Laura E. Benjamin, Ph.D.
Associate Professor of Pathology
Associate Director, CVBR
Beth Israel Deaconess Medical Center
Harvard Medical School

330 Brookline Avenue, RN227D
Boston, MA 02215

Office: 617-667-5964
Fax: 617-667-3616


Laura Benjamin earned a Ph.D. in Molecular Biology from the University of Pennsylvania in 1995. She then performed her postdoctoral study at the Hebrew University-Hadassah Medical School with Eli Keshet. In 1999, Dr. Benjamin joined the Harvard Faculty as an Assistant Professor in the Department of Pathology at Beth Israel Deaconess Medical Center, and later became an Associate Professor in 2005. In 2008, Dr. Benjamin became the Associate Director of the Center for Vascular Biology Research.

Research Interests: Mechanisms of Blood & Lymphatic Angiogenesis


Basic Research - My research has focused on the study of molecular mechanisms that regulate vascular morphogenesis and function. My early work focused on the microvascular remodeling process in angiogenesis of both developmental and tumor vascular beds. This work highlighted the importance of VEGF as a survival factor for a remodeling vasculature and the role of pericytes in relieving VEGF dependence. More recent studies in my laboratory have focused on the role of important signaling pathways in the tumor vasculature and how regulation of those pathways contributes to tumor progression. In particular, our emphasis has been on the AKT pathway, which plays important roles in maintaining endothelial survival and governing microvascular permeability. We have ongoing projects on AKT regulation and the function of downstream signaling. We also have a real interest in exploring the impact of developing therapeutics in the tumor stroma with the notion that many of these rely on stromal responses as components of their efficacy. Going forward we are committing a significant portion of our energy to the study of the lymphatic vasculature from the perspective of novel regulatory pathways that control lymphangiogenesis to the role of lymphatic dysfunction in disease. We have identified novel molecular pathways that differentially impact vascular and lymphatic gene expression. In this context we are investigating lymphatic contributions to the pathologies associated with diabetes as well as cancer metastasis and response to cancer therapy.

New and Noteworthy Publications:

Bergers G, Benjamin LE. Tumorigenesis and the angiogenic switch. Nat Rev Cancer. 2003.(6):401-10. This is a review outlining concepts of angiogenesis and anti-angiogenesis in cancer.

Adini I, Rabinowitz I,Sun JF, Prendergast GP, and Benjamin LE. RhoB controls Akt trafficking and stage-specific survival of endothelial cells during vascular development. Genes Dev. 2003 17: 2721-2732. This study was the first report of the role of RhoB in angiogenic sprouting and linked RhoB to Akt regulation.

Sun JF, Phung T, Shiojima I, Felske T, Feng D, Kornaga T, Dor T, Adini, I. Dvorak AM, Walsh K, and Benjamin LE. Microvascular patterning is controlled by fine-tuning the Akt signal. Track II, PNAS 2005. Jan 4;102(1):128-33. This was our first description of endothelial Akt signaling and described the transgenic mouse model we continue to study. This manuscript used the endothelial inducible Akt transgene to demonstrate the ability of Akt signaling to impact developmental microvascular remodeling.

Phung TL, Ziv K, Dabydeen D, Eyiah-Mensah G, Riveros M, Perruzzi C, Sun J-F, Monahan-Early R, Shiojima I, Nagy JA, Lin MI, Walsh K, Dvorak AM, Briscoe DM, Neeman M, Sessa WC, Dvorak HF, Benjamin LE. Pathological angiogenesis is induced by sustained Akt signaling and inhibited by rapamycin. Cancer Cell. 2006 This manuscript described the consequences of sustained Akt signaling in the vasculature on both the structure and function of blood vessels. The main point in this study was that sustained signaling was capable of reproducing many of the abnormalities we associate with tumor blood vessels and that blocking this pathway induced structural and functional ‘normalization’ of those vessels.

Phung TL, Eyiah-Mensah G, O’Donnell R, Shechter S, Walsh K, Kupperwasser C, and Benjamin LE. Endothelial Akt signaling is rate limiting for rapamycin inhibition of mouse mammary tumor progression. Cancer Res. 2007 Jun 1;67(11):5070-5. This study tested the hypothesis that rapamycin’s anti-tumor effects were in part due to alteration of Akt signaling in the tumor vasculature.