title: Overlapping genes may control reprogramming of mouse somatic cells into induced pluripotent stem cells (iPSCs) and breast cancer stem cells.
abstract: Recent findings suggest the possibility that tumors originate from cancer cells with stem cell properties. The cancer stem cell (CSC) hypothesis provides an explanation for why existing cancer therapies often fail in eradicating highly malignant tumors and end with tumor recurrence. Although normal stem cells and CSCs both share the capacity for self-renewal and multi-lineage differentiation, suggesting that CSC may be derived from normal SCs, the cellular origin of transformation of CSCs is debatable. Research suggests that the tightly controlled balance of self-renewal and differentiation that characterizes normal stem cell function is dis-regulated in cancer. Additionally, recent evidence has linked an embryonic stem cell (ESC)-like gene signature with poorly differentiated high-grade tumors, suggesting that regulatory pathways controlling pluripotency may in part contribute to the somatic CSC phenotype. Here, we introduce expression profile bioinformatic analyses of mouse breast cells with CSC properties, mouse embryonic stem (mES) and induced pluripotent stem (iPS) cells with an emphasis on how study of pluripotent stem cells may contribute to the identification of genes and pathways that facilitate events associated with oncogenesis. Global gene expression analysis from CSCs and induced pluripotent stem cell lines represent an ideal model to study cancer initiation and progression and provide insight into the origin cancer stem cells. Additionally, insight into the genetic and epigenomic mechanisms regulating the balance between self-renewal and differentiation of somatic stem cells and cancer may help to determine whether different strategies used to generate iPSCs are potentially safe for therapeutic use.
authors.affiliation: ITB-CNR, Segrate Milan, Italy. ettore.mosca@itb.cnr.it
authors.forename: Ettore
authors.initials: E
authors.lastname: Mosca
authors.forename: Cinzia
authors.initials: C
authors.lastname: Cocola
authors.forename: Davood
authors.initials: D
authors.lastname: Sabour
authors.forename: Paride
authors.initials: P
authors.lastname: Pelucchi
authors.forename: Giovanni
authors.initials: G
authors.lastname: Bertalot
authors.forename: Orazio
authors.initials: O
authors.lastname: Palumbo
authors.forename: Massimo
authors.initials: M
authors.lastname: Carella
authors.forename: Martin
authors.initials: M
authors.lastname: Götte
authors.forename: Hans R
authors.initials: HR
authors.lastname: Schöler
authors.forename: Rolland
authors.initials: R
authors.lastname: Reinbold
authors.forename: Ileana
authors.initials: I
authors.lastname: Zucchi
authors.forename: Luciano
authors.initials: L
authors.lastname: Milanesi
mesh_terms: D000818:Animals; D014408:Biomarkers, Tumor / Q000235:genetics* / Q000378:metabolism; D002454:Cell Differentiation; D002461:Cell Line, Transformed; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic / Q000235:genetics* / Q000378:metabolism; D053595:Embryonic Stem Cells / Q000166:cytology / Q000378:metabolism; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D005807:Genes, Overlapping; D057026:Induced Pluripotent Stem Cells / Q000166:cytology / Q000378:metabolism*; D008321:Mammary Glands, Animal; D051379:Mice; D009363:Neoplasm Proteins / Q000235:genetics* / Q000378:metabolism; D014411:Neoplastic Stem Cells / Q000378:metabolism* / Q000473:pathology
chemical_list: D014408:Biomarkers, Tumor; D009363:Neoplasm Proteins