Institute for Medicine and Engineering

The mission of the Institute for Medicine and Engineering (IME) is to stimulate fundamental research at the interface between biomedicine and engineering/physical/computational sciences leading to innovative applications in biomedical research and clinical practice. The IME was created in 1996 by the Schools of Medicine (SOM) and Engineering and Applied Science (SEAS) to pursue opportunities for collaborative research. The IME has been successful in obtaining over $80 million in extramural grants, and funded programs. These include a research center in Cell Studies of Pulmonary Artery Hypertension, and a Penn Center for Molecular Discovery.

Membership: The Institute houses 11 core faculty, 6 from the School of Medicine and 5 from SEAS, who were recruited to form the basis for the IME; however, the Institute extends beyond the core group to include 106 members from various schools including School of Medicine, SEAS and Arts and Sciences faculty. The Institute interacts with 24 other Centers or departments.

Multi-disciplinary Research: The IME mission to foster research at the interface of medicine and engineering is met (i) through 8 central investigators who span these disciplines in both schools, (ii) through the core facilities, pilot grant programs, research training, and educational events involving its very wide membership (of 106). The research conducted by central investigators is quite broad, ranging from cell and molecular biology to tissue engineering, biophysics and nanobiology/medicine. Having established a strong basic research foundation the Institute is now expanding translational programs in medicine and engineering.

Strategic Importance: The IME relates directly to 3 major themes of the SOM Research Strategic Plan: Cancer, Neurosciences and Cardiovascular Biology. The University Strategic Plan identifies the link between engineering and medicine as one of the key drivers of success and recommends "fostering advances in engineering, computing, chemistry, mathematics and behavioral sciences that can be applied to life sciences." Because of the multi-disciplinary nature of the Institute, it is well positioned to take advantage of the new NIH roadmap. Because of its unique interface with SEAS, the IME is a strong force in faculty retention by providing unique directions and connections for research among faculty.

 

 

 

 

School of Engineering and Applied Science

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  • Publication
    Autocrine laminin-5 ligates {alpha}6{beta}4 integrin and activates RAC and NF{kappa}B to mediate anchorange-independent survival of mammary tumors
    (2003-12-22) Zahir, Nastaran; Lakins, Johnathon N; Chatterjee, Chandrima; Ming, WenYu; Chatterjee, Chandrima; Weaver, Valerie M.; Marinkovich, Matthew P; Weaver, Valerie M.
    Invasive carcinomas survive and evade apoptosis despite the absence of an exogenous basement membrane. How epithelial tumors acquire anchorage independence for survival remains poorly defined. Epithelial tumors often secrete abundant amounts of the extracellular matrix protein laminin 5 (LM-5) and frequently express α6β4 integrin. Here, we show that autocrine LM-5 mediates anchorage independent survival in breast tumors through ligation of a wild-type, but not a cytoplasmic tail–truncated α6β4 integrin. α6β4 integrin does not mediate tumor survival through activation of ERK or AKT. Instead, the cytoplasmic tail of β4 integrin is necessary for basal and epidermal growth factor–induced RAC activity, and RAC mediates tumor survival. Indeed, a constitutively active RAC sustains the viability of mammary tumors lacking functional β1 and β4 integrin through activation of NFκB, and overexpression of NFκB p65 mediates anchorage-independent survival of nonmalignant mammary epithelial cells. Therefore, epithelial tumors could survive in the absence of exogenous basement membrane through autocrine LM-5–α6β4 integrin–RAC–NFκB signaling.