Acute promyelocytic leukemia classification
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]
Classification
Risk classification
- Low-risk disease: Low-risk disease is defined as the presence of less than 10000 white blood cells per microliter and greater than 40000 platelets per microliter in the peripheral blood.[1] Treatment of low-risk disease involves non-chemotherapy-based regimens, such as the combination of all-trans retinoic acid and arsenic trioxide.[1]
- Intermediate-risk disease: Intermediate-risk disease is defined as the presence of less than 10000 white blood cells per microliter and less than 40000 platelets per microliter in peripheral blood.[2]
- High-risk disease: High-risk disease is defined as the presence of greater than 10000 white blood cells per microliter in peripheral blood, regardless of the platelet count.[1] Platelet count is typically less than 40000 cells per microliter, though platelet count is not a formal criterion in the classification of acute promyelocytic leukemia.
Origin-based classification
- De novo disease: De novo acute promyelocytic leukemia is the most common subtype. This refers to development of the disease in the absence of prior cytotoxic therapy or prior precursor conditions. De novo acute promyelocytic leukemia is due to a sporadic events in cells, without prior DNA-damaging insults. This is in contrast to therapy-related disease.
- Therapy-related disease: Therapy-related disease refers to the development of acute promyelocytic leukemia in patients who were previously treated with DNA-damaging or genotoxic agents for other conditions, such as other cancers. The most common DNA-damaging agents that cause therapy-associated acute promyelocytic leukemia are topoisomerase inhibitors and alkylating agents. Therapy-related acute promyelocytic leukemia is typically seen in patients with a history of breast cancer who received cyclophosphamide or patients with a history of a germ cell tumor who have received etoposide. The prognosis of therapy-related disease is worse than that of de novo disease, with a 5-year survival of less than 10 years.[3] The 4-year overall survival for therapy-related disease is 24.5%, compared to 39.5% for de novo disease.
- Topoisomerase II inhibitors: This class of chemotherapeutics causes early-onset leukemia, with a typical latency of 2-3 years from the receipt of the topoisomerase inhibitor. Cytogenetics from the leukemia diagnosis typically shows the MLL rearrangement (chromosome 11q23).
- Alkylating agents: This class of chemotherapeutics causes late-onset leukemia, with a typical latency of greater than 7 years from the receipt of the alkylating agent. Cytogenetics from the leukemia diagnosis typically shows monosomy 5 or monosomy 7. Mutational analyses might show a TP53 mutation.
- Other chemotherapeutic agents: Although other chemotherapy medications are not classically associated with therapy-related acute promyelocytic leukemia, there have been cases of such associations. In a patient with gastric cancer treated with oxaliplatin and capecitabine, acute promyelocytic leukemia developed after a latency period of 4 years.[3] The leukemic cells had chromosomal abnormalities, suggesting that the secondary neoplasm was chemotherapy-induced rather than de novo.
References
- ↑ 1.0 1.1 1.2 Coombs CC, Tavakkoli M, Tallman MS (2015). "Acute promyelocytic leukemia: where did we start, where are we now, and the future". Blood Cancer J. 5: e304. doi:10.1038/bcj.2015.25. PMC 4450325. PMID 25885425.
- ↑ McCulloch D, Brown C, Iland H (2017). "Retinoic acid and arsenic trioxide in the treatment of acute promyelocytic leukemia: current perspectives". Onco Targets Ther. 10: 1585–1601. doi:10.2147/OTT.S100513. PMC 5359123. PMID 28352191.
- ↑ 3.0 3.1 Zhang YC, Zhou YQ, Yan B, Shi J, Xiu LJ, Sun YW; et al. (2015). "Secondary acute promyelocytic leukemia following chemotherapy for gastric cancer: a case report". World J Gastroenterol. 21 (14): 4402–7. doi:10.3748/wjg.v21.i14.4402. PMC 4394105. PMID 25892894.