Premium
Do we understand the genetic mechanisms of oncogenesis? Keynote address for honey harbor meeting on cellular and molecular biology of neoplasia, October 2–6, 1983
Author(s) -
Temin Howard M.
Publication year - 1984
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041210403
Subject(s) - carcinogenesis , retrovirus , biology , gene , genetics , transfection , organism , mutation , cancer , cell , computational biology , cancer research
Different experiments with viruses and transfection now support the classical view that cancer is the result of a multistep process. This analysis further indicates that some of these steps involve mutations affecting the qualitative and quantitative expression of dominant transforming genes or oncogenes. These mutations are spontaneous or induced and of various kinds, including base pair changes, deletions, translocations, and amplifications. The actions of the active transforming genes or oncogenes lead to the properties of the tumor cell. However, these activities are effective only in the appropriate cell with targets for the products of the oncogenes and without inhibitors. Because there will be multiple genetic changes in tumor cells, it is difficult to determine which changes are significant for the oncogenesis. Retrovirus vectors may be useful in this determination. In addition, our present methods of analysis may be missing certain of the multiple steps in oncogenesis, in particular, those involved with tissue-, organ-, and organism-specific controls.