Evidence map›Paper›PMID 34445588›Full record

ReviewInternational journal of molecular sciences2021

Molecular Mechanisms of Chemoresistance Induced by Cisplatin in NSCLC Cancer Therapy.

Jolanta Kryczka, Jakub Kryczka, Karolina H Czarnecka-Chrebelska, Ewa Brzeziańska-Lasota

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed
0.1field-weighted citation impact, top 54% 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

133 citing papers in PubMed, 1 citations in OpenAlex.

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73 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

4 authors at 1 institution in 1 country.

Jolanta KryczkaDepartment of Biomedicine and Genetics, Medical University of Lodz, 92-213 Lodz, Poland.ORCID 0000-0002-7342-7342
Jakub KryczkaInstitute of Medical Biology, Polish Academy of Sciences, 93-232 Lodz, Poland.ORCID 0000-0002-5719-4139
Karolina H Czarnecka-ChrebelskaDepartment of Biomedicine and Genetics, Medical University of Lodz, 92-213 Lodz, Poland.ORCID 0000-0003-4013-513X
Ewa Brzeziańska-LasotaDepartment of Biomedicine and Genetics, Medical University of Lodz, 92-213 Lodz, Poland.ORCID 0000-0002-0882-1458
Medical University of Lodz · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer cells utilise several mechanisms to increase their survival and progression as well as their resistance to anticancer therapy: deregulation of growth regulatory pathways by acquiring grow factor independence, immune system suppression, reducing the expression of antigens activating T lymphocyte cells (mimicry), induction of anti-apoptotic signals to counter the action of drugs, activation of several DNA repair mechanisms and driving the active efflux of drugs from the cell cytoplasm, and epigenetic regulation by microRNAs (miRNAs). Because it is commonly diagnosed late, lung cancer remains a major malignancy with a low five-year survival rate; when diagnosed, the cancer is often highly advanced, and the cancer cells may have acquired drug resistance. This review summarises the main mechanisms involved in cisplatin resistance and interactions between cisplatin-resistant cancer cells and the tumour microenvironment. It also analyses changes in the gene expression profile of cisplatin sensitive vs. cisplatin-resistant non-small cell lung cancer (NSCLC) cellular model using the GSE108214 Gene Expression Omnibus database. It describes a protein-protein interaction network that indicates highly dysregulated TP53, MDM2, and CDKN1A genes as they encode the top networking proteins that may be involved in cisplatin tolerance, these all being upregulated in cisplatin-resistant cells. Furthermore, it illustrates the multifactorial nature of cisplatin resistance by examining the diversity of dysregulated pathways present in cisplatin-resistant NSCLC cells based on KEGG pathway analysis.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCisplatinGene Expression Regulation, NeoplasticHumansLung NeoplasmsTumor MicroenvironmentAntineoplastic AgentsCisplatinchemoresistance molecular mechanismscisplatinDNA repair mechanismsnon-small cell lung cancertumour microenvironment

Identifiers

PMID34445588
PMCPMC8396273
OpenAlexW3179083918

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.