Evidence map›Paper›PMID 36498921›Full record

ArticleInternational journal of molecular sciences2022

MIG-6 Is Critical for Progesterone Responsiveness in Human Complex Atypical Hyperplasia and Early-Stage Endometrial Cancer.

Olivia Jeong, Russell R Broaddus, Bruce A Lessey, John I Risinger, Mark I Hunter, Tae Hoon Kim

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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 at 4 institutions in 1 country.

Olivia JeongDepartment of Obstetrics, Gynecology & Reproductive Biology, College of Human Medicine, Michigan State University, Grand Rapids, MI 49503, USA.
Russell R BroaddusDepartment of Pathology and Laboratory Medicine, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
Bruce A LesseyDepartment of Obstetrics and Gynecology, Atrium Health Wake Forest Baptist, Winston-Salem, NC 27157, USA.
John I RisingerDepartment of Obstetrics, Gynecology & Reproductive Biology, College of Human Medicine, Michigan State University, Grand Rapids, MI 49503, USA.
Mark I HunterDepartment of Obstetrics, Gynecology and Women's Health, University of Missouri, Columbia, MO 65211, USA.
Tae Hoon KimDepartment of Obstetrics, Gynecology & Reproductive Biology, College of Human Medicine, Michigan State University, Grand Rapids, MI 49503, USA.
Michigan State University · USAtrium Health Wake Forest Baptist · USUniversity of Missouri · USUniversity of North Carolina at Chapel Hill · US

Funding

Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BROADDUS, RUSSELL R · 2003 to 2020
$32.0M
NCI NIH HHS P50CA09825NCI NIH HHS P50 CA098258
6 · The paper itself

Abstract

Women with complex atypical hyperplasia (CAH) or early-stage endometrioid endometrial cancer (EEC) are candidates for fertility preservation. The most common approach is progesterone (P4) therapy and deferral of hysterectomy until after completion of childbearing. However, P4 therapy response rates vary, and molecular mechanisms behind P4 resistance are poorly understood. One potential molecular cause of P4 resistance is a loss or attenuation of PGR expression. Mitogen-inducible gene 6 (MIG-6) is critical for P4 responsiveness. MIG-6 protein expression in the endometrial epithelial and stromal cells from women with CAH and EEC was significantly lower compared to women without CAH or EEC. The P4-responsive women (10/15) exhibited an increase of MIG-6 expression in epithelial and stromal cells compared to P4-resistant women (5/15). In addition, immunohistochemical analysis for PGR results showed that stromal PGR levels are significantly higher in P4-responsive women compared to P4-resistant women, whereas epithelial PGR expression was not different. A reverse correlation of MIG-6 and pAKT levels was observed in early-stage EEC patients. Studies strongly suggest that loss of MIG-6 and PGR and activation of pAKT lead to P4 resistance in CAH and EEC. These results will help to elucidate the molecular mechanism leading to P4 resistance in CAH and EEC.

Indexed as

Adaptor Proteins, Signal TransducingCarcinoma, EndometrioidEndometrial NeoplasmsProgesteroneEndometriumFemaleHumansHyperplasiaIntracellular Signaling Peptides and ProteinsReceptors, ProgesteroneTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingERRFI1 protein, humanIntracellular Signaling Peptides and ProteinsProgesteroneReceptors, ProgesteroneTumor Suppressor Proteinsendometrial cancerendometrial hyperplasiafertility-sparing treatmentMIG-6progesterone receptorprogesterone resistance

Identifiers

PMID36498921
PMCPMC9738720
OpenAlexW4309979456

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.