Dr. Daniel G. Anderson is appointed at the David H. Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology. He received his PhD in molecular genetics from the University of California at Davis. At MIT, he pioneered the use of robotic methods for the development of smart biomaterials for drug delivery and tissue engineering. He has developed robotic technology allowing rapid nanoliter scale synthesis and testing of 1000's of biomaterials with stem cells. The advanced drug delivery systems he has developed provide new methods for nanoparticulate and microparticulate drug delivery, non-viral gene therapy, siRNA delivery, and vaccines. His work has resulted in the publication of over 70 papers and pending patents. These patents have led to a number of licenses to pharmaceutical, chemical and biotechnology companies.

Dr. Brown received his MD from Johns Hopkins University in 1982, followed by an internal medicine residency at Brigham and Women's Hospital and a fellowship in medical oncology at Dana Farber Cancer Institute. He conducted postdoctoral research at the Massachusetts Institute of Technology from 1987 to 1990. In 1989, he joined the staff of DFCI, where his molecular studies focus on the role of the estrogen receptor in breast cancer and the androgen receptor in prostate cancer. Estrogen plays a critical role in the development of the normal breast and in breast cancer. The biochemical mechanisms underlying these processes, however, remain largely unknown. The overall aim of current research is to build on recent advances in the molecular understanding of estrogen receptor (ER) action to better define the role played by estrogen in the normal breast and in breast cancer.

I have worked with the late Dr. Judah Folkman for the past 30 years. When I joined with him in 1977, the only endothelial cells available for research were from large vessels. We were the first to isolate and culture capillary endothelial cells from bovine adrenal capillaries. This was closely followed by the isolation of human foreskin capillary endothelial cells. The isolation of these cells made a significant contribution to the field of tumor angiogenesis, and with this accomplishment came the training of researchers in this isolation technique from all over the world. These cells have afforded us the ability to evaluate in vitro both stimulators and inhibitors of angiogenesis. Over the years, I have isolated and characterized many tumor cells from various human and mouse tumors.

Another contribution our laboratory made to the field of angiogenesis was the development of the corneal pocket assay. This assay affords a direct evaluation of both angiogenesis and lymphangiogenesis in vivo. Taken together, these assays and techniques have allowed us to take full therapeutic advantage of the anti-angiogenic strategy.

More recently, our lab has begun to focus on LAM disease. I am hoping that my expertise in cell biology and angiogenesis will allow me to make contributions towards the understanding and treatment of LAM disease through the isolation and characterization of LAM smooth muscle and LAM derived lymphatic endothelial cells.

Relevant Publications:

• Kaipainen A, Kieran MW, Huang S, Butterfield C, Bielenberg D, Mostoslavsky G, Mulligan R, Folkman J, Panigrahy D. PPARalpha deficiency in inflammatory cells suppresses tumor growth. PLoS ONE. 2007; 2(2):e260.
• Chang LK, Garcia-Cardena G, Farnebo F, Fannon M, Chen EJ, Butterfield C, Moses MA, Mulligan RC, Folkman J, Kaipainen A. Dose-dependent response of FGF-2 for lymphangiogenesis. Proc Natl Acad Sci U S A. 2004; 101(32):11658-63.
• Browder T, Butterfield CE, Kraling BM, Shi B, Marshall B, O'Reilly MS, Folkman J. Antiangiogenic scheduling of chemotherapy improves efficacy against experimental drug-resistant cancer. Cancer Res. 2000; 60(7):1878-86.

John (Sean) Clohessy received his undergraduate training the University of Limerick in Ireland, and upon completion of a M.Sc. in Biological Sciences at Dublin City University, he pursued Ph.D. studies under the supervision of Dr. Hugh Brady at the Institute of Child Health, University College London. In 2005 he was awarded a Ph.D. in Molecular and Cellular Biology for his thesis on the role of Bcl-2 family proteins in apoptosis. Since 2004, Dr. Clohessy has been a post-doctoral fellow in the laboratory of Dr. Pier Paolo Pandolfi, which recently moved from Memorial Sloan Kettering Cancer Center in New York to the Division of Genetics at BIDMC/Harvard Medical School.

Jennifer D. Cook was born on 11 August 1973 in Bentonville, Arkansas. Jennifer did her undergraduate studies at the University of Arkansas and graduated in 2000 with a B.S. in Biology. Jennifer completed her dissertation research under the supervision of Dr. Cheryl Walker at the University of Texas, M.D. Anderson Cancer Center and was awarded her Ph.D. in Biomedical Research in 2006. Jennifer is currently a post-doctoral fellow in the laboratory of Dr. Myles Brown at the Dana Farber Cancer Institute, Harvard Medical School in Boston, Massachusetts.

Relevant Publications:

• Estrogen Receptor Target Gene: An Evolving Concept.
• Genome-wide analysis of estrogen receptor binding sites
• Estradiol and tamoxifen stimulate LAM-associated angiomyolipoma cell growth and activate both genomic and nongenomic signaling pathways

Ian Eslick is a PhD candidate at the Media Laboratory of the Massachusetts Institute of Technology. His current research areas encompass Human-Computer Interfaces, Artificial and Collective Intelligence, Visualization and Software Engineering. Ian is developing technology platforms to enable user communities to collaborate in the acquisition and analysis of complex datasets without requiring significant expertise with computers.

Prior to his doctorate program at MIT, Ian was the founding President of Silicon Spice, a telecommunications semiconductor startup incorporated in 1996. His company was acquired by Broadcom Corporation in 2000 where he continued as a Director of Software Engineering. Under the Broadcom label, the company's products became the market leader in carrier-class voice telephony with significant penetration in the US, Europe and Asia.

Ian is also an advisor to venture capital and startup companies in the semiconductor, software, and non-profit sectors. He holds over a dozen patents in semiconductor architecture, real-time software, and systems technology.

Dr. Finlay obtained her medical degree from University College Dublin, Ireland in 1990. She received her Internal Medicine training in St Vincents University Hospital, Dublin, Ireland. She obtained her MD thesis examining the role of Matrix Metalloproteinases in pathogenesis of COPD and Emphysema from University College Dublin Ireland in 1996. She received her higher training in Pulmonary and Critical Care Medicine at Tufts-New England Medical Center, Boston, Massachusetts. She is currently an Associate Professor of Medicine at T-NEMC. As a Pulmonary and Critical Care physician, she has a strong clinical interest in Emphysema and lymphangioleiomyomatosis (LAM). She has been the recipient of the LAM Foundation Fellowship and Established Investigator awards. Dr Finlay's basic research interests focus on the mechanisms that control cell growth in tuberin null cells. In particular, her research has focused on the signaling mechanisms employed by growth factors and estrogen that lead to smooth muscle cell proliferation in tuberin null states such as lymphangioleiomyomatosis (LAM) and therapeutic modalities that could potentially inhibit growth in tuberin null states.

• 1. The regulation of PDGF production and ERK activation by estrogen is associated with TSC-2 gene expression. Finlay G.A., Hunter D., Walker C., Paulson K.E., Fanburg B.L. Am J Physiol, Cell Physiol 2003: 285: C409-C418.
• 2. Estrogen-induced smooth muscle cell growth is regulated by tuberin and associated with altered activation of PDGFR-beta and ERK-1/2. Finlay, GA., York, B., Karas RH., Fanburg, BL., Zhang, HB., Kwiatkowski DJ., Noonan, DJ. J Biol Chem 2004: 279, 23114-22.
• 3. Selective inhibition of growth of Tuberous Sclerosis Complex 2 (TSC2)-null cells by atorvastatin is associated with impaired Rheb and Rho GTPase function and reduced mammalian target of rapamycin (mTOR)/S6 Kinase activity. Geraldine A. Finlay, Amy M. Malhowski, Yingling Liu, Barry L. Fanburg, David J. Kwiatkowski and Deniz Toksoz. Cancer Res. 2007 Oct 15;67(20):9878-86.

Caroline Heckman is a senior research scientist at the Biomedicum Helsinki working with Prof. Kari Alitalo in the Molecular/Cancer Biology Program at the University of Helsinki. Her training includes an undergraduate degree from the University of Chicago before moving on to the University of Texas MD Anderson Cancer Center where she earned her PhD in 1996. From there she went on to Stanford University as a postdoctoral fellow and later as a staff scientist working in the laboratory of Prof. Linda Boxer to elucidate the molecular mechanisms involved in the development of B cell lymphomas and identifying new targets for therapy. Her current research interests include the identification and characterization of the mediators and mechanisms of lymphatic metastasis, as well as the evaluation of current therapeutic options for metastatic disease. More recent research efforts have focused on lymphangioleiomyomatosis and its association with the lymphatic system. Using LAM patient samples she is currently exploring new possibilities for LAM treatment.

Medical Oncologist Elizabeth Petri Henske, MD is a Senior Member and attending physician at Fox Chase Cancer Center in Philadelphia. Her research focuses on understanding the cause and treatment of tuberous sclerosis complex (TSC), a genetic disorder that leads to benign tumors in multiple organs, and the related disorder, lymphangiomyomatosis (LAM). Her work points to a substantial overlap between the biology of cancer and TSC and suggests that certain biologic therapies being developed for cancer patients will be effective for TSC and LAM patients.

Dr. Henske graduated summa cum laude from Yale University and attended Harvard Medical School. She came to Fox Chase in 1996 after serving as assistant professor of medicine at Harvard Medical School. She was trained in Internal Medicine and Hematology-Oncology at the Massachusetts General Hospital.

She was elected to membership in the American Society for Clinical Investigation in 2005. She has received the LAM Foundation Scientific Advancement Award (2001), the Rothberg Institute for Childhood Diseases "Courage" Award (2002), the Tuberous Sclerosis Alliance's Manuel Gomez Award for "extraordinary scientific and humanitarian efforts to find a cure for Tuberous Sclerosis" (2005), and the Medtronic Prize from the Society for Women's Health Research (2007) for "an outstanding scientist whose work has led or will lead directly to the improvement of women's health." Dr. Henske is Chairperson of the NIH "Cellular and Molecular Biology of the Kidney" study section and the DOD Neurofibromatosis Integration Panel, and Chair-elect of the Tuberous Sclerosis Alliance International Professional Advisory Board.

Relevant Publications:

• Estrogen-Induced Activation of Mammalian Target of Rapamycin Is Mediated via Tuberin and the Small GTPase Ras Homologue Enriched in Brain
• Rheb Inhibits C-Raf Activity and B-Raf,C-Raf Heterodimerization
• Estradiol and tamoxifen stimulate LAM-associated angiomyolipoma cell growth and activate both genomic and nongenomic signaling pathways

Vera P. Krymskaya, Ph.D., Associate Professor of Medicine in the Pulmonary, Allergy and Critical Care Division at the University of Pennsylvania School of Medicine, has dedicated the last several years of her career to combating Lymphangioleiomyomatosis (LAM). Krymskaya's lab was responsible for the breakthrough step of discovering the function of the Tuberous Sclerosis Complex 2 (TSC2) gene. Dr. Krymskaya linked mutational inactivation of TSC2 in human LAM cells to the constitutive activation of mTOR/S6K1 signaling pathway and abnormal LAM cell growth. Dr. Krymskaya has also dramatically advanced translational LAM research by demonstrating that rapamycin inhibits LAM cell growth. This discovery identified rapamycin as a promising therapeutic strategy for LAM patients, and paved the way for rapamycin.

• Goncharova, EA and Krymskaya, VP: Pulmonary Lymphangioleiomyomatosis (LAM): Progress and Current Challenges Journal of Cellular Biochemistry. Wiley-Liss, Inc. 103: 369-382, 2008
• Krymskaya, VP: Smooth Muscle-Like Cells in Pulmonary Lymphangioleiomyomatosis (LAM). Proceedings of the American Thoracic Society 5: 119-126, 2008.

Dr. David Kwiatkowski is Professor of Medicine at Harvard Medical School and Senior Physician at Brigham and Women's Hospital. He has worked on tuberous sclerosis and related conditions for 17 years, including identification of the TSC1 gene in 1997. His current research interests include the human molecular genetics of TSC, the genetic basis of LAM, signaling pathways and functions of TSC1 and TSC2, development of mouse models of TSC and LAM, and exploration of therapeutic strategies for TSC and LAM in mouse models.

• Estrogen Enhances whereas Tamoxifen Retards Development of Tsc Mouse Liver Hemangioma: A Tumor Related to Renal Angiomyolipoma and Pulmonary Lymphangioleiomyomatosis
• PDGFRs are critical for P13K/Akt activation and negatively regulated by mTOR
• Efficacy of a Rapamycin Analog (CCI-779) and IFN- in Tuberous Sclerosis Mouse Models

Dr. Elena Lesma obtained her PhD in Pharmacology from University of Milano, Italy, with a thesis on the opioid modulation of the cortical plasticity through G proteins focused on signal transduction. She had a postdoctoral training at the Pulmonary-Critical Care Medicine Branch, NHLBI, NIH, Bethesda, Maryland in the laboratory of Dr. Joel Moss. She joined the pharmacological laboratories directed by Dr. Gorio in the Dept. of Medicine and Surgery at the University of Milano where she is currently an Assistant Professor. Dr. Lesma's research is focused on cellular and biochemical mechanisms underlying the aberrant proliferation of TSC and LAM cells and identification of a molecular target to treat the diseases.

• Isolation and Growth of Smooth Muscle-Like Cells Derived from Tuberous Sclerosis Complex-2 Human Renal Angiomyolipoma

Dr. McCormack is Professor and Director of the Division of Pulmonary and Critical Care Medicine at the University of Cincinnati. He received his training in Internal Medicine at the University of Michigan and completed his Pulmonary and Critical Care Medicine Fellowship at the University of Colorado. He has an active NIH and VA Merit funded research program focused on the role of the alveolar epithelium in innate immunity and pulmonary fibrosis. His clinical interest is pulmonary fibrosis, especially as it relates to genetic lung disorders such as lymphangioleiomyomatosis. He co-directs the NCRR funded Rare Lung Disease Consortium. He has published approximately 80 peer reviewed papers, reviews and textbook chapters. He has been the Scientific Director of the Lymphangioleiomyomatosis Foundation since it was founded in 1995. Dr. McCormack is a Career Investigator of the American Lung Association and a member of the American Society for Clinical Investigation.

Joel Moss, MD, PhD, is Deputy Chief of the Translational Medicine Branch, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, Maryland. He graduated from Brandeis University (1967), summa cum laude, and received M.D.- Ph.D. (Biochemistry) degrees from New York University School of Medicine (1972). Following internship and residency (medicine; Johns Hopkins), he completed post-doctoral and pulmonary fellowships (NHLBI). At the NHLBI since 1974, he has co-authored over 500 scientific papers, edited/co-authored several books, and is a co-inventor of biotechnology patents. Dr. Moss was a member of the NHLBI Institutional Review Board from 1988-2006, and Chair from 1995-2006. Subjects of his research include lymphangioleiomyomatosis (LAM), with emphasis on roles of the LAM cell and susceptibility/modifier genes on disease progression.

• Meningiomans in Lymphangioleiomyomatosis
• Molecular and genetic analysis of disseminated neoplastic cells in lymphangioleiomyomatosis
• Maximal Oxygen Uptake and Severity of Disease in Lymphangioleiomyomatosis

Michael Nurok, MD, PhD is a founding member of the LAM Treatment Alliance. He lives in Cambridge, Massachusetts with his wife, LAM Treatment Alliance Executive Director Amy Farber, and daughter Charlotte. Dr. Nurok is a practicing Critical Care physician and Cardio-thoracic anesthesiologist at Brigham and Women's Hospital, Harvard Medical School in Boston.

Dr. Padera received B.S. degrees in both Biomedical Engineering and Chemical Engineering from Northwestern University in 1991, a Ph.D. in Medical Engineering and Medical Physics from the Harvard-MIT Division of Health Sciences and Technology (HST) in 1998 and an M.D. from Harvard Medical School in 2000. The Ph.D. involved research on material-tissue interaction, neovascularization and mass transport, and was performed under the direction of Dr. Robert Langer at MIT. After medical school, he received his residency training in Anatomic Pathology at the Brigham and Women's Hospital, with further fellowship training in cardiovascular, pulmonary, orthopedic and autopsy pathology, and spent a year as a medical device pathology fellow under Dr. Frederick Schoen. He has co-authored approximately 40 original publications in the areas of biomaterials, tissue engineering and pathology, and has co-authored several book chapters on cardiovascular pathology and cardiovascular medical devices. He is an attending pathologist at Brigham and Women's Hospital, an assistant professor of pathology at HMS and affiliated faculty within HST. His current clinical responsibilities include cardiac and pulmonary surgical pathology, autopsy pathology and perinatal congenital heart disease pathology. He is the associate director of the first-year HST pathology course at Harvard Medical School and teaches in many other pre-clinical medical courses as well as in engineering courses at MIT. The major focus of his research is in medical device pathology and device development, particularly in the cardiovascular system.

Craig Douglas Peacock is currently a Research Associate at the Kimmel Cancer Center at Johns Hopkins University. He holds a BSc in Microbiology/Biochemistry and a PhD in Viral Immunology from the University of Western Australia. He has completed two post-doctoral fellowships, his first in 2003 from the University of Massachusetts in Viral Immunology and his second in 2006 from Johns Hopkins University in Oncology. He has been a member of the American Society of Hematology since 2005 and the Association of Cancer since 2006.

Relevant Publications:

• Peacock CD., Wang Q., Gesell GS., Corcoran-Schwartz IM., Jones E., Kim J., Devereux DL., Rhodes JT., Huff CA., Beachy PA., Watkins DN. and Matsui W. Hedgehog signaling maintains a tumor stem cell compartment in multiple myeloma. PNAS. 2007; 104(10): 4048-4053.
• Watkins DN. and Peacock CD. Small cell lung cancer: Carcinoma or primitive neural tumor? ASCO Educational Book. 2007.
• Peacock CD. and Watkins DN. Cancer stem cells and the ontogeny of lung cancer. In Press. Journal of Clinical Oncology. 2007.
• Rudin CM., Hann CL., Peacock CD. and Watkins DN. Novel therapeutic approaches to small cell lung cancer. In Press. Journal of the National Comprehensive Cancer Network. 2007.
• Matsui M., Wang Q., Barber JP., Smith BD., Borrello I., McNiece I., Lin L., Ambinder RF., Peacock CD., Watkins DN., Huff CA. and Jones RJ. Clonogenic multiple myeloma progenitors, stem cell properties and drug resistance. Cancer Research. 2008; 68(1): 190-197.

Dr. Peter is currently an Instructor in Medicine at Brigham and Women's Hospital and Harvard Medical School, where his biomedical interests include the application of stem cell technologies to pulmonary disease.

A graduate of the Weizmann Institute of Science in Israel, Dr. Peter obtained a PhD in Molecular Genetics in 2001 where he investigated the effects of oxidative stress on the hereditary disorder ataxia telangiectasia. He is currently teaching at Harvard University and researching methods to isolate and characterize multipotential cell populations from lung tissue. The overall aim of his research is to understand alveolar repair mechanisms to develop novel cell-based therapies in degenerative disease.

Relevant Publications:

• Peter Y. Tracheotomy: a method for transplantation of stem cells to the lung. JoVE (2007).
• Williams L, Peter Y. Adult stem cells of the lung in organ dysfunction. J Organ Dysfunct. 3:31-5 (2007).

Dr. Gustavo Pacheco-Rodriguez is currently a Staff Scientist in the Translational Medicine Branch of the National Heart, Lung, and Blood Institute (NHLBI) at the National Institutes of Health (NIH), where his biomedical research interests include human genetics, molecular aspects of protein-protein interactions, and their regulatory functions in human diseases.

A graduate of the University of North Texas Health Science Center in Fort Worth, Dr. Pacheco-Rodriguez obtained a Ph.D. in Biochemistry in 1997 where he investigated enzymatic processes involved in DNA damage and repair. He did postdoctoral research in molecular aspects of protein trafficking at the NIH from 1997 until 2001 under the mentorship of Dr. Martha Vaughan. He joined the Pulmonary-Critical Medicine Branch of the NHLBI as a Staff Scientist in 2001. He has worked in the laboratory of Dr. Joel Moss to characterize cell surface markers that aid in the identification of circulating metastatic lymphangioleiomyomatosis (LAM) cells. Currently, Dr. Pacheco-Rodriguez's major focus is in the elucidation of molecular mechanisms that characterize the abnormal growth of smooth muscle cells as well as identification of molecules involved in metastasis.

Dr. Pacheco-Rodriguez has identified CD44v6, a hyaluronic acid receptor, as a marker for the LAM cell (Cancer Research 2007), and has contributed to the identification of circulating LAM cells in blood, urine and chyle (PNAS 2004). He has also identified a renin-angiotensin system of the LAM cells (AJRCMB 2006), and identified MCP-1 as a paracrine growth factor for TSC2 null cells (JEM 2005).

Relevant Publications:

• TSC2 Loss in Lymphangioleiomyomatosis Cells Correlated with Expression of CD44v6, a Molecular Determinant of Metastasis
• Molecular and genetic analysis of disseminated neoplastic cells in lymphangioleiomyomatosis

Robert Sackstein, M.D., Ph.D. received his undergraduate degree from Harvard College, Summa cum Laude in biology, and his M.D. and Ph.D. degrees from Harvard Medical School, where he also received the James Tolbert Shipley Prize for outstanding research. He then completed internal medicine training and fellowships in immunology and hematology at the University of Miami, and received the Young Investigator Award for Excellence in the Field of Hematology from the International Society for Experimental Hematology. Dr. Sackstein is a bone marrow transplant physician and he also performs basic research to find new methods to improve the outcomes for patients undergoing bone marrow transplants. His laboratory efforts have helped define the molecular effectors of lymphocyte migration in graft-versus-host disease, and he is widely recognized for his contributions to the field of glycobiology and for the discovery of HCELL, a glycoform of CD44 that is a potent E-selectin ligand expressed on human hematopoietic stem cells. He is an Associate Professor of Dermatology and of Medicine at Harvard Medical School, and serves as the Head of the Translational Research Program of the Bone Marrow Transplantation Unit at the Massachusetts General Hospital, and is a Bone Marrow Transplant Physician at Brigham and Women's Hospital and the Dana-Farber Cancer Institute.

Relevant Publications:

• Shear flow-dependent integration of apical and subendothelial chemokines in T-cell transmigration: implications for locomotion and the multistep paradigm
• The lymphocyte homing receptors: gatekeepers of the multistep paradigm
• Ex vivo glycan engineering of CD44 programs human multipotent mesenchymal stromal cell trafficking to bone

Instructor, Harvard Medical School and Research Associate, Department of Surgery and Vascular Biology Program, Children's Hospital Boston

I received my undergraduate degree in Chemistry from the University of California, Santa Cruz and my doctorate degree in Pharmacology from the University of North Carolina at Chapel Hill (Advisor: Dr. Rudy Juliano). My research focused on understanding collaborative signaling pathways between integrin receptors and G-protein coupled receptors in endothelial cells. In 2000, I began my postdoctoral training (Dr. Bruce Zetter, Children's Hospital Boston). My research focused on the mechanism of thrombospondin's inhibitory effect on migration in endothelial cells. Thrombospondin 1 (TSP1) is an endogenous antiangiogenic protein, and some of its effects are mediated by binding of the type-1 repeat (TSR) domains to the cell surface receptor CD36. However, I showed that TSP1 and a TSR-containing peptide inhibited VEGF-induced migration of HUVEC, cells which do not express CD36. My studies led to the finding that Β1 integrins are a critical receptor in TSR-mediated inhibition of HUVEC migration. Thus, inhibition of migration by TSP1 appears to involve both CD36 and Β1 integrins and can be mediated solely by Β1 integrins in cells lacking CD36.

In 2006 I joined Dr. Folkman's laboratory as an Instructor of Surgery at Harvard Medical School and an investigator in the Vascular Biology Program at Children's Hospital. My major area of research has been in understanding the mechanism of several angiogenesis inhibitors in endothelial cell migration in different vascular beds. More recently, my research interests have included the study of LAM, a rare but progressive cystic lung disease characterized by abnormal and potentially metastatic growth of atypical smooth muscle-like LAM cells within lungs and axial lymphatics. I am focused on the isolation, characterization, expansion and functional studies of both the smooth muscle-like LAM cells and the LAM-associated lymphatic endothelial cells, and in investigating the role of angiogenic regulators in LAM disease.

Relevant Publications:

• Short, S. M., J. L. Boyer, and R. L. Juliano. (2000) Integrins regulate the linkage between upstream events in G protein-compled receptor signaling to mitogen-activated protein kinase. J. Biol Chem. 275 (17):12970-7
• Short, S. M., A. Derrien, R.P. Narsimhan, J. Lawler, D.E. Ingber, and B.R. Zetter. (2005) Inhibition of endothelial cell migration by thrombospondin-1 type-1 repeats is mediated by Beta-1 integrins. J. Cell Biol. 168(4):643-653.
• Italiano, J. E. Jr., J. L. Richardson, S. Patel-Hett, E. Battinelli, A. Zaslavsky, S. Short, S. Ryeom, J. Folkman, and G. L. Klement. (2008) Angiogenesis is regulated by a novel mechanism: pro- and ant-angiogenic proteins are organized into separate platelet alpha-granules and differentially released. Blood. 111(3):1227-33

Roland Stauber is professor of molecular and cellular oncology at the University Hospital in Mainz. After completing his training in Germany he worked at the NIH/NCI program directed by Dr. Vande Woude. His is dedicated in fostering interdisciplinary research among clinical and basic scientist in order to developing novel translation therapeutic strategies. As such, he was coordinating the CancerNet of the German National Genome Research Network. His laboratory is applying systematic genomic technologies to extract disease relevant information from patient material. By subsequently employing adequate in vitro and in vivo model systems, he identified novel proteins and molecular mechanism involved in tumor promotion, metastasis and therapy resistance. Joining the national Network of Chemical-Biology, his group is using cell based high-throughput screening assays to identify therapeutically relevant small molecule inhibitors. In particular, he is interested in dissecting the cellular networks regulated by the Survivin/Chromosomal Passenger Complex and exploiting their implications and therapeutic potential for LAM pathophysiology.

Relevant Publications:

• Knauer, S. K., Bier, C., Habtemichael, N., and Stauber, R. H. (2006). The Survivin-Crm1 interaction is essential for chromosomal passenger complex localization and function. EMBO Rep 7(12), 1259-65.
• Knauer, S. K., Kramer, O. H., Knosel, T., Engels, K., Rodel, F., Kovacs, A. F., Dietmaier, W., Klein-Hitpass, L., Habtemichael, N., Schweitzer, A., Brieger, J., Rodel, C., Mann, W., Petersen, I., Heinzel, T., and Stauber, R. H. (2007). Nuclear export is essential for the tumor-promoting activity of survivin. Faseb J 21(1), 207-16.
• Knauer, S. K., Moodt, S., Berg, T., Liebel, U., Pepperkok, R., and Stauber, R. H. (2005). Translocation biosensors to study signal-specific nucleo-cytoplasmic transport, protease activity and protein-protein interactions. Traffic 6(7), 594-606.
• Stauber, R. H., Mann, W., and Knauer, S. K. (2007). Nuclear and cytoplasmic survivin: molecular mechanism, prognostic, and therapeutic potential. Cancer Res 67(13), 5999-6002.

Dr. Cheryl Lyn Walker is the Ruth and Walter Sterling Professor of Carcinogenesis in the Department of Carcinogenesis, UT MD Anderson Cancer Center. She holds joint academic appointments in the College of Pharmacy at the University of Texas at Austin and in the College of Veterinary Medicine at Texas A&M University. She is also Director of the Genetics and Epigenetics of Early Life Exposures Focus Area for the National Institute for Environmental Health Sciences Center for Research on Environmental Disease.

Dr. Walker is currently Vice-President, Elect for the Society of Toxicology and is a member of the International Scientific Advisory Board for the Tuberous Sclerosis Alliance and the Scientific Advisory Board for the LAM Foundation. Previously, Dr. Walker has held appointments from the Department of Health and Human Services to the Board of Scientific Councilors of the National Toxicology Program and is a former Chair of the Environmental Genomics and Carcinogenesis Panel for the Congressionally mandated US-Japan Cooperative Medical Exchange Program. She is also a former member of the Board of Scientific Councilors of the National Cancer Institute and the National Academy of Sciences Committee on Emerging Issues and Data on Environmental Contaminants.

Dr. Walker's research is focused on the role of tumor suppressor genes in cancer and proliferative smooth muscle diseases including uterine leiomyoma and LAM. Her laboratory is actively investigating how signal transduction pathways, such as the PI3K pathway, become perturbed as a result of loss of function of tumor suppressor genes involved in kidney and uterine cancer including TSC-2 and PTEN. She has developed several unique animal models for studying the molecular defects that cause cancer, which are widely used for preclinical studies to identify new therapeutic interventions for several diseases, including LAM. Dr. Walker also has research interests in the area of mechanisms by which endogenous hormones and xenoestrogens in the environment promote disease.

Relevant Publications:

• Uterine Fibroids - The Elephant in the Room
• Interaction between genetic susceptibility and early-life environmental exposure determines tumor-suppressor-gene penetrance

Dr Watkins is an MD PhD gradute from the University of Western Australia, and trainined in pulmonology/critical care medicine before moving to the United States to pursue a career in basic cancer research. He is currently Assistant Professor of Oncology at the Johns Hopkins University Kimmel Cancer Center where he studies the basic and translational aspects of embryonic signaling pathways in cancer stem cell biology. His laboratory specializes in the development of xenograft models of cancer by direct transplanation of human cells into immunodeficient mice in order to study diseases such as leukemia, myeloma and lung cancer.

Postgraduate Training: Post Doctoral, Oncology, Johns Hopkins Kimmel Cancer Center, Baltimore, MD

Relevant Publications:

• Widespread requirement for Hedgehog ligand stimulation in growth of digestive tract tumours
• Hedgehog Signaling Progenetor Phenotype in Small-Cell Lung Cancer
• Hedgehog signalling within airway epithelial progenitors and in small-cell lung cancer

Vicky Holets Whittemore, Ph.D., is Vice President and Chief Scientific Officer at the Tuberous Sclerosis Alliance in Silver Spring, MD. Her nephew was diagnosed with Tuberous Sclerosis Complex (TSC) in 1985. Vicky and her son were diagnosed with TSC in 1990. Vicky received a B.S. in Zoology from Iowa State University in 1977 and a Ph.D. in Anatomy from the University of Minnesota in 1982. She did postdoctoral fellowships at the University of California, Irvine and the Karolinska Institute in Stockholm, and was on the faculty of University of Miami School of Medicine from 1986-1993. She served on the Board of Directors of the TS Alliance from 1987-1993, and joined the staff of the Tuberous Sclerosis Alliance in 1994 where she has worked to build the interest and support of TSC research. She is the co-editor of the third edition of Tuberous Sclerosis Complex, and is currently co-editing the fourth edition with two of her colleagues. She has authored more than 30 scientific publications. She serves on the Review Committee for the Collaboration, Education, Translational Testing (CETT) Program for the Office of Rare Diseases at the National Institutes of Health, and serves as the Vice-Chair of the Board of Directors of the National Coalition for Health Care Professional Education in Genetics (NCHPEG), and as a member of the National Advisory Council of the National Institute of Neurological Disorders and Stroke, National Institute of Health.

Lunyin Yu is an Instructor of Medicine at Harvard Medical School and working in Pulmonary & Critical Care Unit Research Laboratory at Massachusetts General Hospital. He has been studying on pulmonary hypertension and lung cancer. His research is focused on anti-proliferative effects of heparin on pulmonary arterial smooth muscle cells and lung cancer cells. He has revealed that p27 gene is critical for heparin inhibition of pulmonary hypertension in vitro and in vivo. He has found that NHE1 gene is a key determinant in development of hypoxic pulmonary hypertension and found a new signaling pathway in NHE1 regulating cell proliferation. He also has demonstrated anti-tumor effect of chemically modified heparin with low anticoagulation activity on lung cancer growth. Recently, his work is to investigate the inhibitory effect of the heparin derivative on lymphangioleiomyomatosis (LAM) cell proliferation.

Prior to joining the MGH, Dr. Yu worked on nutrition and cancer research at Beth Israel Deaconess Medical Center, Harvard Medical School. He had been engaged in cancer research, pathology teaching and pathological diagnosis in the Department of Pathology at Wuhan University School of Medicine before came to the United States.

Dr. Yu is the author of 40 scientific articles. He earned his M.D. and M. Sc. in Pathology from Wuhan University School of Medicine in Wuhan, China.

Relevant Publications:

• Yu L, Quinn DA, Garg HG and Hales CA. Cyclin-dependent Kinase inhibitor p27, but not p21, is required for inhibition of hypoxia-induced pulmonary hypertension and remodeling by heparin in mice. Circ Res. 2005; 97(9):937-945.
• Yu L, Quinn DA, Garg HG, Hales CA. Gene expression of cyclin-dependent kinase inhibitors and effect of heparin on their expression in mice with hypoxia-induced pulmonary hypertension. Biochem Biophys Res Commun. 2006; 345(4):1565-1572.
• Yu L, Quinn DA, Garg HG and Hales CA. Deficiency of NHE1 Gene Prevents Hypoxia-Induced Pulmonary Hypertension and Vascular Remodeling. Am. J. Respir. Crit. Care Med. 2008 Feb 28 [Epub ahead of print]

Amy is the founder and Executive Director of the LAM Treatment Alliance. She was diagnosed with LAM in April of 2005, and founded the LAM Treatment Alliance with the goal of fast tracking research to find a treatment for LAM. Amy is trained as a social scientist focused on the study of medicine/science, the law and society. She received her BA in political science from U.C. Berkeley and her PhD from Harvard University. She has completed a Fellowship in Medical Ethics at Harvard Medical School. She is currently an Instructor in the Department of Social Medicine at Harvard Medical School. Amy lives in Cambridge, MA with her husband, Michael Nurok, and their daughter Charlotte.