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Gene expression profiling of rat endometrial cancer

ABSTRACT: Transcriptional profiling of rat EAC - comparison of non-/pre-malignant endometrium with endometrial tumors Endometrial cancer develops from the endometrium of the uterus and is the most common pelvic malignancy diagnosed in women in the western countries. Similar to all cancer diseases, endometrial cancer is a genetic disorder that results from complex patterns of genetic and epigenetic alterations involved in the malignant transformation. The genetic heterogeneity inherent in the human population, differences in the environment and life styles poses enormous difficulties when analyzing the complex patterns of genetic alterations contributing to cancer etiology. Inbred animal models constitute unique experimental genetic tools as the genetic heterogeneity and the influence of environmental factors can be readily reduced. The BDII/Han rat model is unique for spontaneous hormonal carcinogenesis since more than 90% of the female virgins spontaneously develop endometrial cancer during their life span. The possibility to perform global gene expression profiling of tumor cells would likely provide important information of the genes and pathways that are involved in EAC susceptibility and carcinogenesis. Keywords: Endometrial tumors developed in crosses with the BDII inbred rat strain (from backcrosses, NUT, and intercrosses, RUT) and Sprague Dawley curley-3 and Brown Norway

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE13003 | GEO | 2008/10/02

SECONDARY ACCESSION(S): PRJNA110929

REPOSITORIES: GEO

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Project description:Global gene expression patterns associated with early stage endometrial cancer have been reported, but changes in molecular expression associated with tumor grade, depth of myometrial invasion, and non-endometrioid histology have not been previously elucidated. Our group hypothesized there are unique genetic events underlying early endometrial carcinogenesis. Ninety-two samples of pathologically reviewed stage I endometrial cancers (80 endometrioid and 12 serous) with a heterogeneous distribution of grade and depth of myometrial invasion (i.e. 9 IAG1, 14 IAG2, 7 IAG3, 14 IBG1, 12 IBG2, 13 IBG3, 7 ICG1, 10 ICG2, and 6 ICG3) were examined in relation to 12 samples of atrophic endometrium from postmenopausal women. Specimens were analyzed using oligonucleotide microarray analysis and a subset of the differentially expressed transcripts was validated using quantitative PCR. Comparison of early stage cancers with normal endometrium samples by the univariate t-test with 10,000 permutations identified 900 genes that were differentially regulated by at least 4-fold at a p value of <0.001. Unsupervised analysis revealed that when compared to normal endometrium, serous and endometrioid stage I cancers appeared to have similar expression patterns. However, when compared in the absence of normal controls, they were distinct. Differential expression analysis revealed a number of transcripts that were common as well as unique to both histologic types. This data uncovers previously unrecognized, novel pathways involved in early stage endometrial cancers and identifys targets for prevention strategies that are inclusive of both endometrioid and serous histologic subtypes. Ninety-one samples of pathologically reviewed stage I endometrial cancers (79 endometrioid and 12 serous) with a heterogeneous distribution of grade and depth of myometrial invasion (i.e. 9 IAG1, 14 IAG2, 7 IAG3, 14 IBG1, 12 IBG2, 13 IBG3, 7 ICG1, 10 ICG2, and 6 ICG3) were examined in relation to 12 samples of atrophic endometrium from postmenopausal women. Specimens were analyzed using oligonucleotide array analysis.

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Gene expression profiling of rat endometrial cancer

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