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Cited by 417Drug Transport and Resistance MechanismsCancer Cells and MetastasisAntibiotic Resistance in Bacteria

Unveiling the mechanisms and challenges of cancer drug resistance

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Khan, Sameer Ullah, Fatima, Kaneez, Aisha, Shariqa, Malik, Fayaz·2024·Cell Communication and Signaling
DOI 10.1186/s12964-023-01302-1PMC PMC10860306
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Abstract

Cancer treatment faces many hurdles and resistance is one among them. Anti-cancer treatment strategies are evolving due to innate and acquired resistance capacity, governed by genetic, epigenetic, proteomic, metabolic, or microenvironmental cues that ultimately enable selected cancer cells to survive and progress under unfavorable conditions. Although the mechanism of drug resistance is being widely studied to generate new target-based drugs with better potency than existing ones. However, due to the broader flexibility in acquired drug resistance, advanced therapeutic options with better efficacy need to be explored. Combination therapy is an alternative with a better success rate though the risk of amplified side effects is commonplace. Moreover, recent groundbreaking precision immune therapy is one of the ways to overcome drug resistance and has revolutionized anticancer therapy to a greater extent with the only limitation of being individual-specific and needs further attention. This review will focus on the challenges and strategies opted by cancer cells to withstand the current therapies at the molecular level and also highlights the emerging therapeutic options -like immunological, and stem cell-based options that may prove to have better potential to challenge the existing problem of therapy resistance. Video Abstract.

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  • Multiple physiological barriers of the tumor microenvironment-dense extracellular matrix, cellular heterogeneity, hypoxic gradients, and elevated interstitial fluid pressure-hinder uniform distribution and accumulation of therapeutics, reducing treatment efficacy.

    “Drug delivery to solid tumors is challenged by multiple physiological barriers arising from the tumor microenvironment, including dense extracellular matrix, cellular heterogeneity, hypoxic gradients, and elevated interstitial fluid pressure. These features hinder the uniform distribution and accumulation of therapeutics, reducing treatment efficacy.”

    From Modeling Tumor Microenvironment Complexity In Vitro: Spheroids as Physiologically Relevant Tumor Models and Strategies for Their Analysis (2025) · cites this paper as [2]

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Cited by

Sorted by citations

Authors
Khan, S. U., Fatima, K., Aisha, S., & Malik, F.
Affiliations
  • The University of Texas MD Anderson Cancer Center (US)
  • Indian Institute of Integrative Medicine (IN)
Corresponding author
  • Khan, Sameer Ullah
  • Malik, Fayaz
ORCID
Venue
Cell Communication and Signaling
Publisher
Springer Science and Business Media LLC
Published
2024-02-12
Volume
22
Issue
1
Pages
109-109
ISSN
1478-811X (ISSN-L)
DOI
10.1186/s12964-023-01302-1
PMC
PMC10860306
OpenAlex
W4391747436
Cited by
417
References
15
Citations by year
2026: 172 · 2025: 188 · 2024: 57
FWCI
22.36
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell Communication and Signaling (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • Greater South Information System
Funders
Department of Biotechnology, Ministry of Science and Technology, India (BT/IN/Swiss/48/FM/2018-19)
Topics
  • Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
  • Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Medicine › Antibiotic Resistance in Bacteria
Keywords
chemoresistance, acquired drug resistance, epigenetic resistance, tumor microenvironment, combination therapy, immune checkpoint inhibitors, precision immunotherapy, cancer stem cells, targeted cancer therapy
MeSH terms
Antineoplastic Agents, Humans, Neoplasms, Drug Resistance, Neoplasm, Proteomics

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