Evidence map›Paper›PMID 41452570›Full record

ReviewMedical oncology (Northwood, London, England)2025

Emerging Anti-Cancer and Repurposed Therapies for Overcoming Multidrug Resistance in Lung Cancer.

Nilay Solanki, Pratham Shah, Sargam Kewalramani, Umang Shah, Mehul Patel, Swayamprakash Patel, Rajesh Maheshwari

Abstract readReview
PubMed Publisher
In one paragraph

Review in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

7 authors.

Nilay SolankiDepartment of Pharmacology, Ramanbhai Patel College of Pharmacy, Charotar University of Science and Technology, CHARUSAT Campus, Changa-388421, Gujarat, India. nilaysolanki.ph@charusat.ac.in.
Pratham ShahDepartment of Pharmacology, Ramanbhai Patel College of Pharmacy, Charotar University of Science and Technology, CHARUSAT Campus, Changa-388421, Gujarat, India.
Sargam KewalramaniDepartment of Pharmacology, Ramanbhai Patel College of Pharmacy, Charotar University of Science and Technology, CHARUSAT Campus, Changa-388421, Gujarat, India.
Umang ShahDepartment of Pharmacology, Ramanbhai Patel College of Pharmacy, Charotar University of Science and Technology, CHARUSAT Campus, Changa-388421, Gujarat, India.
Mehul PatelDepartment of Pharmacology, Ramanbhai Patel College of Pharmacy, Charotar University of Science and Technology, CHARUSAT Campus, Changa-388421, Gujarat, India.
Swayamprakash PatelDepartment of Pharmacology, Ramanbhai Patel College of Pharmacy, Charotar University of Science and Technology, CHARUSAT Campus, Changa-388421, Gujarat, India.
Rajesh MaheshwariDepartment of Pharmacy, Sumandeep Vidyapeeth Deemed to be University, Piparia, Vadodara-391760, Gujarat, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multidrug resistance (MDR) still constitutes a significant barrier to the effective treatment of lung cancer and makes a significant contribution to the poor clinical results. MDR is explained by a set of mechanisms; increase of drug efflux, metabolism, increase of DNA repair potential, inhibition of apoptotic signals, mutation or post-translational modification of drug targets. These cell intrinsic mechanisms are even aggravated by tumour-microenvironment-induced factors, epigenetics dysregulation, survival of cancer stem cells and intratumour heterogeneity, which has made resistance highly adaptive and multifactorial. In order to address this complexity emerging therapeutic strategy is dual. The former element deals with new targeted agents which are able to counter an oncogene-mediated resistance. These include next-generation tyrosine kinase inhibitors (TKIs), KRAS12C inhibitors, bispecific antibodies including ivonescimab, and they all are specific to inhibit predominant signalling cascades that promote tumoral proliferation and resistance. The second element is drug repurposing whereby it exploits already established pharmacological drugs with already a clear safety record to attack non-oncogenic vulnerabilities linked with MDR. Pharmacological modulators of autophagy including statins, disulfiram, and lysosomotropic agents (e.g., chloroquine) target metabolic vulnerabilities such as mitochondrial bioenergetics and redox homeostasis. By mitigating oxidative stress and immune evasion, these compounds act as chemo sensitizers that potentiate the efficacy of tyrosine kinase inhibitors (TKIs) and immunotherapies, effectively overcoming adaptive drug resistance. Real-time monitoring of resistance evolution can be achieved with liquid biopsies, such as circulating tumor DNA and exosomal cargo, whereas MDR-related biomarkers can be used to stratify a patient. Analytical models that are built using artificial-intelligence also guide rational combination-therapy design and the chosen selection of treatments that are personalized. Also, inhalable nano formulations and targeted drug-delivery systems optimize the bioavailability of the formulation by pulmonary determination and ameliorates the systemic toxicity. A combination of these therapeutic approaches will provide a more accurate and flexible way of conquering MDR in lung cancer.

Indexed as

Antineoplastic AgentsDrug RepositioningDrug Resistance, MultipleDrug Resistance, NeoplasmLung NeoplasmsHumansAntineoplastic AgentsAnti-cancer drugsDrug repurposingImmunotherapiesKRAS inhibitorsMultidrug resistance (MDR)Non-small cell lung cancer (NSCLC)Tyrosine kinase inhibitors

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Registered trials

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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.