Basic Science and Molecular Genetics of Prostate Cancer Aggressiveness - 29/06/21
Doi : 10.1016/j.ucl.2021.04.004
Matthew J. Schiewer, PhD a, b, ⁎ 
, Karen E. Knudsen, MBA, PhD c, d, e, f
, Karen E. Knudsen, MBA, PhD c, d, e, f a Department of Urology, Urology Research Laboratory, Thomas Jefferson University, Sidney Kimmel Cancer Center, 233 South 10th Street BLSB 804, Philadelphia, PA 19107, USA
b Department of Cancer Biology, Urology Research Laboratory, Thomas Jefferson University, Sidney Kimmel Cancer Center, 233 South 10th Street BLSB 804, Philadelphia, PA 19107, USA
c Department of Cancer Biology, Thomas Jefferson University, 233 South 10th Street BLSB 1050, Philadelphia, PA 19107, USA
d Department of Urology, Thomas Jefferson University, 233 South 10th Street BLSB 1050, Philadelphia, PA 19107, USA
e Department of Medical Oncology, Thomas Jefferson University, 233 South 10th Street BLSB 1050, Philadelphia, PA 19107, USA
f Department of Radiation Oncology, Thomas Jefferson University, 233 South 10th Street BLSB 1050, Philadelphia, PA 19107, USA
∗Corresponding author. 233 South 10th Street BLSB 804, Philadelphia, PA 19107.233 South 10th Street BLSB 804PhiladelphiaPA19107
Résumé |
Androgen receptor function, tumor cell plasticity, loss of tumor suppressors, and defects in DNA repair genes affect aggressive features of prostate cancer. Prostate cancer development, progression, and aggressive behavior are often attributable to function of the androgen receptor. Tumor cell plasticity, neuroendocrine features, and loss of tumor suppressors lend aggressive behavior to prostate cancer cells. DNA repair defects have ramifications for prostate cancer cell behavior.
Le texte complet de cet article est disponible en PDF.Keywords : Prostate cancer, Androgen receptor, Cellular plasticity, NEPC, DNA repair
Plan
© 2021
Elsevier Inc. Tous droits réservés.
Vol 48 - N° 3
P. 339-347 - août 2021 Retour au numéro
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