Results 121 to 130 of about 1,437,206 (304)

Emerging role of ARHGAP29 in melanoma cell phenotype switching

open access: yesMolecular Oncology, EarlyView.
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster   +3 more
wiley   +1 more source

PYCR1 inhibition in bone marrow stromal cells enhances bortezomib sensitivity in multiple myeloma cells by altering their metabolism

open access: yesMolecular Oncology, EarlyView.
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert   +13 more
wiley   +1 more source

Insulin Resistance and Metabolic Syndrome [PDF]

open access: yesArteriosclerosis, Thrombosis, and Vascular Biology, 2012
The Centers for Disease Control (CDC) reported that diabetes mellitus affected 8.3% of the United States population in 2011. Type 2 diabetes mellitus is insidious; of the 25.8 million persons affected, the CDC indicated that ≈7 million were undiagnosed subjects.1 The health care costs and burden of diabetes mellitus are substantial; although ...
openaire   +2 more sources

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

open access: yesMolecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu   +18 more
wiley   +1 more source

Comparison of various steady state surrogate insulin resistance indices in diagnosing metabolic syndrome

open access: yesDiabetology & Metabolic Syndrome, 2019
Background Insulin resistance is core cause of metabolic syndrome. Determining insulin resistance is one of the foremost requirements imperative to understanding the pathophysiology of disease.
Sikandar Hayat Khan   +5 more
doaj   +1 more source

Insulin Resistance: From Theory To Practice [PDF]

open access: yes, 2006
Insulin resistance is at the core of the well recognised metabolic syndrome and possibly many other ailments commonly seen in the modern society. While the quantification of insulin resistance remains a difficult task, the problems associated with it are
Kakkilaya Bevinje, Dr. Srinivas
core   +1 more source

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

open access: yesMolecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak   +8 more
wiley   +1 more source

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

open access: yesMolecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié   +16 more
wiley   +1 more source

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