Derangement of growth and differentiation control in oncogenesis
- 2 January 2002
- Vol. 24 (1) , 83-90
- https://doi.org/10.1002/bies.10036
Abstract
Human neoplasms develop following the progressive accumulation of genetic and epigenetic alterations to oncogenes and tumor suppressor genes. These alterations confer a growth advantage to the cancer cell, leading to its clonal proliferation, invasion into surrounding tissues, and spread to distant organs. Genes that are altered in neoplasia affect three major biologic pathways that normally regulate cell growth and tissue homeostasis: the cell cycle, apoptosis, and differentiation. While each of these pathways can be defined by a unique set of molecular events, they are not biologically separate. Rather, they function more as an integrated molecular network, and perturbations in one pathway can have profound consequences on another. Insights into what distinguishes the regulation of growth and differentiation in a normal cell versus a cancer cell have led to the development of novel anticancer therapies. BioEssays 24:83–90, 2002. © 2002 John Wiley & Sons, Inc.Keywords
This publication has 50 references indexed in Scilit:
- A Mechanism of Intracellular Timing and its Cooperation with Extracellular Signals in Controlling Cell Proliferation and Differentiation, an Amended HypothesisJournal of Theoretical Biology, 2001
- Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or AmplificationScience, 2001
- 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 ChromosomeNew England Journal of Medicine, 2001
- The role of the Bcl-2 family in the regulation of outer mitochondrial membrane permeabilityCell Death & Differentiation, 2000
- Exit from G1 and S Phase of the Cell Cycle Is Regulated by Repressor Complexes Containing HDAC-Rb-hSWI/SNF and Rb-hSWI/SNFCell, 2000
- The Hallmarks of CancerCell, 2000
- Disruption of p53 in human cancer cells alters the responses to therapeutic agentsJournal of Clinical Investigation, 1999
- Centrosome Amplification and a Defective G2–M Cell Cycle Checkpoint Induce Genetic Instability in BRCA1 Exon 11 Isoform–Deficient CellsMolecular Cell, 1999
- Cip/Kip cyclin-dependent kinase inhibitors: brakes of the cell cycle engine during developmentBioEssays, 1999
- The multistep nature of cancerTrends in Genetics, 1993