Evidence map›Paper›PMID 27748285›Full record

ArticleThe Indian journal of medical research2016

PI3K/Akt/mTOR signaling & its regulator tumour suppressor genes

Annu Makker, Madhu Mati Goel, Abbas Ali Mahdi, Vikram Bhatia, Vinita Das, Anjoo Agarwal, Amita Pandey

Open access · diamondAbstract read
In one paragraph

Article in The Indian journal of medical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 19 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Annu MakkerPost-Graduate Department of Pathology, King George's Medical University, Lucknow, India.
Madhu Mati GoelPost-Graduate Department of Pathology, King George's Medical University, Lucknow, India.
Abbas Ali MahdiDepartment of Biochemistry, King George's Medical University, Lucknow, India.
Vikram BhatiaPost-Graduate Department of Pathology, King George's Medical University, Lucknow, India.
Vinita DasDepartment of Obstetrics & Gynecology, King George's Medical University, Lucknow, India.
Anjoo AgarwalDepartment of Obstetrics & Gynecology, King George's Medical University, Lucknow, India.
Amita PandeyDepartment of Obstetrics & Gynecology, King George's Medical University, Lucknow, India.
King George's Medical University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

objectivesDespite their high occurrence and associated significant level of morbidity manifesting as spectrum of clinical symptoms, the pathogenesis of uterine leiomyomas (ULs) remains unclear. We investigated expression profile of tumour suppressor genes PTEN (phosphatase and tensin homolog deleted on chromosome ten) and LKB1 (liver kinase B1), and key signaling components of P13K (phosphatidylinositol 3-kinase)/Akt (protein kinase B)/mTOR (mammalian target of rapamycin) pathway in leiomyomas and adjacent normal myometrium in women of reproductive age, to explore the possibility of targeting this pathway for future therapeutic implications.

methodsReal time PCR (qPCR) was used to quantify relative gene expression levels of PTEN, Akt1, Akt2, mTOR, LKB1 and VEGFA (vascular endothelial growth factor A) in leiomyoma as compared to adjacent normal myometrium. Immunohistochemistry was subsequently performed to analyze expression of PTEN, phospho-Akt, phospho-mTOR, phospho-S6, LKB1 and VEGFA in leiomyoma and adjacent normal myometrium.

resultsSignificant upregulation of PTEN (2.52 fold; P=0.03) and LKB1 (3.93 fold; P0.01), and downregulation of VEGFA (2.95 fold; P=0.01) genes were observed in leiomyoma as compared to normal myometrium. Transcript levels of Akt1, Akt2 and mTOR did not vary significantly between leiomyoma and myometrium. An increased immunoexpression of PTEN (P=0.015) and LKB1 (P<0.001) and decreased expression of VEGFA (P=0.01) was observed in leiomyoma as compared to myometrium. Immunostaining for activated (phosphorylated) Akt, mTOR and S6 was absent or low in majority of leiomyoma and myometrium. INTERPRETATION &

conclusionsUpregulation of PTEN and LKB1 in concert with negative or low levels of activated Akt, mTOR and S6 indicates that PI3K/Akt/mTOR pathway may not play a significant role in pathogenesis of leiomyoma.

Indexed as

AdultAMP-Activated Protein Kinase KinasesFemaleGene Expression Regulation, NeoplasticHumansLeiomyomaMiddle AgedNeoplasm ProteinsPhosphatidylinositol 3-KinasesPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionTOR Serine-Threonine KinasesTumor Suppressor ProteinsAMP-Activated Protein Kinase KinasesMTOR protein, humanNeoplasm ProteinsPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanSTK11 protein, humanTOR Serine-Threonine KinasesTumor Suppressor ProteinsVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID27748285
PMCPMC5080920
OpenAlexW2531420581

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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 OpenQuestion graph.