Results 121 to 130 of about 384,141 (378)

Gene amplifications associated with the development of hormone- resistant prostate cancer [PDF]

open access: yes, 2003
Purpose: Hormone resistance remains a significant clinical problem in prostate cancer with few therapeutic options. Research into mechanisms of hormone resistance is essential.
Bartlett, J.M.S.   +3 more
core  

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

Targeting C-myc G-Quadruplex: Dual Recognition by Aminosugar-Bisbenzimidazoles with Varying Linker Lengths

open access: yesMolecules, 2013
G-quadruplexes are therapeutically important biological targets. In this report, we present biophysical studies of neomycin-Hoechst 33258 conjugates binding to a G-quadruplex derived from the C-myc promoter sequence.
Nihar Ranjan, Dev P. Arya
doaj   +1 more source

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

Pediatric Cancers: Development and Treatment Methods

open access: yes, 2018
Pediatric cancers are cancers that develop in kids and adolescents ages 0-19. Pediatric cancers usually develop in three ways: through inherited gene mutations, parental exposure to toxins, and acquired gene mutations.
Walker, MaKayla M.
core  

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

Proteasomal targeting of a viral oncogene abrogates oncogenic phenotype and enhances immunogenicity [PDF]

open access: bronze, 2003
Judy Tellam   +4 more
openalex   +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

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