Abstract
It is proposed here that malignancies of the central nervous system (CNS) are capable of recruiting non-malignant CNS precursor cells and that doing so worsens the course of the disease. In particular, the argument is put forward that such tumors can activate resident neural stem cells, attract them or their progeny to the tumor site, and induce them to proliferate. What begins as a normal wound repair response by the recruited cells can eventually result in augmentation of the tumor. In support of this hypothesis, evidence consistent with the ideas proposed is presented. Since these recruited cells are non-malignant, it should be possible to interfere with this process. This would not necessarily remove the threat posed by the cancer, but could beneficially impact patients by slowing progression. Interfering with recruitment could simultaneously serve to block autocrine stimulation by tumor cells. In contrast, introducing exogenous stem cells could exacerbate the recruitment process unless measures are taken to preclude this possibility. Finally, it is worth noting that the situation described in the current hypothesis might apply to a variety of other stem and precursor cell-containing systems throughout the body.
Keywords: Cancer, stem cells, brain tumors, astrocytoma, retinoblastoma, growth factors, neural precursor cells, wound repair, cellular migration, tropism
Current Stem Cell Research & Therapy
Title: Recruitment of Endogenous Neural Progenitor Cells by Malignant Neoplasms of the Central Nervous System
Volume: 2 Issue: 2
Author(s): Henry Klassen
Affiliation:
Keywords: Cancer, stem cells, brain tumors, astrocytoma, retinoblastoma, growth factors, neural precursor cells, wound repair, cellular migration, tropism
Abstract: It is proposed here that malignancies of the central nervous system (CNS) are capable of recruiting non-malignant CNS precursor cells and that doing so worsens the course of the disease. In particular, the argument is put forward that such tumors can activate resident neural stem cells, attract them or their progeny to the tumor site, and induce them to proliferate. What begins as a normal wound repair response by the recruited cells can eventually result in augmentation of the tumor. In support of this hypothesis, evidence consistent with the ideas proposed is presented. Since these recruited cells are non-malignant, it should be possible to interfere with this process. This would not necessarily remove the threat posed by the cancer, but could beneficially impact patients by slowing progression. Interfering with recruitment could simultaneously serve to block autocrine stimulation by tumor cells. In contrast, introducing exogenous stem cells could exacerbate the recruitment process unless measures are taken to preclude this possibility. Finally, it is worth noting that the situation described in the current hypothesis might apply to a variety of other stem and precursor cell-containing systems throughout the body.
Export Options
About this article
Cite this article as:
Klassen Henry, Recruitment of Endogenous Neural Progenitor Cells by Malignant Neoplasms of the Central Nervous System, Current Stem Cell Research & Therapy 2007; 2 (2) . https://dx.doi.org/10.2174/157488807780599257
DOI https://dx.doi.org/10.2174/157488807780599257 |
Print ISSN 1574-888X |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-3946 |
![](/images/wayfinder.jpg)
- Author Guidelines
- Bentham Author Support Services (BASS)
- 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
- Announcements
Related Articles
-
Oncolytic Viruses: Programmable Tumour Hunters
Current Gene Therapy Current Targets for Anticancer Drug Discovery
Current Drug Targets RNA Interference (RNAi) Patents and Human Health Related Applications of RNAi
Recent Patents on DNA & Gene Sequences Histone Deacetylase Inhibitors: Molecular and Biological Activity as a Premise to Clinical Application
Current Drug Metabolism Drug Transporters and Multiple Drug Resistance in the Most Common Pediatric Solid Tumors
Current Drug Metabolism Silimarin and Cancer
Anti-Cancer Agents in Medicinal Chemistry A Closer Look at Protein Transduction Domains as a Tool in Drug Delivery
Current Nanoscience Pathogenesis and Treatment of Secondary Hyperparathyroidism in Dialysis Patients: The Role of Paricalcitol
Current Vascular Pharmacology Instructions from the Vascular System - Directing Neural Stem Cell Fate in Health and Disease
Current Medicinal Chemistry Stress Hormone-Mediated DNA Damage Response -- Implications for Cellular Senescence and Tumour Progression
Current Drug Targets IP6 & Inositol in Cancer Prevention and Therapy
Current Cancer Therapy Reviews New Insights Into the Molecular Mechanisms of Action of Bisphosphonates
Current Pharmaceutical Design Gene Delivery for Cancer Therapy
Current Drug Delivery Novel Therapeutic Strategies for Dementia
CNS & Neurological Disorders - Drug Targets Bone Morphogenetic Proteins and its Receptors; Therapeutic Targets in Cancer Progression and Bone Metastasis?
Current Pharmaceutical Design TGF-β1 Signalling, Connecting Aberrant Inflammation and Colorectal Tumorigenesis
Current Pharmaceutical Design Biochemical Mechanisms of Cisplatin Cytotoxicity
Anti-Cancer Agents in Medicinal Chemistry Modulation of Cellular Function by TAT Mediated Transduction of Full Length Proteins
Current Protein & Peptide Science Pharmacological Modulation of p53 Function in Cancer Therapy
Current Signal Transduction Therapy Adrenoceptors: Non Conventional Target for Breast Cancer?
Current Medicinal Chemistry