Fero Laboratory

Laboratory of Matthew Fero, MD, FACP

fero-wA major focus of my lab has been the interaction of of cell cycle regulators and microRNA in the development of complex tissues, and to understand how these processes go awry in cancer. 

We have pioneered the discovery of genes that cooperate with the p27/cyclin D pathway in lymphomagenesis. This work culminated in the discovery of miR-106a~363Xpcl1, a gene on the X-chromosome which encodes a cluster of miRNAs. Our recent work shows that miR-106a~363Xpcl1 is a potent oncogene and that it cooperates with p27 loss to induce lymphomas. We are interested in the potential to target non-coding RNAs and cell cycle regulators as novel cancer treatments.

In contrast to cancer control, where our goal is to limit unregulated cellular proliferation, the field of tissue regeneration seeks to induce cell growth where it is needed to restore function to a damaged organ. To understand p27’s role blocking cellular regeneration of post-mitotic tissues I have collaborated with investigators around the globe. We have shown that p27 is a critical regulator of post-mitotic cellular quiescence.

Cyclin-dependent kinases, or CDKs, drive the cell cycle. Their inhibitors, called CDK inhibitors or CKIs, regulate them and thus regulate the cell cycle. One important CKI is p27.

In addition to my primary research interest in cancer pathogenesis, I have expertise in the development of patient derived xenografts. This enables the creation of mouse cancer models that are custom designed to match individual patients. By coupling PDX model development with human clinical trials, we can test new drugs or new twists on established therapies more quickly and safely than in people. In particular, our aim is to establish new therapeutic avenues for hematologic malignancies, including advanced cellular therapies such as stem cell transplantation, cell cycle regulators, and immune modulatory therapy.

We are expert in the use of transgenic mouse models and human tumor xenograft models to elucidate the interactions of cancer genes, carcinogenic compounds, and novel therapeutic agents.

 

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