Evidence map›Paper›PMID 29790226›Full record

ArticleGenes, chromosomes & cancer2018

Comparative analysis of AKT and the related biomarkers in uterine leiomyomas with MED12, HMGA2, and FH mutations.

Jia Xie, Julianne Ubango, Yanli Ban, Debabrata Chakravarti, J Julie Kim, Jian-Jun Wei

Open access · greenAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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  13. Pathogenomics of Uterine Fibroids Development.International journal of molecular sciences · 2019
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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 1 institution in 1 country.

Jia XieDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
Julianne UbangoDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
Yanli BanDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
Debabrata ChakravartiDepartment of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
J Julie KimDepartment of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
Jian-Jun WeiDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.ORCID 0000-0003-0281-2793
Northwestern University · US

Funding

Uterine Leiomyoma Research Center ProgramP01HD057877 · NICHD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BULUN, SERDAR E. · 2009 to 2019
$12.2M
GF P01HD57877NICHD NIH HHS P01 HD057877
6 · The paper itself

Abstract

Uterine leiomyomas (ULM) are histologically and molecularly heterogeneous and clinically they grow at vastly different rates. Several driver gene mutations have been identified in ULM, including MED12 mutations, HMGA2 overexpression, and biallelic FH inactivation. ULM with different driver mutant genes may use different molecular pathways, but currently no clear correlation between gene mutations and growth related pathways has been established. To better define this relationship, we collected ULM with MED12 (n = 25), HMGA2 (n = 15), and FH (n = 27) mutations and examined the sex steroid hormone, cell cycle, and AKT pathway genes by immunohistochemistry. While ER and PR were highly expressed in all types of ULM, FH ULM showed lower ER expression and higher PR expression. HMGA2 tumors had significantly higher levels of AKT signaling and mitogenic activity than other ULM types. HMGA2 activated AKT signaling through upregulation of IGF2BP2. Silencing HMGA2 in ULM cells resulted in downregulation of AKT and upregulation of p16 and p21, which eventually led to cell senescence. HMGA2 overexpression in ULM is not only related to tumor development but also plays a role in controlling cellular proliferation through the AKT pathway.

Indexed as

Biomarkers, TumorFemaleFumarate HydrataseGene Expression Regulation, NeoplasticHMGA2 ProteinHumansImmunohistochemistryLeiomyomaMediator ComplexMiddle AgedMutationOncogene Protein v-aktSignal TransductionTissue Array AnalysisUterine NeoplasmsBiomarkers, TumorFumarate HydrataseHMGA2 ProteinHMGA2 protein, humanMED12 protein, humanMediator ComplexOncogene Protein v-aktAKT pathwaycell cycleFHHMGA2leiomyomaMED12

Identifiers

PMID29790226
PMCPMC6128746
OpenAlexW2803339238

What OpenQuestion holds

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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.