Stephen L. Hauser

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Stephen L. Hauser
Dr. Stephen Hauser.jpg
Born (1949-12-14) December 14, 1949 (age 73)
New York, New York, U.S.
NationalityAmerican
Alma mater Harvard Medical School
Known for multiple sclerosis research
bioethics
AwardsJohn Dystel Prize for Multiple Sclerosis Research (2008)
Charcot Award (2013)
Scientific career
Fields Neurology, neuroimmunology
Institutions University of California, San Francisco

Stephen L. Hauser is a professor of the Department of Neurology at the University of California, San Francisco (UCSF) specializing in immune mechanisms and multiple sclerosis (MS). He has contributed to the establishment of consortia that have identified more than 50 gene variants that contribute to MS risk. [1]

Contents

Research

Hauser is a principal investigator of a multinational effort to identify genetic effects on MS. He is part of the team that identified that humoral immune mechanisms are important in the pathogenesis of MS lesions, leading to the development of B-cell based therapies for MS. He has contributed to the establishment of nationwide and international genetics consortia that have identified more than 50 gene variants that contribute to MS risk. [1]

Using comparative genomics between African-American and Caucasian MS populations, Hauser's group was able to identify HLA-DRB1 as the primary MS signal in the MHC, [2] and also fine map other secondary loci in this region.

In 2007, as a senior organizer of the International Multiple Sclerosis Genetics Consortium (IMSGC), he helped identify the first two non-HLA genes involved in MS susceptibility, IL-2R (CD25) and IL-7R (CD127). [3]

In 2010, his laboratory published the complete genome sequences and the epigenome of identical twins discordant for MS. By mid-2011 more than fifty MS-associated risk alleles were identified, and by now nearly the entire array of common variants associated with MS susceptibility have been mapped. [1]

Hauser has also focused on the role of the B cell and immunoglobulin in the pathogenesis of the disease. He developed and characterized an MS disease model that replicated the core feature of vesicular demyelination previously observed in MS, and demonstrated that this pathology resulted from the synergistic effects of autoreactive T-cells and pathogenic autoantibodies.[ citation needed ] In 1999 he published work identifying specific myelin reactivity of these autoantibodies deposited in areas of myelin damage in MS brains. [4]

Hauser has translated this finding into a new potential therapy for MS. He led a large-scale clinical trial with rituximab, [5] a chimeric monoclonal antibody that depletes CD20+ B cells, and demonstrated robust efficacy in relapsing remitting MS. A second trial in primary progressive MS reported in 2009 that rituximab may be similarly effective in patients with primary progressive MS who also have evidence of ongoing inflammatory CNS disease. More recently, a third clinical trial with a fully humanized anti-CD20 monoclonal antibody, ocrelizumab, replicated the results of the rituximab trial in relapsing remitting MS. [6] With the MS Bioscreen project, Hauser has pioneered precision medicine for complex diseases like MS, creating an "actionable digital growth-chart for complex traits" [7]

Service

In 2010 Hauser was appointed to the Presidential Commission for the Study of Bioethical Issues. [8] He is a co-editor of the textbook Harrison's Principles of Internal Medicine [9] and past editor-in-chief of the Annals of Neurology . [10] [ failed verification ]

Education

Hauser trained in internal medicine at the New York Hospital-Cornell Medical Center, in neurology at the Massachusetts General Hospital (MGH), and in immunology at Harvard Medical School and the Institute Pasteur in Paris, France, and was a faculty member at Harvard Medical School before moving to UCSF. [11]

Awards and honors

Hauser received the 2013 Charcot Award from the Multiple Sclerosis International Federation, [12] the Jacob Javits Neuroscience Investigator Award, [13] and the John-Dystel Prize for Multiple Sclerosis Research. [14] In 2011 he delivered the Robert Wartenberg Lecture at the American Academy of Neurology, an honor given for excellence in clinically relevant research. [15]

Hauser is the chair of the Committee on Gulf War and Health Outcomes for the Institute of Medicine [16] and a Fellow of the American Academy of Arts and Sciences and the Association of American Physicians. [17]

Related Research Articles

<span class="mw-page-title-main">Multiple sclerosis</span> Disease that damages the myelin sheaths around nerves

Multiplesclerosis (MS) is a degenerative disease in which the insulating covers called myelin sheaths, of nerve cells in the brain and spinal cord are damaged. This damage disrupts the ability of parts of the nervous system to transmit signals, resulting in a range of signs and symptoms, including physical, mental, and sometimes psychiatric problems. Specific symptoms can include double vision, visual loss, muscle weakness, and trouble with sensation or coordination. MS takes several forms, with new symptoms either occurring in isolated attacks or building up over time. In the relapsing forms of MS, between attacks, symptoms may disappear completely, although some permanent neurological problems often remain, especially as the disease advances.

<span class="mw-page-title-main">Interferon beta-1a</span> Cytokine in the interferon family

Interferon beta-1a is a cytokine in the interferon family used to treat multiple sclerosis (MS). It is produced by mammalian cells, while interferon beta-1b is produced in modified E. coli. Some research indicates that interferon injections may result in an 18–38% reduction in the rate of MS relapses.

<span class="mw-page-title-main">Fingolimod</span> Chemical compound

Fingolimod, sold under the brand name Gilenya, is an immunomodulating medication, mostly used for treating multiple sclerosis (MS). Fingolimod is a sphingosine-1-phosphate receptor modulator, which sequesters lymphocytes in lymph nodes, preventing them from contributing to an autoimmune reaction. It has been reported to reduce the rate of relapses in relapsing-remitting multiple sclerosis by approximately one-half over a two-year period.

<span class="mw-page-title-main">Natalizumab</span> Medication used to treat multiple sclerosis and Crohns disease

Natalizumab, sold under the brand name Tysabri among others, is a medication used to treat multiple sclerosis and Crohn's disease. It is a humanized monoclonal antibody against the cell adhesion molecule α4-integrin. It is given by intravenous infusion. The drug is believed to work by reducing the ability of inflammatory immune cells to attach to and pass through the cell layers lining the intestines and blood–brain barrier.

Interferon beta-1b is a cytokine in the interferon family used to treat the relapsing-remitting and secondary-progressive forms of multiple sclerosis (MS). It is approved for use after the first MS event. Closely related is interferon beta 1a, also indicated for MS, with a very similar drug profile.

<span class="mw-page-title-main">Cladribine</span> Pharmaceutical drug

Cladribine, sold under the brand name Leustatin, among others, is a medication used to treat hairy cell leukemia and B-cell chronic lymphocytic leukemia. Cladribine, sold under the brand name Mavenclad, is used for the treatment of adults with highly active forms of relapsing-remitting multiple sclerosis.

<span class="mw-page-title-main">Alemtuzumab</span> Medication used to treat chronic lymphocytic leukemia (CLL)

Alemtuzumab, sold under the brand names Campath and Lemtrada among others, is a medication used to treat chronic lymphocytic leukemia (CLL) and multiple sclerosis. In CLL, it has been used as both a first line and second line treatment. In MS it is generally only recommended if other treatments have not worked. It is given by injection into a vein.

Experimental autoimmune encephalomyelitis, sometimes experimental allergic encephalomyelitis (EAE), is an animal model of brain inflammation. It is an inflammatory demyelinating disease of the central nervous system (CNS). It is mostly used with rodents and is widely studied as an animal model of the human CNS demyelinating diseases, including multiple sclerosis (MS) and acute disseminated encephalomyelitis (ADEM). EAE is also the prototype for T-cell-mediated autoimmune disease in general.

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease that affects the central nervous system (CNS). Several therapies for it exist, although there is no known cure.

<span class="mw-page-title-main">Glatiramer acetate</span> Medication

Glatiramer acetate, sold under the brand name Copaxone among others, is an immunomodulator medication used to treat multiple sclerosis. Glatiramer acetate is approved in the United States to reduce the frequency of relapses, but not for reducing the progression of disability. Observational studies, but not randomized controlled trials, suggest that it may reduce progression of disability. While a conclusive diagnosis of multiple sclerosis requires a history of two or more episodes of symptoms and signs, glatiramer acetate is approved to treat a first episode anticipating a diagnosis. It is also used to treat relapsing-remitting multiple sclerosis. It is administered by subcutaneous injection.

Inflammatory demyelinating diseases (IDDs), sometimes called Idiopathic (IIDDs) due to the unknown etiology of some of them, are a heterogenous group of demyelinating diseases - conditions that cause damage to myelin, the protective sheath of nerve fibers - that occur against the background of an acute or chronic inflammatory process. IDDs share characteristics with and are often grouped together under Multiple Sclerosis. They are sometimes considered different diseases from Multiple Sclerosis, but considered by others to form a spectrum differing only in terms of chronicity, severity, and clinical course.

Ocrelizumab, sold under the brand name Ocrevus, is a medication used for the treatment of multiple sclerosis (MS). It is a humanized anti-CD20 monoclonal antibody. It targets CD20 marker on B lymphocytes and is an immunosuppressive drug. Ocrelizumab binds to an epitope that overlaps with the epitope to which rituximab binds.

<span class="mw-page-title-main">Laquinimod</span> Chemical compound

Laquinimod is an experimental immunomodulator developed by Active Biotech and Teva. It is being investigated as an oral treatment for multiple sclerosis (MS).

Research in multiple sclerosis may find new pathways to interact with the disease, improve function, curtail attacks, or limit the progression of the underlying disease. Many treatments already in clinical trials involve drugs that are used in other diseases or medications that have not been designed specifically for multiple sclerosis. There are also trials involving the combination of drugs that are already in use for multiple sclerosis. Finally, there are also many basic investigations that try to understand better the disease and in the future may help to find new treatments.

<span class="mw-page-title-main">Dirucotide</span> Chemical compound

Dirucotide (also known as MBP8298) was developed by two research scientists (Dr. Kenneth G. Warren, MD, FRCP(C) & Ingrid Catz, Senior Scientist) at the University of Alberta for the treatment of Multiple Sclerosis (MS). Dirucotide is a synthetic peptide that consists of 17 amino acids linked in a sequence identical to that of a portion of human myelin basic protein (MBP). The sequence of these 17 amino acids is

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<span class="mw-page-title-main">Alastair Compston</span> British neurologist (born 1948)

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There are several ways for pharmaceuticals for treating multiple sclerosis (MS) to reach the market.

Rhonda Renee Voskuhl is an American physician, research scientist, and professor. She is a member of the Brain Research Institute (BRI) at the David Geffen School of Medicine at UCLA and is the director of its Multiple Sclerosis Program. Voskuhl has published numerous scientific articles in academic journals and has served in the role of principal investigator for several treatment trials investigating potential treatments for multiple sclerosis (MS).

Anne Cross is an American neurologist and neuroimmunologist and the Section Head of Neuroimmunology at Washington University School of Medicine in St. Louis, Missouri. Cross holds the Manny and Rosalyn Rosenthal–Dr. John L. Trotter Endowed Chair in Neuroimmunology at WUSTL School of Medicine and co-directs the John L Trotter Multiple Sclerosis Clinic at Barnes-Jewish Hospital. Cross is a leader in the field of neuroimmunology and was the first to discover the role of B cells in the pathogenesis of multiple sclerosis in animals and then in humans. Cross now develops novel imaging techniques to observe inflammation and demyelination in the central nervous systems of MS patients for diagnosis and disease management.

References

  1. 1 2 3 The International Multiple Sclerosis Genetics Consortium & The Wellcome Trust Case Control Consortium 2; et al. (2011). "Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis". Nature . 476 (7359): 136–144. Bibcode:2011Natur.476..214T. doi:10.1038/nature10251. PMC   3182531 . PMID   21833088.
  2. ↑ Jorge R. Oksenberg; et al. (2004). "Mapping multiple sclerosis susceptibility to the HLA-DR locus in African Americans". American Journal of Human Genetics . 74 (1): 160–167. doi:10.1086/380997. PMC   1181903 . PMID   14669136.
  3. ↑ The International Multiple Sclerosis Genetics Consortium; et al. (2007). "Risk alleles for multiple sclerosis identified by a genomewide study". The New England Journal of Medicine. 357 (9): 851–62. doi: 10.1056/NEJMoa073493 . PMID   17660530. S2CID   25757453.
  4. ↑ Genain CP, Hauser SL.; Hause (2001). "Experimental allergic encephalomyelitis in the New World monkey Callithrix jacchus". Immunological Reviews. 183: 159–72. doi:10.1034/j.1600-065x.2001.1830113.x. PMID   11782255. S2CID   42786895.
  5. ↑ Hauser, SL; Waubant, E; Arnold, DL; Vollmer, T; Antel, J; Fox, RJ; Bar-Or, A; Panzara, M; Sarkar, N; Agarwal, S; Langer-Gould, A; Smith, CH; Hermes Trial, Group (2008). "B-cell depletion with rituximab in relapsing-remitting multiple sclerosis". The New England Journal of Medicine . 358 (7): 676–88. doi:10.1056/NEJMoa0706383. PMID   18272891. S2CID   38840028.
  6. ↑ Kappos, Ludwig; Li, David; Calabresi, Peter A; O'Connor, Paul; Bar-Or, Amit; Barkhof, Frederik; Yin, Ming; Leppert, David; Glanzman, Robert; Tinbergen, Jeroen; Hauser, Stephen L (2011). "Ocrelizumab in relapsing-remitting multiple sclerosis: A phase 2, randomised, placebo-controlled, multicentre trial". The Lancet . 378 (9805): 1779–87. doi:10.1016/S0140-6736(11)61649-8. PMID   22047971. S2CID   21500502.
  7. ↑ Gourraud P.-A.; Henry R. G.; Cree B. A. C.; Crane J. C.; Lizee A.; Olson M. P.; Santaniello A. V.; Datta E.; Zhu A. H.; Bevan C. J.; Gelfand J. M.; Graves J. S.; Goodin D. S.; Green A. J.; von Büdingen H.-C.; Waubant E.; Zamvil S. S.; Crabtree-Hartman E.; Nelson S.; Baranzini S. E.; Hauser S. L. (2014). "Precision medicine in chronic disease management: The multiple sclerosis BioScreen". Ann Neurol. 76 (5): 633–642. doi:10.1002/ana.24282. PMC   4214886 . PMID   25263997.
  8. ↑ "Stephen L. Hauser, M.D." Presidential Commission for the Study of Bioethical Issues. Retrieved 2014-01-22.
  9. ↑ "Harrison's Principles of Internal Medicine, 18e". AccessMedicine. McGraw-Hill Medical. 2013-10-31. Retrieved 2014-01-22.
  10. ↑ "About This Journal". Annals of Neurology. Wiley Online Library. doi: 10.1002/(ISSN)1531-8249 .
  11. ↑ UCSF profile, ucsf.edu; accessed April 20, 2015.
  12. ↑ "Charcot Award". Multiple Sclerosis International Foundation. 2013-03-15. Retrieved 2014-01-23.
  13. ↑ "Stephen Hauser: Executive Profile & Biography". Bloomberg Businessweek . Bloomberg. Retrieved 2014-01-23.[ dead link ]
  14. ↑ "John Dystel Prize". National MS Society. Retrieved 2014-01-23.
  15. ↑ "Department of Neurology: Honors and Awards". UCSF Department of Neurology. Retrieved 2014-01-23.
  16. ↑ "Stephen Hauser". Directory. Institute of Medicine. 2013-09-19. Archived from the original on 2010-04-16. Retrieved 2014-01-22.
  17. ↑ "Member Directory". Association of American Physicians. Retrieved 2014-01-23.
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