A mechanism for androgen receptor-mediated prostate cancer recurrence after androgen deprivation therapy.

By C. Gregory, B. He, Raymond T. Johnson, O. H. Ford, J. Mohler, F. S. French, E. M. Wilson. Cancer Research, 2001

653 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/7d6ed36b4eb26204d8884077f7f226797649985d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Michael Stanbrough
G. Bubley
Carolyn L. Smith
K. Ross
J. Mohler
Todd R. Golub
S. Balk
B. O’Malley

Citations in the corpus

The Androgen Axis in Recurrent Prostate Cancer (2004, background): “Increased expression of androgen receptor coactivators TIF2 and SRC1 in recurrent prostate cancer increased androgen receptor transactivation in response to weaker androgens such as androstenedione (52).”
Coregulator function: a key to understanding tissue specificity of selective receptor modulators. (2004, background): “Although it may be tempting to speculate, based on these studies, that alterations in corepressors are responsible for acquisition of abnormal hormone responses, prostate cancer recurrence after androgen deprivation therapy has been associated with increased expression of SRC-1 and TIF2 coactivators”
Gene expression analysis of human prostate carcinoma during hormonal therapy identifies androgen-responsive genes and mechanisms of therapy resistance. (2004, background): “This data and other published series 24–26 suggest that strong expression of the AR is present in most cases of AARPC and for many tumors the increase in AR transcript levels occurs by mechanisms other than gene amplification.”
Increased expression of genes converting adrenal androgens to testosterone in androgen-independent prostate cancer. (2006, background): “Further mechanisms that may stimulate AR transcriptional activity in androgen-independent prostate cancer include increased expression of transcriptional coactivator proteins and activation of signal transduction pathways that can enhance AR responses to low levels of circulating androgens, includin”
Androgens and cardiovascular disease. (2003, unknown): “creases cellular androgen sensitivity (59).”