Results 41 to 50 of about 70,416 (256)

The Ribosomal Protein L28 Gene Induces Sorafenib Resistance in Hepatocellular Carcinoma

open access: yesFrontiers in Oncology, 2021
BackgroundSorafenib is the first molecular-targeted drug for the treatment of advanced hepatocellular carcinoma (HCC). However, its treatment efficiency decreases after a short period of time because of the development of drug resistance.
Yi Shi   +6 more
doaj   +1 more source

Phase Ii Study of Combining Sorafenib with Metronomic Tegafur/Uracil for Advanced Hepatocellular Carcinoma

open access: yes, 2011
BACKGROUND & AIMS: Sorafenib, a multi-kinase inhibitor with anti- angiogenic activity, was recently approved for the treatment of advanced hepatocellular carcinoma (HCC).
HSU, CHIH-HUNG;SHEN, YING-CHUN;LIN, ZONG-ZHE;CHEN, PEI-JER;SHAO, YU-YUN;DING, YEA-HUI;HSU, CHIUN;CHENG, ANN-LII   +1 more
core   +1 more source

Inhibition of Dickkopf-1 enhances the anti-tumor efficacy of sorafenib via inhibition of the PI3K/Akt and Wnt/β-catenin pathways in hepatocellular carcinoma

open access: yesCell Communication and Signaling, 2023
Background Sorafenib improves the overall survival in patients with advanced hepatocellular carcinoma (HCC). Dickkopf-1 (DKK1) is commonly overexpressed in HCC.
Sang Hyun Seo   +12 more
doaj   +1 more source

ABCC5 facilitates the acquired resistance of sorafenib through the inhibition of SLC7A11-induced ferroptosis in hepatocellular carcinoma

open access: yesNeoplasia: An International Journal for Oncology Research, 2021
Sorafenib is a first-line molecular-target drug for advanced hepatocellular carcinoma (HCC), and reducing sorafenib resistance is an important issue to be resolved for the clinical treatment of HCC.
Wenbin Huang   +12 more
doaj   +1 more source

Blockade of STAT3 activation by sorafenib derivatives through enhancing SHP-1 phosphatase activity

open access: yes, 2017
Previously, we demonstrated that the multiple kinase inhibitor sorafenib mediates the repression of phospho-STAT3 in hepatocellular carcinoma cells.
陳昆鋒;陳培哲   +1 more
core   +1 more source

Patient‐Reported Outcomes with Selpercatinib Treatment Among Patients with RET‐Mutant Medullary Thyroid Cancer in the Phase I/II LIBRETTO‐001 Trial

open access: yesThe Oncologist, EarlyView., 2021
Abstract Background Medullary thyroid cancer (MTC) standard of care includes multikinase inhibitors (MKIs), which can exacerbate disease‐related diarrhea, primarily because of non‐RET kinase inhibition. We report diarrhea and other patient‐reported outcomes (PROs) with selpercatinib, a highly selective RET inhibitor, among patients with RET‐mutant MTC ...
Lori J. Wirth   +10 more
wiley   +1 more source

UBQLN1 mediates sorafenib resistance through regulating mitochondrial biogenesis and ROS homeostasis by targeting PGC1β in hepatocellular carcinoma

open access: yesSignal Transduction and Targeted Therapy, 2021
The treatment for hepatocellular carcinoma (HCC) is promising in recent years, but still facing critical challenges. The first targeted therapy, sorafenib, prolonged the overall survival by months.
Junjie Xu   +11 more
doaj   +1 more source

ABHD12 contributes to tumorigenesis and sorafenib resistance by preventing ferroptosis in hepatocellular carcinoma

open access: yesiScience, 2023
Summary: Sorafenib induces ferroptosis, making it a useful treatment against advanced liver hepatocellular carcinoma (LIHC). However, sorafenib resistance is extremely common among LIHC patients.
Mengxing Cai   +6 more
doaj   +1 more source

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

open access: yesMolecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober   +16 more
wiley   +1 more source

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim   +7 more
wiley   +1 more source

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