Chronic myelogenous leukemia historical perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: James Nasr[2]
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Overview
In the 1840s, the first cases of chronic myelogenous leukemia (splenomegaly with high leukocyte count) was reported in France, Germany, and Scotland. In 1960, the association of Philadelphia chromosome with the pathogenesis of chronic myelogenous leukemia was first discovered. In 1973, (9;22) translocation was first discovered. Definition of the breakpoint cluster region (BCR) on chromosome 22 was first reported in 1984 and the demonstration of the BCR-ABL transcript in CML was first discovered in 1985. CML was previously classified into five subtypes. This has been replaced with a newer model, where it was classified into three phases. In 2022, the World Health Organisation eliminated one of these phases, leaving two remaining categories. From 1980 on wards allogeneic stem cell transplantation (SCT) became the treatment of choice for eligible patients. In 1998, the era of tyrosine kinase inhibitors (TKI) began. TKIs have drastically changed the therapeutic landscape of CML, converting it from a fatal leukemia to a chronic, highly manageable disease.
Historical Perspective
Important dates in chronic myelogenous leukemia:
- The early history of leukemia reaches back 200 years.[1]
- In 1811, Peter Cullen defined a case of splenitis acutus with un explainable milky blood.
- Alfred Velpeau, mentioned the leukemia associated symptoms, and observed pus in the blood vessels (1825).
- Alfred Donné, demonstrated a maturation arrest of the white blood cells (1844).
- John Bennett named the disease leucocythemia, based on the microscopic collection of purulent leucocytes (1845).
- In 1845, Edinburgh pathologist, John Hughes Bennett, presented a “Case of Hypertrophy of the Spleen and Liver in which Death Took Place from Suppuration of the Blood” in the Edinburgh Medical Journal.[2]
- Few weeks later, Rudolf Virchow, in Berlin published a similar case.
- In 1872, Ernst Neumann stated that leukemia cells originated in the bone marrow.
- The next decades described the pathophysiologic differentiation into myeloid versus lymphoid and acute versus chronic leukemias.
- In 1973, (9;22) translocation was discovery by Philadelphia cytogeneticists Peter Nowel and David Hungerford of an abnormally small G-group chromosome that we know as the Philadelphia chromosome (Ph).[3]
- In 1986 Janet Rowley established that Ph was the product of a reciprocal translocation between chromosomes 9 and 22 which were termed as BCR and ABL.
- This then lead to discovery of unregulated tyrosine kinase activity is critical to BCR-ABL’s ability to transform cells.
Historical Classification of chronic myelogenous leukemia:
- CML was previously classified into five subtypes: chronic granulocytic leukaemia (CGL), juvenile CML, chronic neutrophilic leukemia (CNL), chronic myelomonocytic leukemia (CMML), and atypical CML (aCML).[4][5]
- CML was then classified into three phases: CML-chronic phase (CML-CP), CML-accelerated phase (CML-AP), and CML-blast phase (CML-BP).[5]
- In 2022, the World Health Organisation (WHO) classification eliminated CML-AP, leaving only two phases: CML-CP and CML-BP.[6]
- However, CML-AP is still being discussed as studies indicate it being a distinct entity with a different prognosis and treatment approached compared to CML-CP and CML-BP.[7][8]
Historical perspective of treatment of chronic myelogenous leukemia:
Treatment of chronic myeloid leukemia evolved over an era as described below.[9]
- In 1865, Heinrich Lissauer, described the use of arsenic in two patients with leukemia.
- In the 1920s, splenic irradiation was performed which resulted in symptomatic relief.
- In 1959, effective control of blood counts became possible with busulfan.
- Ten years later, hydroxyurea was discovered.
- In mid 1970's, a breakthrough was achieved when the Seattle group described the disappearance of the Ph chromosome in CML patients who underwent allotransplant.
- Interferon-α was discovered to stimulate cytogenetic responses and resultant long-term survival, however, only in a few patients.
- In 1992, Alexander Levitzki, proposed the use of ABL inhibitor.
- At about the same time, scientists at Ciba-Geigy synthesized, a strong inhibitor of ABL that was named GCP57148B and is now known as imatinib.
- For that 20% to 30% who fail imatinib, second-line inhibitors are an effective salvage therapy.
- However, once the disease has progressed beyond the chronic phase, allotransplant is still the recommended.
- Unfortunately, leukemia often persists in the best responders and the therapies directed at the BCR-ABL tyrosine kinase are unable to cure since they can not destroy CML stem cells.
History of Tyrosine Kinase Inhibitors (TKI) therapy in CML:
In 2001, the US Food and Drug Administration (FDA) approved the first BCR::ABL1 TKI, imatinib.[10]
- The FDA has approved 5 additional BCR::ABL1 TKIs since 2001.[11]
- Due to the BCR::ABL1 TKIs, the 10-year overall survival rate has increased from less than 20% to around 85%. [12]
- Although survival benefits are broadly similar among available agents, newer TKIs may enable faster achievement of deep molecular responses.
- Imatinib is the only first-generation TKI.[13]
- Second-generation TKIs include dasatinib, bosutinib, and nilotinib.[14]
- Third-generation TKIs include ponatinib and asciminib.[14]
References
- ↑ Kampen KR (January 2012). "The discovery and early understanding of leukemia". Leuk. Res. 36 (1): 6–13. doi:10.1016/j.leukres.2011.09.028. PMID 22033191.
- ↑ Nowell PC (August 2007). "Discovery of the Philadelphia chromosome: a personal perspective". J. Clin. Invest. 117 (8): 2033–5. doi:10.1172/JCI31771. PMC 1934591. PMID 17671636.
- ↑ NOWELL PC, HUNGERFORD DA (November 1961). "Chromosome studies in human leukemia. II. Chronic granulocytic leukemia". J. Natl. Cancer Inst. 27: 1013–35. PMID 14480645.
- ↑ Shepherd PC, Ganesan TS, Galton DA (December 1987). "Haematological classification of the chronic myeloid leukaemias". Baillieres Clin. Haematol. 1 (4): 887–906. PMID 3332855.
- ↑ 5.0 5.1 Arber DA, Orazi A, Hasserjian R, Thiele J, Borowitz MJ, Le Beau MM, Bloomfield CD, Cazzola M, Vardiman JW (May 2016). "The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia". Blood. 127 (20): 2391–405. doi:10.1182/blood-2016-03-643544. PMID 27069254.
- ↑ Khoury, J.D., Solary, E., Abla, O. et al. The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Myeloid and Histiocytic/Dendritic Neoplasms. Leukemia 36, 1703–1719 (2022). https://doi.org/10.1038/s41375-022-01613-1
- ↑ Senapati, J., Jabbour, E., Kantarjian, H. et al. Pathogenesis and management of accelerated and blast phases of chronic myeloid leukemia. Leukemia 37, 5–17 (2023). https://doi.org/10.1038/s41375-022-01736-5
- ↑ Kantarjian, H.M. and Tefferi, A. (2023), Classification of accelerated phase chronic myeloid leukemia in the era of the BCR::ABL1 tyrosine kinase inhibitors: A work in progress. Am J Hematol, 98: 1350-1353. https://doi.org/10.1002/ajh.27007
- ↑ Deininger, M. W. (2008). "Chronic Myeloid Leukemia: An Historical Perspective". Hematology. 2008 (1): 418–418. doi:10.1182/asheducation-2008.1.418. ISSN 1520-4391.
- ↑ Pfirrmann M, Baccarani M, Saussele S, Guilhot J, Cervantes F, Ossenkoppele G, Hoffmann VS, Castagnetti F, Hasford J, Hehlmann R, Simonsson B. Prognosis of long-term survival considering disease-specific death in patients with chronic myeloid leukemia. Leukemia. 2016 Jan;30(1):48-56. doi: 10.1038/leu.2015.261. Epub 2015 Sep 29. PMID: 26416462.
- ↑ Hochhaus A, Larson RA, Guilhot F, Radich JP, Branford S, Hughes TP, Baccarani M, Deininger MW, Cervantes F, Fujihara S, Ortmann CE, Menssen HD, Kantarjian H, O'Brien SG, Druker BJ; IRIS Investigators. Long-Term Outcomes of Imatinib Treatment for Chronic Myeloid Leukemia. N Engl J Med. 2017 Mar 9;376(10):917-927. doi: 10.1056/NEJMoa1609324. PMID: 28273028; PMCID: PMC5901965.
- ↑ Hehlmann, R., Lauseker, M., Saußele, S. et al. Assessment of imatinib as first-line treatment of chronic myeloid leukemia: 10-year survival results of the randomized CML study IV and impact of non-CML determinants. Leukemia 31, 2398–2406 (2017). https://doi.org/10.1038/leu.2017.253
- ↑ Senapati, J., Sasaki, K., Issa, G.C. et al. Management of chronic myeloid leukemia in 2023 – common ground and common sense. Blood Cancer J. 13, 58 (2023). https://doi.org/10.1038/s41408-023-00823-9
- ↑ 14.0 14.1 Jabbour E, Kantarjian H, Cortes J. Use of second- and third-generation tyrosine kinase inhibitors in the treatment of chronic myeloid leukemia: an evolving treatment paradigm. Clin Lymphoma Myeloma Leuk. 2015 Jun;15(6):323-34. doi: 10.1016/j.clml.2015.03.006. Epub 2015 Mar 24. PMID: 25971713; PMCID: PMC5141582.