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Juvenile myelomonocytic leukemia (JMML) is a rare form of chronic leukemia (cancer of the blood) that affects children, commonly those aged four and younger. [2] The name JMML now encompasses all diagnoses formerly referred to as juvenile chronic myeloid leukemia (JCML), chronic myelomonocytic leukemia of infancy, and infantile monosomy 7 syndrome.
The 5-year event free survival, disease-free survival, and overall survival rate in the phase 3 clinical study in DS-AMKL were 79, 89, 84 percent, respectively. [13] Other studies that use a treatment regimen similar to that used in the phase 3 clinical study report overall survival rates of ~80% [7] and long-term survivals of 74-91%. [9]
The 5-year survival rate for children with leukemia is 83.6% in the USA. This means that 83.6% of children diagnosed with leukemia live for 5 years or more after their diagnosis. This is greatly improved from a 5-year survival rate of 36.5% in 1975. The improvement is largely attributed to advances in therapy, particularly therapy for ALL.
Acute myelomonocytic leukemia (AMML) is a form of acute myeloid leukemia that involves a proliferation of CFU-GM myeloblasts and monoblasts.AMML occurs with a rapid increase amount in white blood cell count and is defined by more than 20% of myeloblast in the bone marrow.
Observation of monosomy 7 within the marrow is well correlated with an increased risk of developing AML and with a very poor prognosis, death generally ensuing within 2 years (unless prompt allogeneic hematopoietic progenitor cell transplant is an option). [9]
Trisomy 8, chromosome 7 abnormalities and complex karyotypes comprise a high risk group. Other cytogenetic abnormalities have intermediate prognoses. Somatic mutations in genes such as ASXL1 and EZH2 are associated with a poor prognosis. [12] CMML has a 20–30% chance of transformation to AML, a lower rate than other similar diseases.
Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, characterized by the rapid growth of abnormal cells that build up in the bone marrow and blood and interfere with normal blood cell production. [1] Symptoms may include feeling tired, shortness of breath, easy bruising and bleeding, and increased risk of infection. [1]
Individuals exhibiting >20% blast cells in blood or bone marrow are diagnosed as having AML. Thus, GATA2 deficiency may also present as AML that was preceded by MPS. [10] [11] [12] In about 70% of the cases, the inactivating GATA2 mutations found in Familial MDS/AML are associated with advanced disease and exhibit monosomy of their 7 chromosome ...