resistance to first-line tyrosine kinase inhibitor therapies, such as sorafenib and lenvatinib, remains a significant clinical challenge
First-pass extracted concept
tyrosine kinase inhibitor resistance in hepatocellular carcinoma
Candidate: concept label1 source documents5 linked claims
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Aliases
TKI resistance in HCC
Evidence Snippets
Supporting Sources
Linked Claims
Aerobic glycolysis is strongly linked to drug resistance in hepatocellular carcinoma.
Quoted textsource-backed
Recent research has revealed a strong link between aerobic glycolysis and drug resistance in HCC.
Metabolic and signaling mechanisms interact synergistically to allow hepatocellular carcinoma cells to survive and proliferate despite targeted therapies, resulting in drug resistance.
Quoted textsource-backed
These mechanisms interact synergistically, allowing HCC cells to endure and proliferate despite targeted therapies, ultimately resulting in drug resistance.
AMPK, HIF-1, and c-Myc signaling pathways play key roles in tumor metabolic regulation relevant to hepatocellular carcinoma drug resistance.
Quoted textsource-backed
Moreover, signaling pathways, such as AMPK, HIF-1, and c-Myc, play key roles in tumor metabolic regulation, influencing energy balance, gene expression under hypoxia, and metabolic pathway control.
Lactate contributes to drug resistance in hepatocellular carcinoma.
Quoted textsource-backed
Lactate, the final product of glycolysis, is also pivotal in contributing to drug resistance in HCC.
Understanding metabolic and signaling regulation of aerobic glycolysis may reveal causes of drug resistance in hepatocellular carcinoma and provide new therapeutic targets and strategies.
Quoted textsource-backed
Therefore, a deeper understanding of these metabolic and signaling regulatory mechanisms will help reveal the fundamental causes of drug resistance in HCC and provide new targets and directions for future therapeutic strategies.