Vol. 44 (1): 8-13, January – February, 2018
doi: 10.1590/S1677-5538.IBJU.2018.0004
DIFFERENCE OF OPINION
Marcelo Langer Wroclawski 1, 2, Flavio Lobo Heldwein 3, 4
1 Hospital Israelita Albert Einstein, São Paulo, SP, Brasil; 2 Faculdade de Medicina do ABC, Santo André, SP, Brasil; 3 Universidade do Sul de Santa Catarina, SC, Brasil; 4 Universidade Federal de Santa Catarina, SC, Brasil
Prostate cancer (PCa) is a heterogeneous disease. After almost a decade of contradictory screening recommendations made by expert and advisory panels (1), prostate cancer has risen again as the second leading cause of cancer death in American males (2).
PCa is androgen dependent. Research on biological effects of testosterone and its relationship with PCa awarded Butenandt with the Nobel Prize in Chemistry in 1939, and Huggins with The Nobel Prize in Physiology or Medicine in 1966 (3, 4). In 1941, Huggins and Hodges observed that castration could cause a decrease of PCa serum marker activity and that administration of exogenous testosterone propionate resulted in its increase. Indeed, different research groups repeatedly showed that PCa culture cells are stimulated by administration of testosterone and that deprivation induces apoptosis (5, 6). These traditional assumptions are the base of metastatic PCa treatment until nowadays.
