Results 91 to 100 of about 26,835 (181)

Antitumor activity of the ERK inhibitor SCH772984 [corrected] against BRAF mutant, NRAS mutant and wild-type melanoma. [PDF]

open access: yes, 2014
BackgroundIn melanoma, dysregulation of the MAPK pathway, usually via BRAF(V600) or NRAS(Q61) somatic mutations, leads to constitutive ERK signaling.
Atefi, Mohammad S   +13 more
core   +1 more source

A phase I pharmacokinetic and pharmacodynamic study of the oral mitogen-activated protein kinase kinase (MEK) inhibitor, WX-554, in patients with advanced solid tumours [PDF]

open access: yes, 2016
Purpose: We performed a multi-centre phase I study to assess the safety, pharmacokinetics (PK) and pharmacodynamics (PD) of the orally available small molecule mitogen-activated protein kinase kinase (MEK) 1/2 inhibitor, WX-554, and to determine the ...
Allen, Rodger   +21 more
core   +2 more sources

Covariate Adjustment in Basket Trials Borrowing Information Across Subgroups

open access: yesStatistics in Medicine, Volume 45, Issue 6-7, March 2026.
ABSTRACT Basket trials are an efficient approach to simultaneously evaluate a single therapy across multiple diseases where patients share a common molecular target. Bayesian hierarchical models (BHMs) are widely used to estimate the treatment effects while accounting for heterogeneity between patient subgroups within a basket trial.
Jiyang Ren   +2 more
wiley   +1 more source

Tumor cell sensitivity to vemurafenib can be predicted from protein expression in a BRAF-V600E basket trial setting

open access: yesBMC Cancer, 2019
Background Genetics-based basket trials have emerged to test targeted therapeutics across multiple cancer types. However, while vemurafenib is FDA-approved for BRAF-V600E melanomas, the non-melanoma basket trial was unsuccessful, suggesting mutation ...
Molly J. Carroll   +3 more
doaj   +1 more source

Photoactivatable prodrugs of antimelanoma agent Vemurafenib [PDF]

open access: yes, 2015
In this study, we report on novel photoactivatable caged prodrugs of vemurafenib. This kinase inhibitor was the first approved drug for the personalized treatment of BRAF-mutated melanoma and showed impressive results in clinical studies.
Bollag G.   +39 more
core   +3 more sources

Vemurafenib: a new treatment for BRAF-V600 mutated advanced melanoma

open access: yesCancer Management and Research, 2012
Rosalie Fisher, James LarkinDepartment of Medical Oncology, Royal Marsden Hospital, London, United KingdomAbstract: The BRAF inhibitor, vemurafenib, has demonstrated improved progression-free and overall survival compared with chemotherapy in a ...
Fisher R, Larkin J
doaj  

The role of BRAF V600 mutation in melanoma

open access: yesJournal of Translational Medicine, 2012
BRAF is a serine/threonine protein kinase activating the MAP kinase/ERK-signaling pathway. About 50 % of melanomas harbors activating BRAF mutations (over 90 % V600E). BRAFV600E has been implicated in different mechanisms underlying melanomagenesis, most
Ascierto Paolo A   +9 more
doaj   +1 more source

Stromal cell effects on melanoma cell drug response [PDF]

open access: yes, 2013
Thesis (M.A.)--Boston UniversityObjective: Melanoma is currently one of the deadliest forms of skin disease in the United States. However in the past decade there have been significant advances in treatment.
Della Penna, Greg
core   +1 more source

Recombinant methioninase (rMETase) is an effective therapeutic for BRAF-V600E-negative as well as -positive melanoma in patient-derived orthotopic xenograft (PDOX) mouse models. [PDF]

open access: yes, 2017
Melanoma is a recalcitrant disease. Melanoma patients with the BRAF-V600E mutation have been treated with the drug vemurafenib (VEM) which targets this mutation.
Chmielowski, Bartosz   +16 more
core   +1 more source

Drug-tolerant persister cancer cells are vulnerable to GPX4 inhibition. [PDF]

open access: yes, 2017
Acquired drug resistance prevents cancer therapies from achieving stable and complete responses. Emerging evidence implicates a key role for non-mutational drug resistance mechanisms underlying the survival of residual cancer 'persister' cells.
Berens, Michael E   +11 more
core   +1 more source

Home - About - Disclaimer - Privacy