Results 91 to 100 of about 727,025 (334)

Next‐generation proteomics improves lung cancer risk prediction

open access: yesMolecular Oncology, EarlyView.
This is one of very few studies that used prediagnostic blood samples from participants of two large population‐based cohorts. We identified, evaluated, and validated an innovative protein marker model that outperformed an established risk prediction model and criteria employed by low‐dose computed tomography in lung cancer screening trials.
Megha Bhardwaj   +4 more
wiley   +1 more source

No cancer predisposition or increased spontaneous mutation frequencies in NEIL DNA glycosylases-deficient mice

open access: yesScientific Reports, 2017
Base excision repair (BER) is a major pathway for removal of DNA base lesions and maintenance of genomic stability, which is essential in cancer prevention. DNA glycosylases recognize and remove specific lesions in the first step of BER. The existence of
Veslemøy Rolseth   +14 more
doaj   +1 more source

Rustless translation [PDF]

open access: yes, 2012
ATP binding cassette proteins are a large and diverse family of molecular machines and include transmembrane transporter, chromosome maintenance and DNA repair proteins, and translation factors.
Karl-Peter Hopfner, Roy
core   +1 more source

Potential therapeutic targeting of BKCa channels in glioblastoma treatment

open access: yesMolecular Oncology, EarlyView.
This review summarizes current insights into the role of BKCa and mitoBKCa channels in glioblastoma biology, their potential classification as oncochannels, and the emerging pharmacological strategies targeting these channels, emphasizing the translational challenges in developing BKCa‐directed therapies for glioblastoma treatment.
Kamila Maliszewska‐Olejniczak   +4 more
wiley   +1 more source

DNA methylation dynamics in aging: How far are we from understanding the mechanisms? [PDF]

open access: yes, 2018
DNA methylation is currently the most promising molecular marker for monitoring aging and predicting life expectancy. However, the mechanisms underlying age-related DNA methylation changes remain mostly undiscovered.Here we discuss the current knowledge ...
Caiafa, Paola   +3 more
core   +1 more source

Effective therapeutic targeting of CTNNB1‐mutant hepatoblastoma with WNTinib

open access: yesMolecular Oncology, EarlyView.
WNTinib, a Wnt/CTNNB1 inhibitor, was tested in hepatoblastoma (HB) experimental models. It delayed tumor growth and improved survival in CTNNB1‐mutant in vivo models. In organoids, WNTinib outperformed cisplatin and showed enhanced efficacy in combination therapy, supporting its potential as a targeted treatment for CTNNB1‐mutated HB.
Ugne Balaseviciute   +17 more
wiley   +1 more source

Predictors of hepatitis B cure using gene therapy to deliver DNA cleavage enzymes: a mathematical modeling approach. [PDF]

open access: yesPLoS Computational Biology, 2013
Most chronic viral infections are managed with small molecule therapies that inhibit replication but are not curative because non-replicating viral forms can persist despite decades of suppressive treatment.
Joshua T Schiffer   +3 more
doaj   +1 more source

Defective DNA repair mechanisms in prostate cancer: impact of olaparib [PDF]

open access: yes, 2017
The field of prostate oncology has continued to change dramatically. It has truly become a field that is intensely linked to molecular genetic alterations, especially DNA-repair defects.
De Felice, Francesca   +4 more
core   +2 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

The role of HECT-type E3 ubiquitin ligases in DNA damage response and repair

open access: yesCell Death Discovery
The post-translational modification ubiquitination consists in a three-step reaction triggered by E1 ubiquitin activating enzymes, E2 ubiquitin conjugating enzymes, and E3 ubiquitin ligases.
Sara Giovannini   +6 more
doaj   +1 more source

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