Results 81 to 90 of about 198,722 (342)
Targeting p38α in cancer: challenges, opportunities, and emerging strategies
p38α normally regulates cellular stress responses and homeostasis and suppresses malignant transformation. In cancer, however, p38α is co‐opted to drive context‐dependent proliferation and dissemination. p38α also supports key functions in cells of the tumor microenvironment, including fibroblasts, myeloid cells, and T lymphocytes.
Angel R. Nebreda
wiley +1 more source
Recommendations for clinical and molecular identification of LS, surgical and endoscopic management of LS‐associated colorectal cancer and preventive measures for cancer were produced. The emphasis was on surgical and gastroenterological aspects of the cancer spectrum.
T. T. Seppälä +18 more
wiley +1 more source
KRAS and BRAF mutations in Iranian colorectal cancer patients: A systematic review and meta-analysis
Background: Mutations in the EGFR signaling pathway play an important role in the development of colorectal cancer (CRC). Mutations in these genes, like KRAS and BRAF, affect the treatment strategies and associated with poor prognosis and relative ...
Abolfazl Yari +4 more
doaj
Impact of depth of response on survival in patients treated with cobimetinib ± vemurafenib: pooled analysis of BRIM-2, BRIM-3, BRIM-7 and coBRIM. [PDF]
BackgroundThis pooled analysis investigated the prognostic value of depth of response in two cohorts of patients with BRAFV600-mutated metastatic melanoma treated with vemurafenib or cobimetinib plus vemurafenib.MethodsThe data were pooled from BRIM-2 ...
Ascierto, Paolo A +12 more
core +2 more sources
Mutant BRAF and MEK inhibitors regulate the tumor immune microenvironment via pyroptosis.
Combinations of BRAF inhibitors and MEK inhibitors (BRAFi + MEKi) are FDA-approved to treat BRAF V600E/K mutant melanoma. Efficacy of BRAFi + MEKi associates with cancer cell death and alterations in the tumor immune microenvironment; however, the links ...
Dan A Erkes +10 more
semanticscholar +1 more source
BACKGROUND BRAF/MEK inhibitor combinations are established treatments for BRAF V600-mutant melanoma based on demonstrated benefits on progression-free survival (PFS) and overall survival (OS). Here, we report an updated analysis of the COLUMBUS (COmbined
P. Ascierto +15 more
semanticscholar +1 more source
Aldehyde dehydrogenase 1A1 (ALDH1A1) is a cancer stem cell marker in several malignancies. We established a novel epithelial cell line from rectal adenocarcinoma with unique overexpression of this enzyme. Genetic attenuation of ALDH1A1 led to increased invasive capacity and metastatic potential, the inhibition of proliferation activity, and ultimately ...
Martina Poturnajova +25 more
wiley +1 more source
Concurrent MEK targeted therapy prevents MAPK pathway reactivation during BRAFV600E targeted inhibition in a novel syngeneic murine glioma model. [PDF]
Inhibitors of BRAFV600E kinase are currently under investigations in preclinical and clinical studies involving BRAFV600E glioma. Studies demonstrated clinical response to such individualized therapy in the majority of patients whereas in some patients ...
Berger, Mitchel S +12 more
core +1 more source
BET and BRAF inhibitors act synergistically against BRAF‐mutant melanoma [PDF]
AbstractDespite major advances in the treatment of metastatic melanoma, treatment failure is still inevitable in most cases. Manipulation of key epigenetic regulators, including inhibition of Bromodomain and extra‐terminal domain (BET) family members impairs cell proliferation in vitro and tumor growth in vivo in different cancers, including melanoma ...
Paoluzzi, Luca +7 more
openaire +2 more sources
Background Previous analysis of COMBI-d (NCT01584648) demonstrated improved progression-free survival (PFS) and overall survival (OS) with combination dabrafenib and trametinib versus dabrafenib monotherapy in BRAF V600E/K-mutant metastatic melanoma ...
G. Long +30 more
semanticscholar +1 more source

