Multiple myeloma historical perspective

Jump to navigation Jump to search

Multiple myeloma Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Multiple Myeloma from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

Staging

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

Echocardiograph and Ultrasound

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Future or Investigational Therapies

Case Studies

Case #1

Multiple myeloma historical perspective On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Multiple myeloma historical perspective

All Images
X-rays
Echo and Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Multiple myeloma historical perspective

CDC on Multiple myeloma historical perspective

Multiple myeloma historical perspective in the news

Blogs on Multiple myeloma historical perspective

Directions to Hospitals Treating Multiple myeloma

Risk calculators and risk factors for Multiple myeloma historical perspective

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 1856, Dr. Heller described precipitation of urinary protein above a temperature of 50 degrees Celcius. This was eventually found to be the Bence Jones protein.
  • 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, Copeland and Geschickter reported the first large case series of multiple myeloma patients. They described 412 patients from 1848 to 1928 and noted that these patients had pathologic fractures, Bence Jones protein in the urine, renal dysfunction, and anemia.[3][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, Gally and Edelman recognized that Bence Jones urinary protein and the serum immunoglobulin light chain had the same amino acid composition. The In the same year, 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 2005, the International Staging System (ISS) was developed and cytogenetic classification was described.
  • 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

  1. Moehler T, Goldschmidt H. Multiple Myeloma. Springer Science & Business Media; 2011. https://books.google.com/books?isbn=3540857729
  2. Moehler T, Goldschmidt H. Multiple Myeloma. Springer Science & Business Media; 2011. https://books.google.com/books?isbn=3540857729
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 Kyle RA, Rajkumar SV (2008). "Multiple myeloma". Blood. 111 (6): 2962–72. doi:10.1182/blood-2007-10-078022. PMC 2265446. PMID 18332230.
  4. 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. 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.


Template:WikiDoc Sources