http://repub.eur.nl/res/aut/29227/ List of Publications en http://repub.eur.nl/static-eur/img/logo.png http://repub.eur.nl http://repub.eur.nl/res/pub/23788/ 1994-06-22T00:00:00Z Normal cells grow, divide, communicate, and differentiate in a coordinated fashion. These highly complex processes are regulated by the programmed expression of different genes. It is generally assumed that tumor formation originates from alterations in genes involved in the control of cell proliferation. To get more insight in the process of tumorigenesis, many studies have focused on the detection of such altered genes followed by the elucidation of the function of the genes involved. Because chromosomal aberrations occur frequently in human cancer, they were suspected to form the basis of the alterations in the genes. Therefore, the earliest studies aimed at the identification of chromosomal breakpoints, were based on known cytogenetic aberrations, such as translocations. In this way, a considerable number of genes has been detected in which structural aberrations occur. The ultimate purpose of these studies was to elucidate the function of the proteins encoded by the altered genes, their role in tumorigenesis and the potentiality to be used as targets for specific tumor-therapy. Aberrant genes and proteins are also highly important from a diagnostic point of view, since they are only expressed in tumor cells. Therefore, the malignant cells distinguish themselves from normal cells by the presence of these particular, tumor-specific genes. As a consequence, aberrant proteins encoded by these genes are also tumor-specific and as such excellent phenotypic tumormarkers, called tumor-specific proteins (TSPs).