Nicholas Chiorazzi

Nicholas Chiorazzi
Nationality American
Education Georgetown University School of Medicine
Occupation Physician, Scientist
Employer The Feinstein Institute for Medical Research
Known for Medical Research
Website

Nicholas Chiorazzi, physician and researcher, is Head of the Karches Center for Chronic Lymphocytic Leukemia Research at The Feinstein Institute for Medical Research in Manhasset, NY.[1]

Education

Dr. Nicholas Chiorazzi received his M.D. from Georgetown University School of Medicine and completed 4 years of internal medicine training in the Cornell Cooperating Hospitals program at North Shore University Hospital and Memorial Sloan-Kettering Cancer Center. He is also trained in Rheumatology and in Allergy-Clinical Immunology.

Academic appointments

Dr. Chiorazzi was a research fellow in immunology at Harvard University in the department of Baruj Benacerraf, M.D., who a few years later shared the Nobel Prize in Physiology or Medicine. Dr. Chiorazzi was then worked with Henry G. Kunkel at The Rockefeller University. At Rockefeller, his time was spent studying human B cells in normal and disease settings. In 1987, Dr. Chiorazzi was appointed Chief of the then newly created Division of Rheumatology & Allergy-Clinical Immunology at North Shore University Hospital. In 2000, he was appointed the first Director and CEO of the Feinstein Institute for Medical Research, a position he held until January 2006. Dr. Chiorazzi is currently Professor of Medicine and of Cell Biology in the Albert Einstein College of Medicine[2] and Head of the Karches Center for Chronic Lymphocytic Leukemia Research at The Feinstein Institute for Medical Research.[1]

Principal scientific contributions

Dr. Chiorazzi's research interests revolve around understanding the activation and maturation of B-lymphocytes in health and disease, in particular chronic lymphocytic leukemia (CLL). Dr. Chiorazzi and his colleagues have demonstrated that: CLL cells are responsive to signals from the internal microenvironment, in particular those delivered by the B-cell antigen receptor (BCR) leading to leukemic cell proliferation and maturation or death; BCR-induced signals are likely delivered by common self antigens and are mediated through sets of BCRs of remarkably similar amino acid structure;[3] patients with CLL segregate into two subgroups based on BCR structure that differ dramatically in clinical outcome;[4] CLL cells proliferate and die in vivo at rates higher than originally appreciated. These findings have led to the view that (auto)antigen drive is a promoting factor in the development and evolution of CLL and have been a pivotal in refining patient prognosis.

Awards and honors

Selected publications

References

  1. 1 2 "Centers of Excellence". Feinstein Institute for Medical Research. Retrieved 1 August 2011.
  2. "Faculty Profile: Nicholas Chi orazzi". Albert Einstein College of Medicine Directory. Retrieved 1 August 2011.
  3. "B-cell chronic lymphocytic leukemia cells express a surface membrane phenotype of activated, antigen-experienced B lymphocytes". Blood. 99 (11): 4087–4093. 2002. doi:10.1182/blood.v99.11.4087. PMID 12010811.
  4. "Telomere length and telomerase activity delineate distinctive replicative features of the B-CLL subgroups defined by immunoglobulin V gene mutations". Blood. 103 (2): 375–382. 2004. doi:10.1182/blood-2003-04-1345. PMID 14504108.
  5. "Membership Lists". The American Society for Clinical Investigation. Retrieved 1 August 2011.
  6. "Membership Directory". Association of American Physicians. Retrieved 1 August 2011.
  7. "Annual Report 2000" (PDF). Lupus NY. Retrieved 1 August 2011.
  8. "Founding Members Page". Association for Patient Oriented Research. Retrieved 1 August 2011.
  9. "Editorial Board". Molecular Medicine. Retrieved 1 August 2011.
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