title: Analysis of gene status in cervical dysplastic lesions and squamous cell carcinoma using tissue microarrays.
abstract: Cervical displasia are classified as CIN-I, CIN-II and CIN-III. It has been observed that in at least 60% of CIN-I and CIN-II, the pathology disappears spontaneously, while around 30% persist at 24 months, 10% progress to CIN-III and 1% develops as a SCC. The factors involved in the evolution of the pathology are not defined, although infection of HPV is a necessary condition, but not the only one. For this reason, the identification of genetic changes is an essential element for understanding the carcinogenic process. It can also serve as a helpful tool for identifying patients who may be susceptible to its evolution and treatment, from patients whose lesions could regress spontaneous and for whom periodic follow-ups would be enough. Fifty three cervical biopsies from patients with dysplasia and ISCC were included in the study. These biopsies were set into nine macroarrays. Eight genes and five proteins were examined in each samples (hTERT, PIK3CA, hTERC, MYC, CCND1, BCL2, ZNF217 and p16) by fluorescence in situ hybridization (FISH) and/or immunohistochemistry (IHC). The results reflected that the genetic alterations of PIK3CA, ZNF217 and CCND1 were associated with the evolution of normal tissue to CIN I, those of hTERC and ERBB with the evolution of LSIL to HSIL, those of hTERT and MYC with the evolution of CIN-II/CIN-III to ISCC, and those of BCL-2 with the inception of ISCC. With regards to proteins, the expression of MYC and CCND1 in the initial stages of the illness would help in the acquisition of the altered cellular phenotype.
authors.affiliation: Pathology Department, Cytogenetic and Molecular Biology Laboratory, Citology Section, Mar Hospital, IMAS, Barcelona, Spain. 93710@imas.imim.es
authors.forename: Carlota
authors.initials: C
authors.lastname: Costa
authors.forename: Blanca
authors.initials: B
authors.lastname: Espinet
authors.forename: Miguel A
authors.initials: MA
authors.lastname: Molina
authors.forename: Rocio
authors.initials: R
authors.lastname: Salgado
authors.forename: Marta
authors.initials: M
authors.lastname: Salido
authors.forename: Teresa
authors.initials: T
authors.lastname: Baró
authors.forename: Pere
authors.initials: P
authors.lastname: Fusté
authors.forename: Gemma
authors.initials: G
authors.lastname: Mancebo
authors.forename: Ramón
authors.initials: R
authors.lastname: Carreras
authors.forename: Francesc
authors.initials: F
authors.lastname: Solé
authors.forename: Sergi
authors.initials: S
authors.lastname: Serrano
authors.forename: Francesc
authors.initials: F
authors.lastname: Alameda
mesh_terms: D001706:Biopsy; D002294:Carcinoma, Squamous Cell / Q000235:genetics*; D016022:Case-Control Studies; D058534:Class I Phosphatidylinositol 3-Kinases; D019938:Cyclin D1 / Q000235:genetics; D018450:Disease Progression; D005260:Female; D005796:Genes; D019254:Genes, bcl-2; D018734:Genes, erbB-2; D016259:Genes, myc; D006801:Humans; D007150:Immunohistochemistry; D017404:In Situ Hybridization, Fluorescence; D020411:Oligonucleotide Array Sequence Analysis / Q000379:methods*; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics; D012313:RNA / Q000235:genetics; D019098:Telomerase / Q000235:genetics; D015534:Trans-Activators / Q000235:genetics; D002578:Uterine Cervical Dysplasia / Q000235:genetics*
chemical_list: C530104:CCND1 protein, human; D015534:Trans-Activators; C113698:ZNF217 protein, human; C422952:telomerase RNA; D019938:Cyclin D1; D012313:RNA; D019869:Phosphatidylinositol 3-Kinases; D058534:Class I Phosphatidylinositol 3-Kinases; C484760:PIK3CA protein, human; C509186:TERT protein, human; D019098:Telomerase