Role of K-ras and Pten in the development of mouse models of endometriosis and endometrioid ovarian cancer

Nature medicine · 2004 · vol. 11(1) , pp. 63–70 · doi:10.1038/nm1173 · PMID:15619626 · W2062495971
article OA: closed CC0 ⤵ 203 in-corpus citations
Limited metadata. Only one source feed has indexed this record so far — no abstract, full text, or open-access copy is available through Endo Lab. The publisher's page (linked below) is the canonical location for the actual content. If you have institutional access, use "Find at my library".
AI-generated summary by claude@2026-06+body, 2026-06-08

Activation of oncogenic K-ras in mice, alone or with Pten deletion, induces peritoneal endometriosis and invasive, metastatic endometrioid ovarian adenocarcinomas.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

AI-generated deep summary by claude@2026-06, 2026-06-08

The study developed genetic mouse models of peritoneal endometriosis and endometrioid ovarian adenocarcinoma driven by activation of an oncogenic K-ras allele, aiming to clarify mechanisms linking endometriosis and endometrioid ovarian cancer. In addition to showing that oncogenic K-ras expression or conditional Pten deletion in the ovarian surface epithelium induces preneoplastic ovarian lesions with endometrioid glandular morphology, the authors report that combining both mutations in the ovary produces invasive, widely metastatic endometrioid ovarian adenocarcinomas with complete penetrance and a latency of about 7 weeks, recapitulating key histomorphology and metastasis features of the human disease. A major limitation explicitly noted in the framing is that these are the first genetic models based on specific driver alterations, so the causal scope is tied to these engineered genotypes. This paper is centrally about endometriosis — it presents genetic mouse models of peritoneal endometriosis and shows how K-ras and Pten cooperate to drive endometrioid ovarian cancer.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Disease Models, Animal Endometriosis Ovarian Neoplasms Protein Tyrosine Phosphatases ras Proteins Tumor Suppressor Proteins Animals Endometriosis Endometriosis Endometriosis Female Mice Ovarian Neoplasms Ovarian Neoplasms Ovarian Neoplasms Protein Tyrosine Phosphatases Protein Tyrosine Phosphatases PTEN Phosphohydrolase ras Proteins ras Proteins

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (39)

Cited by (50)

Source provenance

crossref
last seen: 2026-05-17T01:00:22.453996+00:00
europepmc
last seen: 2026-06-16T06:07:01.518242+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:12:26.305326+00:00
License: CC0 · commercial use OK