Acute promyelocytic leukemia classification
|
Acute promyelocytic leukemia Microchapters |
|
Differentiating Acute promyelocytic leukemia from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Acute promyelocytic leukemia classification On the Web |
|
American Roentgen Ray Society Images of Acute promyelocytic leukemia classification |
|
Directions to Hospitals Treating Acute promyelocytic leukemia |
|
Risk calculators and risk factors for Acute promyelocytic leukemia classification |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]
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.
- 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.
- 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.
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.