Description from BioProject: "In this study, we ablated, individually and in combination, Brca1, Brca2 and Palb2 along with one copy of Trp53 in the mouse mammary gland. We also studied spontaneous tumor development in Palb2 mutant mice with a mutation that disengages the BRCA1-PALB2 interaction, in Trp53 wt, heterozygous and homozygous null backgrounds. Whole exome sequencing was conducted for 35...

Figshare Summary: "This metadata record provides details of the data supporting the claims of the related article: “Genetic interactions among Brca1, Brca2, Palb2 and Trp53 in mammary tumor development”. The related study conducted parallel conditional knockout (CKO) of Brca1, Palb2 and Brca2, individually and in combination, along with one copy of Trp53, in the mammary gland of nulliparous female...

Summary from Dryad: "Abstract: The mechanisms underlying ETS-driven prostate cancer initiation and progression remain poorly understood due to a lack of model systems that recapitulate this phenotype. We generated a genetically engineered mouse with prostate-specific expression of the ETS factor, ETV4, at lower and higher protein dosages through mutation of its degron. Lower-level expression of...

Summary from GEO: "The tumor suppressor p53 is mutated in the majority of human cancers, including pancreatic ductal adenocarcinoma (PDAC)1,2. Wild-type p53 accumulates in response to cellular stress and acts to regulate the expression of genes that influence cell fate and constrain tumorigenesis2. p53 also can modulate cellular metabolism3, though it remains unclear how the metabolic effects of...

Summary from GEO: "Cellular senescence involves a stable cell cycle arrest coupled to a secretory program that, in some instances, stimulates the immune clearance of senescent cells. Using an immune competent tumor model in which senescence triggers CD8 T cell-mediated tumor rejection, we show that senescence also remodels cell surface proteome to alter how they sense environmental factors, as exemplified...

Summary from GEO: "Cellular senescence involves a stable cell cycle arrest coupled to a secretory program that, in some instances, stimulates the immune clearance of senescent cells. Using an immune competent tumor model in which senescence triggers CD8 T cell-mediated tumor rejection, we show that senescence also remodels cell surface proteome to alter how they sense environmental factors, as exemplified...

Characterization of the surface proteome changes between proliferating and senescent liver cancer cells induced by p53 restoration.