Multiple myeloma historical perspective
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Haytham Allaham, M.D. [2] Shyam Patel [3]
Overview
Multiple myeloma was first discovered by Dr. Samuel Solly, a surgeon working in St.Thomas hospital in London in 1844.[1]The Bence Jones protein was first discovered by Dr. Henry Bence Jones and found to be associated with multiple myeloma in 1850; And the term “Bence Jones protein” was first used by Fleischer in 1880. PMID:29194778
Historical Perspective
- In 1844, Dr. Samuel Solly reported the first case of multiple myeloma. He was a a surgeon working in St. Thomas Hospital at London.[2][3] Dr. Solly treated patients with rhubard and orange peel.
- In 1845, abnormal urinary proteins were found to be associated with multiple myeloma. These were eventually coined as Bence Jones proteins. Dr. T. Watson treated patients with steel and quinine.
- In 1850, Dr. Henry Bence Jones first described the Bence Jones protein and found it to be associated with multiple myeloma.[4]
- In 1895, plasma cells were first described. It was later found that plasma cell proliferation was the cellular basis for multiple myeloma.[3]
- In 1928, the first large case series of multiple myeloma patients was reported.[3]
- In 1939, the monoclonal protein spike (M-spike) was described on protein electrophoresis. The M-spike was noted to be the gamma-globulin region.[3]
- In 1947, Dr. N. Alwall treated multiple myeloma patients with urethane.
- In 1956, light chains were recognized to be a component of multiple myeloma.[3]
- In the 1960s, the chemotherapy agent melphalan was shown to improve overall survival in multiple myeloma.[5]
- In 1958, Dr. N. Blokhin first used melphalan as a chemotherapy agent to treat multiple myeloma.[3]
- In 1961, the use of thalidomide was prohibited since it was found to be associated with birth defects.[5]
- In 1962, R.E. Maas demonstrated that corticosteroids could be used to treat multiple myeloma.[3]
- In 1975, the Durie-Salmon staging system was developed.[3]
- In 1983, T.J. McElwain and R.L. Powles showed that autologous stem cell transplant could be used to treat multiple myeloma.[3]
- In the 1990s, it was shown that high-dose therapy with autologous stem cell rescue led to improved patient outcomes.[5]
- In 1999, Singhal and colleagues showed that thalidomide had a 32% response rate in a phase II clinical trial of relapsed/refractory multiple myeloma.
- In 2003, the proteasome inhibitor bortezomib was approved by the U.S. Food and Drug Administration for the treatment of multiple myeloma.
- In 2014, the International Myeloma Working Group (IMWG) revised the diagnostic criteria for active multiple myeloma to include bone marrow [[plasma cell burden of 60% or greater, serum free light chain ratio of involved-to-uninvolved light chain of 100 or greater, and greater than 1 bony lesion on MRI measuring at least 5mm. The advent of the 2014 diagnostic criteria increased the proportion of patients diagnosed with active multiple myeloma.
References
- ↑ Moehler T, Goldschmidt H. Multiple Myeloma. Springer Science & Business Media; 2011. https://books.google.com/books?isbn=3540857729
- ↑ Moehler T, Goldschmidt H. Multiple Myeloma. Springer Science & Business Media; 2011. https://books.google.com/books?isbn=3540857729
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 Kyle RA, Rajkumar SV (2008). "Multiple myeloma". Blood. 111 (6): 2962–72. doi:10.1182/blood-2007-10-078022. PMC 2265446. PMID 18332230.
- ↑ Kyle RA, Steensma DP (2011). "History of multiple myeloma". Recent Results Cancer Res. 183: 3–23. doi:10.1007/978-3-540-85772-3_1. PMID 21509678.
- ↑ 5.0 5.1 5.2 Hong J, Lee JH (2016). "Recent advances in multiple myeloma: a Korean perspective". Korean J Intern Med. 31 (5): 820–34. doi:10.3904/kjim.2015.408. PMC 5016289. PMID 27604794.