Signaling Pathways and Metabolic Adaptation in Cancer: New Targeting Options for Cancer Therapies

Dear Colleagues,

Signaling pathways are involved in many biological processes such as cell proliferation, differentiation and survival. Abnormal cell signaling drives malignant cell division, metastasis and invasion. Oncogenic mutations, amplification or gene fusions involving upstream receptor tyrosine kinases (e.g.: EGFR, ERBB2) and downstream signaling factors (e.g.: KRAS, BRAF, PIK3CA) cause constitutive signaling activation through the RAS-ERK and PI3K-AKT pathways in human cancers.

The recent identification of KRAS-G12C inhibitors and strategies improving inhibition of RAS regulators/effectors (e.g.: SHP2, RAF, MEK inhibitors) has led to significant achievements in RAS-targeted therapy. Strenuous effort has also been committed to improving inhibitors targeting PI3K-AKT-mTOR signaling, with some success in treating advanced cancers. Despite exciting initial responses, targeted therapies eventually fail in advanced cancers, as tumors develop resistance and relapse. Substantial evidence suggests the development of resistance to chemotherapy and targeted therapies is closely linked to metabolic alterations. Important advances in combinational therapy have been achieved by exploiting metabolic dependencies emitted from signaling disruption.

This Special Issue welcomes submissions from diverse areas of cancer biology concerned with signaling pathways, related vulnerabilities and resistance mechanisms, with the purpose of stimulating intriguing perspectives that may lead to the enhanced therapeutic efficacy of treatment for cancers.

Dr. Jianfeng Huang
Guest Editor

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• MAPK signaling
• RAS
• PI3K-AKT-mTOR
• EGFR
• RTK
• cancer metabolism
• drug resistance
• targeted cancer therapy