Results 61 to 70 of about 78,382 (206)

New developments in the treatment of metastatic melanoma – role of dabrafenib–trametinib combination therapy [PDF]

, 2014
Development of selective inhibitors of BRAF has improved the survival of patients with BRAF-mutant melanoma. The progression-free survival after treatment with a BRAF inhibitor is modest, however, and BRAF inhibitors induce cutaneous toxicity, likely due
Luke, Jason J, Ott, Patrick A
core   +1 more source

Eruptive Melanocytic Nevi in the Setting of Encorafenib, Cetuximab, and Binimetinib Combination Therapy: A Case Report

Case Reports in Dermatology
Introduction: The development of new and changing melanocytic lesions has been increasingly reported as an adverse dermatologic toxicity of BRAF inhibitor therapy.
Karen Lam, Gregory A. Gates, Daniel Q. Bach, Kyle Cheng   +3 more
doaj   +1 more source

Efficacy of dabrafenib/trametinib in pancreatic ductal adenocarcinoma with BRAF NVTAP deletion: A case report

Frontiers in Oncology, 2022
Studies have been actively conducted to identify actionable mutations and incorporate them into clinical practice in pancreatic ductal adenocarcinoma (PDAC), which is known to have a poor prognosis with traditional cytotoxic chemotherapy.
Ji Eun Shin, Ho Jung An, Hyung Soon Park, Hyunho Kim, Byoung Yong Shim   +4 more
doaj   +1 more source

FOXD3 Regulates VISTA Expression in Melanoma. [PDF]

, 2020
Immune checkpoint inhibitors have improved patient survival in melanoma, but the innate resistance of many patients necessitates the investigation of alternative immune targets.
Aplin, Andrew E., Berger, Adam C., Chervoneva,, Davies, Michael A., Erkes, Dan A., Fisher, David E., Gershenwald, Jeffrey E., Knecht, Meghan, Lo, Jennifer A., McCue, Peter A., Mollaee, Mehri, Purwin, Timothy J., Rosenbaum, Sheera R., Zhong, Zhijiu   +13 more
core   +1 more source

The Histone Deacetylase Inhibitor ITF2357 (Givinostat) Targets Oncogenic BRAF in Melanoma Cells and Promotes a Switch from Pro-Survival Autophagy to Apoptosis

Biomedicines, 2022
Histone deacetylase inhibitors (HDACI) are epigenetic compounds that have been widely considered very promising antitumor agents. Here, we focus on the effects of the pan-HDAC inhibitor ITF2357 (Givinostat) in comparison with SAHA (Vorinostat) in ...
Adriana Celesia, Antonietta Notaro, Marzia Franzò, Marianna Lauricella, Antonella D’Anneo, Daniela Carlisi, Michela Giuliano, Sonia Emanuele   +7 more
doaj   +1 more source

High-throughput identification of genotype-specific cancer vulnerabilities in mixtures of barcoded tumor cell lines. [PDF]

, 2016
Hundreds of genetically characterized cell lines are available for the discovery of genotype-specific cancer vulnerabilities. However, screening large numbers of compounds against large numbers of cell lines is currently impractical, and such experiments
A Basu, Alykhan F Shamji, Andrew Crenshaw, Andrew L Kung, Aristotle M Mannan, Aviad Tsherniak, Bang Wong, Barbara A Weir, Bradley R Taylor, C Ditchfield, Channing Yu, D Peck, E Comer, Griselda Metta Yvone, J Barretina, J Du, JM Korn, Joshua Z Gould, JP Koivunen, JT Lowe, Kenneth N Ross, KT Flaherty, LA Marcaurelle, Levi A Garraway, M Carmena, Melissa A Marton, MI Davis, Michael A Foley, Michelle A Palmer, MJ Garnett, MK Muellner, ML Sos, MW Karaman, NC Turner, OD Abaan, Pablo Tamayo, PD Andrews, SL Schreiber, SM Wilhelm, Stuart L Schreiber, SV Sharma, Todd R Golub, U McDermott, Wendy Winckler, XD Zhang, Yan-Ling Zhang   +45 more
core   +2 more sources

LSD1 inhibition attenuates targeted therapy-induced lineage plasticity in BRAF mutant colorectal cancer

Molecular Cancer
Background BRAF activating mutations occur in approximately 10% of metastatic colorectal cancer (CRCs) and are associated with worse prognosis in part due to an inferior response to standard chemotherapy.
Christopher A. Ladaika, Averi Chakraborty, Ashiq Masood, Galen Hostetter, Joo Mi Yi, Heather M. O’Hagan   +5 more
doaj   +1 more source

MEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAFV600E amplification whereas KRASG13D amplification promotes EMT-chemoresistance

Nature Communications, 2019
Colorectal cancer cells can acquire resistance to MEK inhibition due to BRAF or KRAS amplification. Here, the authors show that while MEK inhibitor withdrawal in BRAF mutant cells restores sensitivity to the inhibitor through the loss of BRAF ...
Matthew J. Sale, Kathryn Balmanno, Jayeta Saxena, Eiko Ozono, Katarzyna Wojdyla, Rebecca E. McIntyre, Rebecca Gilley, Anna Woroniuk, Karen D. Howarth, Gareth Hughes, Jonathan R. Dry, Mark J. Arends, Pilar Caro, David Oxley, Susan Ashton, David J. Adams, Julio Saez-Rodriguez, Paul D. Smith, Simon J. Cook   +18 more
doaj   +1 more source

IGFBP-3 inhibits Wnt signaling in metastatic melanoma cells. [PDF]

, 2016
In previous works, we have shown that insulin-like growth factor-binding protein-3 (IGFBP-3), a tissue and circulating protein able to bind to IGFs, decreases drastically in the blood serum of patients with diffuse metastatic melanoma.
Londei, Paola, Martella, M, Naspi, A, Panasiti, Vincenzo, Polinari, Dorina, Rosa Alba, R, Sancillo, L, Zingariello, M   +7 more
core   +1 more source

New developments in the treatment of metastatic melanoma – role of dabrafenib–trametinib combination therapy

Drug, Healthcare and Patient Safety, 2014
Jason J Luke, Patrick A Ott Melanoma Disease Center, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA Abstract: Development of selective inhibitors of BRAF has improved the survival of patients with BRAF-mutant melanoma.
Luke JJ, Ott PA
doaj