Richard Fang
Program: Unspecified
Current advisor:
Undergraduate university: University of Pittsburgh
Research summary
Breast cancer remains the leading diagnosed cancer in women, and distal metastasis of primary breast tumors is the leading cause of mortality. The lung is among the most frequent sites of breast cancer metastasis, yet the mechanisms that prime this transformation are not well understood. Cellular senescence is a state of stably-arrested proliferation, accompanied by high metabolic activity. Senescent cells often secrete a variety of bioactive molecules, collectively termed the senescence-associated secretory phenotype (SASP). The SASP can have diverse effects on the tumor microenvironment, including promoting or inhibiting tumor growth, remodeling the extracellular matrix (ECM), and modulating inflammation.
Previous work from the Stewart Lab demonstrated that senescent cancer-associated fibroblasts (CAFs) remodel the breast tumor ECM to suppress natural killer (NK) cell cytotoxicity and enhance tumor progression. Building on this, I employed the MMTV-PyMT;INK-ATTAC mouse model, a model enabling targeted depletion of senescent cells, to investigate the role of senescent macrophages in the lung and their contribution to metastatic tumor progression.
Graduate publications