Bailey.Glen at 21:27, 4 December 2023

2023-12-04T21:27:24Z

← Older revision		Revision as of 16:27, 4 December 2023
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	==Definition / Description of Disease==		==Definition / Description of Disease==

	This is a distinct entity in the World Health Organization (WHO) classification system within the section of [[Acute Myeloid Leukemia (AML), Not Otherwise Specified]]<ref name=":0">Arber DA, et al., (2017). Acute myeloid leukaemia,NOS in WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J Editors. IARC Press: Lyon, France, p156-158.</ref>. This entity does ''not'' meet the criteria for inclusion in any of the other AML groups (i.e. AML with Recurrent Genetic Abnormalities, AML with Myelodysplasia-Related Changes, or Therapy-Related Myeloid Neoplasms).		This is a distinct entity in the World Health Organization (WHO) classification system within the section of [[HAEM4:Acute Myeloid Leukemia (AML), Not Otherwise Specified]]<ref name=":0">Arber DA, et al., (2017). Acute myeloid leukaemia,NOS in WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J Editors. IARC Press: Lyon, France, p156-158.</ref>. This entity does ''not'' meet the criteria for inclusion in any of the other AML groups (i.e. AML with Recurrent Genetic Abnormalities, AML with Myelodysplasia-Related Changes, or Therapy-Related Myeloid Neoplasms).

	• Recognized as a distinct entity in 1987<ref>{{Cite journal\|last=Lee\|first=M. S.\|last2=Chang\|first2=K. S.\|last3=Trujillo\|first3=J. M.\|last4=McCredie\|first4=K. B.\|last5=Keating\|first5=M. J.\|last6=Freireich\|first6=E. J.\|last7=Stass\|first7=S. A.\|date=1987\|title=T-cell receptor gamma chain gene rearrangement in acute myelogenous leukemia--evidence for lymphoid lineage prematurity\|url=https://www.ncbi.nlm.nih.gov/pubmed/2848796\|journal=Hematologic Pathology\|volume=1\|issue=2\|pages=93–98\|issn=0886-0238\|pmid=2848796}}</ref>		• Recognized as a distinct entity in 1987<ref>{{Cite journal\|last=Lee\|first=M. S.\|last2=Chang\|first2=K. S.\|last3=Trujillo\|first3=J. M.\|last4=McCredie\|first4=K. B.\|last5=Keating\|first5=M. J.\|last6=Freireich\|first6=E. J.\|last7=Stass\|first7=S. A.\|date=1987\|title=T-cell receptor gamma chain gene rearrangement in acute myelogenous leukemia--evidence for lymphoid lineage prematurity\|url=https://www.ncbi.nlm.nih.gov/pubmed/2848796\|journal=Hematologic Pathology\|volume=1\|issue=2\|pages=93–98\|issn=0886-0238\|pmid=2848796}}</ref>

Bailey.Glen at 18:46, 3 November 2023

2023-11-03T18:46:01Z

← Older revision		Revision as of 13:46, 3 November 2023
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			{{DISPLAYTITLE:Acute Myeloid Leukemia (AML) with Minimal Differentiation}}


			<blockquote class='blockedit'>{{Box-round\|title=PREVIOUS EDITION\|This page from the 4th edition of Haematolymphoid Tumours is being updated. See 5th edition [[HAEM5:Table_of_Contents\|Table of Contents]].
			}}</blockquote>
	==Primary Author(s)*==		==Primary Author(s)*==

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	==Notes==		==Notes==
	<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.		<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.
			[[Category:HAEM4]] [[Category:DISEASE]]

	[[Category:~~Recently Added Pages~~]]

Bailey.Glen: Created page with "==Primary Author(s)*== Celeste Eno, PhD, Cedars Sinai Medical Center, Los Angeles, Fabiola Quintero-Rivera, MD, FACMG, University of California Irvine TOC ==Cancer C..."

2023-11-03T18:05:31Z

Created page with "==Primary Author(s)*== Celeste Eno, PhD, Cedars Sinai Medical Center, Los Angeles, Fabiola Quintero-Rivera, MD, FACMG, University of California Irvine __TOC__ ==Cancer C..."

New page

==Primary Author(s)*==

Celeste Eno, PhD, Cedars Sinai Medical Center, Los Angeles, Fabiola Quintero-Rivera, MD, FACMG, University of California Irvine

__TOC__

==Cancer Category/Type==

[[AML|Acute Myeloid Leukemia]]

==Cancer Sub-Classification / Subtype==

Acute Myeloid Leukemia (AML) with minimal differentiation

==Definition / Description of Disease==

This is a distinct entity in the World Health Organization (WHO) classification system within the section of [[Acute Myeloid Leukemia (AML), Not Otherwise Specified]]<ref name=":0">Arber DA, et al., (2017). Acute myeloid leukaemia,NOS in WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues, Revised 4th edition. Swerdlow SH, Campo E, Harris NL, Jaffe ES, Pileri SA, Stein H, Thiele J Editors. IARC Press: Lyon, France, p156-158.</ref>. This entity does ''not'' meet the criteria for inclusion in any of the other AML groups (i.e. AML with Recurrent Genetic Abnormalities, AML with Myelodysplasia-Related Changes, or Therapy-Related Myeloid Neoplasms).

• Recognized as a distinct entity in 1987<ref>{{Cite journal|last=Lee|first=M. S.|last2=Chang|first2=K. S.|last3=Trujillo|first3=J. M.|last4=McCredie|first4=K. B.|last5=Keating|first5=M. J.|last6=Freireich|first6=E. J.|last7=Stass|first7=S. A.|date=1987|title=T-cell receptor gamma chain gene rearrangement in acute myelogenous leukemia--evidence for lymphoid lineage prematurity|url=https://www.ncbi.nlm.nih.gov/pubmed/2848796|journal=Hematologic Pathology|volume=1|issue=2|pages=93–98|issn=0886-0238|pmid=2848796}}</ref>

• Rare subtype of acute leukemia without evidence of morphological or cytochemical myeloid differentiation

• Characterize as myeloid through use of immunohistochemistry, flow cytometry or EM cytochemistry

• More than 20% myeloid blasts in bone marrow or peripheral blood

• Less than 3% MPO or Sudan black B positivity by light-microscopic enzyme cytochemical analysis<ref name=":1">{{Cite journal|last=Kaleem|first=Z.|last2=White|first2=G.|date=2001|title=Diagnostic criteria for minimally differentiated acute myeloid leukemia (AML-M0). Evaluation and a proposal|url=https://www.ncbi.nlm.nih.gov/pubmed/11392885|journal=American Journal of Clinical Pathology|volume=115|issue=6|pages=876–884|doi=10.1309/D2BR-C0V5-LEYD-HA2D|issn=0002-9173|pmid=11392885}}</ref>

• No definitive evidence of lymphoid differentiation

==Synonyms / Terminology==

AML M0 (FAB classification)

==Epidemiology / Prevalence==

Approximately <5% AML cases. Affects all age groups though most patients are infants or older adults.

==Clinical Features==

• Patients present with evidence of bone marrow failure

• Anemia

• Thrombocytopenia

• Neutropenia

• Some patients present with leukocytosis and numerous circulating blasts

==Sites of Involvement==

Bone Marrow: hematopoietic stem cell

==Morphologic Features==

• Blasts are usually medium–sized with dispersed nuclear chromatin

• Markedly hypercellular bone marrow with poorly differentiated blasts

• Round or slightly indented nuclei with one or two nucleoli

• Agranular cytoplasm with variable degree of basinophila

• No Auer rods

• Residual normal population of maturing neutrophils may be present

• Less frequently, blasts are small, with more dispersed chromatin, inconspicuous nucleoli and scant cytoplasm resembling that of lymphoblasts.

• MPO and CAE and Sudan Black B staining is negative

==Immunophenotype==

POSITIVE

• For any one of the myelomonocytic lineage antigens not expressed on normal B- or T-lymphoid cells: CD13, CD14, CD15, CD33, or CD64

• Or MPO positive detected by ultrastructural cytochemical analysis, immunohistochemical analysis or flow cytometric analysis<ref name=":1" />

• Most cases express early hematopoetic associated antigens: CD34, HLA-DR

• Approximately 60% of cases express CD33

• Blast cells express at mostly two myeloid-associated markers, CD13 and KIT (CD117)<ref>{{Cite journal|last=Thalhammer-Scherrer|first=Renate|last2=Mitterbauer|first2=Gerlinde|last3=Simonitsch|first3=Ingrid|last4=Jaeger|first4=Ulrich|last5=Lechner|first5=Klaus|last6=Schneider|first6=Barbara|last7=Fonatsch|first7=Christa|last8=Schwarzinger|first8=Ilse|date=2002|title=The immunophenotype of 325 adult acute leukemias: relationship to morphologic and molecular classification and proposal for a minimal screening program highly predictive for lineage discrimination|url=https://www.ncbi.nlm.nih.gov/pubmed/11888077|journal=American Journal of Clinical Pathology|volume=117|issue=3|pages=380–389|doi=10.1309/C38D-D8J3-JU3E-V6EE|issn=0002-9173|pmid=11888077}}</ref>

• 50% case Nuclear TdT is positive (may be of favorable prognostic significance)

• CD7 positive in 40% cases

• CD4 may have expression<ref>{{Cite journal|last=Bennett|first=J. M.|last2=Catovsky|first2=D.|last3=Daniel|first3=M. T.|last4=Flandrin|first4=G.|last5=Galton|first5=D. A.|last6=Gralnick|first6=H. R.|last7=Sultan|first7=C.|date=1981|title=The morphological classification of acute lymphoblastic leukaemia: concordance among observers and clinical correlations|url=https://www.ncbi.nlm.nih.gov/pubmed/6938236|journal=British Journal of Haematology|volume=47|issue=4|pages=553–561|doi=10.1111/j.1365-2141.1981.tb02684.x|issn=0007-1048|pmid=6938236}}</ref>

• Pediatric cases: CD33 bright

NEGATIVE:

• Lack antigens associated with myeloid and monocytic maturation: CD11b, CD14,3 CD153, CD36, CD41, CD61, CD64 and CD65

• CD38 and/or HLA-DR may be decreased

• No monocytic differentiation: no coexpression of CD64 and CD36

• Blasts are negative for the B-cell and T-cell cytoplasmic lymphoid markers CD5, cCD3, cCD79a and cCD22

• MPO negative by cytochemistry, but maybe positive in some blasts by flow cytometry or immunohistochemistry.

• Glycophorin A

• Pediatric cases: Negative for TdT, CD34 and CD13 (weak)

==Chromosomal Rearrangements (Gene Fusions)==

There is no recurrent rearrangements in this entity.

• t(7;12)(q36;p13), cytogenetically cryptic, leads to ''MNX1'' deregulation and a poor prognosis.

- The morphology of cases is variable, but a significant portion is AML with minimal differentiation or without maturation most common in children<ref>{{Cite journal|last=Tosi|first=S.|last2=Harbott|first2=J.|last3=Teigler-Schlegel|first3=A.|last4=Haas|first4=O. A.|last5=Pirc-Danoewinata|first5=H.|last6=Harrison|first6=C. J.|last7=Biondi|first7=A.|last8=Cazzaniga|first8=G.|last9=Kempski|first9=H.|date=2000|title=t(7;12)(q36;p13), a new recurrent translocation involving ETV6 in infant leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/11066076|journal=Genes, Chromosomes & Cancer|volume=29|issue=4|pages=325–332|doi=10.1002/1098-2264(2000)9999:99993.0.co;2-9|issn=1045-2257|pmid=11066076}}</ref><ref name=":2">{{Cite journal|last=Silva|first=F. P. G.|last2=Morolli|first2=B.|last3=Storlazzi|first3=C. T.|last4=Zagaria|first4=A.|last5=Impera|first5=L.|last6=Klein|first6=B.|last7=Vrieling|first7=H.|last8=Kluin-Nelemans|first8=H. C.|last9=Giphart-Gassler|first9=M.|date=2008|title=ETV6 mutations and loss in AML-M0|url=https://www.ncbi.nlm.nih.gov/pubmed/18305557|journal=Leukemia|volume=22|issue=8|pages=1639–1643|doi=10.1038/leu.2008.34|issn=1476-5551|pmid=18305557}}</ref>.

- This translocation has also been reported in ALL

• t(10;11)(p12;q14) has an intermediate to poor prognosis<ref>{{Cite journal|last=Cancer Genome Atlas Research Network|last2=Ley|first2=Timothy J.|last3=Miller|first3=Christopher|last4=Ding|first4=Li|last5=Raphael|first5=Benjamin J.|last6=Mungall|first6=Andrew J.|last7=Robertson|first7=A. Gordon|last8=Hoadley|first8=Katherine|last9=Triche|first9=Timothy J.|date=2013|title=Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/23634996|journal=The New England Journal of Medicine|volume=368|issue=22|pages=2059–2074|doi=10.1056/NEJMoa1301689|issn=1533-4406|pmc=3767041|pmid=23634996}}</ref> .

- Most cases show immature morphology.

- This translocation has also been reported in many other hematological malignancies<ref>{{Cite journal|last=Caudell|first=D.|last2=Aplan|first2=P. D.|date=2008|title=The role of CALM-AF10 gene fusion in acute leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/18094714|journal=Leukemia|volume=22|issue=4|pages=678–685|doi=10.1038/sj.leu.2405074|issn=1476-5551|pmc=2366104|pmid=18094714}}</ref>.

{| class="wikitable sortable"
|-
!Chromosomal Rearrangement!!Genes in Fusion (5’ or 3’ Segments)!!Pathogenic Derivative!!Prevalence
|-
|t(7;12)(q36;p13)||5’ HLXB9 – 3’ ETV6||der(12)||Rare

|-
|t(10;11)(p12;q14)||5’ CALM – 3’ AF10|| ||Rare
|}

==Characteristic Chromosomal Aberrations / Patterns==

• No specific chromosomal abnormality is identified

• Complex karyotype<ref name=":3">{{Cite journal|last=Klaus|first=Mirjam|last2=Haferlach|first2=Torsten|last3=Schnittger|first3=Susanne|last4=Kern|first4=Wolfgang|last5=Hiddemann|first5=Wolfgang|last6=Schoch|first6=Claudia|date=2004|title=Cytogenetic profile in de novo acute myeloid leukemia with FAB subtypes M0, M1, and M2: a study based on 652 cases analyzed with morphology, cytogenetics, and fluorescence in situ hybridization|url=https://www.ncbi.nlm.nih.gov/pubmed/15527902|journal=Cancer Genetics and Cytogenetics|volume=155|issue=1|pages=47–56|doi=10.1016/j.cancergencyto.2004.03.008|issn=0165-4608|pmid=15527902}}</ref>

• Unbalanced abnormalities

• Most common: del(5q) or t(5q) and loss of chromosome 7 or del(7q)<ref name=":3" /><ref name=":4">{{Cite journal|last=Cuneo|first=A.|last2=Ferrant|first2=A.|last3=Michaux|first3=J. L.|last4=Boogaerts|first4=M.|last5=Demuynck|first5=H.|last6=Van Orshoven|first6=A.|last7=Criel|first7=A.|last8=Stul|first8=M.|last9=Dal Cin|first9=P.|date=1995|title=Cytogenetic profile of minimally differentiated (FAB M0) acute myeloid leukemia: correlation with clinicobiologic findings|url=https://www.ncbi.nlm.nih.gov/pubmed/7780152|journal=Blood|volume=85|issue=12|pages=3688–3694|issn=0006-4971|pmid=7780152}}</ref> the presence of these abnormalities would place the case in the category of AML with myelodysplasia-related changes per new WHO classification (2017).

• Near tetraploid karyotypes<ref name=":5">{{Cite journal|last=Béné|first=M. C.|last2=Bernier|first2=M.|last3=Casasnovas|first3=R. O.|last4=Castoldi|first4=G.|last5=Doekharan|first5=D.|last6=van der Holt|first6=B.|last7=Knapp|first7=W.|last8=Lemez|first8=P.|last9=Ludwig|first9=W. D.|date=2001|title=Acute myeloid leukaemia M0: haematological, immunophenotypic and cytogenetic characteristics and their prognostic significance: an analysis in 241 patients|url=https://www.ncbi.nlm.nih.gov/pubmed/11380465|journal=British Journal of Haematology|volume=113|issue=3|pages=737–745|doi=10.1046/j.1365-2141.2001.02801.x|issn=0007-1048|pmid=11380465}}</ref>

• Pediatric: Chromosome 5 aberrations, trisomy 21 and hypodiploidy more common in AML M0 than non-M0 counterparts<ref name=":6">{{Cite journal|last=Barbaric|first=Draga|last2=Alonzo|first2=Todd A.|last3=Gerbing|first3=Robert B.|last4=Meshinchi|first4=Soheil|last5=Heerema|first5=Nyla A.|last6=Barnard|first6=Dorothy R.|last7=Lange|first7=Beverly J.|last8=Woods|first8=William G.|last9=Arceci|first9=Robert J.|date=2007|title=Minimally differentiated acute myeloid leukemia (FAB AML-M0) is associated with an adverse outcome in children: a report from the Children's Oncology Group, studies CCG-2891 and CCG-2961|url=https://www.ncbi.nlm.nih.gov/pubmed/17158236|journal=Blood|volume=109|issue=6|pages=2314–2321|doi=10.1182/blood-2005-11-025536|issn=0006-4971|pmc=1852193|pmid=17158236}}</ref>

==Genomic Gain/Loss/LOH==
• +4 sole; intermediate/poor prognosis

• +8<ref name=":3" />

• +10 sole; intermediate/poor prognosis<ref>Johansson B and Harrison CJ (2015). Cancer Cytogenetics: Chromosomal and molecular genetic aberrations of tumor cells, 4th edition. Heim S and Mitelman F, Editors, Wiley-Blackwell: p62-84.</ref>

• 11q gain MLL amplification; poor prognosis<ref name=":3" />

• +13 sole; poor prognosis<ref name=":3" /><ref name=":4" /><ref name=":7">{{Cite journal|last=Silva|first=Fernando P. G.|last2=Lind|first2=Alexandra|last3=Brouwer-Mandema|first3=Geeske|last4=Valk|first4=Peter J. M.|last5=Giphart-Gassler|first5=Micheline|date=2007|title=Trisomy 13 correlates with RUNX1 mutation and increased FLT3 expression in AML-M0 patients|url=https://www.ncbi.nlm.nih.gov/pubmed/17650443|journal=Haematologica|volume=92|issue=8|pages=1123–1126|doi=10.3324/haematol.11296|issn=1592-8721|pmid=17650443}}</ref> and associated with TdT expression<ref>{{Cite journal|last=Patel|first=Keyur P.|last2=Khokhar|first2=Faisal A.|last3=Muzzafar|first3=Tariq|last4=James You|first4=M.|last5=Bueso-Ramos|first5=Carlos E.|last6=Ravandi|first6=Farhad|last7=Pierce|first7=Sherrie|last8=Medeiros|first8=L. Jeffrey|date=2013|title=TdT expression in acute myeloid leukemia with minimal differentiation is associated with distinctive clinicopathological features and better overall survival following stem cell transplantation|url=https://www.ncbi.nlm.nih.gov/pubmed/22936064|journal=Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc|volume=26|issue=2|pages=195–203|doi=10.1038/modpathol.2012.142|issn=1530-0285|pmc=5485410|pmid=22936064}}</ref>

• +14<ref name=":3" />

• del(11q)

• Loss and haploinsufficiency of ''ETV6'' through deletion may be a leukemogenic step in AML-M0<ref name=":2" />

==Gene Mutations (SNV/INDEL)==

• Co-existence of gene mutations is common

• ''FLT3'' Mutations: ITD and TKD, 16-22% of cases

• RAS: ''K-RAS'' and ''N-RAS''

• ''IDH1'' and ''IDH2'' mutations<ref name=":8">{{Cite journal|last=Kao|first=Hsiao-Wen|last2=Liang|first2=Der-Cherng|last3=Wu|first3=Jin-Hou|last4=Kuo|first4=Ming-Chung|last5=Wang|first5=Po-Nan|last6=Yang|first6=Chao-Ping|last7=Shih|first7=Yu-Shu|last8=Lin|first8=Tung-Huei|last9=Huang|first9=Yu-Hui|date=2014|title=Gene mutation patterns in patients with minimally differentiated acute myeloid leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/25022553|journal=Neoplasia (New York, N.Y.)|volume=16|issue=6|pages=481–488|doi=10.1016/j.neo.2014.06.002|issn=1476-5586|pmc=4198802|pmid=25022553}}</ref>

• Loss and haploinsufficiency of ETV6 result of heterozygous/homozygous mutations may be a leukemogenic step in AML-M0<ref name=":2" />

• Mutations of ''RUNX1'' occur in ~30% of cases<ref name=":7" />, and correlates with the presence of trisomy 13 and increased ''FLT3'' expression. ''De novo'' cases with RUNX1 mutations are now classified as the provisional entity of AML with mutated RUNX1 in the 2017 WHO<ref name=":0" />.

==Epigenomics (Methylation)==

• High frequency of gene mutations in epigenetic modifiers implies that epigenetic deregulation and may lead to the pathogenesis of AML-M0<ref name=":8" />.

• Histone acetylation and methylation patterns for patients with primary AML (all types) is ongoing<ref>Hellenbrecht A. ChIP- Chip microarrays to study the epigenome in leukemia. Available at: <nowiki>https://www.leukemia-net.org/content/leukemias/aml/aml_information/chip_microarrays/index_eng.html</nowiki>. Accessed June 20, 2018.</ref>.

==Genes and Main Pathways Involved==

Put your text here

==Diagnostic Testing Methods==

• Bone Marrow and peripheral blood examination for >20% blasts

• Cytochemical analysis, MPO and/or Sudan black B staining (undetectable - 3% positivity) for MPO

• Flow analysis:
o Lack of expression of lymphoid-specific antigens cyCD3 for T cells and cyCD79 and cyCD22 for B cells
o Positivity for any one of the myelomonocytic lineage antigens known not to be expressed on normal T-lymphoid cells (such as CD13, CD14, CD15, CD33, or CD64)

• Conventional G-banding cytogenetics

• FISH in cases of ''MLL'' (''KMT2A'') amplification and cryptic translocations involving ''ETV6''

==Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications)==

• Adverse outcome in children. May relate to a lack of more favorable AML cytogenetic abnormalities, such as t(8;21) and inv 16 and presence of high-risk abnormalities (i.e. chromosome 5)<ref name=":6" />.

• Patients treated with only chemotherapy in conventional doses.

• Stem cell transplantation may contribute to a longer remission and prolongation of the survival<ref name=":5" />.

• MDR1/p-170 protein is positive in blasts and mediates multidrug resistance in adults. This protein functions as a barrier, reducing intracellular concentrations of chemotherapeutics<ref>{{Cite journal|last=Campos|first=L.|last2=Guyotat|first2=D.|last3=Jaffar|first3=C.|last4=Solary|first4=E.|last5=Archimbaud|first5=E.|last6=Treille|first6=D.|date=1992|title=Correlation of MDR1/P-170 expression with daunorubicin uptake and sensitivity of leukemic progenitors in acute myeloid leukemia|url=https://www.ncbi.nlm.nih.gov/pubmed/1353726|journal=European Journal of Haematology|volume=48|issue=5|pages=254–258|doi=10.1111/j.1600-0609.1992.tb01803.x|issn=0902-4441|pmid=1353726}}</ref><ref>{{Cite journal|last=Wuchter|first=C.|last2=Karawajew|first2=L.|last3=Ruppert|first3=V.|last4=Büchner|first4=T.|last5=Schoch|first5=C.|last6=Haferlach|first6=T.|last7=Ratei|first7=R.|last8=Dörken|first8=B.|last9=Ludwig|first9=W. D.|date=1999|title=Clinical significance of CD95, Bcl-2 and Bax expression and CD95 function in adult de novo acute myeloid leukemia in context of P-glycoprotein function, maturation stage, and cytogenetics|url=https://www.ncbi.nlm.nih.gov/pubmed/10602414|journal=Leukemia|volume=13|issue=12|pages=1943–1953|doi=10.1038/sj.leu.2401605|issn=0887-6924|pmid=10602414}}</ref>.

==Familial Forms==

Put your text here

==Other Information==

Differential Diagnosis: Acute Lymphoblastic Leukemia (more common), mixed phenotype acute leukemia, leukemic phase of large cell lymphoma (less common)

==Links==

Put your links here

==References==
<references />

==Notes==
<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page. If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage). Additional global feedback or concerns are also welcome.

[[Category:Recently Added Pages]]

HAEM4:Acute Myeloid Leukemia (AML) with Minimal Differentiation - Revision history

Bailey.Glen at 21:27, 4 December 2023

Bailey.Glen at 18:46, 3 November 2023

Bailey.Glen: Created page with "==Primary Author(s)*== Celeste Eno, PhD, Cedars Sinai Medical Center, Los Angeles, Fabiola Quintero-Rivera, MD, FACMG, University of California Irvine __TOC__ ==Cancer C..."

Bailey.Glen: Created page with "==Primary Author(s)*== Celeste Eno, PhD, Cedars Sinai Medical Center, Los Angeles, Fabiola Quintero-Rivera, MD, FACMG, University of California Irvine TOC ==Cancer C..."