HAEM5:Myeloid neoplasm post cytotoxic therapy: Difference between revisions

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<blockquote class='blockedit'>{{Box-round|title=v4:Clinical Features|The content below was from the old template. Please incorporate above.}}
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Two subsets of tMNs are generally recognized clinically:
Two subsets of tMNs are generally recognized clinically:
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Bone marrow and blood. Initial presentation as extramedullary myeloid sarcoma has been reported.
Bone marrow and blood. Initial presentation as extramedullary myeloid sarcoma has been reported.


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==Sites of Involvement==
==Sites of Involvement==
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<blockquote class='blockedit'>{{Box-round|title=v4:Immunophenotype|The content below was from the old template. Please incorporate above.}}
<blockquote class='blockedit'>{{Box-round|title=v4:Immunophenotype|The content below was from the old template. Please incorporate above.}}</blockquote>


-Immunophenotypic findings reflect the heterogeneity of the underlying morphology.
-Immunophenotypic findings reflect the heterogeneity of the underlying morphology.
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-p53 positive cells in bone marrow biopsies have been demonstrated to correlate well with TP53 mutations and with a poor prognosis.
-p53 positive cells in bone marrow biopsies have been demonstrated to correlate well with TP53 mutations and with a poor prognosis.


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==Chromosomal Rearrangements (Gene Fusions)==
==Chromosomal Rearrangements (Gene Fusions)==
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NA
NA
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* Individual Region Genomic Gain/Loss/LOH
* Individual Region Genomic Gain/Loss/LOH
* Characteristic Chromosomal Patterns
* Characteristic Chromosomal Patterns
* Gene Mutations (SNV/INDEL)}}
* Gene Mutations (SNV/INDEL)}}</blockquote>


Prognosis is generally poor, common reported 5 year survival rates are <10%.
Prognosis is generally poor, common reported 5 year survival rates are <10%.
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Patients with therapy related APL with PML-RARA should be managed with the same urgency as ''de novo'' APL.
Patients with therapy related APL with PML-RARA should be managed with the same urgency as ''de novo'' APL.


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==Individual Region Genomic Gain / Loss / LOH==
==Individual Region Genomic Gain / Loss / LOH==
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<blockquote class='blockedit'>{{Box-round|title=v4:Genomic Gain/Loss/LOH|The content below was from the old template. Please incorporate above.}}
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NA
NA
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==Characteristic Chromosomal Patterns==
==Characteristic Chromosomal Patterns==
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<blockquote class='blockedit'>{{Box-round|title=v4:Characteristic Chromosomal Aberrations / Patterns|The content below was from the old template. Please incorporate above.}}</blockquote>


-Leukemic cells of >90% of patients with tMN show an abnormal karyotype.
-Leukemic cells of >90% of patients with tMN show an abnormal karyotype.
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A small percentage of tMN patients have a reported normal karyotype.
A small percentage of tMN patients have a reported normal karyotype.


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==Gene Mutations (SNV / INDEL)==
==Gene Mutations (SNV / INDEL)==
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NA
NA
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NA
NA


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==Epigenomic Alterations==
==Epigenomic Alterations==
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<blockquote class='blockedit'>{{Box-round|title=v4:Genes and Main Pathways Involved|The content below was from the old template. Please incorporate above.}}</blockquote>


Thought to be the consequence of mutation events in hematopoietic stem cells induced by cytotoxic therapy or selection of a myeloid clone with a mutator phenotype. Only a small proportion of patients treated with identical protocols develop tMN, suggesting that some individuals may have predisopistion due to mutations in DNA damage sensing or prepair genes, or polymorphisms in genes that affect drug metabolism, transport, or repair.
Thought to be the consequence of mutation events in hematopoietic stem cells induced by cytotoxic therapy or selection of a myeloid clone with a mutator phenotype. Only a small proportion of patients treated with identical protocols develop tMN, suggesting that some individuals may have predisopistion due to mutations in DNA damage sensing or prepair genes, or polymorphisms in genes that affect drug metabolism, transport, or repair.


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==Genetic Diagnostic Testing Methods==
==Genetic Diagnostic Testing Methods==