Abstract
Bone marrow (BM) suppression is an important dose-limiting side effect of chemotherapy and radiotherapy for cancer. Although acute myelosuppression is an immediate concern for patients undergoing cancer therapy, its management has been improved significantly in recent years by the use of various hematopoietic growth factors. However, many patients receiving chemotherapy and/or ionizing radiation (IR) also develop residual (or long-term) BM injury (a sustained decrease in HSC reserves due to an impairment in HSC self-renewal) after the recovery from acute myelosuppression. Unlike acute myelosuppression, residual BM injury is latent and long lasting and shows little tendency for recovery. Following additional hematopoietic stress such as subsequent cycles of consolidation cancer treatment or autologous BM transplantation, residual BM injury can deteriorate to become a hypoplastic or myelodysplastic syndrome. This article review some of the new developments in elucidating the cellular and molecular mechanisms whereby chemotherapy and radiotherapy cause residual BM injury. Particularly, we discuss the role of induction of hematopoietic stem cell (HSC) senescence via the p53-p21Cip1/Waf1 and/or p16Ink4a-RB pathways in the induction of the injury and the therapeutic potential of molecularly targeting these pathways for amelioration of chemotherapy- and radiotherapy-induced long-term BM toxicity.
Keywords: Ionizing radiation, chemotherapy, myelosuppression, hematopoietic stem cells, senescence
Current Cancer Therapy Reviews
Title: Cancer Therapy-Induced Residual Bone Marrow Injury: Mechanisms of Induction and Implication for Therapy
Volume: 2 Issue: 3
Author(s): Yong Wang, Virginia Probin and Daohong Zhou
Affiliation:
Keywords: Ionizing radiation, chemotherapy, myelosuppression, hematopoietic stem cells, senescence
Abstract: Bone marrow (BM) suppression is an important dose-limiting side effect of chemotherapy and radiotherapy for cancer. Although acute myelosuppression is an immediate concern for patients undergoing cancer therapy, its management has been improved significantly in recent years by the use of various hematopoietic growth factors. However, many patients receiving chemotherapy and/or ionizing radiation (IR) also develop residual (or long-term) BM injury (a sustained decrease in HSC reserves due to an impairment in HSC self-renewal) after the recovery from acute myelosuppression. Unlike acute myelosuppression, residual BM injury is latent and long lasting and shows little tendency for recovery. Following additional hematopoietic stress such as subsequent cycles of consolidation cancer treatment or autologous BM transplantation, residual BM injury can deteriorate to become a hypoplastic or myelodysplastic syndrome. This article review some of the new developments in elucidating the cellular and molecular mechanisms whereby chemotherapy and radiotherapy cause residual BM injury. Particularly, we discuss the role of induction of hematopoietic stem cell (HSC) senescence via the p53-p21Cip1/Waf1 and/or p16Ink4a-RB pathways in the induction of the injury and the therapeutic potential of molecularly targeting these pathways for amelioration of chemotherapy- and radiotherapy-induced long-term BM toxicity.
Export Options
About this article
Cite this article as:
Wang Yong, Probin Virginia and Zhou Daohong, Cancer Therapy-Induced Residual Bone Marrow Injury: Mechanisms of Induction and Implication for Therapy, Current Cancer Therapy Reviews 2006; 2 (3) . https://dx.doi.org/10.2174/157339406777934717
DOI https://dx.doi.org/10.2174/157339406777934717 |
Print ISSN 1573-3947 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6301 |
Call for Papers in Thematic Issues
Current progress in Protein Degradation and Cancer Therapy
argeted Protein Degradation is gaining momentum in cancer therapy, it facilitate targeting undruggable proteins, it overcome cancer resistance and avoid undesirable side effects. Thus small molecules degraders have emerged as novel therapeutic strategy. Targeted protein degradation (TPD), the process of eliminating a protein of interest hold a great promise for ...read more
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Meet Our Executive Editor
Current HIV Research Meet Our Editorial Board Member
Current Green Chemistry Thromboembolic Complications in Malignant Haematological Disorders
Current Vascular Pharmacology Withdrawal Notice: Design and Analysis of Optimization and Tuning in Data Warehouses Using Bitmap Indexes
Recent Advances in Computer Science and Communications FOXM1-Dependent Transcriptional Regulation of EZH2 Induces Proliferation and Progression in Prostate Cancer
Anti-Cancer Agents in Medicinal Chemistry STAT3 as a Therapeutic Target for Glioblastoma
Anti-Cancer Agents in Medicinal Chemistry Creating A Standard of Care for Fertility Preservation
Current Women`s Health Reviews Modulation of Nitric Oxide Pathway by Multiligands/RAGE Axis: A Crossing Point on the Road to Microvascular Complication in Diabetes
Current Enzyme Inhibition Treatment and Response to Statins: Gender-related Differences
Current Medicinal Chemistry Genome and Transcriptome Analysis of Neuroblastoma Advanced Diagnosis from Innovative Therapies
Current Pharmaceutical Design Crude Methanol Extract of Rosin Gum Exhibits Specific Cytotoxicity against Human Breast Cancer Cells via Apoptosis Induction
Anti-Cancer Agents in Medicinal Chemistry Anticancer Antifolates: Current Status and Future Directions
Current Pharmaceutical Design Evidence for Anti-Cancer Properties of Blueberries: A Mini-Review
Anti-Cancer Agents in Medicinal Chemistry MiR-22-3p Regulates Amyloid β Deposit in Mice Model of Alzheimer's Disease by Targeting Mitogen-activated Protein Kinase 14
Current Neurovascular Research Squalene as Novel Food Factor
Current Pharmaceutical Biotechnology Calpain Inhibition: A Therapeutic Strategy Targeting Multiple Disease States
Current Pharmaceutical Design Radioiodinated Agents for Imaging Multidrug Resistant Tumors
Medicinal Chemistry Advances in Nanocarriers for Anticancer Drugs Delivery
Current Medicinal Chemistry Noninvasive Diagnosis of Chemotherapy Related Cardiotoxicity
Current Cardiology Reviews Development of a Radiolabeled Amlodipine Analog for L-type Calcium Channel Imaging
Current Radiopharmaceuticals