Evidence map›Paper›PMID 31280421›Full record

ReviewMolecular biology reports2019

Cell signaling and cancer: a mechanistic insight into drug resistance.

Munmun Panda, Bijesh K Biswal

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Synergistic Effects of PI3K Inhibition on Arsenic Trioxide Cytotoxicity in Acute Promyelocytic Leukemia Cells: A New Portrait of Idelalisib as an Adjuvant Therapy.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2023
    Article
  20. 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

2 authors at 1 institution in 1 country.

Munmun PandaCancer Drug Resistance Laboratory, Department of Life Science, National Institute of Technology, Sundargarh, Rourkela, Odisha, 769008, India.
Bijesh K BiswalCancer Drug Resistance Laboratory, Department of Life Science, National Institute of Technology, Sundargarh, Rourkela, Odisha, 769008, India. biswalb@nitrkl.ac.in.ORCID http://orcid.org/0000-0002-5609-7660
National Institute of Technology Rourkela · IN

Funding

Department of Science and technology, Science and Engineering Research Board (DST, SERB), New Delhi, India ECR/2016/000792
6 · The paper itself

Abstract

Drug resistance is a major setback for advanced therapeutics in multiple cancers. The increasing prevalence of this resistance is a growing concern and bitter headache for the researchers since a decade. Hence, it is essential to revalidate the existing strategies available for cancer treatment and to look after a novel therapeutic approach for target based killing of cancer cells at the genetic level. This review outlines the different mechanisms enabling resistance including drug efflux, drug target alternation, alternative splicing, the release of the extracellular vesicle, tumor heterogeneity, epithelial-mesenchymal transition, tumor microenvironment, the secondary mutation in the receptor, epigenetic alternation, heterodimerization of receptors, amplification of target and amplification of components rather than the target. Furthermore, existing evidence and the role of various signaling pathways like EGFR, Ras, PI3K/Akt, Wnt, Notch, TGF-β, Integrin-ECM signaling in drug resistance are explained. Lastly, the prevention of this resistance by a contemporary therapeutic strategy, i.e., a combination of specific signaling pathway inhibitors and the cocktail of a cancer drug is summarized showing the new treatment strategies.

Indexed as

Antineoplastic AgentsCell Line, TumorDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionGenes, erbB-1HumansMAP Kinase Signaling SystemNeoplasmsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesTumor MicroenvironmentWnt Signaling PathwayAntineoplastic AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAberrant signalingCancerCross-resistanceDrug resistanceTherapeutics

Identifiers

PMID31280421
OpenAlexW2954345285

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.