Keywords: quiescence, stem cells, regeneration, iPS cells, chromatin, mouse genetics, cancer.

The accumulation of genetic and epigenetic alterations transforms normal cells into cancer cells. But how does cancer initiate and progress? In the hierarchy from stem cells to terminally differentiated cells present in adult tissues, what cell types have the potential to act as target cells for cancer? And how do these mutant cells become cancer stem cells? Key issues in the cancer field are to identify the target cells for cancer initiation and to determine the nature and consequences of cancer-initiating lesions.

To address these basic questions, we study the mechanisms of action of key cancer pathways, including the Ras, p53, and RB pathways. Recent work in the lab has focused on regulators of Ras signaling in lung adenocarcinoma and pancreatic cancer. We also investigate the mechanisms of small cell lung cancer (SCLC) initiation and progression following loss of RB and p53. The lab is interested in both basic molecular and cellular aspects of cancer growth as well as the development of novel therapeutic approaches.

 

 

Many cancer genes play a role in embryonic development and differentiation. More specifically, accumulating evidence that RB family members interact with chromatin remodeling factors. Based on these observations, a second focus of the lab is to investigate the role of cancer pathways, including the RB pathway in embryonic stem cells (from mice and humans) as well as during the reprogramming of iPS cells and during regeneration using the flatworm Schmidtea mediterranea as a model organism. We are particularly interested in investigating links between the basic cell cycle machinery and factors involved in cellular reprogramming as well as lineage fate decisions.

 

 
 
 

 

 

Last modified: March 10, 2013