Evidence mapPaperPMID 40106332Full record

ArticleEndocrine-related cancer2025

ob/ob obese mice promote tumorigenesis of endometrial cancer associated with Pten deficiency.

Keun Cheon Kim, Amanda Hull, Eric Johannsen, Mark I Hunter, Tae Hoon Kim, Jae-Wook Jeong

Abstract read
In one paragraph

Article in Endocrine-related cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Keun Cheon Kim
Amanda Hull
Eric Johannsen
Mark I Hunter
Tae Hoon Kim

Funding

The role of cholesterol biosynthesis in metastatic and recurrent endometrialcancerR01CA264944 · NCI · UNIVERSITY OF MISSOURI-COLUMBIA · 2023 to 2025
$1.1M
NCI NIH HHS R01 CA264944
6 · The paper itself

Abstract

Obesity refers to the condition of being overweight due to abnormal fat accumulation and is highly associated with the development of various cancers. Endometrial cancer is the most diagnosed gynecologic cancer. Obesity is a strong risk factor for endometrial cancer. However, the etiological and pathophysiological effects of obesity on endometrial cancer have not been fully understood. To determine the effect of obesity on tumorigenesis in endometrial cancer, we examined the effect of obesity on tumorigenesis using genetically engineered mouse models, including an obesity model (ob/ob), an endometrial cancer model (Pgrcre/+Ptenf/f ; Ptend/d ), and an endometrial cancer with obesity model (Pgrcre/+Ptenf/fob/ob; Ptend/dob/ob). Histopathological analysis was performed on the uteri of the three groups during tumorigenesis. From 1.5 months of age, the body and uterine weight of Ptend/dob/ob mice were significantly higher than those of the Ptend/d mice. Ptend/dob/ob mice had higher tumor grade with myometrial invasion at 1.5 and 2 months than Ptend/d mice. The levels of phospho-histone H3, a proliferation marker and phospho-STAT3 were significantly increased in the endometrial cancer of Ptend/dob/ob mice compared to Ptend/d mice. Our results suggest that obesity accelerates the progression of endometrial cancer associated with Pten mutation.

Indexed as

CarcinogenesisEndometrial NeoplasmsObesityPTEN PhosphohydrolaseAnimalsDisease Models, AnimalFemaleMiceMice, ObesePTEN PhosphohydrolasePten protein, mouseendometrial cancerleptinmouse modelobesityPTEN

Identifiers

PMID40106332
PMCPMC11957430

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.