Myelodysplastic/Myeloproliferative Neoplasms Treatment (PDQ®): Treatment - Health Professional Information [NCI]

Treatment of Juvenile Myelomonocytic Leukemia

Disease Overview

Note: Juvenile myelomonocytic leukemia (JMML) was classified as a myelodysplastic syndrome (MDS) under the French-American-British scheme.[11] The World Health Organization classification removed JMML from MDS, placing it in the new category, myelodysplastic/myeloproliferative neoplasms (MDS/MPN).[11,22,33]

JMML (also known as juvenile chronic myelomonocytic leukemia) is a rare hematopoietic malignancy of childhood accounting for 2% of all childhood leukemias.[44] A number of clinical and laboratory features distinguish JMML from adult-type chronic myeloid leukemia, a disease noted only occasionally in children. In children presenting with clinical features suggestive of JMML, a definitive diagnosis requires the following:[55,66,77]

Major criteria (all three required)

• No Philadelphia chromosome or BCR::ABL fusion gene.
• Peripheral blood monocytosis is greater than 1 × 10⁹ /L.
• Fewer than 20% blasts (including promonocytes) in the blood and bone marrow.

Minor criteria (two or more required)

• Fetal hemoglobin (Hb F) increased for age.
• Immature granulocytes in the peripheral blood.
• White blood cell count is greater than 1 × 10⁹ /L.
• Clonal chromosomal abnormality (e.g., monosomy 7).
• Granulocyte-macrophage colony-stimulating factor (GM-CSF) hypersensitivity of myeloid progenitors in vitro.

The clinical features of JMML at the time of initial presentation may include the following:[55,66,77,88,99]

• Constitutional symptoms (e.g., malaise, pallor, and fever) or evidence of an infection.
• Symptoms of bronchitis or tonsillitis (in approximately 50% of cases).
• Bleeding diathesis.
• Maculopapular skin rashes (in 40%–50% of cases).
• 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.
• Cytomegalovirus.
• Human herpesvirus 6.
• Histoplasma.
• Mycobacteria.
• Toxoplasma.

Laboratory testing can distinguish whether JMML or infectious diseases have affected the clinical and hematologic findings.[55,66,1010,1111,1212]

JMML typically presents in young children (median age approximately 1 year) and occurs more commonly in boys (male to female ratio approximately 2.5:1). The cause for JMML is not known.[66,77] Children with neurofibromatosis type 1 (NF1) are at increased risk for developing JMML, and up to 14% of cases of JMML occur in children with NF1.[99,1313]

Morphologically, the peripheral blood picture in this disease shows leukocytosis, anemia, and frequently, thrombocytopenia.[66,77,88,99,1414,1515] The median reported white blood cell count varies from 25 × 10⁹ /L to 35 × 10⁹ /L. In 5% to 10% of children with JMML, however, it is greater than 100 × 10⁹ /L. The leukocytosis is comprised of neutrophils, promyelocytes, myelocytes, and monocytes. Blasts, including promonocytes, usually account for less than 5% of the white blood cells and always for less than 20%. Nucleated red blood cells are seen frequently. Thrombocytopenia is typical and may be severe.[66,77,88,99,1414,1515] Bone marrow findings include the following:[66,77,99,1414,1515]

• Hypercellularity with granulocytic proliferation.
• Hypercellularity with erythroid precursors (in some patients).
• Monocytes comprising 5% to 10% of marrow cells (30% or more in some patients).
• Minimal dysplasia.
• Reduced numbers of megakaryocytes.

A distinctive characteristic of JMML leukemia cells is their spontaneous proliferation in vitro without the addition of exogenous stimuli, an ability that results from the leukemia cells being hypersensitive to GM-CSF.[1616,1717] No Philadelphia chromosome or BCR::ABL fusion gene exists. Although cytogenetic abnormalities, including monosomy 7, occur in 30% to 40% of patients, none is specific for JMML.[66,1515,1818] In JMML associated with NF1, loss of the normal NF1 allele is common, and loss of heterozygosity for NF1 has been observed in some patients with JMML who lack the NF1 phenotype.[1818] This genetic alteration results in a loss of neurofibromin, a protein that is involved in the regulation of the RAS family of oncogenes.[1818] Point mutations in RAS have been reported to occur in the leukemic cells of 20% of patients with JMML.[66,1919]

The median survival times for JMML vary from approximately 10 months to more than 4 years, depending partly on the type of therapy chosen.[88,99,2020] Prognosis is related to age at the time of diagnosis. The prognosis is better in children younger than 1 year at the time of diagnosis. Children older than 2 years at the time of diagnosis have a much worse prognosis.[66,88] A low platelet count and a high Hb F level have been associated with a worse prognosis.[99,1414] Approximately 10% to 20% of cases may evolve to acute leukemia.[88,99]

Treatment Overview

No consistently effective therapy is available for JMML. Historically, more than 90% of patients have died despite the use of chemotherapy.[2121] Patients appeared to follow three distinct clinical courses:

1. Rapidly progressive disease and early demise.
2. Transiently stable disease followed by progression and death.
3. Clinical improvement that lasted for as long as 9 years before progression or, rarely, long-term survival.

A recent retrospective review described 60 children with JMML treated with chemotherapy (nonintensive and intensive) and/or bone marrow transplant (BMT) using sibling or unrelated human leukocyte antigen (HLA)-matched donor marrow or autologous marrow. The median survival was 4.4 years.[88][Level of evidence C1]

BMT seems to offer the best chance of cure for JMML.[44,99,2020,2121,2222,2323] A summary of the outcome of 91 patients with JMML treated with BMT in 16 different reports is as follows: 38 patients (41%) were still alive at the time of reporting, including 30 of the 60 (50%) patients who received grafts from HLA-matched or one-antigen mismatched familial donors, 2 of 12 (17%) with mismatched donors, and 6 of 19 (32%) with matched unrelated donors.[44]

In a retrospective study investigating the role of BMT for chronic myelomonocytic leukemia (CMML), 43 children with CMML and given BMT were evaluated. In 25 cases, the donor was a HLA-identical or a one-antigen-disparate relative, in four cases a mismatched family donor, and in 14 cases a matched unrelated donor. Conditioning regimens consisted of total-body radiation therapy and chemotherapy in 22 patients, whereas busulfan with other cytotoxic drugs were used in the remaining patients. Six of 43 patients (14%), five of whom received transplants from alternative donors, had graft failure. Probabilities of transplant-related mortality for children transplanted from HLA-identical/one-antigen-disparate relatives or from matched unrelated donors/mismatched relatives were 9% and 46%, respectively. The probability of relapse for the entire group was 58%; the 5-year event-free survival (EFS) rate was 31%. The authors of this study concluded that children with CMML and an HLA-compatible relative should receive a transplant as early as possible.[2020][Level of evidence C2]

In a retrospective review from Japan, the records of 27 children with JMML who underwent allogeneic hematopoietic stem cell transplant (SCT) were examined to determine the role of different variables that potentially influence outcome. The source of grafts was HLA-identical siblings in 12 cases, HLA-matched unrelated individuals in 10 cases, and HLA-mismatched donors in five cases. Total-body radiation therapy was used in 18 cases. At 4 years after SCT, EFS and overall survival (OS) rates were 54.2% (+/- 11.2% standard error [SE]) and 57.9% (+/- 11.0% SE), respectively. Six patients died of relapse and three died of complications. Patients with abnormal karyotypes showed a significantly lower OS than those with normal karyotypes (P < .001). Patients younger than 1 year showed a significantly higher OS than those older than 1 year. Other variables studied were not associated with OS. A multivariate analysis of these factors indicated that the abnormal karyotype was the only significant risk factor for lower OS.[2424][Level of evidence C1] Five of 10 patients with JMML responded to the oral administration of isotretinoin (i.e., two complete responses, three partial responses); median duration of response was 37 months. Treatment with isotretinoin was associated with a decrease in spontaneous colony formation and in GM-CSF hypersensitivity.[2525]

Molecular-targeting therapies under evaluation include the use of farnesyltransferase inhibitors that prevent RAS protein maturation, which may result in increased tumor cell apoptosis and inhibition of tumor cell growth.[1717,2626]

Current Clinical Trials

Use our advanced clinical trial searchadvanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General informationGeneral information about clinical trials is also available.

References:

1. Orazi A, Germing U: The myelodysplastic/myeloproliferative neoplasms: myeloproliferative diseases with dysplastic features. Leukemia 22 (7): 1308-19, 2008.
2. Emanuel PD: Myelodysplasia and myeloproliferative disorders in childhood: an update. Br J Haematol 105 (4): 852-63, 1999.
3. Hasle H, Niemeyer CM, Chessells JM, et al.: A pediatric approach to the WHO classification of myelodysplastic and myeloproliferative diseases. Leukemia 17 (2): 277-82, 2003.
4. Aricò M, Biondi A, Pui CH: Juvenile myelomonocytic leukemia. Blood 90 (2): 479-88, 1997.
5. Niemeyer CM, Fenu S, Hasle H, et al.: Response: differentiating myelomonocytic leukemia from infectious disease. Blood 91(1): 365-367.
6. Vardiman JW, Pierre R, Imbert M, et al.: Juvenile myelomonocytic leukaemia. In: Jaffe ES, Harris NL, Stein H, et al., eds.: Pathology and Genetics of Tumours of Haematopoietic and Lymphoid Tissues. IARC Press, 2001. World Health Organization Classification of Tumours, 3, pp 55-7.
7. Emanuel PD: Juvenile myelomonocytic leukemia and chronic myelomonocytic leukemia. Leukemia 22 (7): 1335-42, 2008.
8. Luna-Fineman S, Shannon KM, Atwater SK, et al.: Myelodysplastic and myeloproliferative disorders of childhood: a study of 167 patients. Blood 93 (2): 459-66, 1999.
9. Niemeyer CM, Arico M, Basso G, et al.: Chronic myelomonocytic leukemia in childhood: a retrospective analysis of 110 cases. European Working Group on Myelodysplastic Syndromes in Childhood (EWOG-MDS) Blood 89 (10): 3534-43, 1997.
10. Lorenzana A, Lyons H, Sawaf H, et al.: Human herpesvirus 6 infection mimicking juvenile myelomonocytic leukemia in an infant. J Pediatr Hematol Oncol 24 (2): 136-41, 2002.
11. Luna-Fineman S, Shannon KM, Lange BJ: Childhood monosomy 7: epidemiology, biology, and mechanistic implications. Blood 85 (8): 1985-99, 1995.
12. Pinkel D: Differentiating juvenile myelomonocytic leukemia from infectious disease. Blood 91 (1): 365-7, 1998.
13. Stiller CA, Chessells JM, Fitchett M: Neurofibromatosis and childhood leukaemia/lymphoma: a population-based UKCCSG study. Br J Cancer 70 (5): 969-72, 1994.
14. Passmore SJ, Hann IM, Stiller CA, et al.: Pediatric myelodysplasia: a study of 68 children and a new prognostic scoring system. Blood 85 (7): 1742-50, 1995.
15. Hess JL, Zutter MM, Castleberry RP, et al.: Juvenile chronic myelogenous leukemia. Am J Clin Pathol 105 (2): 238-48, 1996.
16. Emanuel PD, Bates LJ, Castleberry RP, et al.: Selective hypersensitivity to granulocyte-macrophage colony-stimulating factor by juvenile chronic myeloid leukemia hematopoietic progenitors. Blood 77 (5): 925-9, 1991.
17. Emanuel PD, Snyder RC, Wiley T, et al.: Inhibition of juvenile myelomonocytic leukemia cell growth in vitro by farnesyltransferase inhibitors. Blood 95 (2): 639-45, 2000.
18. Side LE, Emanuel PD, Taylor B, et al.: Mutations of the NF1 gene in children with juvenile myelomonocytic leukemia without clinical evidence of neurofibromatosis, type 1. Blood 92 (1): 267-72, 1998.
19. Flotho C, Valcamonica S, Mach-Pascual S, et al.: RAS mutations and clonality analysis in children with juvenile myelomonocytic leukemia (JMML). Leukemia 13 (1): 32-7, 1999.
20. Locatelli F, Niemeyer C, Angelucci E, et al.: Allogeneic bone marrow transplantation for chronic myelomonocytic leukemia in childhood: a report from the European Working Group on Myelodysplastic Syndrome in Childhood. J Clin Oncol 15 (2): 566-73, 1997.
21. Freedman MH, Estrov Z, Chan HS: Juvenile chronic myelogenous leukemia. Am J Pediatr Hematol Oncol 10 (3): 261-7, 1988 Fall.
22. Sanders JE, Buckner CD, Thomas ED, et al.: Allogeneic marrow transplantation for children with juvenile chronic myelogenous leukemia. Blood 71 (4): 1144-6, 1988.
23. Smith FO, King R, Nelson G, et al.: Unrelated donor bone marrow transplantation for children with juvenile myelomonocytic leukaemia. Br J Haematol 116 (3): 716-24, 2002.
24. Manabe A, Okamura J, Yumura-Yagi K, et al.: Allogeneic hematopoietic stem cell transplantation for 27 children with juvenile myelomonocytic leukemia diagnosed based on the criteria of the International JMML Working Group. Leukemia 16 (4): 645-9, 2002.
25. Castleberry RP, Emanuel PD, Zuckerman KS, et al.: A pilot study of isotretinoin in the treatment of juvenile chronic myelogenous leukemia. N Engl J Med 331 (25): 1680-4, 1994.
26. Rowinsky EK, Windle JJ, Von Hoff DD: Ras protein farnesyltransferase: A strategic target for anticancer therapeutic development. J Clin Oncol 17 (11): 3631-52, 1999.

Treatment of Atypical Chronic Myeloid Leukemia

Disease Overview

Atypical chronic myeloid leukemia (aCML) is a leukemic disorder that exhibits both myelodysplastic and myeloproliferative features at the time of diagnosis.

Atypical CML is characterized pathologically by the following:[11]

• Peripheral blood leukocytosis with increased numbers of mature and immature neutrophils.
• Prominent dysgranulopoiesis.
• No Philadelphia chromosome or BCR::ABL fusion gene.
• Neutrophil precursors (e.g., promyelocytes, myelocytes, and metamyelocytes) accounting for more than 10% of white blood cells.
• Minimal absolute basophilia with basophils accounting for less than 2% of white blood cells.
• Absolute monocytosis with monocytes typically account for less than 10% of white blood cells.
• Hypercellular bone marrow with granulocytic proliferation and granulocytic dysplasia.
• Fewer than 20% blasts in the blood or bone marrow.
• Thrombocytopenia.

Clinical features of aCML include the following:[11,22,33,44]

• Anemia. For more information on anemia, see FatigueFatigue.
• Thrombocytopenia.
• Splenomegaly (in 75% of cases).

Although cytogenetic abnormalities are found in as many as 80% of the patients with aCML, none is specific.[11,22,33,55] No Philadelphia chromosome or BCR::ABL fusion gene exists.

The exact incidence of aCML is unknown. The median age at the time of diagnosis of this rare leukemic disorder is in the seventh or eighth decade of life.[11,22,33]

Morphologically, aCML is characterized by myelodysplasia associated with bone marrow and peripheral blood patterns similar to chronic myeloid leukemia, but cytogenetically it lacks a Philadelphia chromosome or BCR::ABL fusion gene.[11] The white blood cell count in the peripheral blood is variable. Median values range from 35 × 10⁹ /L to 96 × 10⁹ /L, and some patients may have white blood cell counts greater than 300 × 10⁹ /L.[11,22,33,55] Blasts in the peripheral blood typically account for less than 5% of the white blood cells. Immature neutrophils usually total 10% to 20% or more.[11] The percentage of monocytes is rarely more than 10%. Minimal basophilia may be present.[11,22,33,55] Nuclear abnormalities, such as acquired Pelger-Huët anomaly, may be seen in the neutrophils. Moderate anemia (often showing changes indicative of dyserythropoiesis) and thrombocytopenia are common.[11,22,33,44] Bone marrow findings include the following: [11,22,33,55]

• Granulocytic hypercellularity.
• Blast count less than 20%.
• Dysgranulopoiesis
• Megakaryocytic dysplasia.
• Erythroid precursors accounting for more than 30% of marrow cells with dyserythropoiesis present (in some cases).

The median survival times for aCML are reported to be less than 20 months, and thrombocytopenia and marked anemia are poor prognostic factors.[11,22] Atypical CML evolves to acute leukemia in approximately 25% to 40% of patients.[11,33] In the remainder, fatal complications include resistant leukocytosis, anemia, thrombocytopenia, hepatosplenomegaly, cerebral bleeding associated with thrombocytopenia, and infection.[33,44]

Treatment Overview

The optimal treatment of aCML is uncertain because of the rare incidence of this chronic leukemic disorder. Treatment with hydroxyurea may lead to short-lived partial remissions of 2 to 4 months in duration.[44] Atypical CML appears to respond poorly to treatment with interferon-alpha.[44]

Current Clinical Trials

Use our advanced clinical trial searchadvanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General informationGeneral information about clinical trials is also available.

References:

1. Orazi A, Germing U: The myelodysplastic/myeloproliferative neoplasms: myeloproliferative diseases with dysplastic features. Leukemia 22 (7): 1308-19, 2008.
2. Hernández JM, del Cañizo MC, Cuneo A, et al.: Clinical, hematological and cytogenetic characteristics of atypical chronic myeloid leukemia. Ann Oncol 11 (4): 441-4, 2000.
3. Costello R, Sainty D, Lafage-Pochitaloff M, et al.: Clinical and biological aspects of Philadelphia-negative/BCR-negative chronic myeloid leukemia. Leuk Lymphoma 25 (3-4): 225-32, 1997.
4. Kurzrock R, Bueso-Ramos CE, Kantarjian H, et al.: BCR rearrangement-negative chronic myelogenous leukemia revisited. J Clin Oncol 19 (11): 2915-26, 2001.
5. Bennett JM, Catovsky D, Daniel MT, et al.: The chronic myeloid leukaemias: guidelines for distinguishing chronic granulocytic, atypical chronic myeloid, and chronic myelomonocytic leukaemia. Proposals by the French-American-British Cooperative Leukaemia Group. Br J Haematol 87 (4): 746-54, 1994.

Treatment of MDS / MPN, Unclassifiable

Disease Overview

Myelodysplastic/myeloproliferative neoplasm, unclassifiable (MDS/MPN-UC) (also known as mixed myeloproliferative/myelodysplastic syndrome, unclassifiable and overlap syndrome, unclassifiable) shows features of both myeloproliferative disease and myelodysplastic disease but does not meet the criteria for any of the other MDS/MPN entities.[11]

Diagnostic criteria for MDS/MPN-UC can be either:[11]

1. The combination of four sets of criteria (a–d):
   1. Clinical, laboratory, and morphologic features of myelodysplastic syndrome (MDS) (e.g., refractory anemia, refractory anemia with ringed sideroblasts, refractory cytopenia with multilineage dysplasia, and refractory anemia with excess of blasts) with fewer than 20% blasts in the blood and bone marrow. For more information on anemia, see FatigueFatigue.
   2. Prominent myeloproliferative features, e.g. platelet count greater than 600 × 10⁹ /L associated with megakaryocytic proliferation, or white blood cell count greater than 13.0 × 10⁹ /L with or without splenomegaly.
   3. No history of an underlying chronic myeloproliferative disorder (CMPD), MDS, or recent cytotoxic or growth factor therapy that could cause the myelodysplastic or myeloproliferative features.
   4. No Philadelphia chromosome or BCR::ABL fusion gene, del(5q), t(3;3)(q21;q26), or inv(3)(q21q26).
2. Mixed myeloproliferative and myelodysplastic features that cannot be assigned to any other category of MDS, CMPD, or MDS/MPN.

Clinical characteristics of MDS/MPN-UC include the following:

• Features of both MDS and CMPD.
• Hepatomegaly.
• Splenomegaly.

The incidence and etiology of MDS/MPN-UC are unknown.

Laboratory features typically include anemia and dimorphic erythrocytes on the peripheral blood smear.[11] Thrombocytosis (platelet count >600 × 10⁹ /L) or leukocytosis (white blood cell count >13 × 10⁹ /L) are present. Neutrophils may exhibit dysplastic features, and giant or hypogranular platelets may be present. Blasts make up less than 20% of the white blood cells and of the nucleated cells of the bone marrow. The bone marrow is hypercellular and may exhibit proliferation in any or all of the myeloid lineages. Dysplastic features are present in at least one cell line.[11]

No cytogenetic or molecular findings are available that are specific for MDS/MPN-UC. In one small series, six of nine patients (those with ringed sideroblasts associated with marked thrombocytosis [RARS-T]) showed a JAK2 V617F mutation causing constitutive activation of the JAK2 tyrosine kinase (a mutation also commonly observed in patients with polycythemia vera, essential thrombocythemia, and idiopathic myelofibrosis).[22] Because of its rare occurrence, the prognosis and predictive factors are unknown.[11]

Treatment Overview

Adult patients with MDS/MPN associated with platelet-derived growth factor receptor gene rearrangements are candidates for imatinib mesylate at standard dosages.[33] Because of its rare occurrence, the literature only minimally addresses other treatment options for MDS/MPN-UC. Supportive care involves treating cytopenias and infection as necessary.

Current Clinical Trials

Use our advanced clinical trial searchadvanced clinical trial search to find NCI-supported cancer clinical trials that are now enrolling patients. The search can be narrowed by location of the trial, type of treatment, name of the drug, and other criteria. General informationGeneral information about clinical trials is also available.

References:

1. Orazi A, Germing U: The myelodysplastic/myeloproliferative neoplasms: myeloproliferative diseases with dysplastic features. Leukemia 22 (7): 1308-19, 2008.
2. Szpurka H, Tiu R, Murugesan G, et al.: Refractory anemia with ringed sideroblasts associated with marked thrombocytosis (RARS-T), another myeloproliferative condition characterized by JAK2 V617F mutation. Blood 108 (7): 2173-81, 2006.
3. GLEEVEC - imatinib mesylate tablet. Novartis Pharmaceuticals Corporation, 2020. Available onlineAvailable online. Last accessed June 13, 2024.

Latest Updates to This Summary (06 / 14 / 2024)

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About This PDQ Summary

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of myelodysplastic/myeloproliferative neoplasms. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions.

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Last Revised: 2024-06-14