DEC-205/NY-ESO-1 Fusion Protein CDX-1401, Poly ICLC, Decitabine, and Nivolumab in Treating Patients With Myelodysplastic Syndrome or Acute Myeloid Leukemia
Conditions: Acute Myeloid Leukemia; Blasts 30 Percent or Less of Bone Marrow Nucleated Cells; Chronic Myelomonocytic Leukemia; High Risk Myelodysplastic Syndrome; Myelodysplastic Syndrome; Refractory Anemia Interventions: Biological: DEC-205/NY-ESO-1 Fusion Protein CDX-1401; Drug: Decitabine; Other: Laboratory Biomarker Analysis; Biological: Nivolumab; Drug: Poly ICLC Sponsors: Roswell Park Cancer Institute; National Cancer Institute (NCI) Not yet recruiting
Myelodysplastic syndromes (MDS) are a heterogeneous group of hematological diseases of ineffective hematopoiesis with a risk for progression to acute myeloid leukemia (AML) [1,2]. More than 80% of individuals with MDS are 65 years old or older at the time of diagnosis ; the average age at diagnosis is 67 years old . Anemia and fatigue are common in MDS, and are often managed through red blood cell transfusions. In addition, MDS can transform into AML requiring intensive chemotherapy and prolonged hospital stays of approximately 30 days , which can lead to severe toxicities and functional impairments [5 –8].
British Journal of Haematology, EarlyView.
Pediatric myelodysplastic syndromes (MDSs) are a heterogeneous group of clonal disorders with an annual incidence of 1 to 4 cases per million, accounting for less than 5% of childhood hematologic malignancies. MDSs in children often occur in the context of inherited bone marrow failure syndromes, which represent a peculiarity of myelodysplasia diagnosed in pediatric patients. Moreover, germ line syndromes predisposing individuals to develop MDS or acute myeloid leukemia have recently been identified, such as those caused by mutations in GATA2, ETV6, SRP72, and SAMD9/SAMD9-L. Refractory cytopenia of childhood (RCC) is the m...
Acquired aplastic anemia (AA) represents bone marrow (BM) failure caused by immune-system-mediated destruction of hematopoietic stem cells (HSCs) . Gene expression profiling of AA HSCs suggests the presence of a stressed and immunologically activated target cell population . Next-generation sequencing studies have identified somatic mutations, particularly in BCOR/BCORL1, PIGA, DNMT3A, and ASXL1, in AA patients [3,4]. Clonal hematopoiesis (CH) in AA is associated with evolution to myelodysplastic syndromes (MDS) or acute myeloid leukemia (AML) .
Myelodysplastic syndromes (MDS) are a group of heterogeneous oligoclonal stem cell disorders characterized by peripheral cytopenia and a risk of transformation into acute myeloid leukemia (AML). Anemia is the most frequent symptom and reflects the impaired erythroid cell maturation.
Conclusion: The prevalence of PHD after PRRT with 177Lu-DOTATATE was 4% in our patient population. The median time at which PHD developed was 41 mo after the first PRRT cycle. The relative risk for developing a hematopoietic neoplasm was 2.7. No risk factors were found for the development of PHD in GEP NET patients.
AbstractMyelodysplastic syndromes (MDS) are heterogeneous clonal disorders ranging from indolent conditions with a near-normal life expectancy to forms approaching acute myeloid leukaemia. Comorbid conditions have rarely been systematically studied among patients with MDS. Older age per se has a negative impact on survival of MDS patients, in particular of those with lower risk. However, age indirectly affects also the survival of higher-risk patients by limiting their eligibility to intensive treatments. In addition, ageing is associated with an increasingly high risk of developing comorbidity, and a high prevalence of co...
Background: Studies of bone marrow cell clonal alterations in patients with Fanconi anemia (FA), a cancer-prone inherited bone marrow failure (BMF) syndrome, have focused on their role in progression from BMF to myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). The role of such alterations on patient outcomes after hematopoietic cell transplantation (HCT) is unknown.
CPX-351 is a dual-drug liposomal encapsulation of cytarabine (C) and daunorubicin (D) that delivers a synergistic 5:1 drug ratio and is FDA-approved for adults with newly diagnosed therapy-related AML or AML with MDS-related changes. In a randomized, phase 3 study (NCT01696084) in patients (pts) 60-75 y with newly diagnosed sAML, CPX-351 significantly improved overall survival (OS) and remission rates vs 7 + 3. RAEB-t AML, often defined as bone marrow blasts 20%-29%, shares many features with myelodysplastic syndrome (MDS).
Conclusion Patients with acute leukaemia and myelodysplastic syndrome/severe aplastic anaemia were at high risk of pulmonary IFI.