title: [Better understanding of the biology of cancer cells].
abstract: Most forms of cancer arise through a Darwinian evolutionary process. The natural selection that ultimately leads to cancer takes place in somatic tissues although it may be triggered by inherited mutations in a small but significant minority. It favors the growth of clones and subclones that are less and less responsive to normal intra- and extracellular growth control mechanisms. The development of molecular biology has led to the identification of many genes that participate in this somatic evolution. They belong to the following groups: Oncogenes, constitutively activated by structural and/or regulatory changes that drive the cell to continuous proliferation; Tumor suppressor genes, that can inhibit the illegitimately activated cell cycle. They contribute to tumor development by loss mutations or permanent down-regulation, e.g. by methylation; Apoptosis inhibitory genes that can contribute to tumor development by raising the apoptotic threshold, and apoptosis promoting genes that can favor the growth of apoptosis prone tumor cells by their loss or inactivation; DNA repair genes whose inactivation can counteract the normal elimination of cells that carry potentially cancer promoting mutations. Inherited mutations in DNA repair genes can lead to familial cancer syndromes. Immortalizing genes that counteract cellular senescence; Angiogenesis promoting genes whose products may stimulate the vascular supply of tumors; Genes whose structural or functional changes may facilitate the escape of tumor cells from immune rejection; The multi-step development of individual tumors can encompass changes in most or all of these genes. They occur independently of each other and without any fixed order or timing. Tumor emancipation from growth control can therefore proceed along various pathways. It follows that each tumor must be regarded as a biologically unique individual.
authors.affiliation: Mikrobiologiskt och tumörbiologiskt centrum, Karolinska institutet, Stockholm.
authors.forename: G
authors.initials: G
authors.lastname: Klein
mesh_terms: D017209:Apoptosis / Q000502:physiology; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000276:immunology / Q000473:pathology; D002872:Chromosome Deletion; D003131:Combined Modality Therapy; D004260:DNA Repair; D004273:DNA, Neoplasm / Q000235:genetics; D016147:Genes, Tumor Suppressor / Q000502:physiology*; D015316:Genetic Therapy; D006801:Humans; D009369:Neoplasms / Q000098:blood supply / Q000235:genetics / Q000276:immunology / Q000473:pathology*; D009857:Oncogenes / Q000502:physiology*; D014178:Translocation, Genetic
chemical_list: D004273:DNA, Neoplasm