Evidence map›Paper›PMID 32866423›Full record

ArticleCancer biology & therapy2020

Rac1 repression reverses chemoresistance by targeting tumor metabolism.

Shanmugasundaram Ganapathy-Kanniappan

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Genomic Index of Sensitivity to Chemotherapy for Triple Negative Breast Cancer.Asian Pacific journal of cancer prevention : APJCP · 2023
    Article
  3. Article
  4. Review
  5. Review
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

1 author at 1 institution in 1 country.

Shanmugasundaram Ganapathy-KanniappanRussell H. Morgan Department of Radiology and Radiological Science, Division of Interventional Radiology, The Johns Hopkins University School of Medicine , Baltimore, MD, USA.ORCID 0000-0001-7176-3804
Johns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor metabolism is exemplified by the increased rate of glucose utilization, a biochemical signature of cancer cells. The enhanced glucose hydrolysis enabled by the augmentation of glycolytic flux and the pentose phosphate pathway (PPP) plays a pivotal role in the growth and survival of neoplastic cells. In a recent report, it has been shown that in human breast cancer the GTP binding protein, Rac1 enables resistance to therapy, particularly against the DNA-damaging therapeutics. Significantly, the findings demonstrate that Rac1-dependent chemoresistance involves the upregulation of glycolytic flux as well as PPP. Using multiple approaches, the study demonstrates that disruption of Rac1 activity sensitizes cancer cells to DNA-damaging agents. More importantly, the data uncover a previously unknown PPP regulatory role of Rac1 in breast cancer. Finally, the authors also show the effectiveness and the feasibility of

Indexed as

Cell Line, TumorHumansMolecular Targeted Therapyrac1 GTP-Binding ProteinTriple Negative Breast Neoplasmsrac1 GTP-Binding ProteinRAC1 protein, humanaldolase Achemoresistanceglucose metabolismpentose phosphate pathway (PPP)Rac1triple-negative breast cancer (TNBC)

Identifiers

PMID32866423
PMCPMC7583477
OpenAlexW3081987367

What OpenQuestion holds

Textmetadata
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.