Evidence map›Paper›PMID 33052041›Full record

ReviewCancer reports (Hoboken, N.J.)2022

Molecular and cellular paradigms of multidrug resistance in cancer.

Foram U Vaidya, Abu Sufiyan Chhipa, Vinita Mishra, Vishal Kumar Gupta, Shiv Govind Rawat, Ajay Kumar, Chandramani Pathak

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer reports (Hoboken, N.J.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 193 citations in OpenAlex.

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  15. HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025
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27 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Foram U VaidyaCell Biology Laboratory, School of Biological Sciences & Biotechnology, Indian Institute of Advanced Research, Gandhinagar, India.ORCID 0000-0003-1093-1514
Abu Sufiyan ChhipaCell Biology Laboratory, School of Biological Sciences & Biotechnology, Indian Institute of Advanced Research, Gandhinagar, India.ORCID 0000-0003-1208-1162
Vinita MishraCell Biology Laboratory, School of Biological Sciences & Biotechnology, Indian Institute of Advanced Research, Gandhinagar, India.
Vishal Kumar GuptaDepartment of Zoology, Banaras Hindu University, Varanasi, India.
Shiv Govind RawatDepartment of Zoology, Banaras Hindu University, Varanasi, India.
Ajay KumarDepartment of Zoology, Banaras Hindu University, Varanasi, India.
Chandramani PathakCell Biology Laboratory, School of Biological Sciences & Biotechnology, Indian Institute of Advanced Research, Gandhinagar, India.ORCID 0000-0002-9389-8096
Indian Institute of Advanced Research · INBanaras Hindu University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe acquisition of resistance to chemotherapy is a major hurdle in the successful application of cancer therapy. Several anticancer approaches, including chemotherapies, radiotherapy, surgery and targeted therapies are being employed for the treatment of cancer. However, cancer cells reprogram themselves in multiple ways to evade the effect of these therapies, and over a period of time, the drug becomes inactive due to the development of multi-drug resistance (MDR). MDR is a complex phenomenon where malignant cells become insensitive to anticancer drugs and attain the ability to survive even after several exposures of anticancer drugs. In this review, we have discussed the molecular and cellular paradigms of multidrug resistance in cancer. RECENT

findingsAn Extensive research in cancer biology revealed that drug resistance in cancer is the result of perpetuated intracellular and extracellular mechanisms such as drug efflux, drug inactivation, drug target alteration, oncogenic mutations, altered DNA damage repair mechanism, inhibition of programmed cell death signaling, metabolic reprogramming, epithelial mesenchymal transition (EMT), inherent cell heterogeneity, epigenetic changes, redox imbalance, or any combination of these mechanisms. An inevitable cross-link between inflammation and drug resistance has been discussed. This review provided insight molecular mechanism to understand the vulnerabilities of cancer cells to develop drug resistance.

conclusionMDR is an outcome of interplays between multiple intricate pathways responsible for the inactivation of drug and development of resistance. MDR is a major obstacle in regimens of successful application of anti-cancer therapy. An improved understanding of the molecular mechanism of multi drug resistance and cellular reprogramming can provide a promising opportunity to combat drug resistance in cancer and intensify anti-cancer therapy for the upcoming future.

Indexed as

Antineoplastic AgentsNeoplasmsDrug Delivery SystemsDrug Resistance, MultipleDrug Resistance, NeoplasmHumansAntineoplastic AgentsCancer metabolismCellular reprogrammingInflammationMulti drug resistance and cancerProgrammed cell deathTumor microenvironment

Identifiers

PMID33052041
PMCPMC9780431
OpenAlexW3092057003

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.