HAEM5:Acute undifferentiated leukaemia: Difference between revisions

{{DISPLAYTITLE:Acute undifferentiated leukaemia}}

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==Primary Author(s)*==

==Clinical Features==

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|'''Signs and Symptoms'''

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|'''Laboratory Findings'''

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In one study of 16 cases of adults with AUL, the median age was 63 years (range: 24-84 years) and patients could achieve clinical remission after allogeneic stem cell transplantation<ref name=":2">{{Cite journal|displayauthors=1|last=Heesch|first=Sandra|last2=Neumann|first2=Martin|last3=Schwartz|first3=Stefan|last4=Bartram|first4=Isabelle|last5=Schlee|first5=Cornelia|last6=Burmeister|first6=Thomas|last7=Hänel|first7=Matthias|last8=Ganser|first8=Arnold|last9=Heuser|first9=Michael|date=2013|title=Acute leukemias of ambiguous lineage in adults: molecular and clinical characterization|url=https://pubmed.ncbi.nlm.nih.gov/23412561|journal=Annals of Hematology|volume=92|issue=6|pages=747–758|doi=10.1007/s00277-013-1694-4|issn=1432-0584|pmid=23412561|via=}}</ref>. In previous studies that weakly suggest ALL induction regimens over AML induction regimens, there may be selection bias in the patients who were well enough to be transplant candidates<ref>{{Cite journal|displayauthors=1|last=Weinberg|first=Olga K.|last2=Hasserjian|first2=Robert P.|last3=Baraban|first3=Ezra|last4=Ok|first4=Chi Young|last5=Geyer|first5=Julia T.|last6=Philip|first6=John K. S. S.|last7=Kurzer|first7=Jason H.|last8=Rogers|first8=Heesun J.|last9=Nardi|first9=Valentina|date=2019|title=Clinical, immunophenotypic, and genomic findings of acute undifferentiated leukemia and comparison to acute myeloid leukemia with minimal differentiation: a study from the bone marrow pathology group|url=https://pubmed.ncbi.nlm.nih.gov/31000771|journal=Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc|volume=32|issue=9|pages=1373–1385|doi=10.1038/s41379-019-0263-3|issn=1530-0285|pmid=31000771|via=}}</ref>.

==Immunophenotype==

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!Finding!!Marker

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Per WHO 2017, AUL blasts should express no more than one membrane marker for any lineage.

!Notes

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|Yes

|No

|Yes

The t(9;22) is diagnostic of CML in the appropriate morphology and clinical context (add reference). This fusion is responsive to targeted therapy such as Imatinib (Gleevec) (add reference).

NA

* Chromosomal Rearrangements (Gene Fusions)

* Individual Region Genomic Gain/Loss/LOH

==Individual Region Genomic Gain / Loss / LOH==

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!Notes

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7

chr7:1- 159,335,973 [hg38]

chr7

|Yes

|No

Presence of monosomy 7 (or 7q deletion) is sufficient for a diagnosis of AML with MDS-related changes when there is ≥20% blasts and no prior therapy (add reference).  Monosomy 7/7q deletion is associated with a poor prognosis in AML (add reference).

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8

chr8:1-145,138,636 [hg38]

chr8

|No

|No

Common recurrent secondary finding for t(8;21) (add reference).

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NA

==Characteristic Chromosomal Patterns==

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!Notes

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Co-deletion of 1p and 18q

|No

|No

See chromosomal rearrangements table as this pattern is due to an unbalanced derivative translocation associated with oligodendroglioma (add reference).

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AUL is associated with a high rate of chromosomal abnormalities, but have no characteristic abnormalities<ref name=":2" />.  

==Gene Mutations (SNV / INDEL)==

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!Notes

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EGFR; Exon 20 mutations

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PHF6 a tumor suppressor gene may have implications in AUL though the evidence is limited.

==Genes and Main Pathways Involved==

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!Gene; Genetic Alteration!!Pathway!!Pathophysiologic Outcome

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Overexpression of BAALC, ERG, and MN1<ref name=":0" />.