Results 61 to 70 of about 239,426 (300)

A mathematical model quantifies proliferation and motility effects of TGF--$\beta$ on cancer cells [PDF]

open access: yes, 2008
Transforming growth factor (TGF) $\beta$ is known to have properties of both a tumor suppressor and a tumor promoter. While it inhibits cell proliferation, it also increases cell motility and decreases cell--cell adhesion.
Arteaga, Carlos L.   +6 more
core   +3 more sources

Exploiting metabolic adaptations to overcome dabrafenib treatment resistance in melanoma cells

open access: yesMolecular Oncology, EarlyView.
We show that dabrafenib‐resistant melanoma cells undergo mitochondrial remodeling, leading to elevated respiration and ROS production balanced by stronger antioxidant defenses. This altered redox state promotes survival despite mitochondrial damage but renders resistant cells highly vulnerable to ROS‐inducing compounds such as PEITC, highlighting redox
Silvia Eller   +17 more
wiley   +1 more source

Bases moleculares del cáncer

open access: yesRepertorio de Medicina y Cirugía, 2011
El cáncer es una enfermedad caracterizada por la proliferación anormal de células neoplásicas, dada en esencia por alteraciones genéticas y epigenéticas.
Otto Gabriel Monzón   +4 more
doaj   +1 more source

The X-linked tumor suppressor TSPX downregulates cancer-drivers/oncogenes in prostate cancer in a C-terminal acidic domain dependent manner. [PDF]

open access: yes, 2019
TSPX is a tumor suppressor gene located at Xp11.22, a prostate cancer susceptibility locus. It is ubiquitously expressed in most tissues but frequently downregulated in various cancers, including lung, brain, liver and prostate cancers.
Chris Lau, Yun-Fai   +4 more
core   +1 more source

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

open access: yesMolecular Oncology, EarlyView.
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala   +15 more
wiley   +1 more source

Post‐operative mortality and recurrence patterns in pancreatic cancer according to KRAS mutation and CDKN2A, p53, and SMAD4 expression

open access: yesThe Journal of Pathology: Clinical Research, 2023
Alterations in KRAS, CDKN2A (p16), TP53, and SMAD4 genes have been major drivers of pancreatic carcinogenesis. The clinical course of patients with pancreatic cancer in relation to these driver alterations has not been fully characterised in large ...
Yohei Masugi   +24 more
doaj   +1 more source

LncRNAs Associated with Neuronal Development and Oncogenesis Are Deregulated in SOD1-G93A Murine Model of Amyotrophic Lateral Sclerosis

open access: yesBiomedicines, 2021
Amyotrophic Lateral Sclerosis (ALS) is a devastating neurodegenerative disease caused in 10% of cases by inherited mutations considered “familial”. An ever-increasing amount of evidence is showing a fundamental role for RNA metabolism in ALS pathogenesis,
Federica Rey   +8 more
doaj   +1 more source

The Nefarious Nexus of Noncoding RNAs in Cancer [PDF]

open access: yes, 2018
The past decade has witnessed enormous progress, which has seen the noncoding RNAs (ncRNAs) turn from the so called dark matter RNA to critical functional molecules, influencing most physiological processes in development and disease contexts.
Anastasiadou, Eleni   +3 more
core   +1 more source

Peroxidasin enables melanoma immune escape by inhibiting natural killer cell cytotoxicity

open access: yesMolecular Oncology, EarlyView.
Peroxidasin (PXDN) is secreted by melanoma cells and binds the NK cell receptor NKG2D, thereby suppressing NK cell activation and cytotoxicity. PXDN depletion restores NKG2D signaling and enables effective NK cell–mediated melanoma killing. These findings identify PXDN as a previously unrecognized immune evasion factor and a potential target to improve
Hsu‐Min Sung   +17 more
wiley   +1 more source

Utilizing Protein Structure to Identify Non-Random Somatic Mutations [PDF]

open access: yes, 2013
Motivation: Human cancer is caused by the accumulation of somatic mutations in tumor suppressors and oncogenes within the genome. In the case of oncogenes, recent theory suggests that there are only a few key "driver" mutations responsible for ...
Cheng, Yuwei   +4 more
core   +2 more sources

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