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Drug Resistance in Cancer: Molecular Mechanisms and Tackling Strategies 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: 30 May 2024 | Viewed by 1860

Special Issue Editor

The Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, VIC 3010, Australia
Interests: drug resistance; Ewing sarcoma; ovarian cancer; ABCB1; LSD1; TP53
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is a highly complex, adaptive condition that can rapidly develop new phenotypic and genotypic profiles to circumvent therapy. Drug resistance threatens the longevity of drugs and restricts the treatment options for patients, and it is highly common in oncology and infectious diseases. The emergence of drug resistance remains the largest impediment in the quest for a curative cancer treatment, with an estimated 90% of all cancer-related deaths being attributed to chemoresistance. The rapidity with which cancer cells can develop resistance to both classical chemotherapy and targeted agents is startling. With the knowledge that each cubic centimeter of a tumour contains up to one billion cancer cells, novel insights into both primary and acquired resistance mechanisms, including drug detoxification, alterations in drug targets, genomic/epigenetic instability, increased ability to repair DNA damage, reduced susceptibility to apoptosis, as well as the influence of the tumour microenvironment and clonal cooperation, are required to substantially alter therapeutic treatment practices and increase the overall survival rates. Some of these resistance pathways lead to multidrug resistance, generating an increasingly challenging clinical problem.

This Special Issue of IJMS will highlight the recent advances in drug resistance, particularly novel mechanisms and targeted strategies to tackle this global medicine concern. Experimental papers, up-to-date review articles, and commentaries are all welcome.

Dr. Kathleen Pishas
Guest Editor

Manuscript Submission Information

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Keywords

  • apoptosis
  • cancer
  • clinical trials
  • chemotherapy
  • drug metabolism
  • drug resistance
  • drug delivery
  • heterogeneity
  • immunotherapy
  • microenvironment

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Published Papers (2 papers)

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Review

22 pages, 694 KiB  
Review
Treatment of Double-Refractory Chronic Lymphocytic Leukemia—An Unmet Clinical Need
Int. J. Mol. Sci. 2024, 25(3), 1589; https://doi.org/10.3390/ijms25031589 - 27 Jan 2024
Viewed by 849
Abstract
Recent years have seen significant improvement in chronic lymphocytic leukemia (CLL) management. Targeting B-cell lymphoma (BCL-2) and Bruton’s kinase (BTK) have become the main strategies to restrain CLL activity. These agents are generally well tolerated, but the discontinuation of these therapies happens due [...] Read more.
Recent years have seen significant improvement in chronic lymphocytic leukemia (CLL) management. Targeting B-cell lymphoma (BCL-2) and Bruton’s kinase (BTK) have become the main strategies to restrain CLL activity. These agents are generally well tolerated, but the discontinuation of these therapies happens due to resistance, adverse effects, and Richter’s transformation. A growing population of patients who have previously used both BTK inhibitors and BCL2 suffer from the constriction of the following regimens. This review explores the resistance mechanisms for both ibrutinib and venetoclax. Moreover, we present innovative approaches evaluated for treating double-refractory CLL. Full article
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14 pages, 708 KiB  
Review
Emerging Roles of YES1 in Cancer: The Putative Target in Drug Resistance
Int. J. Mol. Sci. 2024, 25(3), 1450; https://doi.org/10.3390/ijms25031450 - 25 Jan 2024
Viewed by 696
Abstract
Src family kinases (SFKs) are non-receptor tyrosine kinases that are recognized as proto-oncogenic products. Among SFKs, YES1 is frequently amplified and overexpressed in a variety of human tumors, including lung, breast, ovarian, and skin cancers. YES1 plays a pivotal role in promoting cell [...] Read more.
Src family kinases (SFKs) are non-receptor tyrosine kinases that are recognized as proto-oncogenic products. Among SFKs, YES1 is frequently amplified and overexpressed in a variety of human tumors, including lung, breast, ovarian, and skin cancers. YES1 plays a pivotal role in promoting cell proliferation, survival, and invasiveness during tumor development. Recent findings indicate that YES1 expression and activation are associated with resistance to chemotherapeutic drugs and tyrosine kinase inhibitors in human malignancies. YES1 undergoes post-translational modifications, such as lipidation and nitrosylation, which can modulate its catalytic activity, subcellular localization, and binding affinity for substrate proteins. Therefore, we investigated the diverse mechanisms governing YES1 activation and its impact on critical intracellular signal transduction pathways. We emphasized the function of YES1 as a potential mechanism contributing to the anticancer drug resistance emergence. Full article
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