Make your appointment or second opinion with Dana-Farber today to meet with an onsite specialist.

Adult Patients:877-442-3324

Pediatric Patients:888-733-4662

Make Appointment OnlineInternational Patients

Online second opinions

Can’t get to Boston? Explore our Online Second Opinion service to get expert advice from Dana-Farber oncologists.

Request a second opinion

Contact & Directions

Email Dana-Farber

Main Number617-632-3000

Toll-Free Number866-408-DFCI (3324)

Maps & DirectionsContact InformationSend us a Question or Comment

How to Help

Discover the ways to give and how to get involved to support Dana-Farber.

Learn More
Give now

    Martin E. Hemler, PhD

    Professor of Pathology, Harvard Medical School

    About Hemler Lab

    Novel adhesion and palmitoylation mechanisms that regulate the tumor microenvironment 

    Cell adhesion is a basic process in cell biology, controlling cell growth, death, differentiation, movement, and tissue organization in normal cells, as well as the proliferation and metastasis of tumor cells. The Hemler Lab focuses on the molecular basis for cell adhesion and migration. In particular, they are interested in the structures and functions of heterodimers in the INTEGRIN family, including studies of the mechanisms whereby integrin functions are rapidly turned on and off, and different integrins link to distinct cellular signaling pathways. In addition, they study other cell surface transmembrane proteins that associate with integrins. Recent studies have shown that transmembrane linker proteins, called tetraspanin proteins, allow the membrane proximal extracellular domains of integrins to play key roles in the recruitment of intracellular signaling enzymes such as protein kinase C, and phosphatidylinositol 4-kinase.

    Recent studies have focused on how certain integrins may be linked to regulation of matrix metalloproteinase (MMP) production, a key process during cell and tissue remodeling and tumor cell metastasis. Most recently, they have generated mutant mice in which the tetraspanin CD151 gene has been deleted to investigate the role of CD151 during tumor progression.