Evidence map›Paper›PMID 31766724›Full record

ReviewGenes2019

A "NOTCH" Deeper into the Epithelial-To-Mesenchymal Transition (EMT) Program in Breast Cancer.

Rohan Kar, Niraj Kumar Jha, Saurabh Kumar Jha, Ankur Sharma, Sunny Dholpuria, Nidhi Asthana, Kundan Chaurasiya, Vivek Kumar Singh, Shuaib Burgee, Parma Nand

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
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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

10 authors at 3 institutions in 1 country.

Rohan KarIndian Institute of Management Ahmedabad (IIMA), Gujarat 380015, India.ORCID 0000-0002-7903-4558
Niraj Kumar JhaDepartment of Biotechnology, School of Engineering & Technology (SET), Sharda University, Greater Noida 201306, India.ORCID 0000-0001-9486-4069
Saurabh Kumar JhaDepartment of Biotechnology, School of Engineering & Technology (SET), Sharda University, Greater Noida 201306, India.
Ankur SharmaDepartment of Life Science, School of Basic Science & Research (SBSR), Sharda University, Greater Noida 201306, India.
Sunny DholpuriaDepartment of Life Science, School of Basic Science & Research (SBSR), Sharda University, Greater Noida 201306, India.
Nidhi AsthanaNational Centre of Experimental Mineralogy & Petrology (NCEMP), University of Allahabad, Prayagraj 2l1002, India.
Kundan ChaurasiyaDepartment of Biotechnology, School of Engineering & Technology (SET), Sharda University, Greater Noida 201306, India.
Vivek Kumar SinghDepartment of Biotechnology, School of Engineering & Technology (SET), Sharda University, Greater Noida 201306, India.
Shuaib BurgeeDepartment of Life Science, School of Basic Science & Research (SBSR), Sharda University, Greater Noida 201306, India.
Parma NandDepartment of Biotechnology, School of Engineering & Technology (SET), Sharda University, Greater Noida 201306, India.
Sharda University · INIndian Institute of Management Ahmedabad · INUniversity of Allahabad · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Notch signaling is a primitive signaling pathway having various roles in the normal origin and development of each multicellular organisms. Therefore, any aberration in the pathway will inevitably lead to deadly outcomes such as cancer. It has now been more than two decades since Notch was acknowledged as an oncogene in mouse mammary tumor virus-infected mice. Since that discovery, activated Notch signaling and consequent up-regulation of tumor-promoting Notch target genes have been observed in human breast cancer. Moreover, consistent over-expression of Notch ligands and receptors has been shown to correlate with poor prognosis in human breast cancer. Notch regulates a number of key processes during breast carcinogenesis, of which, one key phenomenon is epithelial-mesenchymal transition (EMT). EMT is a key process for large-scale cell movement during morphogenesis at the time of embryonic development. Cancer cells aided by transcription factors usurp this developmental program to execute the multi-step process of tumorigenesis and metastasis. In this review, we recapitulate recent progress in breast cancer research that has provided new perceptions into the molecular mechanisms behind Notch-mediated EMT regulation during breast tumorigenesis.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsBreast NeoplasmsFemaleHumansReceptors, NotchSignal TransductionReceptors, Notchbreast cancercytokineEMThypoxiainvasionmetastasisNotchPI3K/Aktsignaling pathway

Identifiers

PMID31766724
PMCPMC6947643
OpenAlexW2989690384

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.