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==Classification==
==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.<ref name="pmid25885425">{{cite journal| author=Coombs CC, Tavakkoli M, Tallman MS| title=Acute promyelocytic leukemia: where did we start, where are we now, and the future. | journal=Blood Cancer J | year= 2015 | volume= 5 | issue=  | pages= e304 | pmid=25885425 | doi=10.1038/bcj.2015.25 | pmc=4450325 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25885425  }} </ref> Treatment of low-risk disease involves non-chemotherapy-based regimens, such as the combination of all-trans retinoic acid and arsenic trioxide.<ref name="pmid25885425">{{cite journal| author=Coombs CC, Tavakkoli M, Tallman MS| title=Acute promyelocytic leukemia: where did we start, where are we now, and the future. | journal=Blood Cancer J | year= 2015 | volume= 5 | issue=  | pages= e304 | pmid=25885425 | doi=10.1038/bcj.2015.25 | pmc=4450325 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25885425  }} </ref>
*'''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.<ref name="pmid25885425">{{cite journal| author=Coombs CC, Tavakkoli M, Tallman MS| title=Acute promyelocytic leukemia: where did we start, where are we now, and the future. | journal=Blood Cancer J | year= 2015 | volume= 5 | issue=  | pages= e304 | pmid=25885425 | doi=10.1038/bcj.2015.25 | pmc=4450325 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25885425  }} </ref> Treatment of low-risk disease involves non-chemotherapy-based regimens, such as the combination of all-trans retinoic acid and arsenic trioxide.<ref name="pmid25885425">{{cite journal| author=Coombs CC, Tavakkoli M, Tallman MS| title=Acute promyelocytic leukemia: where did we start, where are we now, and the future. | journal=Blood Cancer J | year= 2015 | volume= 5 | issue=  | pages= e304 | pmid=25885425 | doi=10.1038/bcj.2015.25 | pmc=4450325 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25885425  }} </ref>
*'''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.
*'''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.<ref name="pmid28352191">{{cite journal| author=McCulloch D, Brown C, Iland H| title=Retinoic acid and arsenic trioxide in the treatment of acute promyelocytic leukemia: current perspectives. | journal=Onco Targets Ther | year= 2017 | volume= 10 | issue=  | pages= 1585-1601 | pmid=28352191 | doi=10.2147/OTT.S100513 | pmc=5359123 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28352191  }} </ref>
*'''High-risk disease''': Low-risk disease is defined as the presence of greater than 10000 [[white blood cells]] per microliter in peripheral blood, regardless of the platelet count.<ref name="pmid25885425">{{cite journal| author=Coombs CC, Tavakkoli M, Tallman MS| title=Acute promyelocytic leukemia: where did we start, where are we now, and the future. | journal=Blood Cancer J | year= 2015 | volume= 5 | issue=  | pages= e304 | pmid=25885425 | doi=10.1038/bcj.2015.25 | pmc=4450325 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25885425  }} </ref> [[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.
*'''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.<ref name="pmid25885425">{{cite journal| author=Coombs CC, Tavakkoli M, Tallman MS| title=Acute promyelocytic leukemia: where did we start, where are we now, and the future. | journal=Blood Cancer J | year= 2015 | volume= 5 | issue=  | pages= e304 | pmid=25885425 | doi=10.1038/bcj.2015.25 | pmc=4450325 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25885425  }} </ref> [[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 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 inhibitors'':
**''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'':
**''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==
==References==

Revision as of 23:18, 29 April 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.

References

  1. 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.
  2. 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.

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