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Treatment Resistant Cancers02:56

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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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Antibiotic resistance is a major public health concern that arises when bacteria evolve mechanisms to withstand the effects of antibiotic treatments. This resistance can be intrinsic, acquired through genetic mutations, or transferred between bacteria via horizontal gene transfer. The development of antibiotic resistance poses significant challenges in treating bacterial infections and necessitates ongoing research to develop new therapeutic strategies.Intrinsic resistance occurs when bacterial...
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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Multidrug Resistance in Leukaemia.

J A Holmes1

  • 1a Dept of Haematology, University of Wales College of Medicine, Heath Park, Cardiff, CP4 4XN.

Leukemia & Lymphoma
|July 28, 2016
PubMed
Summary
This summary is machine-generated.

Multidrug resistance (MDR) complicates hematological malignancy treatment, reducing chemotherapy effectiveness. Circumventing MDR mechanisms offers potential for chemosensitizing resistant leukemia cells, improving patient outcomes.

Keywords:
Multidrug resistance (MDR)chemotherapyleukaemia

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Area of Science:

  • Hematology
  • Cancer Biology
  • Pharmacology

Background:

  • Cytotoxic agent resistance is a major challenge in treating hematological malignancies.
  • Acquired multidrug resistance (MDR) leads to cross-resistance against various chemotherapeutic drugs.
  • Multiple drug resistance mechanisms are implicated in clinically resistant leukemia.

Purpose of the Study:

  • To explore the role of drug resistance mechanisms in hematological malignancies.
  • To investigate the potential therapeutic benefits of circumventing multidrug resistance (MDR) in leukemia.
  • To highlight the need for further research into in vivo efficacy of MDR-reversing agents.

Main Methods:

  • Review of established drug resistance mechanisms in leukemia.
  • Analysis of in vitro studies on MDR-reversing agents.
  • Discussion of the clinical relevance and in vivo efficacy of MDR circumvention strategies.

Main Results:

  • Leukemic cells may employ MDR mechanisms for survival and proliferation.
  • Circumventing MDR could render resistant leukemia cells chemosensitive and potentially curable.
  • In vitro MDR reversal agents show promise, but in vivo efficacy requires further demonstration.

Conclusions:

  • Drug resistance significantly complicates hematological malignancy treatment.
  • Understanding and targeting MDR mechanisms is crucial for improving therapeutic outcomes.
  • Further investigation into the in vivo effectiveness of MDR circumvention is warranted.