Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Inactivation of<i>Brca2</i>cooperates with<i>Trp53</i><sup>R172H</sup>to induce invasive pancreatic ductal adenocarcinomas in mice

1 Jun 2011

Abstract excerpt

An inactivating germline mutation in BRCA2 is the most common known genetic basis for familial pancreatic cancer (FPC), accounting for 5-10% of inherited cases. A genetically engineered mouse model of pancreatic ductal adenocarcinoma (PDAC) arising on the backdrop of Brca2 deficiency is likely to elucidate valuable diagnostic and therapeutic insights for FPC. Both Brca2 alleles were conditionally deleted during...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cancer Genomics and Diagnostics
Share to Epigenetics and DNA Methylation
Share to Pancreatic and Hepatic Oncology Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 21455033
DOI: 10.4161/cbt.11.11.15534

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Inactivation of<i>Brca2</i>cooperates with<i>Trp53</i><sup>R172H</sup>to induce invasive pancreatic ductal adenocarcinomas in micePMID 21455033Read ↗

Genetically Engineered Mouse Models of Pancreatic Cancer: The KPC Model (<i>LSL‐Kras<sup>G12D/+</sup>;LSL‐Trp53<sup>R172H/+</sup>;Pdx‐1‐Cre</i>), Its Variants, and Their Application in Immuno‐oncology Drug DiscoverySemantic proximity Read ↗

Loss of p53 tumor suppression function drives invasion and genomic instability in models of murine pancreatic cancerSemantic proximity Read ↗

Differences between KC and KPC pancreatic ductal adenocarcinoma mice models, in terms of their modeling biology and their clinical relevance.Semantic proximity Read ↗

Inactivation of Brca2 Promotes Trp53-Associated but Inhibits KrasG12D-Dependent Pancreatic Cancer Development in MiceSemantic proximity Read ↗

Mouse models of pancreatic cancerSemantic proximity Read ↗

Murine models for familial pancreatic cancer: Histopathology, latency and drug sensitivity among cancers of Palb2, Brca1 and Brca2 mutant mouse strains.Semantic proximity Read ↗

A pipeline for rapidly generating genetically engineered mouse models of pancreatic cancer using in <i>vivo</i> CRISPRCas9 mediated somatic recombinationSemantic proximity Read ↗

Pancreatic cancer: translating lessons from mouse models and hereditary syndromes.Semantic proximity Read ↗

Genetically engineered mouse models of pancreatic adenocarcinomaSemantic proximity Read ↗

Genetically engineered mouse models of pancreatic cancer: unravelling tumour biology and progressing translational oncologySemantic proximity Read ↗

Germline Brca2 heterozygosity promotes Kras(G12D) -driven carcinogenesis in a murine model of familial pancreatic cancer.Semantic proximity Read ↗

CDKN2B deletion is essential for pancreatic cancer development instead of unmeaningful co-deletion due to juxtaposition to CDKN2ASemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.