作者: Daniel Satgé
DOI: 10.1002/9780470015902.A0024465
关键词:
摘要: According to the somatic mutation theory (SMT) of cancer, mutations observed in cancerous tissues directly cause malignancy. However, a close look at experimental data and observations about human diseases show many discrepancies with theory, including lack specificity so-called ‘cancer genes’ that are mutated noncancerous tissues, not cancers; rarity malignancies some genetic conditions deoxyribonucleic acid repair anomalies high number initial early carcinogenesis. Above all, abnormal proliferations altered tissue architecture before specific detected strongly support idea correlation between carcinogenesis modifications is more complex probably less determining than has been theorised by SMT. Other theories take into account microenvironment, such as organisation field promising paths towards an understanding oncogenesis. Key Concepts: Initial found cancer much frequently expected from random event. Proliferative architectural organs occur. Mutations present tissues. Mutations all cells cancer/tumour. Tissues maintain their respective phenotypes despite mutations. Some DNA deficiency have no increased risk others appear be protected against particular types. Cancers can induced transplanting normal unusual environment for tissue. Cancer reverted when implanted microenvironment this type cells. Keywords: somatic mutation; mutation rate; carcinogenesis; somatic theory; tissue theory; oncogene; tumour suppressor gene; Down syndrome; microenvironment