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Citation for the 1997 Fred Conrad Koch Award of The Endocrine Society to Wylie Vale |
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Professor and Head of the Clayton Foundation
Laboratories for Peptide Biology at the Salk Institute. This award is
made in recognition of his continued scholarship in endocrine research,
his effective mentorship of young scientists, and his active leadership
in the Society’s affairs.
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Beginning in 1981 with the isolation and characterization of CRH, the neuropeptide that integrates endocrine, visceral, and behavioral responses to stressors, other advances quickly followed. This impressive list includes: the characterization of hypothalamic GH-releasing hormone (GHRH); the discovery of activin A and the cloning of its receptor; the first established serine kinase. More recently, Wylie’s group cloned two classes of CRH receptors, a binding protein for CRH and a potential ligand for the second CRF receptor, urocortin. All of these are critical findings that have spawned independent fields of investigation. Each of these discoveries was not merely a feat of peptide and protein chemistry and molecular biology; rather, all were associated with significant relevant physiologic observations, new insights into fundamental neuroendocrine control mechanisms, and appropriate collaborations with clinical investigators to explore both their pathophysiology and therapeutic implications. In this latter regard, the Vale Department has been a model in establishing critical bench-to-bedside links leading not only to important therapeutic applications but also important pharmaceutical and industrial opportunities. Such collaborations unearthed the therapeutic value of paradoxical desensitization of gonadotrope secretion by GnRH agonists, leading to an effective means of "biochemical castration." This observation has now provided the basis for important new treatments for precocious puberty, prostate cancer, endometriosis, and polycystic ovarian disease, generating new treatments for thousands of patients. In recognition of these scientific accomplishments, Dr. Vale has received the Edwin B. Astwood Lectureship of The Endocrine Society, the Van Meter-Armour Prize Award of the American Thyroid Association, and the Vincent du Vigneaud Award of the American Peptide Society, and in 1992, Dr. Vale was elected to the National Academy of Sciences.
Similarly, the training, mentoring, and scientific generative activities of Dr. Vale and his group have been equally remarkable. Over the past 25 years, they have trained dozens of graduate and postdoctoral students from throughout the world, many of whom have returned to their native countries to establish independent centers of endocrine excellence following the effective model established by Wylie at the Salk Institute. In addition to his dynamic Directorship of the Clayton Foundation Laboratories for Peptide Biology, Dr. Vale has twice served as the Chairman of the Salk Institute Faculty and held numerous leadership positions within The Endocrine Society, including membership on the Council and serving as its President in 1992. He is currently President of the International Society of Endocrinology.
Despite these impressive accomplishments and the high intensity, sustained productivity they obviously require, Wylie has always remained a warm and engaging colleague, an unfailingly helpful collaborator, and an engaging friend who always has both time and special knack for advising peers and colleagues. To know Wylie is either to be engaged with him in a vigorous scientific discussion, to experience his insightful wit, or to feel the warmth of his collaborative concern. To know Wylie is also to know the importance that he holds of being a good father and husband and to experience the warmth and hospitality of his wife, Betty, and two daughters, Elizabeth and Susannah, all of whom Wylie holds as his first importance in life. Thus, it is a great pleasure to award the Koch Award to Wylie Vale, outstanding scientist, generative mentor, dynamic leader, and valued colleague and friend.
William F. Crowley, Jr., M.D.
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Citation for the 1997 Ernst Oppenheimer Memorial Award of The Endocrine Society to Pamela L. Mellon |
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Dr.
Mellon has made critical contributions to our understanding of the
regulation and development of the pituitary and hypothalamus and the
control of reproductive hormone genes. She is Professor of Reproductive
Medicine and Neuroscience at the University of California, San
Diego, School of Medicine.
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Dr. Mellon’s research interests are the molecular regulation and development of the neuroendocrine system. She has focused on the control of reproductive function by the hypothalamus and pituitary. Using targeted oncogenesis in transgenic mice, Dr. Mellon has created numerous cultured cell models for pituitary endocrine cells and hypothalamic neurons. The impact of the development of these models has been enormous, creating entirely new directions for molecular research in reproductive neuroendocrinology.
The creation of a series of pituitary cell lines representing sequential stages in development within several of the anterior pituitary endocrine cell lineages has allowed Dr. Mellon and her colleagues to significantly illuminate the developmental and hormonal regulation of hormone gene expression, synthesis, and secretion. One highlight of this research was the demonstration that the nuclear orphan receptor, Steroidogenic Factor I, regulates expression of the luteinizing hormone genes. Another major advance was the cloning of the GnRH receptor gene. The most recent development of thyrotrope and gonadotrope cell lines promises to continue this rich avenue of discovery.
The creation of immortal hypothalamic GnRH neurons has facilitated rapid advances in understanding the roles of neurotransmitters and transcriptional regulators in hypothalamic function. For example, this model allowed the demonstration that the GnRH pulse generator is intrinsic to the GnRH neuron because pulsatile secretion is reproduced by these clonal cells in culture. Dr. Mellon has also demonstrated the roles of POU-homeodomain and GATA transcription factors in neuron-specific regulation of the GnRH gene. A particularly novel advance has been the demonstration that the neurotransmitter cascade of glutamate, nitric oxide, and cGMP activate cGMP-dependent kinase to regulate gene expression in GnRH neurons. In addition to Dr. Mellon’s own important contributions, her generous provision of cells to researchers around the world has transformed the study of reproductive hormones at the cellular and molecular level.
On a personal note, Dr. Mellon and her husband, Dr. James Posakony, Professor of Biology at the University of California, San Diego, live near the beach in Del Mar. Their first child was born in April 1997. Dr. Mellon’s interests include cultivating orchids and traveling to historical and tropical locations and will now focus on her new daughter.
In summary, The Endocrine Society is proud to award the 1997 Ernst Oppenheimer Memorial Award to Pamela, whose scientific contributions to understanding the development of the pituitary and the regulation of GnRH in the hypothalamus, have been landmark in impact and quality. Together with the earlier Weitzman Award, the Oppenheimer Award represents not only the Society’s recognition of Pamela’s outstanding contributions, but also our expectation of future excellence from this remarkable endocrine investigator.
Samuel S. C. Yen, M.D., D.Sc.
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Citation for the 1997 Robert H. Williams Distinguished Leadership Award of The Endocrine Society to Dr. Hiroo Imura |
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was born in 1931 in Yokaichi
City, a small town near Kyoto. He received his M.D. degree in 1954 from
Kyoto University. During his internship and residency, he encountered
patients with Addison’s disease and Cushing’s syndrome, stimulating
an interest in endocrinology. He earned his Doctor of Medical Science
degree from Kyoto University in 1962 for studies on plasma bioactive
ACTH levels and responses to ACTH stimulation in patients with
glucocorticoid-induced hypothalamic-pituitary-adrenal suppression.
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He early investigated opioid peptides in human tissues and fluids, especially leumorphin, a potent six-receptor agonist derived from dynorphin. These studies prompted his interest in fluid balance and blood pressure control. He collaborated with Kazuwa Nakao beginning in 1984 to study atrial natriuretic peptide (ANP), a newly discovered cardiac hormone, human brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP), endothelins, and their receptors. They showed that ANP is also expressed in the ventricles of the failing heart and that BNP is a ventricular hormone in many species and a clinically useful marker of ventricular overload and myocardial infarction. Noting increased expression of CNP in proliferating endothelial cells, they postulated an endothelial natriuretic peptide system regulating vascular remodeling. They demonstrated the brain natriuretic peptide system is important in central control of fluid balance and blood pressure, antagonizing angiotensin II’s action, and postulated complementary roles for the central and peripheral natriuretic and renin-angiotensin systems in fluid homeostasis. In addition to his contributions to cardiovascular endocrinology, he has studied regulation of GH and PRL secretion, endocrine-immune interactions, pancreatic and gastrointestinal hormone physiology and diabetes. Dr. Imura’s research has employed techniques ranging from molecular biology to clinical investigation and resulted in over 800 original articles and 40 books, book chapters, and reviews.
His contributions have been recognized by the Sir Henry Dale Medal of the British Endocrine Societies, the Takeda Medical Award from the Takeda Science Foundation, the Erwin von Baelz Award from Boehringer Sohn Ingelheim, the Medical Award from the Japan Medical Association, and the Oceania Medal from the Society for Endocrinology. He has received an honorary Doctor of Laws degree from Brown University, is a member of the Japanese Academy, and is a Foreign Honorary Member of the American Academy of Arts and Sciences.
Dr. Imura has served as Professor at Kobe University and Professor and Chair of the Second Department of Medicine at Kyoto University School of Medicine for twenty years, during which he trained 245 postdoctoral fellows in endocrinology and metabolism.
He has served on the editorial boards of Clinical Endocrinology, Endocrinologia Japonica, Frontiers in Neuroendocrinology, Hypertension, Journal of Endocrinological Investigation, Journal of Neuroendocrinology, Molecular Aspects of Medicine, Molecular Biology and Medicine, Molecular and Cellular Endocrinology, Neuroendocrinology, Peptides, and The New England Journal of Medicine; as President of the Western Section of the Japan Endocrine Society; Councilor, Council Chair and President of the Japan Endocrine Society; Councilor and President of the Japan Diabetic Society; Vice-President of the 7th Asia and Oceania Congress of Endocrinology; Chair of the Program Organizing Committee of the 7th International Congress of Endocrinology; Chair of the Local Organizing Committee for the 8th International Congress of Endocrinology, a memorable meeting held in Kyoto; Councilor of the International Society of Neuroendocrinology; and Executive Committee Chair, President and Honorary President of the International Society of Endocrinology. He organized a TransPacific Symposium that was first held at the 1997 Endocrine Society Annual Meeting.
In addition to serving as department chair in one of Japan’s two most prestigious universities, Dr. Imura was Dean of the Faculty of Medicine and has been President of Kyoto University since 1991. In this role, he is in the forefront of a movement to revamp the university system in Japan to produce future world-class scientists.
During his exceptional career, Dr. Imura has provided enlightened leadership in endocrinology for his university, his country, and the international endocrine community. In recognition of his many contributions, The Endocrine Society has named Dr. Hiroo Imura the recipient of the 1997 Robert H. Williams Distinguished Leadership Award.
David N. Orth, M.D.
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Citation for the 1997 Edwin B. Astwood Lecture Award of The Endocrine Society to John D. Baxter |
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was born in Lexington, Kentucky,
where he attended high school and the University of Kentucky. He
distinguished himself at both institutions by his academic and athletic
records. He was the star of the track team at both institutions. His
outstanding academic performance at the University led to his election
to Phi Beta Kappa and to his graduation cum laude in 1962. He chose a
career in medicine and graduated from the Yale Medical School in 1966.
During medical school, he continued to receive prizes acknowledging his
academic prowess. He was elected to Alpha Omega Alpha and served as
Class Marshal. Of interest was the fact that, during medical school,
John received the Parker Prize, which was awarded to the student
showing the best qualifications for a career as a successful
practitioner. Although the practice of medicine never did become the
dominant theme of his professional life, the award foreshadowed John’s
continuing interest and commitment to clinical medicine. He also
graduated cum laude from Yale Medical School.
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During these years, Dr. Baxter’s area of research spanned an ever increasing range of contemporary endocrinology. His initial studies represented an extension of his mentor’s work in the molecular basis of glucocorticoid action. His interests subsequently broadened to include the molecular biology and actions of mineralocorticoids, adrenocorticotropin, renin, GH, chorionic somatotropin, PRL, epidermal growth factor, atrial natriuretic factor, and endorphin. Further, he contributed significantly to evolutionary theory by comparing the genomic changes that underpin hormonal action in several species.
In the course of this research, Dr. Baxter made numerous important observations relating to the molecular basis of hormone action. These included the identification of specific messenger RNAs regulated by thyroid hormone and glucocorticoids, the demonstration that thyroid hormone causes the bending of the receptor, the first demonstration of a cellular glucocorticoid response element, and the first demonstration of negative glucocorticoid receptor control through competition for DNA binding.
However, his most important contribution to the receptor area may have
been made only recently. The December 14, 1995, issue of
Nature contained the first demonstration of
three-dimensional structure at atomic resolution of a small molecule
liganded to its receptor. The example was T3 bound to the
TR-
-1 receptor. Dr. Baxter coordinated the efforts of a team of
investigators represented by biophysicists, endocrinologists, and
biochemists. This structural analysis may pave the way for
understanding at an atomic level the most detailed mechanism by which
thyroid hormone initiates its action. Such insights may in turn lead to
the synthesis of new classes of "designer" drugs for the treatment
of disease.
Dr. Baxter is the recipient of multiple prizes and awards in recognition of these contributions. These include a Research Career Development Award from the NIH, the George W. Thorn Award for Research from the Howard Hughes Medical Institute, repre-sentation in the Hall of Distinguished Alumni of the University of Kentucky, a Citation for Distinguished Service from the American Society for Clinical Investigation, the Dautrebande Prize awarded by Queen Fabiola of Belgium for research in the field of molecular biology, the Goldblatt Award from the American Heart Association for his work on hypertension, and the Henry Christian Award from the American Federation for Clinical Research.
Dr. Baxter’s success as an investigator can also be gauged by his influence on the career of his trainees. Thirty of his trainees now occupy faculty positions at distinguished universities, two are departmental chairs, and many have been recognized in their own right by the receipt of prestigious awards for their research.
Jack H. Oppenheimer, M.D.
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Citation for the 1997 Gerald D. Aurbach Lecture Award of The Endocrine Society to Edward M. Brown |
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with the Gerald D. Aurbach Lecture Award in recognition
of his outstanding contributions to the field of mineral
metabolism.
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Showing great initiative, Ed adapted a cell dispersal method used by Kevin Catt’s lab at NIH to the study of parathyroid cells. His objective was to create a system suitable for detailed studies on the regulation of PTH secretion. At the time, it was appreciated from in vivo studies that PTH secretion was inhibited by extracellular ionized calcium, but the mechanism of inhibition was entirely obscure. Ed succeeded in setting up the dispersed cell system and was able to demonstrate that, in addition to calcium, PTH secretion is regulated by a variety of hormones. He found that dopamine stimulated secretion in bovine cells, an observation that led to the discovery of D1 (stimulatory) receptors.
In a pattern that has continued throughout his investigative career, Ed quickly applied the insights gained from his basic research to clinical problems. He was able to adapt his dispersed cell system to the study of pathologic parathyroid glands removed during surgery. Using this approach, he provided compelling evidence for a difference in sensitivity of PTH secretion to calcium in cells from hyperplastic vs. adenomatous glands. This observation was of practical significance, as he showed that cells that failed to shut off PTH secretion even at high calcium caused recurrent hyperparathyroidism if autotransplanted into patients who had undergone total parathyroidectomy.
After five years at NIH, Ed returned to the Brigham Hospital, setting up an independent research program focused on understanding how PTH secretion is regulated. While still at NIH, he had already shown that cAMP is a key second messenger of the effects of stimulatory neurotransmitters in parathyroid cells, but his data also showed that changes in cAMP alone could not adequately account for the inhibitory effect of extracellular calcium. In a series of key papers, Ed showed convincingly that inhibition of PTH secretion by extracellular calcium is associated with a rise in cytosolic ionized calcium. He showed that extracellular calcium effects were mimicked by other divalent and trivalent cations and by polycations such as neomycin. Because several of these cations were not cell-permeable, he suggested boldly that extracellular calcium might modulate PTH secretion by binding to a cell-surface receptor rather than by a mechanism involving transport of calcium across the cell membrane. In a landmark paper in 1991 in Physiological Reviews, he set out his hypothesis on the existence of a cell-surface "calcium-sensing" receptor.
At this point in his career, Ed showed the courage and perseverance evidenced by only a handful of scientists. He pursued a sabbatical in which he trained himself in molecular biology to accomplish his goal of cloning the putative calcium-sensing receptor. The paper published in 1993 in Nature documenting his success is sure to become a classic. Not only had he isolated a complementary DNA for a parathyroid calcium-sensing receptor (a member of the G protein-coupled receptor superfamily), but he also found that the receptor was expressed in several other tissues including brain and kidney. This has opened up an entirely new field of study and suggests the possibility that there may exist additional receptors regulated by extracellular ions.
A further bonus of this discovery was the observation that the human calcium-sensing receptor gene localizes to the same site on chromosome 3 that harbors the gene mutated in the autosomal dominantly inherited disease, familial (benign) hypocalciuric hypercalcemia (FBHH). This immediately suggested the receptor gene as a candidate for the FBHH gene, and in collaboration with the Seidman lab at the Brigham, Ed found mutations in the calcium receptor gene in individuals with FBHH. This provided compelling evidence for the physiologic importance of the receptor because the reduction in calcium sensitivity both in the parathyroid and kidney that is characteristic of FBHH could now be explained by a loss of function of one allele of the receptor gene. Furthermore, homozygous mutations in the receptor gene were shown to cause the rare condition of severe neonatal hyperparathyroidism. In addition to their diagnostic significance, identification of receptor mutations in FBHH offers key insights into the structure and function of the receptor. Ed has also identified gain of function mutations in the receptor in individuals with autosomal dominant hypoparathyroidism. A single amino acid substitution at a key residue apparently activates the receptor even at ambient low extracellular calcium concentrations. The consequence is inappropriate inhibition of PTH secretion. This extraordinary recent work shows no sign of abating; Ed’s lab is actively addressing a series of crucial questions, e.g. how does calcium bind to and activate the receptor, how does the receptor inhibit PTH secretion, and what is the function of the receptor in neurons and other cells? It is clear that Ed will continue to be at the forefront of efforts to answer these and related questions.
With all of his accomplishments, Ed remains a remarkably modest individual, ready to share credit, and more interested in scientific progress than personal recognition. Nonetheless, Ed has been recognized repeatedly and deservedly for his outstanding achievements. He has been elected to the American Society for Clinical Investigation as well as the Association of American Physicians. He has received the Fuller Albright Award of the American Society for Bone and Mineral Research, and the Research Prize of the Austrian Society for Bone and Mineral Research. He has been promoted to full Professor at Harvard Medical School. Ed has truly carried on the legacy of Gerry Aurbach’s pioneering work on PTH, mimicking so closely Gerry’s style in terms of brilliant scientific achievements, being an outstanding teacher and colleague, and retaining throughout a sense of humility. He is eminently deserving of the Gerald D. Aurbach Lecture Award.
Allen M. Spiegel, M.D.
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Citation for the 1997 Clinical Investigator Award of The Endocrine Society to George P. Chrousos |
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with the 1997 Clinical
Investigator Award in recognition of his contributions to our
understanding of the molecular mechanisms modulating the
hypothalamic-pituitary-adrenal (HPA) axis in health and disease. After
graduating from the Faculty of Medicine at Athens University and
completing house staff training in pediatrics in Athens and at New York
University Medical Center, Dr. Chrousos moved to the NIH in 1978 and
has essentially spent his entire research career there. Currently, Dr.
Chrousos is the Chief of the Section on Pediatric Endocrinology and
Director of the Pediatric Endocrinology Program in the National
Institute of Child Health and Human Development at the NIH.
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Dr. Chrousos further examined the interactions between the immune
system and the HPA axis. He found that several cytokines, including
interleukin I, tumor necrosis factor-, and interleukin-6, as well as
several lipid mediators of inflammation, induce profound stimulation of
the HPA axis by activation of the CRH neuron. Thus, it appears that
this neuron represents a crucial link between the immune and central
nervous systems.
Dr. Chrousos and his colleagues also cloned the regulatory region of the human CRH gene. They found a cAMP-binding protein-responsive element and several other key elements of the gene, including evidence for estrogenic regulation of this gene, which may explain the differential gender responsiveness of the HPA axis responsiveness observed in most species.
Additional research revealed that CRH is secreted locally at inflammatory sites and that CRH itself participates directly in the inflammatory response as a major proinflammatory agent. Dr. Chrousos identified "immune" or "tissue" CRH in many types of inflammation, including that associated with rheumatoid arthritis, thyroiditis, ulcerative colitis, and uveitis, suggesting that CRH is a general and ubiquitous inflammatory "cytokine."
Dr. Chrousos mapped the gene of the ACTH receptor to the short arm of chromosome 18 and studied families with hereditary isolated glucocorticoid deficiency, also known as congenital insensitivity to ACTH, for possible defects of this gene. He found that point mutations in key functional areas of the molecule caused the disease and that heterozygote carriers have exaggerated CRH-induced ACTH responses.
In the past few years, Dr. Chrousos and his group have studied the molecular mechanisms of adrenal tumorigenesis. They found a monoclonal origin of adrenocortical tumors and identified p53 mutations in one-third of adrenal malignant tumors. They also studied the genetics and molecular pathophysiology of Carney Complex, a multiple neoplasia and lentiginosis syndrome involving the adrenal glands and transmitted in an autosomal dominant fashion. They mapped the defective gene to the short arm of chromosome 2 and that the gene was most likely an oncogene rather than a tumor suppressor gene.
Dr. Chrousos has exceptional abilities in conducting and teaching of basic and clinical investigation, always working in difficult areas of clinical importance. He has trained a substantial number of investigators who have already risen to leadership positions in academia, both in the U.S. and abroad. He has made many pioneering and seminal contributions to endocrinology that opened new avenues of research. Attesting to the caliber of his research contributions, Dr. Chrousos is an elected member of the American Society for Clinical Investigation and the Association of American Physicians. In 1987, he received The Endocrine Society’s Richard Weitzman Award, which recognizes outstanding achievements in the fields of endocrinology and metabolism by an exceptionally promising young investigator. Also more recently, Dr. Chrousos received the Superior Service Award of the Public Health Service for "pioneering studies on the regulation of HPA axis function, leading to new insights into the pathophysiology of adrenal diseases and novel diagnostic strategies." Dr. Chrousos richly deserves the Clinical Investigator Award for outstanding contributions to our understanding the molecular mechanisms of disorders of the HPA, combining both bench and clinical research approaches in his work.
Judith L. Vaitukaitis, M.D.
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Citation for the 1997 Sidney H. Ingbar Distinguished Service Award of The Endocrine Society to William Rosner |
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William Rosner is probably the leading figure in steroid-protein
interaction. A native New Yorker, Dr. Rosner received his undergraduate
education at the University of Wisconsin, his M.D. degree from the
Albert Einstein College of Medicine, Bronx, New York, and his training
as an internist at Chapel Hill, North Carolina, and at Bellevue
Hospital in Manhattan. In 1964, he joined the laboratory of N. P.
Christy in the Department of Medicine at Columbia University’s College
of Physicians and Surgeons. During his fellowship and for the three
decades thereafter, Rosner honed his skills as a clinical
endocrinologist and investigator, became a seasoned internist and
teacher, trained himself in depth as a biochemist and biophysicist, and
published, independently and with his group, over a hundred original
studies in journals of the highest quality (The Journal of
Biological Chemistry, The Journal of Clinical Investigation,
Endocrinology, and Proceedings of the National Academy of Sciences of
the United States of America). His work has won him election to
this Society, the American Society for Clinical Investigation, the New
York Academy of Sciences, and, unusual for a physician, to the American
Society for Biochemistry and Molecular Biology. His high standing as a
scientist has been recognized by appointment to prestigious posts:
membership in the Endocrinology Study Section (NIH), Editor-in-Chief of
Steroids, Chairman of the Special NIH Study Section on
Regulation of Prostate Growth, and Consultant in Endocrinology to
Cancer and Leukemia Group B. Simultaneously, he has directed the
Division of Endocrinology at Columbia’s St. Luke’s/Roosevelt Hospital
Center, engaged in a limited practice in endocrinology, rigorously
taught students, residents, and fellows, and served effectively on
numerous University and Hospital committees, advancing academically
from Instructor to tenured Professor of Medicine at Columbia in the
short space of 15 years.
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Rosner’s invaluable services to The Endocrine Society form the major basis for the 1997 Ingbar Award. He has served on a half dozen Society committees and will shortly assume the role of Chairman of the Publications Committee. During his tenure as a member and later as Chairman of the Finance Committee, his efforts transformed the Society. Dr. David Orth accepted the position of Secretary-Treasurer only on condition that Dr. Rosner chair the Finance Committee, as did Orth’s successor, Dr. Robert Jaffe. In those years (1988–1995) the Society’s net assets grew from $2.6 to over $5 million, revenues from $1.6 to $11 million, and expenses from $1.6 to $9.3 million. The Society almost doubled in size to 8,000 members; Dr. Rosner totally reorganized and expanded its Council and committee structure, took on self-publication of all its four journals, restructured several other annual meetings, thought through the financial basis for hosting the 10th International Congress of Endocrinology (1996), increased the central office staff from 5 to 27, doubled its office space, and moved into new quarters, all while protecting and expanding its cash reserves and investment portfolio. It was Dr. Rosner who continually and indefatigably supplied thorough analyses of annual budgets, the long-range view of where the Society was heading, the prudent management of our investments, the thoughtful consideration of cost vs. benefit, and the willingness to say "No" to good causes that the Society simply could not afford, even when Rosner’s negative but necessary position was unpopular.
For these imaginative and unique contributions, for his astonishing, unflagging, and productive energy, his skills in managing and persuading people, and for his practical wisdom and unswerving devotion, The Endocrine Society is proud to give this Distinguished Service Award to William Rosner, who has worked for us in a manner that does honor to himself and to the memory of Sidney H. Ingbar.
Nicholas P. Christy, M.D.
(The writer takes pleasure in expressing his indebtedness to President-Elect David N. Orth, whose detailed description and analysis of Dr. Rosner’s work for the Society provided indispensable information.)
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Citation for the 1997 Richard E. Weitzman Memorial Award of The Endocrine Society to Donald P. McDonnell |
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Associate Professor, Department of Pharmacology, at
Duke University Medical Center. Donald has established his expertise as
a molecular endocrinologist through his pioneering experiments,
bringing the power of yeast genetics to bear upon problems in mammalian
cells and human tissues. By clever shuttling of approaches and reagents
back and forth between the lower and higher organisms, McDonnell
brought forth innovations in our thinking about the intranuclear
receptor superfamily. Most importantly, Donald has shared his expertise
and reagents widely within the field, and especially among members of
the Society. His conceptual advances have led himself and others to
provide a novel molecular understanding to the functions of sex
hormones in particular. As an emerging national spokesperson for
research into human disease, he has effectively bridged the chasm
between basic science and clinical research. Finally, from his
perspective within and allied with the pharmaceutical industry, Donald
brings a unique approach to using his talented research efforts to
devise new and more effective drugs for clinical use.
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In his first academic position, he turned his attention to the sex hormone receptors, overexpressing both estrogen and progesterone receptors in yeast, and adopted the yeast genetics tools to studies of these proteins. Mutational analysis of PR allowed his group to discover a PR mutation in which the antagonist RU38486 functioned as an agonist, whereas progesterone binding was completely eliminated. This observation led to the seminal view that a ligand’s definition as an agonist or antagonist was entirely context-sensitive. This concept allowed a simple yeast screen to be developed, through which receptor-modulating compounds could be found via high-throughput assays in yeast and mammalian cells. Donald left academics and accepted a scientific position at Ligand Pharmaceuticals, where he exploited the receptor mutation screening concept to develop nonsteroidal sex hormone mimetics.
As has often been the case in Donald’s career, an important conceptual advance resulted from this new drug discovery interest. Through mutational analysis of the estrogen receptor, McDonnell and his colleagues devised ER mutants lacking specific trans-activation domains, whose activity was altered in specific cells but not affected in other cells. This concept resulted in a paradigm useful to define ER ligands in terms of their tissue-selective activity. That concept provided an assay to use for discovery of coactivator proteins, expected to be the molecular mediators of tissue selectivity. Returning to yeast genetics, McDonnell proceeded to isolate mutant lines from which specific receptor-accessory protein genes could be identified. Confirmation of the genes in human cells brought further understanding to the mechanism of tissue-selective gene expression.
Donald returned to academics in 1994, when he accepted a position in the Pharmacology Department of Duke University. There his infectious enthusiasm and aggressive research style have attracted numerous students and fellows. He has turned his attention to the cornerstone of pharmacology, i.e. predicting biologic activity from molecular knowledge of the ligands. He has again capitalized upon his ability to shuttle both experimentally and conceptually between yeast and human cells, to begin to determine what hormone contacts account for selective activities in certain cells. In view of Dr. McDonnell’s molecular biology upbringing, his pharmaceutical past and pharmacologic present, there is little doubt that Dr. Weitzman would approve of this recipient, and would surely agree, "the future looks better still."
William T. Schrader, Ph.D.
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