Commitment of cells to programmed cell death via the mitochondrial pathway of apoptosis is governed by the BCL-2 protein family, comprising anti- and proapoptotic BCL-2 proteins. Of note, BCL2 family of proteins have been shown to play important roles in tumorigenesis as well as in the response of cancers to conventional chemotherapies and targeted therapies, including kinase inhibitors and BH3 mimetics. Nevertheless, our understanding of the precise mechanisms of apoptotic signaling networks in response to targeted therapies continue to evolve.
Resistance to therapy poses a prominent problem for the successful treatment of cancer, and there is a vast flow of information emerging in the field of drug resistance to cancer. Furthermore, improved clinical models, in particular patient-derived xenografts, and high-throughput screens, are providing in-depth understanding of how cancer cells evolve to resist treatment.
Specific subtopics will include, but are not limited to:
• Cell death signaling in targeted cancer therapies
• Mechanisms of resistance in targeted cancer therapies
• Cancer models and biomarkers for predicting cell death response in targeted cancer therapies
• Tumor microenvironment and response to targeted cancer therapies
• Non-apoptotic cell death signaling in targeted cancer therapies
Commitment of cells to programmed cell death via the mitochondrial pathway of apoptosis is governed by the BCL-2 protein family, comprising anti- and proapoptotic BCL-2 proteins. Of note, BCL2 family of proteins have been shown to play important roles in tumorigenesis as well as in the response of cancers to conventional chemotherapies and targeted therapies, including kinase inhibitors and BH3 mimetics. Nevertheless, our understanding of the precise mechanisms of apoptotic signaling networks in response to targeted therapies continue to evolve.
Resistance to therapy poses a prominent problem for the successful treatment of cancer, and there is a vast flow of information emerging in the field of drug resistance to cancer. Furthermore, improved clinical models, in particular patient-derived xenografts, and high-throughput screens, are providing in-depth understanding of how cancer cells evolve to resist treatment.
Specific subtopics will include, but are not limited to:
• Cell death signaling in targeted cancer therapies
• Mechanisms of resistance in targeted cancer therapies
• Cancer models and biomarkers for predicting cell death response in targeted cancer therapies
• Tumor microenvironment and response to targeted cancer therapies
• Non-apoptotic cell death signaling in targeted cancer therapies