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      The Different Mechanisms of Cancer Drug Resistance: A Brief Review

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          Abstract

          Anticancer drugs resistance is a complex process that arises from altering in the drug targets. Advances in the DNA microarray, proteomics technology and the development of targeted therapies provide the new strategies to overcome the drug resistance. Although a design of the new chemotherapy agents is growing quickly, effective chemotherapy agent has not been discovered against the advanced stage of cancer (such as invasion and metastasis). The cancer cell resistance against the anticancer agents can be due to many factors such as the individual’s genetic differences, especially in tumoral somatic cells. Also, the cancer drug resistance is acquired, the drug resistance can be occurred by different mechanisms, including multi-drug resistance, cell death inhibiting (apoptosis suppression), altering in the drug metabolism, epigenetic and drug targets, enhancing DNA repair and gene amplification. In this review, we outlined the mechanisms of cancer drug resistance and in following, the treatment failures by common chemotherapy agents in the different type of cancers.

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          Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome.

          Brian J Druker, Charles L. Sawyers, Hagop Kantarjian … (2001)
          BCR-ABL, a constitutively activated tyrosine kinase, is the product of the Philadelphia chromosome. This enzyme is present in virtually all cases of chronic myeloid leukemia (CML) throughout the course of the disease, and in 20 percent of cases of acute lymphoblastic leukemia (ALL). On the basis of the substantial activity of the inhibitor in patients in the chronic phase, we evaluated STI571 (formerly known as CGP 57148B), a specific inhibitor of the BCR-ABL tyrosine kinase, in patients who had CML in blast crisis and in patients with ALL who had the Ph chromosome. In this dose-escalating pilot study, 58 patients were treated with STI571; 38 patients had a myeloid blast crisis and 20 had ALL or a lymphoid blast crisis. Treatment was given orally at daily doses ranging from 300 to 1000 mg. Responses occurred in 21 of 38 patients (55 percent) with a myeloid-blast-crisis phenotype; 4 of these 21 patients had a complete hematologic response. Of 20 patients with a lymphoid blast crisis or ALL, 14 (70 percent) had a response, including 4 who had complete responses. Seven patients with a myeloid blast crisis continue to receive treatment and remain in remission from 101 to 349 days after starting the treatment. All but one patient with a lymphoid blast crisis or ALL has relapsed. The most frequent adverse effects were nausea, vomiting, edema, thrombocytopenia, and neutropenia. The BCR-ABL tyrosine kinase inhibitor STI571 is well tolerated and has substantial activity in the blast crises of CML and in Ph-positive ALL.
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            Acute lymphoblastic leukaemia.

            Hiroto Inaba, Mel F Greaves, Charles Mullighan (2013)
            Acute lymphoblastic leukaemia occurs in both children and adults but its incidence peaks between 2 and 5 years of age. Causation is multifactorial and exogenous or endogenous exposures, genetic susceptibility, and chance have roles. Survival in paediatric acute lymphoblastic leukaemia has improved to roughly 90% in trials with risk stratification by biological features of leukaemic cells and response to treatment, treatment modification based on patients' pharmacodynamics and pharmacogenomics, and improved supportive care. However, innovative approaches are needed to further improve survival while reducing adverse effects. Prognosis remains poor in infants and adults. Genome-wide profiling of germline and leukaemic cell DNA has identified novel submicroscopic structural genetic changes and sequence mutations that contribute to leukaemogenesis, define new disease subtypes, affect responsiveness to treatment, and might provide novel prognostic markers and therapeutic targets for personalised medicine. Copyright © 2013 Elsevier Ltd. All rights reserved.
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              Childhood Acute Lymphoblastic Leukemia: Progress Through Collaboration.

              Ching-Hon Pui, Jun J Yang, Stephen P. Hunger … (2015)
              To review the impact of collaborative studies on advances in the biology and treatment of acute lymphoblastic leukemia (ALL) in children and adolescents.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Adv Pharm Bull
                Journal ID (iso-abbrev): Adv Pharm Bull
                Journal ID (publisher-id): Adv Pharm Bull
                Journal ID (pmc): APB
                Journal ID (publisher-id): TBZMED
                Title: Advanced Pharmaceutical Bulletin
                Publisher: Tabriz University of Medical Sciences
                ISSN (Print): 2228-5881
                ISSN (Electronic): 2251-7308
                Publication date (Print): September 2017
                Publication date (Electronic): 25 September 2017
                Volume: 7
                Issue: 3
                Pages: 339-348
                Affiliations
                1Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
                2Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
                Author notes
                [* ] Corresponding author: Behzad Baradaran, Tel: +98 41 33371440, Fax: +98 41 33371311, baradaranb@ 123456tbzmed.ac.ir
                Article
                DOI: 10.15171/apb.2017.041
                PMC ID: 5651054
                PubMed ID: 29071215
                SO-VID: 939b1bad-fedd-4851-87f3-9b3660e42bce
                Copyright © ©2017 The Authors.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution (CC BY), which permits unrestricted use, distribution, and reproduction in any medium, as long as the original authors and source are cited. No permission is required from the authors or the publishers.

                History
                Date received : 26 February 2017
                Date revision received : 19 July 2017
                Date accepted : 22 July 2017
                Page count
                Figures: 2, Tables: 2, References: 88, Pages: 10
                Categories
                Subject: Review Article

                Keywords: drug resistance,cancer,multi-drug resistance,microrna,epigenetic,cell death inhibiting
                Data availability:
                Keywords: drug resistance, cancer, multi-drug resistance, microrna, epigenetic, cell death inhibiting

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