Dataset Information

Whole proteome analysis of mesonephric-derived cancers describes new potential biomarkers

ABSTRACT: Mesonephric carcinomas (ME) and Female Adnexal Tumors of probable Wolffian Origin (FATWO) are thought to derive from remnants of the Wolffian/mesonephric ducts – anlages of the male reproductive tract. Mesonephric-like carcinomas (MLC) show identical morphology to ME of the cervix, but occur in the uterus and ovary without convincing mesonephric remnants. ME, MLC and FATWO are challenging to diagnose due to their morphologic similarities to Müllerian tumors, resulting in a lack of evidence-based and tumor-specific treatment regimens. In order to identify potential diagnostic biomarkers, we performed whole proteomic analysis on 9 ME/MLC and 56 endometrial carcinomas (EC). ME and MLC proteomes showed significant overlap with few distinguishing protein markers.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Uterine Endometrium, Mesonephric Duct

DISEASE(S): Wolffian Duct Adenocarcinoma

SUBMITTER: Gian Luca Negri

LAB HEAD: Gregg Morin

PROVIDER: PXD020879 | Pride | 2020-11-02

REPOSITORIES: Pride

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Whole-proteome analysis of mesonephric-derived cancers describes new potential biomarkers.

Gibbard Evan E Cochrane Dawn R DR Pors Jennifer J Negri Gian Luca GL Colborne Shane S Cheng Angela S AS Chow Christine C Farnell David D Tessier-Cloutier Basile B McAlpine Jessica N JN Morin Gregg B GB Schmidt Dietmar D Kommoss Stefan S Kommoss Friedrich F Keul Jacqueline J Gilks Blake B Huntsman David G DG Hoang Lynn L

Human pathology 20201026

Mesonephric carcinomas (MEs) and female adnexal tumors of probable Wolffian origin (FATWO) are derived from embryologic remnants of Wolffian/mesonephric ducts. Mesonephric-like carcinomas (MLCs) show identical morphology to ME of the cervix but occur in the uterus and ovary without convincing mesonephric remnants. ME, MLC, and FATWO are challenging to diagnose due to their morphologic similarities to Müllerian/paramesonephric tumors, contributing to a lack of evidence-based and tumor-specific tr ...[more]

PMID: 33121982

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Project description:Full title: comparison of the genomic (arrayCGH) profiles of endometrial cancer with and without prior prolonged tamoxifen treatment for primary breast cancer Purpose: Tamoxifen has been a very effective treatment for breast cancer for several decades, however, at the same time increases the risk of endometrial cancer, especially after prolonged exposure. In addition, tamoxifen has been associated with a higher proportion of unfavorable uterine tumor subtypes (carcinosarcomas and serous adenocarcinomas) with worse survival. We investigated whether endometrial tumors, which developed after prolonged tamoxifen treatment for breast cancer, are genetically different from endometrial tumors without preceding tamoxifen exposure. Experimental design: Array CGH was used on archival formalin-fixed paraffin embedded (FFPE) endometrial tumors to determine genomic aberrations. We compared the genomic profiles of 52 endometrial tumors from breast cancer patients after long-term (>=2 years) tamoxifen use (endometrioid adenocarcinomas n=26, carcinosarcomas n=14 and serous adenocarcinomas n=12) with endometrial tumors from unexposed breast cancer patients (n=45). Genomic profiles were correlated with tamoxifen exposure, tumor subtypes and histopathological characteristics of the endometrial tumors. Results: The common uterine corpus cancers of the endometrioid subtype show few genomic aberrations. Tumors with many genomic aberrations were in general ER-negative. In contrast, carcinosarcomas and serous adenocarcinomas showed many aberrations, however they were indistinguishable from each other. Tumors that developed after prolonged tamoxifen use did not show more or different aberrations than unexposed tumors. This was true for all tumor subtypes. Conclusion: Endometrial carcinomas that develop after prolonged tamoxifen use can not be distinguished from non-users on basis of their tumor genomic profile. 52 endometrial tumors from breast cancer patients after long-term (>=2 years) tamoxifen use (endometrioid adenocarcinomas n=26, carcinosarcomas n=14 and serous adenocarcinomas n=12) and 45 endometrial tumors from unexposed breast cancer patients

Project description:BACKGROUND: Despite the moderate incidence of papillary renal cell carcinoma; (PRCC), there is a disproportionately limited understanding of its underlying genetic programs. There is no effective therapy for metastatic PRCC, and patients are often excluded from kidney cancer trials. A morphological classification of PRCC into Type 1 and Type 2 tumors has been recently proposed, but its biological relevance remains uncertain. PATIENTS AND METHODS. We studied the gene expression profiles of 34 cases of PRCC using Affymetrix HGU133 Plus 2.0 arrays (54,675 probe sets) using both unsupervised and supervised analysis. Comparative genomic microarray analysis (CGMA) was used to infer cytogenetic aberrations, and pathways were ranked with a curated database. Expression of selected genes was validated by immunohistochemistry in 34 samples, with 15 independent tumors. RESULTS. We identified 2 highly distinct molecular PRCC subclasses with morphologic correlation. The first class, with excellent survival, corresponded to 3 histological subtypes: Type 1, low-grade Type 2 and mixed Type 1/low-grade Type 2 tumors. The second class, with poor survival, corresponded to high-grade Type 2 tumors (n=11). Dysregulation of G1/S and G2/M checkpoint genes were found in Class 1 and Class 2 tumors respectively, alongside characteristic chromosomal aberrations. We identified a 7-transcript predictor that classified samples on cross-validation with 97% accuracy. Immunohistochemistry confirmed high expression of cytokeratin 7 in Class 1 tumors, and of topoisomerase IIa in Class 2 tumors. CONCLUSIONS. We report 2 molecular subclasses of PRCC, which are biologically and clinically distinct, which may be readily distinguished in a clinical setting. Experiment Overall Design: 34 individual samples analyzed, no technical replicates. Based on histologic features and Fuhrman grading system, we designated four categories of tumors: type 1 (n = 14) characterized by small tumor cells of low Fuhrman grade (2); type 2A (n = 4) characterized by large eosinophilic tumor cells of low Fuhrman grade (2); combined type 1 and 2A (n = 5); and type 2B (n = 11) characterized by large eosinophilic tumor cells with Fuhrman grade.

Dataset Information

Whole proteome analysis of mesonephric-derived cancers describes new potential biomarkers

Publications

Whole-proteome analysis of mesonephric-derived cancers describes new potential biomarkers.

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