[Molecular mechanisms of oncogenic transformation: what’s new?]

Blanchard, J. M.

Bull Cancer

2002-01 / vol 89 / pages 9-16


During the past two years, new molecular targets have been discovered which link cell cycle, cell proliferation and cellular growth. It has become more and more evident that whereas gain-of-function mutations in specific genes can lead to cancer, genomic instability plays also an important role in tumour progression. With examples taken from the recent literature, we describe in this short review crucial findings on the molecular mechanisms controlling cell cycle and proliferation. We illustrate how specific combinations of proto-oncogenes alterations can result in tissue-specific tumours. Finally, impairment of the interactions of a cancer cell with its surrounding neighbours is also shown to participate in the progression toward aggressive phenotypes.

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Humans; Animals; Mice; Neoplasm Metastasis; Rats; Cell Cycle/*physiology; Disease Progression; Cell Division/physiology; Cyclin-Dependent Kinase Inhibitor p21; *CDC2-CDC28 Kinases; Antineoplastic Agents, Phytogenic/metabolism; Cell Transformation, Neoplastic/genetics/pathology; Cyclin D1/physiology; Cyclin E/physiology; Cyclin-Dependent Kinase 2; Cyclin-Dependent Kinase Inhibitor p16/physiology; Cyclin-Dependent Kinases/physiology; Cyclins/metabolism; Drug Resistance; Fusion Proteins, bcr-abl/physiology; Mutation/*physiology; Neoplasm Proteins/physiology; Neoplasms/*genetics/*pathology; Neovascularization, Pathologic/physiopathology; Neural Cell Adhesion Molecules/physiology; Paclitaxel/metabolism; Protein-Serine-Threonine Kinases/physiology; Radiation Tolerance; Thrombospondins/physiology; Transforming Growth Factor beta/physiology; Tuberous Sclerosis/genetics/pathology

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