Results 111 to 120 of about 5,711,116 (385)

The anticancer effect of the HDAC inhibitor belinostat is enhanced by inhibitors of Bcl‐xL or Mcl‐1 in ovarian cancer

Molecular Oncology, EarlyView.
The pan‐HDAC inhibitor belinostat increases the expression of the pro‐apoptotic proteins Bim, Puma, and Noxa and induces apoptosis in ovarian cancer cell lines and patient‐derived tumor organoids when used at high concentrations. Moreover, inhibiting the anti‐apoptotic proteins Bcl‐xL or Mcl‐1 sensitizes these preclinical models to the cytotoxic effect
Cécilia Thomine, Sterenn Guillemot, Louis‐Bastien Weiswald, Romane Florent, Edwige Abeilard, Florence Giffard, Emilie Brotin, Mélanie Briand, Enora Dolivet, Laurent Poulain, Marie Villedieu   +10 more
wiley   +1 more source

Circulating tumor DNA monitoring and blood tumor mutational burden in patients with metastatic solid tumors treated with atezolizumab

Molecular Oncology, EarlyView.
In patients treated with atezolizumab as a part of the MyPathway (NCT02091141) trial, pre‐treatment ctDNA tumor fraction at high levels was associated with poor outcomes (radiographic response, progression‐free survival, and overall survival) but better sensitivity for blood tumor mutational burden (bTMB).
Charles Swanton, Russell W. Madison, Candice Francheska B. Tambaoan, Funda Meric‐Bernstam, Christopher J. Sweeney, Razelle Kurzrock, Howard A. Burris III, David R. Spigel, Hanna Tukachinsky, Jason Hughes, Julia Malato, Bongin Yoo, Tania Szado, Cheryl Schwab, Lincoln W. Pasquina, Amaya Gasco, Katja Schulze, Claire F. Friedman   +17 more
wiley   +1 more source

Cholesterol and the risk of grade-specific prostate cancer incidence: evidence from two large prospective cohort studies with up to 37 years' follow up [PDF]

, 2012
<b>Background</b> High cholesterol may be a modifiable risk factor for prostate cancer but results have been inconsistent and subject to potential "reverse causality" where undetected disease modifies cholesterol prior to diagnosis.<p ...
A Jemal, AG Renehan, AM Mondul, AM Mondul, Carole Hart, CL Hart, CL Hart, DA Lawlor, David S Morrison, DM Boudreau, DR Browning, E Giovannucci, EA Platz, EA Platz, EL Korn, F Bravi, F Bray, G Davey Smith, G Davey Smith, GD Batty, General Register Office, Hing Leung, HM Van, HY Oh, J Green, JD Kark, JD Neaton, Kashif Shafique, Khaver Qureshi, KM Dale, L Zhuang, L Zuccolo, LE Johns, LJ Schouten, MH Hager, MJ Resnick, ML Turley, MM Thompson, MR Freeman, National Heart, Lung and Blood Institute, P Knekt, PD Baade, Philip McLoone, RA Hiatt, RM White, TE Strandberg, VM Hawthorne, WA Sakr, Y Ben-Shlomo   +48 more
core   +2 more sources

Screening for Prostate Cancer: US Preventive Services Task Force Recommendation Statement

Journal of the American Medical Association (JAMA), 2018
Importance In the United States, the lifetime risk of being diagnosed with prostate cancer is approximately 13%, and the lifetime risk of dying of prostate cancer is 2.5%. The median age of death from prostate cancer is 80 years.
D. Grossman, S. Curry, D. Owens, Kirsten Bibbins-Domingo, A. Caughey, K. Davidson, Chyke A Doubeni, M. Ebell, J. Epling, A. Kemper, A. Krist, Martha Y. Kubik, C. Landefeld, C. Mangione, Michael Silverstein, M. Simon, A. Siu, Chien-Wen Tseng   +17 more
semanticscholar   +1 more source

The subcellular distribution of phosphorylated Y‐box‐binding protein‐1 at S102 in colorectal cancer patients, stratified by KRAS mutational status and clinicopathological features

Molecular Oncology, EarlyView.
This study identifies nuclear YB‐1 S102 phosphorylation as a marker associated with KRAS and FBXW7 mutations in colorectal cancer. Mutated KRAS correlates specifically with nuclear, not cytoplasmic, S102 YB‐1. These findings provide the first ex vivo evidence of this link in CRC and suggest future studies should assess the prognostic and therapeutic ...
Konstanze Lettau, Stephan Forchhammer, Birgit Fehrenbacher, Lejla Mahmutovic, Marcus Scharpf, Gunnar Blumenstock, Martin Schaller, Irina Bonzheim, Shayan Khozooei, Mahmoud Toulany   +9 more
wiley   +1 more source

AZGP1 Protein Expression in Hormone-Naïve Advanced Prostate Cancer Treated with Primary Androgen Deprivation Therapy

Diagnostics, 2020
Biomarkers for predicting the risk of castration-resistant prostate cancer (CRPC) in men treated with primary androgen deprivation therapy (ADT) are lacking.
Mads Dochedahl Winther, Gitte Kristensen, Hein Vincent Stroomberg, Kasper Drimer Berg, Birgitte Grønkær Toft, James D. Brooks, Klaus Brasso, Martin Andreas Røder   +7 more
doaj   +1 more source

AR-V7 and resistance to enzalutamide and abiraterone in prostate cancer.

New England Journal of Medicine, 2014
BACKGROUND The androgen-receptor isoform encoded by splice variant 7 lacks the ligand-binding domain, which is the target of enzalutamide and abiraterone, but remains constitutively active as a transcription factor.
E. Antonarakis, Changxue Lu, Hao Wang, Brandon S. Luber, M. Nakazawa, J. Roeser, Yan Chen, Tabrez A Mohammad, Yidong Chen, Helen L. Fedor, T. Lotan, Qizhi Zheng, A. D. De Marzo, J. Isaacs, W. Isaacs, R. Nadal, C. Paller, S. Denmeade, M. Carducci, M. Eisenberger, Jun Luo   +20 more
semanticscholar   +1 more source

BMP antagonist CHRDL2 enhances the cancer stem‐cell phenotype and increases chemotherapy resistance in colorectal cancer

Molecular Oncology, EarlyView.
Overexpression of CHRDL2 in colon cancer cells makes them more stem‐like and resistant to chemo‐ and radiotherapy. CHRDL2‐high cells have upregulation of the WNT pathway, genes involved in the DNA damage response (DDR) pathway and epithelial‐to‐mesenchymal transition (EMT). This leads to quicker repair of damaged DNA and more cell migration.
Eloise Clarkson, Annabelle Lewis
wiley   +1 more source

Sexual well-being and diurnal cortisol after prostate cancer treatment. [PDF]

, 2020
Sexual dysfunction and psychological distress are common after prostate cancer. Research has not examined the role of neuroendocrine markers of stress (e.g. cortisol).
Gaffey, Allison E, Hoyt, Michael A, Lawsin, Catalina J, Litwin, Mark S, Wang, Ashley W   +4 more
core  

Divergent clonal evolution of castration resistant neuroendocrine prostate cancer

Nature Network Boston, 2016
An increasingly recognized resistance mechanism to androgen receptor (AR)-directed therapy in prostate cancer involves epithelial plasticity, in which tumor cells demonstrate low to absent AR expression and often have neuroendocrine features.
H. Beltran, D. Prandi, J. Mosquera, M. Benelli, L. Puca, J. Cyrta, C. Marotz, Eugenia G. Giannopoulou, B. V. Chakravarthi, S. Varambally, S. Tomlins, D. Nanus, S. Tagawa, E. V. Van Allen, O. Elemento, A. Sboner, L. Garraway, M. Rubin, F. Demichelis   +18 more
semanticscholar   +1 more source