CMS & NCTS Joint Activity - Cancer as a mini-evolutionary process
Cancers result from the accumulation of inherited and somatic
mutations in oncogenes and tumor suppressor genes. Those mutations
increase the net reproductive rate of cells. Many aspects of
carcinogenesis can be handled as evolutionary processes.
[1] Chromosomal instability (CIN) is a feature of most human cancers.
From the mathematical analysis of situations where inactivation of
one or two tumor suppressor genes is required for tumorigenesis, we
conclude that CIN is likely to emerge first and then enhance the risk
of cancer.
[2] Most epithelial tissues have common architecture -- a tissue is
organized into numerous small compartments, and within each
compartment includes a few stem cells and numerous differentiated
cells. This design can slow down delay the onset of cancer.
[3] The ABL tyrosine kinase inhibitor imatinib in chronic myeloid
leukemia (CML) serves as a model for molecularly targeted therapy of
cancer. We show that a four-compartment model can explain the kinetics
of the molecular response to imatinib in a 169-patient data set. We
also calculate the probability of developing imatinib resistance
mutations.
2010-01-06 15:00 ~ 2010-01-06 16:00
Prof. Yoh Iwasa (Department of Biology, Kyushu University)