CANB610:Functional Genomics: Difference between revisions
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==Discussion Points== | ==Discussion Points== | ||
== Nathalie: == | |||
# Metabolic changes generally don’t seem to fall into the category of early, “driving” lesions during tumorigenesis. Cancer cells require the metabolic changes to adapt their energy consumption and production to their erratic growth and abnormal microenvironment. However, it is unlikely that a metabolic change could be selected for in a normal cell, and allow that cell to become cancerous. Does this make metabolic targets more suitable for later stages of cancer that have generated an abnormal, hypoxic environment? Should we always strive to target the earliest lesion to completely eradicate the cancer, or can it be just as effective to target a secondary requirement? | |||
# Are the metabolic pathways that a cancer cell can alter to accomplish growth and survival more limited than the signaling pathways that can be deregulated to the same end? Could drugs targeting metabolic pathways be applicable more widely that, for example, receptor kinase inhibitors? | |||
# Are resistance mutations more or less likely to arise when a metabolic enzyme is targeted versus a more classic driver, like a receptor kinase? | |||
Latest revision as of 10:49, 9 February 2012
Discussion Points
Nathalie:
- Metabolic changes generally don’t seem to fall into the category of early, “driving” lesions during tumorigenesis. Cancer cells require the metabolic changes to adapt their energy consumption and production to their erratic growth and abnormal microenvironment. However, it is unlikely that a metabolic change could be selected for in a normal cell, and allow that cell to become cancerous. Does this make metabolic targets more suitable for later stages of cancer that have generated an abnormal, hypoxic environment? Should we always strive to target the earliest lesion to completely eradicate the cancer, or can it be just as effective to target a secondary requirement?
- Are the metabolic pathways that a cancer cell can alter to accomplish growth and survival more limited than the signaling pathways that can be deregulated to the same end? Could drugs targeting metabolic pathways be applicable more widely that, for example, receptor kinase inhibitors?
- Are resistance mutations more or less likely to arise when a metabolic enzyme is targeted versus a more classic driver, like a receptor kinase?
