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Chronic Myelomonocytic Leukemia


Chronic myelomonocytic leukemia is a clonal hematopoietic stem cell disorder characterized by features typical of myelodysplastic syndromes and myeloproliferative neoplasms. Affected individuals present with monocytosis, cytopenias, and extramedullary manifestations like lymphadenopathy and hepatosplenomegaly.

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CMML is generally diagnosed in the elderly, but the clinical presentation of affected individuals varies largely. Most symptoms are due to hematological alterations, and the latter may be seen in a hemogram. Thus, CMML is usually not suspected until blood sample analyses reveal chronic monocytosis.

In detail, the following signs and symptoms may be associated with bone marrow suppression:

Furthermore, CMML patients frequently present with lymphadenopathy and hepatosplenomegaly. Infiltration of extramedullary tissues by leukemic cells and development of solid tumors is rare, but not unheard of [12]. They may indicate imminent transformation to acute myeloid leukemia, though.

Comorbidities are present in most cases and may blur the clinical picture.

Easy Bruising
  • bruising or bleeding Pain or a feeling of fullness below the ribs Diagnosis The following tests and procedures may be used: Physical exam and history Complete blood count (CBC) with differential Peripheral blood smear Blood chemistry studies Bone marrow[uvahealth.com]
  • A shortage of blood platelets (thrombocytopenia) can lead to easy bruising and bleeding. Some people notice frequent or severe nosebleeds or bleeding from their gums. Other symptoms can include weight loss, fever, and loss of appetite.[cancer.org]
  • Low numbers of platelets, which can cause bleeding and easy bruising with no apparent cause, a condition called thrombocytopenia. Risk Factors Doctors don't know why some cells become chronic myelomonocytic leukemia (CMML) cells and others don't.[lls.org]
  • A low number of blood platelets ( thrombocytopenia ) that can lead to problems with easy bruising and bleeding, frequent or severe nosebleeds or bleeding from the gums.[aamds.org]
  • Splenomegaly is frequently seen and may be massive. A 56-year-old man with stable CMML and moderate splenomegaly presented to the emergency department with generalized abdominal pain and abrupt drop in hemoglobin.[ncbi.nlm.nih.gov]
  • These patients are vulnerable to hepatic toxicity and graft failure after HSCT because of their increased likelihood of portal hypertension, massive splenomegaly, and extensive bone marrow fibrosis related to their disease.[ncbi.nlm.nih.gov]
  • We describe a 67-year-old man with a 3-year history of CMML who had been managed on single-agent azacitidine with stable disease before developing splenomegaly and acute onset skin lesions.[ncbi.nlm.nih.gov]
  • In a CMML patient with splenomegaly, who was treated with the JAK1/2 inhibitor ruxolitinib off label, we can demonstrate a spleen response and the disappearance of constitutional symptoms which was associated with a decrease in autonomous CFU-GM formation[ncbi.nlm.nih.gov]
  • Four of the five patients presented with leukocytosis and splenomegaly, and an increased number of ringed sideroblasts was observed in two cases.[ncbi.nlm.nih.gov]
Pleural Effusion
  • Other less frequent signs and symptoms consist of anaemia , fever , weight loss , night sweats , infection , bleeding , synovitis , lymphadenopathy , skin rashes, pleural effusion , pericardial effusion and peritoneal effusion . [7] [11] [12] Cause [[en.wikipedia.org]
  • Similarly, clinically meaningful responses, including improvement of life threatening pericardial and pleural effusions, as well as cytopenias were reported for the topoisomerase‐II inhibitor etoposide [ 52 ].[intechopen.com]
  • Here is reported the case of an elderly woman that, after surgical intervention, showed an important anemia, leucocytosis and thrombocytopenia. The leucocytosis was accompanied with clean increase of the monocytes.[ncbi.nlm.nih.gov]
  • Bone marrow examination of a 66-year-old woman with severe anemia revealed PRCA and was suspicious for CMML. There was no HLA-matched sibling for bone marrow transplantation.[ncbi.nlm.nih.gov]
  • Absolute neutropenia was the dominant feature at presentation, with mild anemia, thrombocytopenia, monocytosis (as a percentage), multilineage dysplasia, and increased myeloblasts, consistent with a diagnosis of refractory anemia with excess blasts (RAEB[ncbi.nlm.nih.gov]
  • […] neutropenia Refractory thrombocytopenia Refractory cytopenia with multilineage dysplasia (RCMD) Refractory anemia with ring sideroblasts (RARS) Refractory anemia with excess blasts (RAEB) MDS associated with isolated del(5q) Childhood myelodysplastic[surgpathcriteria.stanford.edu]
  • She had been diagnosed with refractory anemia and subsequently developed CMML with cytogenetic abnormalities including t(3;8)(q26;q24).[ncbi.nlm.nih.gov]
  • We report on a familial Mediterranean fever (FMF) patient homozygous for p.M694V in the MEFV gene who developed chronic myelomonocytic leukemia (CMML) leading to an uncontrolled and fatal inflammatory syndrome.[ncbi.nlm.nih.gov]
  • A 67-year-old woman presented with fever, purpura, and confusion.[ncbi.nlm.nih.gov]
  • It is the commonest hereditary fever syndrome with recurrent episodes of fever accompanied by abdominal, chest and joint pain.[ojrd.biomedcentral.com]
  • Glucocorticoid (GC) therapy occasionally relieves tumor-related fever and promotes tumor reduction in patients with chronic myelomonocytic leukemia (CMML).[ncbi.nlm.nih.gov]
  • Dose-limiting toxicities (DLTs) consisted of grade 3 fatigue, grade 3 typhilitis, grade 3 syncope and grade 3 QTc prolongation).[ncbi.nlm.nih.gov]
  • We ask about general symptoms (anxious mood, depressed mood, fatigue, pain, and stress) regardless of condition. Last updated: November 30, 2018[patientslikeme.com]
  • We ask about general symptoms (anxious mood, depressed mood, fatigue, pain, and stress) regardless of condition. Last updated: March 23, 2018[patientslikeme.com]
  • Can be variable but many patients tend to present with fatigue, weight loss, fever, and night sweats. It is usually characterised by accumulation of monocytes in the blood and bone marrow, dysplastic haematopoiesis.[radiopaedia.org]
Weight Loss
  • Over several months, the patient's symptoms progressed, which resulted in significant weight loss. The patient's course of disease was ultimately complicated by acute disseminated encephalomyelitis and death.[ncbi.nlm.nih.gov]
  • Can be variable but many patients tend to present with fatigue, weight loss, fever, and night sweats. It is usually characterised by accumulation of monocytes in the blood and bone marrow, dysplastic haematopoiesis.[radiopaedia.org]
  • Symptoms can include fatigue, weight loss, fever, and abdominal pain. Treatment may include chemotherapy, radiation, supportive care, surgery, or stem cell transplant.[patientslikeme.com]
  • […] tend to be: Older Male Previously exposed to certain substances at work or in the environment, including radiation Treated in the past with certain anticancer drugs Symptoms You may experience: Fever for no known reason Infection Feeling very tired Weight[uvahealth.com]
  • A 53-year-old woman with CMML and newly diagnosed cervical lymphadenopathy underwent whole-body PET/CT for evaluation of extramedullary disease. PET demonstrated marked tracer uptake in cervical lymph nodes.[ncbi.nlm.nih.gov]
  • […] infiltration by malignant cells, intrarenal leukostasis, tumor lysis syndrome, thrombotic microangiopathy, cryoglobulinemia, paraprotein deposition disease, chemotherapy-induced tubular or vascular toxicity, radiation injury, and ureteral obstruction from lymphadenopathy[dovepress.com]
  • Neck exam revealed tenderness over the right neck without lymphadenopathy or jugular venous distention or thyroid tenderness. Cardiac exam revealed only tachycardia. No ecchymosis was noted over the skin or mucous membranes.[omicsgroup.org]
  • Other less frequent signs and symptoms consist of anaemia , fever , weight loss , night sweats , infection , bleeding , synovitis , lymphadenopathy , skin rashes, pleural effusion , pericardial effusion and peritoneal effusion . [7] [11] [12] Cause [[en.wikipedia.org]
  • Lymphadenopathy (in approximately 75% of cases). Hepatosplenomegaly (in most cases). The clinical and laboratory features of JMML can closely mimic a variety of infectious diseases, including the following: Those caused by the Epstein-Barr virus.[cancer.gov]
Abdominal Pain
  • This report should alert physicians to consider this diagnosis in patients with CMML and acute abdominal pain.[ncbi.nlm.nih.gov]
  • The most common non-hematological toxicities of any grade, regardless of association with drug, were fatigue, diarrhea, dysphonia, dyspnea, hypertension, constipation, and abdominal pain.[ncbi.nlm.nih.gov]
  • Symptoms can include fatigue, weight loss, fever, and abdominal pain. Treatment may include chemotherapy, radiation, supportive care, surgery, or stem cell transplant.[patientslikeme.com]
  • Diarrhea, abdominal pain, and gastrointestinal bleeding can be seen in patients with either disorder, depending on the location and extent of disease.[nature.com]
  • If the liver gets too big (called hepatomegaly), it causes discomfort in the upper right part of the abdomen.[cancer.org]
  • […] chromosome negative CML 80% of cases arise de novo; 20% arise from prior myelodysplasia, occasionally with monocytosis ( Am J Clin Pathol 2006;126:789 ) Splenomegaly in 30 - 50% with rare rupture ( Am J Hematol 2007;82:405 , Am J Surg Pathol 1983;7:197 ), hepatomegaly[pathologyoutlines.com]
  • Symptoms, when present, are the consequences of cytopenias (notably anemia, which is invalidating in a third of patients), and/or of extramedullary hematopoiesis, notably splenomegaly but also hepatomegaly, skin infiltration, gum infiltration, and serous[atlasgeneticsoncology.org]
  • Common signs and symptoms include fatigue, splenomegaly and hepatomegaly, weight loss, fevers, and night sweats. About 50% of patients have normal or slightly decreased white blood cell count (WBC) with monocytosis.[oncologynurseadvisor.com]
  • Hepatosplenomegaly may be present.[ 4 , 5 ] Autoimmune phenomena, including pyoderma gangrenosum, vasculitis, and idiopathic thrombocytopenia have been observed in CMML.[ 11 ] Care should be taken to identify cases of CMML with eosinophilia, a subtype[cancer.gov]
  • Hepatosplenomegaly is more frequent (25–50% of patients) in the myeloproliferative variant [ 21 ]. Many patients experience constitutional symptoms, fatigue, night sweats and occasionally bone pain.[intechopen.com]
Buttock Pain
  • A 64-year-old female patient, admitted to our hospital with buttock pain alternating left and right, was found to have sacroiliitis and spondylitis by contrast magnetic resonance imaging.[ncbi.nlm.nih.gov]
Night Sweats
  • Can be variable but many patients tend to present with fatigue, weight loss, fever, and night sweats. It is usually characterised by accumulation of monocytes in the blood and bone marrow, dysplastic haematopoiesis.[radiopaedia.org]
  • If you have symptoms, they may include: Fatigue Weight loss Night sweats Fever Pain or a feeling of fullness below the ribs on the left side Tests that examine the blood and bone marrow diagnose CML.[icdlist.com]
  • Patients may present with symptoms related to cytopenias and/or an underlying hypercatabolic state with drenching night sweats, splenomegaly, and weight loss.[ncbi.nlm.nih.gov]
  • Most patients present with fatigue, weight loss, night sweats, and fevers. Patients typically have an increased white count (MPN feature), although a subset does present with normal or only modestly elevated leukocytes.[clinicaladvisor.com]
  • Case 1 was a 61-year-old female patient admitted to our hospital because of skin petechiae and purpura for 6 days.[ncbi.nlm.nih.gov]
  • […] carry oxygen) Shortness of breath Pale skin Weakness and fatigue Lack of appetite Bleeding in excess (even when you get a minor cut) Sinus infections Skin infections Urinary tract infections ( UTIs ) Headaches Fatigue Bruising easily Night sweats Fevers Petechiae[webmd.com]
  • Petechiae (flat, pinpoint spots under the skin caused by bleeding). Pain or a feeling of fullness below the ribs.[northshore.org]
  • […] routine assessment Early satiety and decreased food intake from encroachment on stomach by enlarged spleen Left upper quadrant abdominal pain from spleen infarction Hepatomegaly The following are signs and symptoms of progressive disease: Bleeding, petechiae[emedicine.medscape.com]
  • Generalized eruptive histiocytosis, described in 1963 by Winklemann and Muller, is a reactive, self-healing form of non-Langerhans histiocytosis.[ncbi.nlm.nih.gov]
Facial Papule
  • An 82-year old Japanese man presented with numerous asymptomatic facial papules clinically simulating rhinophyma.[ncbi.nlm.nih.gov]


Laboratory analyses of blood samples may prompt an initial suspicion of CMML. In order to confirm that hypothesis, bone marrow specimens have to be examined, too. Furthermore, routine cytogenetics, fluorescence in situ hybridization (FISH) or molecular biological techniques have to be applied to rule out chromosomal anomalies and gene defects indicative of differential diagnoses.

The following algorithm has been proposed for the diagnosis of CMML [13]:

  • Confirmation of persistent monocytosis with cell counts >1 × 10⁹/l
  • Confirmation of additional hematological alterations, e.g., anemia, neutropenia, eosinophilia, leukocytosis, thrombocytopenia, while a medical history of a hematopoietic disorder or systemic chemotherapy is as indicative of CMML as the former
  • In case all these criteria are fulfilled, a bone marrow biopsy should be carried out
  • Otherwise, differential diagnoses like chronic myeloid leukemia (positive for Philadelphia chromosome), chronic eosinophilic leukemia (rearrangement of platelet-derived growth factor receptor-α or β), infection and autoimmune disease should be ruled out by analyzing peripheral blood specimens before a bone marrow biopsy is realized
  • Estimation of peripheral blasts and bone marrow blasts in order to distinguish CMML-1, CMML-2, and acute myeloid leukemia

This workup aims at clarifying whether all diagnostic criteria, as proposed by the World Health Organization, are fulfilled. In detail, these criteria are:

  • Persistent monocytosis as defined above
  • Absence of Philadelphia chromosome or variants of the BCR-ABL fusion gene which encodes for a constitutively active tyrosine kinase
  • Absence of rearrangement of genes encoding for platelet-derived growth factor receptor subunits α and β
  • Peripheral blasts and bone marrow blasts <20%
  • Dysplasia in one or more myeloid lineages, or: detection of cytogenetic or molecular anomalies consistent with CMML in hematopoietic stem cells, or: exclusion of all other causes of monocytosis
Pericardial Effusion
  • Although CMML cells disappeared from the peripheral blood, the pericardial effusion still persisted. This case indicates that pericardial effusion is a possible and life-threatening complication in CMML patients despite stably controlled leukocytes.[ncbi.nlm.nih.gov]
  • Ibrahim MI, Maslak PG, Heaney ML, George MS,Downey RJ, Tallman MS (2009) Chronic myelomonocyticleukemia (CMML) associated with symptomatic pericardial effusion. J ClinOncol 29.[esciencecentral.org]
  • Two months later, her aphasia returned with accompanying pericardial effusion, biopsy-proven leptomeningeal inflammation, and left elbow arthritis responsive to prednisone. Rheumatoid factor was transiently elevated at 21.8 IU/mL (range 0.0-20.0).[springerplus.springeropen.com]
  • Other less frequent signs and symptoms consist of anaemia , fever , weight loss , night sweats , infection , bleeding , synovitis , lymphadenopathy , skin rashes, pleural effusion , pericardial effusion and peritoneal effusion . [7] [11] [12] Cause [[en.wikipedia.org]
Pleural Effusion
  • Other less frequent signs and symptoms consist of anaemia , fever , weight loss , night sweats , infection , bleeding , synovitis , lymphadenopathy , skin rashes, pleural effusion , pericardial effusion and peritoneal effusion . [7] [11] [12] Cause [[en.wikipedia.org]
  • Similarly, clinically meaningful responses, including improvement of life threatening pericardial and pleural effusions, as well as cytopenias were reported for the topoisomerase‐II inhibitor etoposide [ 52 ].[intechopen.com]


Drug therapy is chosen for the majority of CMML patients, especially in a case of CMML-1. Hypomethylating agents like azacitidine and decitabine are primarily administered to control MDS-like symptoms; chemotherapeutics such as hydroxyurea and etoposide are used to remedy MPN-like complications. Response rates are 40 and 30% for azacitidine and decitabine, respectively. Hydroxyurea has been shown to be more effective than etiposide [14]. Hypomethylating or cytoreductive therapy may also precede hematopoietic stem cell transplantation.

To date, hematopoietic stem cell transplantation remains the only curative treatment. It is indicated in case of CMML-2 and whenever the general condition of the patient allows for this approach, i.e., its usability is mainly limited by the age of CMML patients and the high prevalence of comorbidities. While stem cell transplantations are associated with a better outcome in younger patients, response rates are still modest. According to a recent multi-center study, little more than half of CMML patients respond to this therapy [15]. Myeloablative regimens are generally chosen to prepare patients younger than 55 years for the procedure, whereas reduced intensity conditioning is recommended for elder individuals.

Supportive care should be provided to all CMML patients and may include the use of erythropoiesis-stimulating agents as well as the transfusion of blood products.


CMML is generally associated with a poor outcome. Recently, median survival times of 13.3 months and an overall three-years survival rate of 19% have been reported [9]. Similar values have been reported elsewhere [3]. Such values do, however, comprise data obtained from patients diagnosed with CMML-1, CMML-2 and those who sustained disease progression to acute myeloid leukemia. A detailed listing of survival times for CMML-1 and CMML-2 is slightly more encouraging since these phases of the disease are associated with median overall survival times of 38 and 24 months, respectively [2]. Moreover, studies regarding the prognosis of CMML patients highlight that there is a considerable heterogeneity with regards to the underlying molecular anomalies and to the provision of adequate treatment. In this context, drug- or radiation-induced CMML may be associated with a better outcome than sporadic cases of the disease [3]. Besides blast counts and bone marrow compromise, monocyte counts >10 × 10⁹/l, leukocyte counts >15 × 10⁹/l, platelet counts <100 × 10⁹/l, hemoglobin concentrations <10 g/dl, ASXL1 mutations as well as age over 65 years have been identified as unfavorable prognostic factors [10] [11].


Both cytogenetic anomalies and gene mutations contribute to disturbances of cell cycle regulation in CMML. Chromosomal aberrations are observed in about 30% of CMML patients, whereas more than 90% of affected individuals show molecular and epigenetic abnormalities [2]. With regards to the former, trisomy 8, trisomy 21, loss of the Y chromosome, monosomy 7 and deletion of the long arms of chromosomes 7 or 20 are among the most common karyotypes. Alterations of sequence segments are as heterogeneous as the aforementioned cytogenetic anomalies and may affect genes encoding for epigenetic regulators (e.g., TET2, ASXL1), transcription factors (e.g., RUNX1), proteins involved in post-translational modification (e.g., SRSF2), and components of intracellular signaling cascades (e.g., RAS). All these gene products are involved in the complex process of hematopoiesis, in the regulation of precursor cell growth, division, differentiation, and death. TET2, for instance, induces the conversion of methylcytosine to 5-hydroxymethylcytosine, a biochemical reaction important in myelopoiesis since the attachment of a methyl and hydroxy group to cytosine is presumed to serve as a signal for increased or reduced gene expression. ASXL1, in contrast, is assumed to enhance the expression of certain genes and suppress the expression of others by modifying chromatin. About half of CMML patients show either TET2 or ASXL1 mutations. Of note, such mutations are not pathognomonic of CMML. Sequence alterations affecting TET2 and ASXL1, for instance, have also been related to myelodysplasia.

In most cases, the precise trigger of malignant transformation of precursor cells is not known. Few cases are ascribed to the administration of alkylating agents or irradiation, though. The former are generally referred to as de novo CMML, the latter as therapy-related CMML [3]. Nine out of ten cases are deemed de novo CMML. It has been speculated that exposure to common carcinogens such as cigarette smoke and ionizing radiation may predispose for CMML. This hypothesis is based on the fact that those environmental factors are known to increase the individual risk of MDS.


The overall incidence of CMML has been estimated to be 0.3 per 100,000 inhabitants in the United States and 0.39 per 100,000 people in Spain [4] [5]. According to the respective studies, CMML is the most common disease classified as myelodysplastic/myeloproliferative neoplasm, with atypical chronic myeloid leukemia and juvenile chronic myeloid leukemia being observed much less frequently. However, CMML only accounts for about 10% of MDS cases. Misdiagnosis of CMML as MDS may have caused an underestimation of incidence rates.

Men are affected more often than women (male-to-female ratio = 1.3), and a trend towards shorter survival in males has been observed. The median age at the time of diagnosis is 65 to 75 years. Few case reports exist on CMML in pediatric patients and young adults. In these patients, CMML is generally induced by chemotherapeutics or radiation therapy.

Sex distribution
Age distribution


The pathogenesis of CMML is incompletely understood, but current knowledge regarding the diversity of cytogenetic and molecular anomalies as well as the clinical presentation of affected individuals implies heterogeneous mechanisms to account for symptom onset. As has been indicated above, TET2 mutations are frequently detected in affected cells obtained from CMML patients. Although a detailed list of genes whose expression is enhanced or suppressed upon failure of TET2 cannot be provided, it has been shown that early dominance of TET2-deficient stem cell clones favors the proliferation of granulomonocytic precursors [6]. The pathophysiological importance of TET2 may also be illustrated by the fact that the presence of TET2 mutations predicts an MSD patient's response to hypomethylating agents [7]. ASXL1 mutations have also been related to an excess proliferation of myeloid precursor cells: While the precise function of its gene product remains unknown, it could be shown that ASXL1 gene defects are associated with reduced histone H3 lysine 27 (H3K27) trimethylation [8].


Most cases of CMML cannot be ascribed to any trigger. However, exposure to cigarette smoke, ionizing radiation, and cytotoxic chemotherapy is known to be related to the onset of MDS. It may be assumed that these factors also play a role in CMML pathogenesis and thus, it is recommended to minimize such exposure as much as possible.


Chronic myelomonocytic leukemia (CMML) is a clonal hematopoietic stem cell disorder. According to the current classification of tumors of the hematopoietic and lymphoid tissues, as published by the World Health Organization, CMML is a myelodysplastic/myeloproliferative neoplasm [1]. This classification responds to the fact that CMML comprises both features of myelodysplasia and myeloproliferative diseases, namely pathological alterations of hematopoiesis and a proliferation of a particular cell type. The clinical hallmark of CMML is monocyte count that exceeds 1 × 10⁹/l and persists for more than three months. Additionally, patients often suffer from anemia, neutropenia, and thrombocytopenia. CMML may transform to acute myeloid leukemia at any time, a condition that is not always treated as an own entity but rather referred to as the blast phase of CMML. Disease progression is associated with a worse prognosis, and the following degrees of severity have been defined accordingly:

  • CMML-1: 5% peripheral blasts including monoblasts and promonocytes, <10% bone marrow blasts
  • CMML-2: 5-19% peripheral blasts including monoblasts and promonocytes and/or 10-19% bone marrow blasts
  • Acute myeloid leukemia: >20% peripheral blasts or bone marrow blasts

Therapeutic regimens are derived from those established for treatment of myelodysplastic syndromes and myeloproliferative neoplasms. To date, the only curative treatment option is hematopoietic stem cell transplantation. CMML is generally associated with a poor outcome.

Patient Information

Chronic myelomonocytic leukemia (CMML) is a hematopoietic disorder, i.e., affected individuals suffer from an impairment of bone marrow function. On the one hand, hematopoietic stem cells and later precursors of blood cells are no longer able to differentiate into functional cells. This condition is referred to as myelodysplasia. On the other hand, stem cells undergo malignant transformation and start to proliferate in an uncontrolled manner. This process is characteristic of blood cancer and further interferes with blood cell maturation.

Symptoms related to CMML thus result from bone marrow suppression. Patients may suffer from lethargy and fatigue due to anemia, be prone to infections because of an immunosuppression due to reduced immune cell counts, and present with a bleeding diathesis caused by lack of platelets. Since these symptoms are very unspecific, detailed analyses of blood and bone marrow specimens are required to diagnose CMML. Findings obtained in those analyses also allow for an estimation of disease severity, which is important at the moment of deciding for a determined treatment regimen. To this end, the general condition of the patient also plays a crucial role.

CMML patients may either receive medication to control symptoms associated with myelodysplasia and myeloproliferation, or they may be recommended for hematopoietic stem cell transplantation. While the latter is the only curative therapy known to date, there are inherent risks to this procedure. Thus, debilitated patients and individuals diagnosed with less severe CMML generally receive drug therapy.



  1. Swerdlow SH, Campo E, Harris NL, et al. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues. 4 ed. Lyon, France: IARC Press; 2013.
  2. Patnaik MM, Tefferi A. Cytogenetic and molecular abnormalities in chronic myelomonocytic leukemia. Blood Cancer J. 2016; 6:e393.
  3. Takahashi K, Pemmaraju N, Strati P, et al. Clinical characteristics and outcomes of therapy-related chronic myelomonocytic leukemia. Blood. 2013; 122(16):2807-2811.
  4. Rollison DE, Howlader N, Smith MT, et al. Epidemiology of myelodysplastic syndromes and chronic myeloproliferative disorders in the United States, 2001-2004, using data from the NAACCR and SEER programs. Blood. 2008; 112(1):45-52.
  5. Osca-Gelis G, Puig-Vives M, Saez M, Gallardo D, Lloveras N, Marcos-Gragera R. Population-based incidence of myeloid malignancies: fifteen years of epidemiological data in the province of Girona, Spain. Haematologica. 2013; 98(8):e95-97.
  6. Itzykson R, Kosmider O, Renneville A, et al. Clonal architecture of chronic myelomonocytic leukemias. Blood. 2013; 121(12):2186-2198.
  7. Bejar R, Lord A, Stevenson K, et al. TET2 mutations predict response to hypomethylating agents in myelodysplastic syndrome patients. Blood. 2014; 124(17):2705-2712.
  8. Abdel-Wahab O, Adli M, LaFave LM, et al. ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression. Cancer Cell. 2012; 22(2):180-193.
  9. Zandberg DP, Huang TY, Ke X, et al. Treatment and outcomes for chronic myelomonocytic leukemia compared to myelodysplastic syndromes in older adults. Haematologica. 2013; 98(4):584-590.
  10. Itzykson R, Kosmider O, Renneville A, et al. Prognostic score including gene mutations in chronic myelomonocytic leukemia. J Clin Oncol. 2013; 31(19):2428-2436.
  11. Patnaik MM, Itzykson R, Lasho TL, et al. ASXL1 and SETBP1 mutations and their prognostic contribution in chronic myelomonocytic leukemia: a two-center study of 466 patients. Leukemia. 2014; 28(11):2206-2212.
  12. Corcoran NM, Tsui A, Costello AJ, Bouchier-Hayes D. Unilateral testicular mass in man with chronic myelomonocytic leukemia: unusual presentation of chronic myelomonocytic leukemia sequela. Urology. 2005; 65(5):1001.
  13. Parikh SA, Tefferi A. Chronic myelomonocytic leukemia: 2013 update on diagnosis, risk stratification, and management. Am J Hematol. 2013; 88(11):967-974.
  14. Wattel E, Guerci A, Hecquet B, et al. A randomized trial of hydroxyurea versus VP16 in adult chronic myelomonocytic leukemia. Groupe Francais des Myelodysplasies and European CMML Group. Blood. 1996; 88(7):2480-2487.
  15. Patnaik MM, Wassie EA, Padron E, et al. Chronic myelomonocytic leukemia in younger patients: molecular and cytogenetic predictors of survival and treatment outcome. Blood Cancer J. 2015; 5:e270.

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Last updated: 2018-06-21 18:25