Evidence map›Paper›PMID 33590419›Full record

ReviewClinical & experimental metastasis2021

TGFβ signaling networks in ovarian cancer progression and plasticity.

Asha Kumari, Zainab Shonibare, Mehri Monavarian, Rebecca C Arend, Nam Y Lee, Gareth J Inman, Karthikeyan Mythreye

Open access · hybridAbstract readReview
In one paragraph

Review in Clinical & experimental metastasis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 82 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 3 institutions in 2 countries.

Asha KumariDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, WTI 320B, 1824 Sixth Avenue South, Birmingham, AL, 35294, USA.
Zainab ShonibareDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, WTI 320B, 1824 Sixth Avenue South, Birmingham, AL, 35294, USA.
Mehri MonavarianDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, WTI 320B, 1824 Sixth Avenue South, Birmingham, AL, 35294, USA.
Rebecca C ArendDepartment of Obstetrics and Gynecology-Gynecologic Oncology, University of Alabama at Birmingham, Birmingham, AL, 35233, USA.
Nam Y LeeDivision of Pharmacology, Chemistry and Biochemistry, College of Medicine, University of Arizona, Tucson, AZ, 85721, USA.
Gareth J InmanCancer Research UK Beatson Institute and Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.
Karthikeyan MythreyeDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, WTI 320B, 1824 Sixth Avenue South, Birmingham, AL, 35294, USA. mythreye@uab.edu.ORCID 0000-0001-5478-0098
University of Alabama at Birmingham · USCancer Research UK Scotland Institute · GBUniversity of Arizona · US

Funding

Role of Sox2 in Stress Adaptations to Ovarian Cancer Anchorage IndependenceR01CA230628 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HEMPEL, NADINE, KARTHIKEYAN, MYTHREYE · 2019 to 2023
$2.1M
Inhibin function in tumor angiogenesisR01CA219495 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI KARTHIKEYAN, MYTHREYE · 2018 to 2023
$1.7M
Role of spectrin signaling complex in angiogenesisR01GM128055 · NIGMS · UNIVERSITY OF ARIZONA · PI LEE, NAM Y · 2019 to 2022
$1.3M
Cancer Research UK 29802NCI NIH HHS R01 CA219495NCI NIH HHS R01 CA230628NIGMS NIH HHS R01 GM128055
6 · The paper itself

Abstract

Epithelial ovarian cancer (EOC) is a leading cause of cancer-related death in women. Late-stage diagnosis with significant tumor burden, accompanied by recurrence and chemotherapy resistance, contributes to this poor prognosis. These morbidities are known to be tied to events associated with epithelial-mesenchymal transition (EMT) in cancer. During EMT, localized tumor cells alter their polarity, cell-cell junctions, cell-matrix interactions, acquire motility and invasiveness and an exaggerated potential for metastatic spread. Key triggers for EMT include the Transforming Growth Factor-β (TGFβ) family of growth factors which are actively produced by a wide array of cell types within a specific tumor and metastatic environment. Although TGFβ can act as either a tumor suppressor or promoter in cancer, TGFβ exhibits its pro-tumorigenic functions at least in part via EMT. TGFβ regulates EMT both at the transcriptional and post-transcriptional levels as outlined here. Despite recent advances in TGFβ based therapeutics, limited progress has been seen for ovarian cancers that are in much need of new therapeutic strategies. Here, we summarize and discuss several recent insights into the underlying signaling mechanisms of the TGFβ isoforms in EMT in the unique metastatic environment of EOCs and the current therapeutic interventions that may be relevant.

Indexed as

Carcinoma, Ovarian EpithelialDisease ProgressionEpithelial-Mesenchymal TransitionFemaleHumansNeoplasm MetastasisOvarian NeoplasmsSignal TransductionSmad ProteinsTransforming Growth Factor betaSmad ProteinsTransforming Growth Factor betaEMTMetastasisOvarian cancerTGFβTumor microenvironment

Identifiers

PMID33590419
PMCPMC7987693
OpenAlexW3129964011

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.