Compendium of Cancer Genome Aberrations

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{{DISPLAYTITLE:Chronic myelomonocytic leukaemia}}
{{DISPLAYTITLE:Chronic myelomonocytic leukaemia}}
[[HAEM5:Table_of_Contents|Haematolymphoid Tumours (WHO Classification, 5th ed.)]]
[[HAEM5:Table_of_Contents|Haematolymphoid Tumours (WHO Classification, 5th ed.)]]


{{Under Construction}}
{{Under Construction}}


<blockquote class='blockedit'>{{Box-round|title=Content Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition Classification|This page was converted to the new template on 2023-12-07. The original page can be found at [[HAEM4:Chronic Myelomonocytic Leukemia (CMML)]].
<blockquote class="blockedit">{{Box-round|title=Content Update To WHO 5th Edition Classification Is In Process; Content Below is Based on WHO 4th Edition Classification|This page was converted to the new template on 2023-12-07. The original page can be found at [[HAEM4:Chronic Myelomonocytic Leukemia (CMML)]].
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|Subtype(s)
|Subtype(s)
|Chronic myelomonocytic leukaemia
|Chronic myelomonocytic leukaemia
|}
==Definition / Description of Disease==
Chronic myelomonocytic leukemia (CMML) is a myelodysplastic/myeloproliferative neoplasm (MDS/MPN) with persistent monocytosis (absolute monocyte count ≥1 x 10<sup>9</sup>/L and ≥10% of leukocytes are monocytes). When myelodysplasia is absent or minimal, clonal evidence(s) of acquired cytogenetic or molecular genetic change(s) in hematopoietic cells, or unexplained monocytosis persisted for ≥3 months supports the diagnosis of CMML.
Before a diagnosis of CMML can be rendered, other well-defined myeloid neoplasms that sometimes present with monocytosis, such as ''BCR-ABL1''-positive chronic myeloid leukemia (especially with p190 fusion) and myeloid/lymphoid neoplasms with rearrangement of ''PDGFRA, PDGFRB'', ''FGFR1'' or ''PCM1-JAK2'' must be ruled out. Dysplastic features are usually seen in at least one myeloid lineage. By definition, the blast percentage must be <20%.
'''CMML can be subdivided into three categories based on the percentage of blasts and promonocytes (considered blast equivalent) in the peripheral blood and bone marrow'''<ref name=":2" />''':'''
'''CMML-0:''' < 2% blasts in the blood and < 5% in the bone marrow; and no Auer rods.
'''CMML-1:''' 2-4% blasts in the blood or 5-9% in the bone marrow; and no Auer rods.
'''CMML-2:''' 5-19% blasts in the blood, 10-19% in the bone marrow or Auer rods are present.
==Synonyms / Terminology==
Put your text here <span style="color:#0070C0">(''Instructions: Include currently used terms and major historical ones, adding “(historical)” after the latter.'') </span>
==Epidemiology / Prevalence==
Historically CMML was classified as a subtype of MDS. The exact incidence of CMML is difficult to calculate based on the published data. Recent studies reported approximate incidence of 0.4 cases per 100,000 population<ref>{{Cite journal|last=Dinmohamed|first=Avinash G.|last2=van Norden|first2=Yvette|last3=Visser|first3=Otto|last4=Posthuma|first4=Eduardus F.M.|last5=Huijgens|first5=Peter C.|last6=Sonneveld|first6=Pieter|last7=van de Loosdrecht|first7=Arjan A.|last8=Jongen-Lavrencic|first8=Mojca|date=2015|title=The use of medical claims to assess incidence, diagnostic procedures and initial treatment of myelodysplastic syndromes and chronic myelomonocytic leukemia in the Netherlands|url=https://linkinghub.elsevier.com/retrieve/pii/S0145212614003774|journal=Leukemia Research|language=en|volume=39|issue=2|pages=177–182|doi=10.1016/j.leukres.2014.11.025}}</ref>. The median patient age at diagnosis is 65-75 years, with a slight male dominance (male-to female ratio of 1.5-3:1)<ref name=":1">Czader, M and Orazi, A. Chapter 45. Myelodysplastic/Myeloproliferative Neoplasms and Related Diseases. In Orazi A, Foucar K, Knowles DM. eds. Knowles Neoplastic Hematopathology. Riverwoods, IL: Wolters Kluwer Health; 2013:1140-1156.</ref><ref name=":0">{{Cite journal|last=Germing|first=Ulrich|last2=Gattermann|first2=Norbert|last3=Minning|first3=Horst|last4=Heyll|first4=Axel|last5=Aul|first5=Carlo|date=1998|title=Problems in the classification of CMML—dysplastic versus proliferative type|url=https://linkinghub.elsevier.com/retrieve/pii/S0145212697001926|journal=Leukemia Research|language=en|volume=22|issue=10|pages=871–878|doi=10.1016/S0145-2126(97)00192-6}}</ref><ref>{{Cite journal|last=Onida|first=Francesco|last2=Kantarjian|first2=Hagop M.|last3=Smith|first3=Terry L.|last4=Ball|first4=Greg|last5=Keating|first5=Michael J.|last6=Estey|first6=Elihu H.|last7=Glassman|first7=Armand B.|last8=Albitar|first8=Maher|last9=Kwari|first9=Monica I.|date=2002|title=Prognostic factors and scoring systems in chronic myelomonocytic leukemia: a retrospective analysis of 213 patients|url=https://ashpublications.org/blood/article/99/3/840/53495/Prognostic-factors-and-scoring-systems-in-chronic|journal=Blood|language=en|volume=99|issue=3|pages=840–849|doi=10.1182/blood.V99.3.840|issn=1528-0020}}</ref>.
==Clinical Features==
Put your text here and fill in the table <span style="color:#0070C0">(''Instruction: Can include references in the table. Do not delete table.'') </span>
{| class="wikitable"
|'''Signs and Symptoms'''
|<span class="blue-text">EXAMPLE:</span> Asymptomatic (incidental finding on complete blood counts)
<span class="blue-text">EXAMPLE:</span> B-symptoms (weight loss, fever, night sweats)
<span class="blue-text">EXAMPLE:</span> Fatigue
<span class="blue-text">EXAMPLE:</span> Lymphadenopathy (uncommon)
|-
|'''Laboratory Findings'''
|<span class="blue-text">EXAMPLE:</span> Cytopenias
<span class="blue-text">EXAMPLE:</span> Lymphocytosis (low level)
|}
<blockquote class='blockedit'>{{Box-round|title=v4:Clinical Features|The content below was from the old template. Please incorporate above.}}</blockquote>
The clinical features are variable and significantly related to blood cell counts<ref name=":1" /><ref name=":2">Arber DA, et al., (2017). Introduction and overview of the classification of myeloid neoplasms, in World Health Organization 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, p82-86.</ref>. Some clinical presentations may be different in dysplastic (WBC count < 13 x 10<sup>9</sup>/L) and proliferative (WBC count ≥ 13 x 10<sup>9</sup>/L) subgroups<ref name=":0" />. In patients with increased white blood cell (WBC) count (~50% of all cases), constitutional symptoms (e.g. weight loss, fever, and night sweats) are common. In cases with cytopenia(s), similar to [[HAEM4:Myelodysplastic Syndromes (MDS)|MDS]], clinical presentations are usually related to insufficient blood cells (anemia, leukopenia and/or thrombocytopenia, e.g. fatigue, infection, and bleeding tendency)<ref>Storniolo AM, Moloney WC, Rosenthal DS, Cox C, Bennett JM. Chronic myelomonocytic leukemia. ''Leukemia''. 1990;4(11):766‐770.</ref>. Hepatosplenomegaly can be present in both subgroups, but are frequently related to leukocytosis. Rare cases with life-threatening hyperleukocytosis have been reported.
<blockquote class="blockedit">
<center><span style="color:Maroon">'''End of V4 Section'''</span>
----
</blockquote>
==Sites of Involvement==
Blood and bone marrow (always involved).
The common sites of extramedullary infiltrate include spleen, liver, skin and lymph nodes<ref name=":1" /><ref name=":2" /><ref>{{Cite journal|last=Vitte|first=Franck|last2=Fabiani|first2=Bettina|last3=Bénet|first3=Claire|last4=Dalac|first4=Sophie|last5=Balme|first5=Brigitte|last6=Delattre|first6=Claire|last7=Vergier|first7=Béatrice|last8=Beylot-Barry|first8=Marie|last9=Vignon-Pennamen|first9=Dominique|date=2012|title=Specific Skin Lesions in Chronic Myelomonocytic Leukemia: A Spectrum of Myelomonocytic and Dendritic Cell Proliferations. A Study of 42 Cases|url=http://content.wkhealth.com/linkback/openurl?sid=WKPTLP:landingpage&an=00000478-201209000-00003|journal=The American Journal of Surgical Pathology|language=en|volume=36|issue=9|pages=1302–1316|doi=10.1097/PAS.0b013e31825dd4de|issn=0147-5185}}</ref>, involvement of other organs, although less common, have also been reported.
==Morphologic Features==
'''Blood:'''
*Monocytosis ≥ 1 x 10<sup>9</sup>/L and monocytes account for ≥ 10% of the leukocytes.
Monocyte morphology ranges from normal to atypical: unusual nuclear segmentation or chromatin patterns, and abnormal cytoplasmic granulation.
*Blasts and promonocytes together must be <20% of the leukocytes.
*Variable changes in other blood cells are usually present.
**WBC count: increased, normal to slightly decreased, with neutropenia
**Granulocytes frequently left-shifted with occasional immature forms (promyelocytes, myelocytes and metamyelocytes, usually < 10% of the leukocytes)
**Dysplastic features in neutrophils (more frequently related to leukopenia): hyposegmented or abnormally segmented nuclei, abnormal cytoplasmic granulation
**Eosinophilia
**Mild anemia, often normocytic or macrocytic, nucleated red blood cells may be seen
**Thrombocytopenia with atypical, large platelets.
[[File:PB 200X.jpg|center|thumb|Blood smear, 200X (Wright stain)]]
'''Bone marrow:'''
*Usually hypercellular (>75% of cases) but rarely can be hypocellular.
*The myeloid to erythroid ratio is generally increased with dysplastic granulocytic hyperplasia.
**Monocytes can be difficult to recognize in the bone marrow, especially when many dysplatic granulocytes are present.
**Cytochemical studies (Alpha-naphthyl butyrate esterase or alpha-naphthyl acetate esterase with fluoride inhibition staining of blood and bone marrow aspirate smears can be useful to facilitate better recognition of the monocytic component.
*Mild dyserythropoiesis (e.g. megaloblastoid changes, abnormal nuclear features and ring sideroblasts) in some cases.
*Dysmegakaryopoiesis are present in many cases.
*Mild to moderate increase in the number of reticulin fibers seen in nearly 30% of cases<ref>{{Cite journal|last=Ratsimbasoa|first=Arsène|last2=Randrianarivelojosia|first2=Milijaona|last3=Millet|first3=Pascal|last4=Soarès|first4=Jean Louis|last5=Rabarijaona|first5=Leon|last6=Rakotoson|first6=Benjamin|last7=Malvy|first7=Denis|last8=Ménard|first8=Didier|date=2006|title=Use of pre-packaged chloroquine for the home management of presumed malaria in Malagasy children|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1592101/|journal=Malaria Journal|volume=5|pages=79|doi=10.1186/1475-2875-5-79|issn=1475-2875|pmc=1592101|pmid=16972985}}</ref>.
*Nodules composed of mature plasmacytoid dendritic cells in the bone marrow biopsy have been reported in 20% of cases<ref>{{Cite journal|last=Orazi|first=Attilio|last2=Chiu|first2=Ronald|last3=O'Malley|first3=Dennis P|last4=Czader|first4=Magdalena|last5=Allen|first5=Susan L|last6=An|first6=Caroline|last7=Vance|first7=Gail H|date=2006|title=Chronic myelomonocytic leukemia: the role of bone marrow biopsy immunohistology|url=http://www.nature.com/articles/3800707|journal=Modern Pathology|language=en|volume=19|issue=12|pages=1536–1545|doi=10.1038/modpathol.3800707|issn=0893-3952}}</ref>.
[[File:BMA 600X.jpg|center|thumb|Bone marrow aspirate smear, 600X (Wright stain)]]
'''Spleen and lymph node:'''
*Red pulp infiltrate in spleen.
*Lymph node infiltrate less common
*Involvement by a diffuse infiltration of plasmacytoid dendritic cells can be seen in lymph node and less commonly in spleen
==Immunophenotype==
The neoplastic monocytic cells frequently show some aberrant immunophenotype. Recognizing monoblasts by immunophenotype can be very challenging.
{| class="wikitable sortable"
|-
!Finding!!Marker
|-
|Positive (universal)||CD13, CD33
|-
|Positive (variable, can be aberrantly decreased)||CD11c, CD13, CD14, CD15, CD16, CD36, CD64, CD64, CD68, HLA-DR
|-
|Positive (aberrant, variable)
|CD56, CD2. Increased CD34+ blasts suggest disease progression
|-
|Negative (universal)||CD3, CD5, CD20, CD79a (T-cell and B-cell markers)
|-
|Negative (subset)||CD14, CD56
|}
|}


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No chromosome rearrangements  specifically associated with CMML.
No chromosome rearrangements  specifically associated with CMML.
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<blockquote class='blockedit'>{{Box-round|title=v4:Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications).|Please incorporate this section into the relevant tables found in:
<blockquote class="blockedit">{{Box-round|title=v4:Clinical Significance (Diagnosis, Prognosis and Therapeutic Implications).|Please incorporate this section into the relevant tables found in:
* Chromosomal Rearrangements (Gene Fusions)
* Chromosomal Rearrangements (Gene Fusions)
* Individual Region Genomic Gain/Loss/LOH
* Individual Region Genomic Gain/Loss/LOH
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Clonal cytogenetic abnormalities are found in 20-40% of CMML cases, but there are no specific abnormalities<ref>{{Cite journal|last=Such|first=E.|last2=Cervera|first2=J.|last3=Costa|first3=D.|last4=Sole|first4=F.|last5=Vallespi|first5=T.|last6=Luno|first6=E.|last7=Collado|first7=R.|last8=Calasanz|first8=M. J.|last9=Hernandez-Rivas|first9=J. M.|date=2011|title=Cytogenetic risk stratification in chronic myelomonocytic leukemia|url=http://www.haematologica.org/cgi/doi/10.3324/haematol.2010.030957|journal=Haematologica|language=en|volume=96|issue=3|pages=375–383|doi=10.3324/haematol.2010.030957|issn=0390-6078|pmc=PMC3046268|pmid=21109693}}</ref>.
Clonal cytogenetic abnormalities are found in 20-40% of CMML cases, but there are no specific abnormalities<ref>{{Cite journal|last=Such|first=E.|last2=Cervera|first2=J.|last3=Costa|first3=D.|last4=Sole|first4=F.|last5=Vallespi|first5=T.|last6=Luno|first6=E.|last7=Collado|first7=R.|last8=Calasanz|first8=M. J.|last9=Hernandez-Rivas|first9=J. M.|date=2011|title=Cytogenetic risk stratification in chronic myelomonocytic leukemia|url=http://www.haematologica.org/cgi/doi/10.3324/haematol.2010.030957|journal=Haematologica|language=en|volume=96|issue=3|pages=375–383|doi=10.3324/haematol.2010.030957|issn=0390-6078|pmc=PMC3046268|pmid=21109693}}</ref>.
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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>
<blockquote class="blockedit">{{Box-round|title=v4:Characteristic Chromosomal Aberrations / Patterns|The content below was from the old template. Please incorporate above.}}</blockquote>


No characteristic chromosome aberrations identified in association with CMML.
No characteristic chromosome aberrations identified in association with CMML.
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|}Note: A more extensive list of mutations can be found in [https://www.cbioportal.org/ <u>cBioportal</u>], [https://cancer.sanger.ac.uk/cosmic <u>COSMIC</u>], and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.
|}Note: A more extensive list of mutations can be found in [https://www.cbioportal.org/ <u>cBioportal</u>], [https://cancer.sanger.ac.uk/cosmic <u>COSMIC</u>], and/or other databases. When applicable, gene-specific pages within the CCGA site directly link to pertinent external content.


<blockquote class='blockedit'>{{Box-round|title=v4:Gene Mutations (SNV/INDEL)|The content below was from the old template. Please incorporate above.}}</blockquote>
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Over 90% of CMML patients studied exhibited one or more mutations<ref name=":2" />. Concurrent mutations in ''TET2'' and ''SRSF2'' appear to be highly specific for this entity<ref name=":3">{{Cite journal|last=Ti|first=Mughal|last2=Nc|first2=Cross|last3=E|first3=Padron|last4=Rv|first4=Tiu|last5=M|first5=Savona|last6=L|first6=Malcovati|last7=R|first7=Tibes|last8=Rs|first8=Komrokji|last9=Jj|first9=Kiladjian|date=2015|title=An International MDS/MPN Working Group's Perspective and Recommendations on Molecular Pathogenesis, Diagnosis and Clinical Characterization of Myelodysplastic/Myeloproliferative Neoplasms|url=https://pubmed.ncbi.nlm.nih.gov/26341525/|language=en|doi=10.3324/haematol.2014.114660|pmc=PMC4800699|pmid=26341525}}</ref><ref>{{Cite journal|last=Gelsi-Boyer|first=Véronique|last2=Trouplin|first2=Virginie|last3=Adélaïde|first3=José|last4=Aceto|first4=Nicola|last5=Remy|first5=Virginie|last6=Pinson|first6=Stephane|last7=Houdayer|first7=Claude|last8=Arnoulet|first8=Christine|last9=Sainty|first9=Danielle|date=2008|title=Genome profiling of chronic myelomonocytic leukemia: frequent alterations of RAS and RUNX1genes|url=http://bmccancer.biomedcentral.com/articles/10.1186/1471-2407-8-299|journal=BMC Cancer|language=en|volume=8|issue=1|doi=10.1186/1471-2407-8-299|issn=1471-2407|pmc=PMC2588460|pmid=18925961}}</ref>. Mutations in certain pathways correlated with clinical classification (dysplastic vs. proliferative)<ref name=":7">{{Cite journal|last=Patel|first=B J|last2=Przychodzen|first2=B|last3=Thota|first3=S|last4=Radivoyevitch|first4=T|last5=Visconte|first5=V|last6=Kuzmanovic|first6=T|last7=Clemente|first7=M|last8=Hirsch|first8=C|last9=Morawski|first9=A|date=2017|title=Genomic determinants of chronic myelomonocytic leukemia|url=http://www.nature.com/articles/leu2017164|journal=Leukemia|language=en|volume=31|issue=12|pages=2815–2823|doi=10.1038/leu.2017.164|issn=0887-6924}}</ref>.
Over 90% of CMML patients studied exhibited one or more mutations<ref name=":2">Arber DA, et al., (2017). Introduction and overview of the classification of myeloid neoplasms, in World Health Organization 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, p82-86.</ref>. Concurrent mutations in ''TET2'' and ''SRSF2'' appear to be highly specific for this entity<ref name=":3">{{Cite journal|last=Ti|first=Mughal|last2=Nc|first2=Cross|last3=E|first3=Padron|last4=Rv|first4=Tiu|last5=M|first5=Savona|last6=L|first6=Malcovati|last7=R|first7=Tibes|last8=Rs|first8=Komrokji|last9=Jj|first9=Kiladjian|date=2015|title=An International MDS/MPN Working Group's Perspective and Recommendations on Molecular Pathogenesis, Diagnosis and Clinical Characterization of Myelodysplastic/Myeloproliferative Neoplasms|url=https://pubmed.ncbi.nlm.nih.gov/26341525/|language=en|doi=10.3324/haematol.2014.114660|pmc=PMC4800699|pmid=26341525}}</ref><ref>{{Cite journal|last=Gelsi-Boyer|first=Véronique|last2=Trouplin|first2=Virginie|last3=Adélaïde|first3=José|last4=Aceto|first4=Nicola|last5=Remy|first5=Virginie|last6=Pinson|first6=Stephane|last7=Houdayer|first7=Claude|last8=Arnoulet|first8=Christine|last9=Sainty|first9=Danielle|date=2008|title=Genome profiling of chronic myelomonocytic leukemia: frequent alterations of RAS and RUNX1genes|url=http://bmccancer.biomedcentral.com/articles/10.1186/1471-2407-8-299|journal=BMC Cancer|language=en|volume=8|issue=1|doi=10.1186/1471-2407-8-299|issn=1471-2407|pmc=PMC2588460|pmid=18925961}}</ref>. Mutations in certain pathways correlated with clinical classification (dysplastic vs. proliferative)<ref name=":7">{{Cite journal|last=Patel|first=B J|last2=Przychodzen|first2=B|last3=Thota|first3=S|last4=Radivoyevitch|first4=T|last5=Visconte|first5=V|last6=Kuzmanovic|first6=T|last7=Clemente|first7=M|last8=Hirsch|first8=C|last9=Morawski|first9=A|date=2017|title=Genomic determinants of chronic myelomonocytic leukemia|url=http://www.nature.com/articles/leu2017164|journal=Leukemia|language=en|volume=31|issue=12|pages=2815–2823|doi=10.1038/leu.2017.164|issn=0887-6924}}</ref>.


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(use the "Cite" icon at the top of the page) <span style="color:#0070C0">(''Instructions: Add each reference into the text above by clicking where you want to insert the reference, selecting the “Cite” icon at the top of the wiki page, and using the “Automatic” tab option to search by PMID to select the reference to insert. If a PMID is not available, such as for a book, please use the “Cite” icon, select “Manual” and then “Basic Form”, and include the entire reference. To insert the same reference again later in the page, select the “Cite” icon and “Re-use” to find the reference; DO NOT insert the same reference twice using the “Automatic” tab as it will be treated as two separate references. The reference list in this section will be automatically generated and sorted''</span><span style="color:#0070C0">''.''</span><span style="color:#0070C0">)</span> <references />


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==Notes==
==Notes==
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<nowiki>*</nowiki>''Citation of this Page'': “Chronic myelomonocytic leukaemia”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/HAEM5:Chronic_myelomonocytic_leukaemia</nowiki>.
<nowiki>*</nowiki>''Citation of this Page'': “Chronic myelomonocytic leukaemia”. Compendium of Cancer Genome Aberrations (CCGA), Cancer Genomics Consortium (CGC), updated {{REVISIONMONTH}}/{{REVISIONDAY}}/{{REVISIONYEAR}}, <nowiki>https://ccga.io/index.php/HAEM5:Chronic_myelomonocytic_leukaemia</nowiki>.
[[Category:HAEM5]][[Category:DISEASE]][[Category:Diseases C]]
[[Category:HAEM5]]
[[Category:DISEASE]]
[[Category:Diseases C]]
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