Our goal is to gain mechanistic understanding how altered expression or function of key mitotic regulators (e.g. GTPases, kinases) can give rise to genetically unbalanced cells that may
initiate tumorigenesis.
In this issue of Developmental Cell, Levine et al. (2017) provide strong evidence that centrosome amplification is sufficient to
initiate tumorigenesis in a mouse model.
We have found that the initiation of pancreatic cancer does not follow the classic paradigm seen in colon cancer where loss of a tumor suppressor gene
initiates tumorigenesis and then acquisition of an oncogene promotes tumor formation.
Not exact matches
The pancreas seems to require two oncogenic events to
initiate and promote
tumorigenesis with tumor suppressors acting later to increase progression to malignant disease.