Acute promyelocytic leukemia classification: Difference between revisions
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**''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). | **''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. | **''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, | **''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.<ref name="pmid25892894">{{cite journal| author=Zhang YC, Zhou YQ, Yan B, Shi J, Xiu LJ, Sun YW et al.| title=Secondary acute promyelocytic leukemia following chemotherapy for gastric cancer: a case report. | journal=World J Gastroenterol | year= 2015 | volume= 21 | issue= 14 | pages= 4402-7 | pmid=25892894 | doi=10.3748/wjg.v21.i14.4402 | pmc=4394105 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25892894 }} </ref> | ||
==References== | ==References== | ||
Revision as of 02:56, 7 May 2018
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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.
- 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]
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.
- ↑ 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.