Related Experiment Video
Updated: May 24, 2026
11:06
Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells
Published on: February 24, 2014
Genomic instability in chronic myeloid leukemia: targets for therapy?
N Muvarak1, P Nagaria, F V Rassool
1Department of Radiation Oncology, University of Maryland School of Medicine, Baltimore, MD 21230, USA.
Current Hematologic Malignancy Reports
|March 20, 2012
Summary
Genomic instability in Philadelphia-positive chronic myeloid leukemia (CML) arises from DNA damage and repair issues, driving disease progression and treatment resistance. Targeting these molecular pathways offers potential new therapies for advanced CML.
Area of Science:
- Hematology
- Molecular Biology
- Genetics
Background:
- Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) involves genetic and cytogenetic abnormalities during disease progression.
- These abnormalities can indicate genes driving blastic transformation, suggesting underlying genomic instability.
- Genomic instability may result from compromised DNA damage and repair responses, leading to advanced CML and therapy resistance.
Purpose of the Study:
- To examine molecular pathways contributing to genomic instability in Ph+ CML.
- To identify potential therapeutic targets within these pathways for advanced CML treatment.
Main Methods:
- Review of molecular pathways implicated in genomic instability in CML.
- Analysis of genetic and cytogenetic abnormalities as markers of disease progression.
- Exploration of DNA damage and repair response mechanisms in CML.
Main Results:
- Identified molecular pathways associated with genomic instability in Ph+ CML.
- Highlighted the role of compromised DNA repair in disease advancement and treatment resistance.
- Established a link between genetic alterations and blastic transformation.
Conclusions:
- Genomic instability is a key factor in advanced Ph+ CML and therapy resistance.
- Molecular pathways driving genomic instability represent promising targets for novel CML therapies.
- Targeting DNA damage and repair mechanisms could overcome treatment resistance in CML.
Related Concept Videos
02:57Targeted Cancer Therapies
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.
There are several types of targeted therapies against specific...
There are several types of targeted therapies against specific...
02:50Combination Therapies and Personalized Medicine
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.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
01:15Differentiation of Common Myeloid Progenitor Cells
Common myeloid progenitors (CMPs) are oligopotent cells that can differentiate into granulocytes and macrophages. Granulocytes and macrophages are essential for protecting the body against bacterial, viral, or fungal infections. They migrate from the bone marrow into the circulating blood to reach specific tissue sites where they differentiate and help in immune surveillance. However, they survive only for a few days and must be continuously made available to the organism to maintain a robust...
02:56Treatment Resistant Cancers
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...
01:11Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
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...
02:40Cancer Stem Cells and Tumor Maintenance
Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...