Evidence map›Paper›PMID 37701602›Full record

ArticleTransactions of the American Clinical and Climatological Association2023

ENDOMETRIAL CARCINOMA: THE INTERPLAY OF GENETICS AND HORMONES.

Lora Hedrick Ellenson

Open access · greenAbstract read
In one paragraph

Article in Transactions of the American Clinical and Climatological Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 80% of its field
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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

1 author.

Lora Hedrick EllensonNew York, New York.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometrial carcinoma is the most common malignancy of the genital tract in females in the United States, and it is one of the few human cancers increasing in incidence and mortality. Numerous studies have found an association of endometrial carcinoma with obesity, diabetes, and unopposed estrogen stimulation. Molecular studies, in our lab and others, have shown that endometrial carcinoma has a high frequency of alterations in the Phosphoinositide 3-kinase (PIK3) pathway, and notably, coexisting abnormalities in more than one member of the pathway are common. We have combined studies on primary human tumors and genetic mouse models to explore the role of the PIK3 pathway and estrogen, and their interactions, in the development and progression of endometrial carcinoma. Abnormalities in the PIK3 pathway do not simply play redundant roles in endometrial carcinoma and, although not required, the presence of estrogen can alter the course of the disease.

Indexed as

Endometrial NeoplasmsPhosphatidylinositol 3-KinasesAnimalsEstrogensFemaleHumansMiceEstrogensPhosphatidylinositol 3-Kinases

Identifiers

PMID37701602
PMCPMC10493730
OpenAlexW4386704672

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.