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
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
BRAF Mutation Heterogeneity in Melanoma Lesions
is missing (Short communication)
Kaori Sakaizawa +3 more
doaj +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
Antitumor activity of the ERK inhibitor SCH772984 [corrected] against BRAF mutant, NRAS mutant and wild-type melanoma. [PDF]
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
CO175 OCTOPUS: Ambispective Observational Study Describing Diagnosis and Treatment Patterns in Adults with Metastatic NSCLC with BRAF V600E Mutation in Clinical Practice, to Assess Treatment Effectiveness and Quality of Life (TIP) [PDF]
David Planchard +9 more
openalex +1 more source
Response to BRAF/MEK Inhibition in A598_T599insV BRAF Mutated Melanoma [PDF]
Approximately 50% of patients with metastatic melanoma harbor an activating BRAF mutation. Tumors with activating mutation <i>BRAF</i> gene proliferate excessively and can be treated with targeted BRAF-inhibitors in combination with MEK inhibitors. The most common BRAF mutation occurs at amino acid position 600. Other <i>BRAF</i>
Sara Bjursten +7 more
openaire +3 more sources
Overview of molecular signatures of senescence and associated resources: pros and cons
Cells can enter a stress response state termed cellular senescence that is involved in various diseases and aging. Detecting these cells is challenging due to the lack of universal biomarkers. This review presents the current state of senescence identification, from biomarkers to molecular signatures, compares tools and approaches, and highlights ...
Orestis A. Ntintas +6 more
wiley +1 more source
The miR-139-5p regulates proliferation of supratentorial paediatric low-grade gliomas by targeting the PI3K/AKT/mTORC1 signalling [PDF]
Paediatric low-grade gliomas (pLGGs) are a heterogeneous group of brain tumours associated with a high overall survival: however, they are prone to recur and supratentorial lesions are difficult to resect, being associated with high percentage of disease
Antonelli, Manila +19 more
core +1 more source
Combined BRAF and MEK Inhibition versus BRAF Inhibition Alone in Melanoma [PDF]
Combined BRAF and MEK inhibition, as compared with BRAF inhibition alone, delays the emergence of resistance and reduces toxic effects in patients who have melanoma with BRAF V600E or V600K mutations.In this phase 3 trial, we randomly assigned 423 previously untreated patients who had unresectable stage IIIC or stage IV melanoma with a BRAF V600E or ...
G. V. Long +34 more
openaire +3 more sources

