen

last: Del Favero


title: MicroRNA expression profiling in laryngeal squamous cell carcinoma (LSCC)

status: Public on Nov 10 2015

first: Chad

last: Creighton

address: One Baylor Plaza, Mail Stop: BCM305

department: Biostatistics, Ducan Cancer Center

summary: In this study, we aimed to explore the role of miR-145, which is downregulated in LSCC, on cancer stem cell potency of laryngeal cancer cells. Using microRNA expression profiling and experimental follow-up studies, we demonstrated the regulatory role of miR-145 in stem cell characteristics of Hep-2 cells. Based on these results, we propose that mir-145 might carry crucial roles in LSCC tumorigenesis, prognosis, metastasis, chemoresistance and recurrence through regulating stem cell properties of tumor cells.

overall_design: LSCC tissue samples and normal tissues were profiled for microRNA expression; cancer tissue profiles were compared with normal tissue profiles.

first: Michael

last: Ittmann

first: Mustafa

last: Ozen

first: Yiqun

last: Zhang


title: LncRNA and mRNA expression profiles from human GES-1 cells in response to Helicobacter pylori infection

status: Public on Nov 03 2015

city: Zhen Jiang

first: Hong

last: ZHU

state: Jiang Su

address: No.301,Xue Fu Road, Jing Kou District

institute: Jiangsu University

summary:
Research on lncRNAs expression profiles in human interactions with Helicobacter pylori (H.pylori) is rare reported. We used HTA2.0 to investigate the expression changes of lncRNAs and mRNAs in human gastric epithelial cells (GES-1 cell line) infected with or without H.pylori infection.
Our study provided a preliminary exploration of lncRNAs expression profiles in H.pylori-infected cell models by microarray. A subset of aberrantly expressed lncRNAs was verified by qRT-PCR. These dysregulated lncRNAs might contribute to the pathological processes during H.pylori infection.

overall_design: We infected GES-1 cells with H.pylori as experimental groups,and cells without H.pylori infection were regarded as control groups. After 24hr-infection, cells of each group were selected for total RNA extraction and hybridization on Affymetrix HTA2.0 arrays. The aberrant expression profiles of lncRNAs and mRNAs were explored by microarray analysis between experimental and control groups.

last: Zhu

first: Shihe

last: Shao

first: Hua

last: Wang


title: AURKA Expression in allogeneic HCT-recipients

status: Public on Nov 29 2015

city: Pittsburgh

first: Warren

middle: David

last: Shlomchik

state: PA

address: 3550 Terrace Street

institute: University of Pittsburgh

summary: Graft versus host disease (GVHD) is the most common complication of hematopoietic stem cell transplant (HCT). However, our understanding of the molecular pathways that cause this disease remains incomplete, leading to inadequate treatment strategies. To address this, we measured the gene expression profile of non-human primate (NHP) T cells during acute GVHD (GSE73723).  Within these profiles we discovered potentially druggable targets not previously implicated in GVHD, prominently including aurora kinase A (AURKA).  In this study, we performed a planned comparison of AURKA gene expression in HCT-recipients with clinical GVHD and compared it to expression in HCT-recipients without clinical GVHD.

overall_design: Samples were obtained from patients enrolled in hematopoietic stem cell transplant (HCT) clinical trials performed at Emory University and the University of Minnesota, with and without GVHD.  Patients from Emory University were enrolled on two contemporaneous IRB-approved clinical trials: (1) The Bone Marrow Immune Monitoring Protocol and (2) The Abatacept Feasibility Study.  The patients from the University of Minnesota were enrolled on an immune monitoring protocol approved by the University of Minnesota IRB. Samples from patients with acute GVHD were identified and then control samples were selected that were matched for sample collection day, preparative regimen intensity, disease, stem cell source, and GVHD prophylaxis.

first: Scott

middle: N

last: Furlan

first: Leslie

last: Kean


title: Transcriptome Analysis of GVHD Reveals Aurora Kinase A as a Targetable Pathway for Disease Prevention

sample_organism:
Macaca mulatta
Homo sapiens

platform_organism:
Macaca mulatta
Homo sapiens


title: The Activation-Induced Assembly of an RNA/Protein Interactome Centered on the Splicing Factor U2AF2 Regulates Gene Expression in Human CD4 T Cells [RIP-array]

status: Public on Nov 04 2015

city: La Jolla

first: Thomas

middle: C

last: Whisenant

state: CA

address: 10550 North Torrey Pines Rd

department: Molecular and Experimental Medicine

institute: The Scripps Research Institute

summary: Activation of CD4 T cells is a reaction to challenges such as microbial pathogens, cancer and toxins that defines adaptive immune responses. The roles of T cell receptor crosslinking, intracellular signaling, and transcription factor activation are well described, but the importance of post-transcriptional regulation by RNA-binding proteins (RBPs) has not been considered in depth. We describe a new model expanding and activating primary human CD4 T cells and applied this to characterizing activation-induced assembly of splicing factors centered on U2AF2. We immunoprecipitated U2AF2 to identify what mRNA transcripts were bound as a function of activation by TCR crosslinking and costimulation. In parallel, mass spectrometry revealed the proteins incorporated into the U2AF2-centered RNA/protein interactome. Molecules that retained interaction with the U2AF2 complex after RNAse treatment were designated as “central” interactome members (CIMs). Mass spectrometry also identified a second class of activation-induced proteins, “peripheral” interactome members (PIMs), that bound to the same transcripts but were not in physical association with U2AF2 or its partners. siRNA knockdown of two CIMs and two PIMs caused changes in activation marker expression, cytokine secretion, and gene expression that were unique to each protein and mapped to pathways associated with key aspects of T cell activation. While knocking down the PIM, SYNCRIP, impacts a limited but immunologically important set of U2AF2-bound transcripts, knockdown of U2AF1 significantly impairs assembly of the majority of protein and mRNA components in the activation-induced interactome. These results demonstrated that CIMs and PIMs, either directly or indirectly through RNA, assembled into activation-induced U2AF2 complexes and play roles in post-transcriptional regulation of genes related to cytokine secretion. These data suggest an additional layer of regulation mediated by the activation-induced assembly of RNA splicing interactomes that is important for understanding T cell activation.

overall_design:
HTA 2.0 microarray results of U2AF2 RIP RNA from a primary CD4 T cell culture after treatment with siRNAs (Control, U2AF1, and SYNCRIP) and 24 hours after anti-CD3/CD28 bead activation

Please note that the Series supplementary 'U2AF2RIP_HTA2_all_siRNA_100414.xlsx' file includes multiple worksheets containing: 1) Differentially expressed genes in ctrl siRNA vs. U2AF1 siRNA; 2) Differntially spliced genes in ctrl siRNA vs. U2AF1 siRNA; 3) Differentially spliced exons in ctrl siRNA vs. U2AF1 siRNA; 4) Differentially expressed genes in ctrl siRNA vs. SYNCRIP siRNA; 5) Differntially spliced genes in ctrl siRNA vs. SYNCRIP siRNA; 6) Differentially spliced exons in ctrl siRNA vs. SYNCRIP siRNA

first: Eigen

middle: R

last: Peralta

first: Lauren

middle: D

last: Aarreberg

first: Nina

last: Gao

first: Steven

last: Head

first: Phillip

last: Ordoukhanian

first: Jamie

last: Williamson

first: Daniel

last: Salomon


title: The ascidian natural product eusynstyelamide B is a novel topoisomerase II poison that induces DNA damage and growth arrest in prostate and breast cancer cells

status: Public on Oct 21 2015

city: Brisbane

first: Colleen

last: Nelson

state: Queensland

address: 199 Ipswich Road

department: Institute of Health and Biomedical Innovation; Vancouver Prostate Centre

institute: Queensland University of Technology; University of British Columbia

summary: As part of an anti-cancer natural product drug discovery program, we recently identified eusynstyelamide B (EB), which displayed cytotoxicity against MDA-MB-231 breast cancer cells. Here, we investigated the mechanism of action of EB in the prostate cancer cell line LNCaP after a treatment with 5 uM for 24 h. Transcriptome profiling followed by pathway analysis suggested that EB activated DNA damage pathways in LNCaP cells. Consistent with this, Chk2 phosphorylation was increased, p21Cip/Waf1 was up-regulated and Cdc2 expression was strongly reduced by EB. Importantly, EB caused DNA double-strand breaks, yet did not directly interact with DNA. Analysis of topoisomerase II-mediated decatenation discovered that EB is a novel topoisomerase II poison.

overall_design: The dataset was derived from three independent biological repeats of each of the three treatment groups: untreated, DMSO-vehicle treated, eusynstyelamide B (EB) treated.

first: Michelle

middle: S

last: Liberio

first: Martin

last: Sadowski

first: Rohan

middle: A

last: Davis

first: Anja

last: Rockstroh

first: Raj

last: Vasireddy

first: Melanie

middle: L

last: Lehman


title: The Activation-Induced Assembly of an RNA/Protein Interactome Centered on the Splicing Factor U2AF2 Regulates Gene Expression in Human CD4 T Cells [total RNA-array]

overall_design:
HTA 2.0 microarray results of total from a primary CD4 T cell culture after treatment with siRNAs (Control, U2AF1, SRRM2, SYNCRIP, and ILF2) and 24 hours after anti-CD3/CD28 bead activation

Please note that the Series supplementary 'TotalRNA_HTA2_all_siRNA_100414.xslx' file has multiple worksheets containing: 1) Differentially expressed genes in ctrl siRNA vs. U2AF1 siRNA; 2) Differntially spliced genes in ctrl siRNA vs. U2AF1 siRNA; 3) Differentially spliced exons in ctrl siRNA vs. U2AF1 siRNA; 4) Differentially expressed genes in ctrl siRNA vs. SRRM2 siRNA; 5) Differntially spliced genes in ctrl siRNA vs. SRRM2 siRNA; 6) Differentially spliced exons in ctrl siRNA vs. SRRM2 siRNA; 7) Differentially expressed genes in ctrl siRNA vs. SYNCRIP siRNA; 8) Differntially spliced genes in ctrl siRNA vs. SYNCRIP siRNA; 9) Differentially spliced exons in ctrl siRNA vs. SYNCRIP siRNA; 10) Differentially expressed genes in ctrl siRNA vs. ILF2 siRNA; 11) Differntially spliced genes in ctrl siRNA vs. ILF2 siRNA; 12) Differentially spliced exons in ctrl siRNA vs. ILF2 siRNA

middle: J


title: Human Lacrimal Gland Gene Expression

status: Public on Jan 03 2017

city: Chicago

first: Mark

last: Maienschein-Cline

state: IL

address: 900 S Ashland Ave, Rm 1058, M/C 937

department: Research Resources Center

institute: University of Illinois at Chicago

type:
Expression profiling by array
Third-party reanalysis

summary: Background: The study of human lacrimal gland biology and development is limited.  Lacrimal gland tissue is damaged or poorly functional in a number of disease states including dry eye disease.  Development of cell based therapies for lacrimal gland diseases requires a better understanding of the gene expression and signaling pathways in lacrimal gland. Differential gene expression analysis between lacrimal gland and other embryologically similar tissues may be helpful in furthering our understanding of lacrimal gland development. Methods: We performed global gene expression analysis of human lacrimal gland tissue using Affymetrix ® gene expression arrays.   Primary data from our laboratory was compared with datasets available in the NLM GEO database for other surface ectodermal tissues including salivary gland, skin, conjunctiva and corneal epithelium. Results: The analysis revealed statistically significant difference in the gene expression of lacrimal gland tissue compared to other ectodermal tissues. The lacrimal gland specific, cell surface secretory protein encoding genes and critical signaling pathways which distinguish lacrimal gland from other ectodermal tissues are described. Conclusions: Differential gene expression in human lacrimal gland compared with other ectodermal tissue types revealed interesting patterns which may serve as the basis for future studies in directed differentiation among other areas.

overall_design: 8 microarray samples co-analyzed with 104 publicly available microarray datasets

first: Vinay

last: Kumar Aakalu

first: Sowmya

last: Parmeswaran

first: Neil

last: Bahroos

first: Dhara

last: Shah

first: Marwan

last: Ali

first: Krishnakumar

last: Subramanian


title: Gene expression profiling in response to radiation treatment in human breast cancer

status: Public on Oct 31 2015

city: Durham

first: Wei

last: Chen

state: NC

address: 101 Science Drive

department: Center for Genomic and Computational Biology

institute: Duke University

summary: Treatment-related morbidities have been linked to the large post-operative treatment volumes required for external beam partial breast irradiation (PBI).  Alternative PBI techniques require equipment that is not readily available.  To address these issues, we designed a phase I trial utilizing widely available technology to 1) evaluate the safety of a single radiation treatment delivered preoperatively to the small-volume, intact breast tumor and 2) identify imaging and genomic markers of radiation response.

overall_design: Women 55 or older with clinically node negative, ER+ and/or PR+, HER2-, T1 invasive carcinomas or low-intermediate grade in situ disease ≤2cm were enrolled (n=32).  Intensity-modulated radiotherapy was used to deliver 15 Gy (n=8, patients 01-08), 18 Gy (n=8, patients 09-16), or 21Gy (n=16, patients 17-32) to the tumor with a 1.5cm margin.  Lumpectomy was performed within 10 days.  Paired pre- and post-radiation MRI images and patient tumor samples were analyzed.

first: Janet

middle: K

last: Horton

last: Dewhirst

first: Sharareh

last: Siamakpour-Reihani


title: Oncogenic activation of RNA binding proteins and c-Myc signaling in hepatocellular carcinoma

status: Public on Sep 23 2015

city: Bethesda

first: Hien

middle: T

last: Dang

address: 37 Convent Drive

department: CCR

institute: National Insitutes of Health/NCI

summary:
Global transcriptomic alterations of both coding and non-coding RNA species are a ubiquitous feature associated with human cancers including hepatocellular carcinoma (HCC). Dysregulation of RNA-binding proteins (RBPs), the key regulators of RNA processing, is one mechanism in which cancer cells select to promote tumorigenesis. We analyzed genomic alterations amongst a family of more than 800 mRNA RBPs (mRBPs) in 1,225 clinical specimens from HCC patients and found that RBPs are significantly activated through gene amplification in a subset of tumors with poor prognosis, suggesting their potential oncogenic roles in HCC progression. Amongst the top candidates, RD binding protein (RDBP) was further characterized for its oncogenic role and effects on the HCC transcriptome. While the activation of RDBP induced an oncogenic phenotype, the abrogation of RDBP in HCC cells significantly decreased cancer associated phenotypes such as cell proliferation, migration/invasion and tumorigenicity in vivo. Further microarray analyses revealed that RDBP-dependent genes were tumor-related with a significant enrichment for c-Myc targets, suggesting interplay between RDBP and c-Myc signaling. Similar data were also found in HCC clinical specimens where c-Myc amplification was uncommon. Consistently, the RDBP-dependent c-Myc target gene signature was able to predict HCC patient survival in two independent cohorts of more than 400 patients. Taken together, our results suggest that oncogenic activation of RDBP is a novel mechanism that contributes to global transcriptome imbalance that is selective for the activation of c-Myc oncogenic signaling in HCC.
We used microarray analysis to determine the affects of siRNA mediated RDBP knockdown in HCC transcriptome in cell lines.

overall_design: Hep3b and Huh1 cells were transfected with RDBP or scramble control siRNA for 48 hours in quadruplicates. Quality control using Spearman or Pearson correlation removes outliers resulting in triplicates for each group

first: Atsushi

last: Takai

first: Zhipeng

last: Zhou

first: Marshonna

last: Forgues

first: Xin

middle: W

last: Wang


title: Multi-platform assessment of transcriptional profiling technologies utilizing a precise probe mapping methodology (Affymetrix_HTA2.0)

status: Public on Sep 28 2015

city: St. Louis

first: Jinsheng

last: Yu

address: 660 S. Euclid Ave.

department: Genetics

institute: Washington University School of Medicine

summary: We present a more extensive and yet precise assessment to elucidate differences and similarities in performance at numerous aspects including signal range, sensitivity to fold-change, and fidelity with TaqMan qRT-PCR. There were three levels of data examined: entire data sets, data derived from gene name annotation oriented subset of 15442 RefSeq genes, and data derived from transcript pattern defined subset of 7034 RefSeq genes.  Our results showed a fair degree of overall correlation between all 6 platforms evaluated; but, to varying degrees, two RNA-seq protocols outperformed three of the microarray platforms in most categories.  Notably, a fourth microarray platform, Agilent, was comparable, or marginally superior, to the RNA-seq protocols within these same assessments.  Furthermore, 3 platforms (Agilent and two RNA-seq methods) demonstrated over 80% concordance with the gold standard TaqMan assay in terms of fold-change accuracy.  Our study suggests that the use of transcript patterns can enhance a number of the observed cross-platform correlations, indicating a potential usefulness for similar evaluations.

overall_design: The study assessed differences and similarities in performance at numerous aspects including signal range, sensitivity to fold-change, and fidelity with TaqMan qRT-PCR. There were three levels of data examined: entire data sets, data derived from gene name annotation oriented subset of 15442 RefSeq genes, and data derived from transcript pattern defined subset of 7034 RefSeq genes.

first: Richard

last: Head


title: Transcriptome data of multiple sclerosis patients receiving fingolimod therapy [HTA-2_0, CD8+ cells, gene level]

status: Public on Sep 19 2015

city: Rostock

first: Michael

last: Hecker

address: Gehlsheimer Str. 20

department: Department of Neurology

institute: University of Rostock

summary:
We analyzed the gene expression patterns of different blood cell types before and during fingolimod treatment in a group of patients with relapsing-remitting multiple sclerosis (RRMS).
Affymetrix Human Transcriptome Arrays (HTA) 2.0 were used to obtain gene expression profiles of immune cell populations from 10 RRMS patients within the first 3 months of fingolimod treatment.
This GEO entry provides the Affymetrix HTA 2.0 microarray data of peripheral blood CD8+ cells, preprocessed according to the gene level workflow.

overall_design:
EDTA blood samples were taken from all patients immediately before first and second fingolimod administration as well as after 3 months of therapy.
Total RNA of CD8+ cells positively selected from each blood sample was extracted, labeled and hybridized to high-density Affymetrix HTA 2.0 microarrays to quantify the transcript levels.

first: Dirk

last: Koczan

first: Uwe

last: Zettl


title: Transcriptome data of multiple sclerosis patients receiving fingolimod therapy [HTA-2_0, CD4+ cells, gene level]

summary:
We analyzed the gene expression patterns of different blood cell types before and during fingolimod treatment in a group of patients with relapsing-remitting multiple sclerosis (RRMS).
Affymetrix Human Transcriptome Arrays (HTA) 2.0 were used to obtain gene expression profiles of immune cell populations from 10 RRMS patients within the first 3 months of fingolimod treatment.
This GEO entry provides the Affymetrix HTA 2.0 microarray data of peripheral blood CD4+ cells, preprocessed according to the gene level workflow.

overall_design:
EDTA blood samples were taken from all patients immediately before first and second fingolimod administration as well as after 3 months of therapy.
Total RNA of CD4+ cells positively selected from each blood sample was extracted, labeled and hybridized to high-density Affymetrix HTA 2.0 microarrays to quantify the transcript levels.


title: Beyond the one-locus-one-miRNA paradigm: microRNA isoforms enable deeper insights into breast cancer heterogeneity

city: Philadelphia

first: Isidore

last: Rigoutsos

address: 1020 Locust Street, Suite M81

department: Sidney Kimmel Medical College

institute: Thomas Jefferson University

summary:
The product of genomic loci coding for micro RNAs (miRNAs) produce many isoforms (isomiRs). IsomiRs differing at their 5’ end have different seed regions and therefore are expected to target different genes. We used microarrays to study the effect of different isomiRs in the context of breast cancer.
The product of genomic loci coding for micro RNAs (miRNAs) produce many isoforms (isomiRs). IsomiRs differing at their 5’ end have different seed regions and therefore are expected to target different genes. We used microarrays to study the effect of different isomiRs in the context of breast cancer.

overall_design: Breast cancer MDA-MB-231 cells were cultured and were subject to a negative control treatment or transfected with one of the three selected isomiRs: the archetype miRNA, the miR-183-5p|2|-2| or the miR-183-5p|+2|+2| isomiR. Each treatment was done in triplicate. RNA was extracted and hybridized on Affymetrix microarrays.

first: Aristeidis

middle: G

last: Telonis

first: Yi

last: Jing


title: ColXα1 and Tumor Infiltrating Lymphocytes: a Marker of Response to Neoadjuvant Therapy in Estrogen Receptor and Human Epidermal Growth Factor Receptor 2 Positive Breast Cancer

status: Public on Sep 08 2015

city: PROVIDENCE

first: Alexander

last: Brodsky

state: RI

address: 593 Eddy St.

department: MCB

institute: Rhode Island Hospital/Brown University

summary:
This study focused on patients with estrogen receptor positive/human epidermal growth factor receptor 2 positive (ER+/HER2+) breast cancer treated with neoadjuvant chemotherapy and HER2-targeted therapy (NAC+H), and was designed to identify novel biomarkers by correlating gene expression, histology and immunohistochemistry with pathologic response.
We performed gene expression profiling on 11 pre-treatment tumors samples: 5 who had no or minimal residual disease residual cancer burden (RCB) score of 0 or 1 and 6 who had significant residual disease (RCB score of 2 or 3).

overall_design: ER2/HER2 postive breast tumors biopsied before neoadjuvant chemotherapy were selected to identify potential biomarkers of pathological complete response (pCR)

first: Yihong

first: Murray

last: Resnick


title: microRNA profiles for lymph node metastasis in T1-stage colorectal cancers.

status: Public on Sep 30 2015

city: seoul

first: SeungHyun

last: Jung

state: seoul

address: catholic university, medical college, banpo-dong

department: Department of Biochemistry

institute: Catholic University of Korea

summary:
If we can more accurately predict the likelihood of regional lymph node metastasis (LNM) for endoscopically resected T1-stage colorectal cancers (CRC), the number of unnecessary additional surgeries can be reduced.
We aimed of identify miRNA markers that can predict LNM-positive tumors among T1-stage CRCs and we also developed a miRNA classifier set for facilitating the accuracy and applicability.

overall_design: Tumor cell rich areas (>70% of tumor cells) were selected and microdissected under a microscope. Total RNA was extracted using the RecoverAll™ Total Nucleic Acid Isolation Kit for FFPE. Then, we examined global miRNA expression profiles from 16 T1-stage CRCs (7 LNM-positive and 9 LNM- negative tumors) using miRNA-array analysis.

first: Seung-Hyun

first: Yeun-Jun

last: Chung


title: Transcriptome data of multiple sclerosis patients receiving fingolimod therapy

summary:
This SuperSeries is composed of the SubSeries listed below.

Using 150 Affymetrix HTA 2.0 microarrays, we profiled the gene expression of 5 cell populations of the peripheral blood from patients with multiple sclerosis in the course of fingolimod treatment.

overall_design:
Refer to individual Series

Please note that HTA 2.0 data can be processed according to two different workflows: exon level (GEO platform GPL17585) and gene level (GEO platform GPL17586). This SuperSeries contains each of the 150 CEL files twice, because they had to be submitted for both, the exon level records and the gene level records.


title: Differentially Expressed LncRNAs Might be Controlling Signaling Pathways by Establishing Interactions with mRNAs and MicroRNAs in Pediatric Astrocytoma

status: Public on Aug 25 2015

city: México.

first: Ruth

last: Ruiz-Esparza

address: Centro Médico Nacional Siglo XXI, IMSS, México,

department: Pediatría

institute: Instituto Mexicano del Seguro Social

summary: In this study was determined the global expression pattern of long non-coding RNAs, mRNAs, and miRNAs in pediatric astrocytoma of different histological grades. The Affymetrix HTA 2.0 array showed expression changes on one hundred-sixty two and two hundred-fifteen long non-coding RNAs in tumors (versus the control) and in GBM (versus low-grade astrocytoma), respectively.

overall_design: A total of seven astrocytic tumors and two control tissues were collected during the period of 2012–2014: four low-grade Ast (three pilocytic Ast (PAst) and one diffuse Ast (DAst)) and four high-grade Ast (four glioblastoma multiforme (GBM)).RNA was extracted from tissue samples using TRIzol (Ambion life technologies, Thermo Scientific Inc.) following the methodology described by Hongbao et al. 2008 and with certain modifications described by Vujovic et al. 2013. For expression analysis, Human Transcriptome Array 2.0 (HTA) (Santa Clara, CA, USA) was employed.  in this study was determined the global expression pattern of long non-coding RNAs, mRNAs, and miRNAs in pediatric astrocytoma of different histological grades. The HTA 2.0 array showed expression changes on one hundred-sixty two and two hundred-fifteen long non-coding RNAs in tumors (versus the control) and in GBM (versus low-grade astrocytoma), respectively.

last: Esparza Garrido

first: Miguel

last: Velázquez Flores


title: Dysregulation of the Transforming Growth Factor Beta Pathway in Induced Pluripotent Stem Cells Generated from Patients with Diamond Blackfan Anemia [HTA-2_0]

status: Public on Aug 31 2015

first: Jingping

last: Ge

address: 3615 CivicCenter Blvd, ARC 303

institute: Children's Hospital of Philadelphia

summary: Diamond Blackfan Anemia (DBA) is an inherited bone marrow failure syndrome with clinical features of red cell aplasia and variable developmental abnormalities. Most affected patients have heterozygous loss of function mutations in ribosomal protein genes but the pathogenic mechanism is still unknown. We generated induced pluripotent stem cells from DBA patients carrying RPS19 or RPL5 mutations. Transcriptome analysis revealed the striking dysregulation of the transforming growth factor beta signaling pathway in DBA lines. Expression of TGF beta target genes, such as TGFBI, BAMBI, COL3A1 and SERPINE1 was significantly increased in the DBA iPSCs. We quantified intermediates in canonical and non-canonical TGF beta pathways and observed a significant increase in the levels of the non-canonical pathway mediator p-JNK in the DBA iPSCs. Moreover, when the mutant cells were corrected by ectopic expression of WT RPS19 or RPL5, levels of p-JNK returned to normal. Surprisingly, nuclear levels of SMAD4, a mediator of canonical TGF beta signaling, were decreased in DBA cells due to increased proteolytic turnover. We also observed the up-regulation of TGF beta 1R, TGF beta 2, CDKN1A and SERPINE1 mRNA, and the significant decrease of GATA1 mRNA in the primitive multilineage progenitors. In summary our observations identify for the first time a dysregulation of the TGF beta pathway in the pathobiology of DBA.

overall_design: 8 Total samples were analyzed, including 4 wild type samples, 2 RPS19 mutant samples, 2 corrected RPS19 mutant samples. We generated the following pairwise comparisons using Partek Softare : RPS19 mutant<WT; RPS19 mutant<corrected RPS19 mutant. Genes with an FDR≤5% and a fold-change ≥2 were selected.

first: Marisa

last: Apicella

first: Jason

last: Mills

first: Loïc

last: Garçon

first: Deborah

last: French

first: Mitchell

last: Weiss

first: Monica

last: Bessler

first: Philip

last: Mason


title: Expression data from The human glioblastoma cell culture resource: validated cell models representing all molecular subtypes (transcript)

status: Public on Aug 20 2015

city: Uppsala

first: Sven

last: Nelander

address: Rudbecklab

institute: Uppsala Universitet

summary: To explore the degree to which the glioma cell lines remained transcriptionally stable under diverse experimental conditions, we transplanted three different lines (U3020MG, U3047MG and U3065MG) intracranially to NOD-SCID mice; explanted the resulting tumors and cultured the cells for two passages, and then isolated RNA from the cell line prior to transplantation (U3020MG-p10, U3047MG-p7, U3065MG-p10), from the xenograft tumor and from the explanted cells.

overall_design: Total RNA extracted from both tumor tissues and glioma cell lines using the miRNeasy Mini kit (Qiagen) was labeled and hybridized on Affymetrix GeneChip Human Transcriptome Array 2.0.  Expression levels were RMA-normalized employing the Affymetrix Expression Console software.

first: Lene

last: Uhrbom


title: Array analysis of wound induced hair neogenesis (late stage)

status: Public on Aug 05 2015

city: Baltimore

first: Luis

middle: Andres

last: Garza

address: 1550 Orleans St. Suite 204 CRBII Koch

department: Dermatology

institute: Johns Hopkins School of Medicine

summary: Mice were wounded and measured for regeneration starting 4 days after wound closure with simultaneous measurement of hair follicle neogenesis and biopsing. At each time point, RNA was collected from one mouse with high number of regenerated follicles and one without regenerated follicles.

overall_design: Whole skin  biopsies of wound scars were submitted for Affymetrix Exon arrays. 3 replicates of mice with high number of regenerated follicles, 3 replicates of mice with no regenerated follicles; each pair taken at a different date after wound closure.

first: Amanda

middle: M

last: Nelson


title: Array analysis of wound induced hair neogenesis

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Antitumor Activity of the Novel Flavonoid Oncamex in Preclinical Breast Cancer Models

status: Public on Sep 01 2015

city: Edinburgh

first: Carlos

last: Martinez-Perez

address: Western General Hospital, Crewe Road South

department: Institute of Genetics and Molecular Medicine

institute: The University of Edinburgh

summary: Introduction: The flavonoid myricetin has been shown to induce cell cycle arrest and mitochondrial-dependent apoptosis in preclinical cancer models. We hypothesised that myricetin-derived flavonoids with redox properties and improved physicochemical attributes that enhance cell uptake and mitochondrial targeting might have increased potential as antitumour agents, since mitochondria are the main site of production of reactive oxygen species (ROS) and redox status is known to regulate the development and advancement of certain cancers. In this study we assessed a small library of novel flavonoids, then focussed on the lead compound, second-generation analogue OncamexTM, its mechanism of action and structure-activity relationships as an anti-proliferative agent. Methods: With this aim, we studied the effect of OncamexTM in a panel of 7 breast cancer cell lines using proliferation, cytotoxicity and apoptosis assays. The redox properties and mitochondrial delivery of the drug were studied using cyclic voltammetry and fluorescence microscopy, respectively. The mechanism of action was further studied using western blotting, gene expression analysis and immunohistochemistry (IHC) of treated xenograft tissue from in vivo mice models. Results: Sulforhodamine B (SRB) proliferation assays demonstrated strong, anti-proliferative properties of OncamexTM, with IC50 values in the low micromolar range. Treatment for 8 h exerted concentration-dependent reduction in cell viability and induction of cytotoxicity and apoptosis, with increased caspase activation. Microarray analysis suggested that OncamexTM regulates changes in cell cycle and apoptosis at gene expression level. Fluorescence microscopy was used to investigate mitochondrial targeting and ROS regulation in treated cells. OncamexTM was found to induce production of superoxide at concentrations which exerted anti-proliferative effects. Initial in vivo studies in mice implanted with a MDA-MB-231 breast cancer xenograft showed that OncamexTM inhibited tumour growth, reducing tissue viability and Ki-67 proliferation, with no overall systemic toxicity. Conclusions: OncamexTM is a novel flavonoid capable of specific delivery to the mitochondria and induction of ROS production. We have shown its antitumor activity in preclinical models of breast cancer, both in vitro and in initial in vivo models, where tumour growth was arrested without inducing toxicity, support the potential of this novel drug for its continued development as an anticancer agent.

overall_design: Total RNA was obtained from 5 breast cancer cell lines subjected to 6 hours of 10µM OncamexTM and matched untreated controls (1% DMSO)


title: Expression data from human primary skeletal muscle myotubes treated with aldosterone, spironolactone, or vehicle.

status: Public on Jul 14 2015

city: Columbus

first: Jill

last: Rafael-Fortney

state: OH

address: 460 W. 12th Ave

department: Physiology & Cell Biology

institute: The Ohio State University

summary: To test for a function effect of mineralocorticoid receptor modulation in skeletal muscle, global gene expression analysis was conducted on human myltubes treated with a mineralocorticoid receptor agonist or antagonist.

overall_design: 9 total samples were analyzed. 3 biological replicates for each of the following treatment groups were included: 1) aldosterone; 2) spironolactone; 3) vehicle (ethanol). Pairwise comparison between groups were carried out and a fold-change ≥2 were selected.

first: Jessica

last: Chadwick


title: A long noncoding RNA regulates sister chromatid cohesion [microarray]

status: Public on Aug 03 2016

city: Pamplona

first: Maite

last: Huarte

state: Navarra

address: c/ Avd Pio XII, 55

institute: Centro de Investigación Médica Aplicada

summary: Long noncoding RNAs (lncRNAs) have appeared to be involved in the most diverse cellular processes through multiple mechanisms. Here we describe a previously uncharacterized human lncRNA, CONCR (cohesion regulator noncoding RNA), transcriptionally activated by MYC, which is upregulated in multiple cancer types. The expression of CONCR is cell cycle-regulated, and it is required for cell cycle progression and DNA replication. Moreover, cells depleted of CONCR show severe defects in sister chromatid cohesion, suggesting an essential role for CONCR in cohesion establishment during cell division. CONCR interacts with and regulates the activity of DDX11, a DNA-dependent ATPase and helicase involved in DNA replication. These findings suggest a novel mechanism of action for CONCR in the modulation of DDX11 enzymatic activity, unveiling the direct involvement of a lncRNA in the establishment of sister chromatid cohesion.

overall_design: Characterization of the function of the long noncoding RNA CONCR. A549 were transfected with a control siRNA or with a combination of two siRNAs targeting CONCR. Three independent siRNA-mediated knockdowns (siRNA CONCR REP1, 2 and 3) and controls (siRNA Control REP1, 2 and 3) were used for the analysis.

first: Francesco

middle: P

last: Marchese

first: Elena

last: Grossi

first: Oskar

last: Marín-Béjar

first: Sanjay

last: Bharti

first: Ivan

last: Raimondi

first: Jovanna

last: González

first: Dannys

last: Martínez-Herrera

first: Alejandro

last: Athie

first: Alicia

last: Amadoz

first: Robert

last: Brosh


title: Expression data from DNMT3A in human gastric cancer

status: Public on Jul 17 2015

city: Nan jing

first: He

last: Cui

address: 87# Dingjiaqiao Road

institute: Southeast University

summary:
DNA methylation is a major epigenetic mechanism that plays an important role in the early tumorigenic process.However, little is known about the roles of DNA methyltransferase 3A (DNMT3A) in gastric carcinogenesis.
We used microarrays to detail the gene expression underlying gastric cancer and identified distinct classes of up-regulated genes during this process.

overall_design: Differential expression profiles between control and MKN45-DNMT3A cells were examined via microarray.

first: Hong

last: Fan


title: Expression data from H1299 cells

status: Public on Jun 05 2015

city: Beijing

first: Jie

last: Li

state: HaiDian Qu

address: Taiping Road 27

department: Biochemistry and Molecular Biology

institute: Institute of Basic Medical Sciences

type:
Expression profiling by array
Non-coding RNA profiling by array
Expression profiling by RT-PCR


title: Epigenome-wide and Transcriptome-wide Analyses Reveal Gestational Diabetes is Associated with Alterations in the Human Leukocyte Antigen Complex [gene expression]

status: Public on Aug 03 2015

city: Los Angeles

first: Alexandra

last: Binder

state: California

address: 650 Charles Young Drive, South

department: Department of Epidemiology

institute: University of California Los Angeles

summary: Gestational diabetes mellitus (GDM) affects approximately 18% of pregnancies in the United States and increases the risk of adverse health outcomes in the offspring. These adult disease propensities may be set by anatomical and molecular alterations in the placenta associated with GDM. To assess the mechanistic aspects of fetal programming, we measured genome-wide methylation (Infinium HumanMethylation450 Beadchips) and expression (Affymetrix Transcriptome Microarrays) in placental tissue of 41 GDM cases and 41 matched pregnancies without maternal complications from the Harvard Epigenetic Birth Cohort. Specific transcriptional and epigenetic perturbations associated with GDM status included alterations in the major histocompatibility complex (MHC) region, which were validated in an independent cohort, the Rhode Island Child Health Study. Gene ontology enrichment among gene regulation influenced by GDM revealed an over-representation of immune response pathways among differential expression, reflecting these coordinated changes in the MHC region. Our study represents the largest investigation of transcriptomic and methylomic differences associated with GDM, providing comprehensive insight into the molecular basis of GDM induced fetal (re)programming.

overall_design: RNA extracted from the placentas (maternal-side) of 30 clinically-confirmed cases of GDM and 25 pregnancies without maternal complications was hybridised to the GeneChip® Human Transcriptome Array 2.0 (Affymetrix). Four samples were run in triplicate.


title: Expression data from Pin1 inhibitor ATRA and Pin1 knockdown

status: Public on Apr 12 2015

city: Boston

first: Kun Ping

last: Lu

state: MA

address: 330 Brookline Ave

institute: Beth Israel Deaconess Medical Center

summary: ATRA was identified as a Pin1 inhibitor via fluorescence polarization-based high throughput screening.  We performed microarray expression profiling to demonstrate the similarity between ATRA and Pin1 KD at the genome-wide level

overall_design: APL NB4 cells in response to ATRRA or inducible Pin1 knockdown for 3 days were collected for RNA extraction and hybridization on Affymetrix microarrays. We sought to validate in genome-wide level whether similarity occurred between ATRA and Pin1 knockdown-treated NB4 cells.

first: Shuo

last: Wei

first: Moris

last: Nehama

first: Marie

last: Bruno-Joseph

first: Hai

last: Hu

first: Mani-Li

last: Luo

first: Kun


title: DDB2 regulates gene expression in ovarian cancer cell lines

status: Public on May 01 2015

first: Qi-En

last: Wang

address: 420 W.12th Avenue

department: Radiation Oncology

summary: DDB2 has been suggested to function as a transcription regulator in various cancer cell lines. We stably overexpressed DDB2 in ovarian cancer cell line A2780-CP70, and compared the gene expression profiles between DDB2-overexpressed and empty vector-transfected cells.

overall_design: Empty vector and DDB2-expressing vector were transfected into A2780-CP70 separately. The stable transfection clones were selected, and gene expression patterns in these clones were investigated through microarray analysis.

first: Ran

last: Zhao

first: Chunhua

last: Han

first: Huabao

first: Xiaoli

last: Zhang


title: Leukemic cell lines expression profile of OTX015 compared to JQ1 and DMSO controls

status: Public on Jun 25 2015

city: Paris

first: Marc

last: Delord

address: Hopital Saint-Louis, 1 avenue Claude Vellefaux

department: Recherche clinique

country: France

institute: Centre hospitalier de Versailles

summary: Gene signature determination of the effect of a new bromodomain inhibitor among a representative set of leukemic cell lines

overall_design: OTX015 vs. DMSO and JQ1 vs. DMSO

first: M

last: Coudé

first: T

last: Braun

first: J

last: Berrou

last: Dupont

first: S

last: Bertrand

first: A

last: Masse

first: E

last: Raffoux

first: R

last: Itzykson

middle: E

last: Riveiro

first: P

last: Herait

last: Baruchel

first: H

last: Dombret

first: C

last: Gardin


title: Genome-wide interactions of mouse-Plasmodium yoelii  parasite and identification of regulators of type I interferon response

status: Public on Jun 01 2015

city: Bethesda

first: Timothy

last: Myers

address: 50 South Drive, Room 5509

department: Research Technologies Branch

institute: National Institute of Allergy and Infectious Diseases

summary: An invading pathogen will trigger specific host responses, which can be explored to identify genes functioning in pathogen recognition and elimination. Here we performed trans-species expression quantitative trait locus (ts-eQTL) analysis using genotypes of the Plasmodium yoelii malaria parasite and phenotypes of mouse gene expression. We significantly (LOD score≥3.0) linked 1,054 host genes to many parasite genetic loci. Clustering genome-wide pattern of LOD scores (GPLSs), which produced results different from those of direct expression level clustering, grouped host genes functioning in related pathways together, allowing accurate functional prediction of unknown genes. As proof of principle, 14 of 15 randomly selected genes unknown, but predicted to function in type I interferon (IFN-I) responses, were experimentally verified using gene over expression, shRNA knockdown, viral infection, and/or infection of KO mice. This study demonstrates an effective strategy for studying gene function, establishes a functional gene database, and identifies regulators in IFN-I pathways.

overall_design: Mouse spleen transcriptome 4-days after infection with 26 different strains of malaria P. yoelii parasites were compared to mock infected controls. The parasites were P. yoelii yoelii 17XNL,  P. yoelii nigeriensis N67, and 24 progeny of a genetic cross between them. Three biological replicates - different mice, for each strain tested.

first: Jian

last: Wu

first: Baowei

last: Cai

first: Wenxiang

last: Sun

first: Ruili

last: Huang

first: Xueqiao

last: Liu

first: Meng

last: Lin

first: Sittiporn

last: Pattaradilokrat

first: Scott

last: Martin

first: Yanwei

last: Qi

first: Sethu

last: Nair

first: Silvia

last: Bolland

first: Jeffrey

middle: I

last: Cohen

first: Christopher

last: Austin

first: Carole

last: Long

first: Rongfu

last: Wang

first: Xin-zhuan

last: Su


title: The LSD1/KDM1A neuro-specific isoform regulates neuronal differentiation through H3K9 demethylation [Affymetrix]

city: Shanghai

first: Ruitu

last: Lyu

address: 138 Yixueyuan Road Xuhui District

institute: Institutes of Biomedical Sciences Fudan University

summary: During brain development, histone-modifying enzymes play an important role by orchestrating transcriptional programs that regulate neuronal maturation. Lysine-Specific Demethylase 1 (LSD1, also named as KDM1A) functions as a transcriptional repressor by removing methyl groups at lysine 4 of histone H3 (H3K4). In neurons, alternative splicing can include an additional exon (exon E8a) within LSD1 transcripts, generating a LSD1+8a neuro-specific isoform. We here report that LSD1+8a isoform does not have the intrinsic ability to demethylate H3K4. LSD1+8a functions as a co-activator on its target genes by removing H3K9 repressive histone marks. We identify the supervillin protein (SVIL) as a LSD1+8a interacting partner and demonstrate that SVIL protein regulates neuronal maturation by controlling LSD1+8a mediated H3K9 demethylation. Thus, our results show that alternative splicing provides a genius mechanism by which LSD1 isoforms can acquire a dual specificity (H3K9 vs H3K4) and therefore differentially control specific gene expression patterns during brain development.

overall_design: In order to find some LSD1+8a regulated genes at differentiated SH-SY5Y cell lines, we infected SH-SY5Y with control or LSD1+8a shRNA, then induced differentiation with RA and BDNF, (Retinoic acid (RA) (Sigma) was added at a final concentration of 10 μM the next day after plating. After 4 days, the cells were washed three times with PBS and incubated with 50 ng/mL of Brain Derived Neural Factor (BDNF) (Millipore) in serum-free medium for 3 days),  we extracted RNA from BDNF induced SH-SY5Y cells for expression analysis.Duplicates were included for Affymetrix Human transcriptome version 2 array.

first: Yang

last: Shi

first: Benoit

last: Laurent

last: Lv


title: Validation of EZH2 targets in GSCs treated with shNT (control), shMELK, shFOXM1, and EZH2 overexpression

status: Public on Apr 16 2015

first: Ichiro

last: Nakano

address: 400w 12th, wisemanhall

institute: Ohio State University

summary:
We demonstrate that the catalytic subunit of Polycomb Repressive Complex 2, EZH2, is targeted by the MELK-FOXM1 complex, which in turn promotes resistance to radiation in GSCs. Clinically, EZH2 and MELK are co-expressed in GBM and significantly induced in post-irradiation recurrent tumors whose expression inversely correlated with patient prognosis. Through gain-and loss-of-function study, our data show that MELK or FOXM1 contributes on GSC radioresistance by regulation of EZH2.
We used microarrays to validate EZH2 target gene expression.

overall_design: GSCs were treated with shNT (control), shMELK, shFOXM1, and EZH2 overexpression. Total RNA was isolated using the Qiagen RNeasy kit (Qiagen).

first: Sunghak

last: Kim


title: Development of microRNA (miRNA) expression signatures for human glioma-initiating cells (GICs)

status: Public on Apr 07 2015

city: Toon

first: Daisuke

last: Yamashita

address: Shitsukawa

department: Neurosurgery

institute: Ehime University Graduate School of Medicine

summary: To identify a novel miRNA that is aberrantly expressed in GICs, we analyzed differences in miRNA expression between the human GICs and glioma cell lines and neural stem cells by miRNA microarrays.

overall_design: We examined the miRNA expression profiles of five human GICs that were obtained from human glioma samples and two human glioma cell lines, U87 and U251, and NSC (neural stem cells) as a control.

first: Toru

last: Kondo


title: Targeting the novel SALL4/CBL-B pathway by HDAC inhibitor MS-275 in lung cancer

status: Public on May 16 2015

city: Singapore

first: Henry

last: Yang

address: 28 Medical Drive

country: Singapore

institute: Cancer Science Institute of Singapore

summary: The overall survival of lung cancer patients remains dismal despite the availability of targeted therapies. Oncofetal protein SALL4 is a novel cancer target. We herein report that SALL4 was aberrantly expressed in a subset of lung cancer patients with poor survival. SALL4 silencing by RNA interference or SALL4 peptide inhibitor treatment led to impaired lung cancer cell growth. Expression profiling on SALL4-knockdown cells demonstrated that both the EGFR and IGF1R signaling pathways were affected. Further studies revealed that SALL4 suppresses these pathways indirectly by repressing CBL-B. Connectivity Map analysis revealed HDAC inhibitor MS-275 as a potential drug in treating SALL4-expressing cancers and this was confirmed using 17 lung cancer cell lines. In summary, we report for the first time that MS-275 can target the novel SALL4/CBL-B pathway in lung cancer. This lays the foundation for future clinical studies to evaluate the therapeutic efficacy of MS-275 in SALL4-positive lung cancer patients.

overall_design: Cells from human lung carcinoma cell line H661  with wildtype scrambled controls or Sall4 knockdown were used for RNA extraction and hybridization on Affymetrix microarrays.

first: Kol

last: Yong

first: Ailing

last: Li

first: Wenbin

last: Ou

first: Wenxiu

last: Zhao

first: Fei

first: Hiro

last: Tatetsu

first: Benedict

last: Yan

first: Lihua

first: Jonathan

last: Fletcher

first: Ross

last: Soo

first: Daniel

last: Tenen

first: Chai


title: Vemurafenib resistance selects for highly malignant brain and lung-metastasizing melanoma cells

status: Public on Mar 20 2015

city: Tel Aviv

first: Metsada

last: Pasmanik-Chor

address: Ramat Aviv

department: Biology

country: Israel

institute: Tel Aviv University

summary:
V600E being the most common mutation in BRAF, leads to constitutive activation of the MAPK signaling pathway. The majority of V600E BRAF positive melanoma patients treated with the BRAF inhibitor vemurafenib showed initial good clinical responses but relapsed due to acquired resistance to the drug. The aim of the present study was to identify possible biomarkers associated with the emergence of drug resistant melanoma cells. To this end we analyzed the differential gene expression of vemurafenib-sensitive and vemurafenib resistant brain and lung metastasizing melanoma cells.
The major finding of this study is that the in vitro induction of vemurafenib resistance in melanoma cells is associated with an increased malignancy phenotype of these cells. Resistant cells expressed higher levels of genes coding for cancer stem cell markers (JARID1B, CD271 and Fibronectin) as well as genes involved in drug resistance (ABCG2), cell invasion and promotion of metastasis (MMP-1 and MMP-2). We also showed that drug-resistant melanoma cells adhere better to and transmigrate more efficiently through lung endothelial cells than drug-sensitive cells. The former cells also alter their microenvironment in a different manner from that of drug-sensitive cells. Biomarkers and molecular mechanisms associated with drug resistance may serve as targets for therapy of drug-resistant cancer.

overall_design: 6 Samples (arrays) were analyzed. We generated pairwise comparisons between Vemurafenib and control DMSO treatments of various metastatic variants, using Partek Genomics Suite. Genes with fold-change difference of  ≥1.25 or <-1.25 were selected.

first: Inna

last: Zubrilov

first: Orit

last: Sagi-Assif

first: Sivan

last: Izraely

first: Tsipi

last: Meshel

first: Shlomit

last: Ben-Menahem

first: Ravit

last: Ginat

first: Clara

last: Nahmias

first: Pierre-Olivier

last: Couraud

first: Dave

last: Hoon

first: Isaac

last: Witz


title: Expression profile of human liver cancer cells with GP73 overexpression or knock down

status: Public on Mar 26 2015

first: Xinxin

last: chen

address: 5 Dong Dan San Tiao

department: Institute of Basic Medical Sciences and School of Basic Medicine

country: China

institute: Peking Union Medical College and Chinese Academy of Medical Sciences

summary:
GP73 contributes to the oncogenesis and development of HCC
We used microarrays to detail the mechanism of GP73 with downstream targets that drive HCC cell growth

overall_design: GP73 were knocked down in MHCC97H cell for RNA extraction and hybridization on Affymetrix microarrays.We sought to obtain the mechanism/interactions of GP73 with downstream proteins/components that drive HCC cell growth

first: Hongbing

last: Zhang

last: Chen

first: Yanan

last: Wang