Project description:A collection of genetically engineered mouse models (GEMM) of colorectal cancer (CRC) were created, and primary tumors from these GEMMs were analyzed. Primary CRC tumors from these GEMMs were genotyped to confirm that they contain the core genetic lesions of interest, including APC, P53, KRAS, and BRAF. Primary tumors from GEMMs with combinations of lesions of interest were analyzed by whole genome expression, and their expression profiles were compared to determine how they segregate. Signatures were then generated from GEMM tumors of interest and compared to human clinical datasets with expression and outcome data. Primary tumors from CRC GEMMs with different combinations of mutant alleles of interested were generated and analyzed. Alleles include mutant forms of APC (A), P53 (P), KRAS (K) and BRAF (B).

2014-07-01 | E-GEOD-50794 | biostudies-arrayexpress

Melanoma GEMM Tumors, untreated or vemurafenib treated

Project description:Melanoma GEMM Tumors, untreated or vemurafenib treated

| PRJNA844332 | ENA

Melanoma GEMM Tumors, untreated or vemurafenib treated (scRNASeq)

Project description:Melanoma GEMM Tumors, untreated or vemurafenib treated (scRNASeq)

| PRJNA523031 | ENA

GEMM CRC collection analysis

2014-07-01 | GSE50794 | GEO

Trial

Project description:Trial Trial

| PRJEB7892 | ENA

Genomic and transcriptomic profiling expands precision cancer medicine: the WINTHER trial (Lung patients)

Project description:Genomic and transcriptomic profiling expands precision cancer medicine: the WINTHER trial (Lung patients)

| PRJNA720621 | ENA

A genetically engineered mouse model (GEMM) of NUT carcinoma (RNA-Seq)

Project description:NUT carcinoma (NC) is a highly aggressive subtype of squamous carcinoma driven by the BRD4-NUT fusion oncoprotein. Closely resembling human NC (hNC), GEMM tumors (mNC) are poorly differentiated squamous carcinomas that express high levels of MYC and metastasize to organs (liver, lung) and regional lymph nodes. Two GEMM-derived cell lines were developed whose transcriptomic and epigenetic landscapes, characterized by RNAseq and CUT&RUN, show striking overlap with those of primary GEMM tumors. As in hNC, BRD4-NUT functions to block differentiation and maintain growth of mNC, as evidenced by BRD4-NUT knockdown and treatment of mNC cell lines with BET bromodomain inhibitors (BETi). Mechanistically, GEMM primary tumor and cell lines form very large H3K27ac-enriched super-enhancers that are unique to hNC, termed megadomains, that are invariably associated with key hNC-defining transcriptional oncogenic targets, Myc and Trp63.

2023-10-04 | GSE241474 | GEO

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