Cytogenetic profile of patients with acute myeloid leukemia and central nervous system disease

Shihadeh, Ferial; Reed, Valerie Klairisa; Faderl, Stefan; Medeiros, L. Jeffrey; Mazloom, Ali; Hadziahmetovic, Mersiha; Kantarjian, Hagop; Allen, Pamela K.; Ballas, Leslie K.; Pierce, Sherry; Dabaja, Bouthaina S.

doi:10.1002/cncr.26253

Cited by 70 publications

(93 citation statements)

References 23 publications

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“…These results suggest that allo-HSCT may decrease the relapse rate and overcome the poor prognosis otherwise associated with CNSþAML. This notion is consistent with the observations of Shihadeh et al [3], in which 4 of 5 patients who survived for more than 18 months received allo-HSCT. The clinical characteristics of patients with CNSþAML in this study were consistent with those seen in previous studies [3][4][5].…”

Section: Discussionsupporting

confidence: 93%

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Outcome of Allogeneic Hematopoietic Stem Cell Transplantation for Acute Myeloid Leukemia Patients with Central Nervous System Involvement

Aoki

Ishiyama

Taniguchi

et al. 2014

Biology of Blood and Marrow Transplantation

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Central nervous system (CNS) involvement in adult acute myeloid leukemia (AML) is rare and associated with poor outcomes. Therefore, CNS involvement in AML is an indicator for allogeneic hematopoietic stem cell transplantation (allo-HSCT). However, the impact of CNS involvement in AML on the outcome of allo-HSCT remains unclear. We performed a large-scale nationwide retrospective analysis to elucidate the outcomes of allo-HSCT on AML with CNS involvement (CNS+AML). Clinical data were collected from a registry database of the Japan Society for Hematopoietic Cell Transplantation. CNS involvement was defined as the infiltration of leukemia cells into the CNS or myeloid sarcoma in the CNS identified at any time from diagnosis to transplantation. One hundred fifty-seven patients with CNS+AML underwent allo-HSCT between 2006 and 2011. The estimated overall survival, cumulative incidence of relapse and nonrelapse mortality at 2 years for CNS+AML (51.2%, 30.2%, and 14.5%, respectively) were comparable with those for AML without CNS involvement (48.6%, 27.4%, and 22.0%, respectively). Univariate and multivariate analyses indicated that the development of chronic graft-versus-host disease, disease status, and cytogenetic risk category were independent prognostic factors for overall survival for CNS+AML. These results suggest that allo-HSCT may improve outcomes in patients with CNS+AML.

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Section: Discussionsupporting

confidence: 93%

“…Predisposing factors for AML with CNS involvement (CNSþAML) include higher level of lactate dehydrogenase and WBC counts at diagnosis, chromosome 16 inversion and chromosome 11 abnormality, French-American-British (FAB) subgroup M4 and M5, and younger age [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Outcome of Allogeneic Hematopoietic Stem Cell Transplantation for Acute Myeloid Leukemia Patients with Central Nervous System Involvement

Aoki

Ishiyama

Taniguchi

et al. 2014

Biology of Blood and Marrow Transplantation

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“…67 An increased risk of CNS involvement in AML occurs with a high WBC, high circulating blast count, high LDH, and younger age. 68 It is more commonly associated with inv(16)(p13q22), chromosome 11 abnormality, or trisomy 8. 68 Monocytic lineage leukemias are also associated with a 5.7-fold increased risk of CNS disease.…”

Section: Can Cns Relapse Be Predicted? Is There a Role For Cns Prophymentioning

confidence: 99%

“…68 It is more commonly associated with inv(16)(p13q22), chromosome 11 abnormality, or trisomy 8. 68 Monocytic lineage leukemias are also associated with a 5.7-fold increased risk of CNS disease. 69 In more than two-thirds of affected AML patients, CNS involvement appears at relapse, either isolated or as part of systemic disease.…”

Section: Can Cns Relapse Be Predicted? Is There a Role For Cns Prophymentioning

confidence: 99%

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How I treat hematologic emergencies in adults with acute leukemia

Zuckerman

Ganzel

Tallman

et al. 2012

Blood

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Acute myeloid leukemia and acute lymphoblastic leukemia remain devastating diseases. Only approximately 40% of younger and 10% of older adults are long-term survivors. Although curing the leukemia is always the most formidable challenge, complications from the disease itself and its treatment are associated with significant morbidity and mortality. Such complications, discussed herein, include tumor lysis, hyperleukocytosis, cytarabine-induced cellebellar toxicity, acute promyelocytic leukemia differentiation syndrome, thrombohemorrhagic syndrome in acute promyelocytic leukemia, L-asparaginase-associated thrombosis, leukemic meningitis, neutropenic fever, neutropenic enterocolitis, and transfussion-associated GVHD. IntroductionAlthough inadequate for the cure of most patients, the initial therapeutic approach to acute myeloid leukemia (AML) is standardized. However, the management of hematologic emergencies is challenging and may be controversial. We present clinical vignettes describing 10 emergencies encountered in practice and the questions such emergencies generate. We then provide our view of how to treat adults supported by studies if available and, if not, by clinical experience and consensus. The approach to these emergencies is as important as the antileukemia therapy, and in no clinical setting is it fairer to say that "the devil is in the details." Tumor lysis syndromeA 23-year-old man with a history of G6PD deficiency is diagnosed with pre-B acute lymphoblastic leukemia (B-ALL). At presentation, his white blood cell count (WBC) is 160 000/L with 90% lymphoblasts and 450/L neutrophils; the hemoglobin is 7.5 g/dL and platelet count is 10 000/L. His electrolytes and renal function are normal, the uric acid is 11.0 mg/dL, and lactate dehydrogenase (LDH) is 1500 IU/L (normal, 100-250 IU/L). Remission induction chemotherapy is planned. Questions What is the risk of tumor lysis syndrome (TLS)? What is the optimal treatment for preventing TLS? What is the role of rasburicase and urine alkalinization?TLS can appear before starting treatment (primary TLS) as a result of high turnover of the malignant cells or, more commonly, a short time after the beginning of treatment (secondary TLS). 1 The risk of developing TLS and its severity is influenced by many factors, including tumor burden, potential for rapid cell lysis, and preexisting nephropathy. 2 In acute leukemias, the risk is dependent on the WBC and the rate of response to therapy. In ALL with WBC Ͼ 100 000/L, the risk for TLS is high. With lower WBC, the risk is moderate and low. 3 A classification system has been developed, 4 which is based on separate definitions for laboratory and clinical TLS. Laboratory TLS loosely is defined as the presence of 2 or more abnormal laboratory values of uric acid, potassium, phosphorus, or calcium at presentation or a 25% change in values from the pretreatment measurements. Clinical TLS is defined as the presence of laboratory TLS plus renal dysfunction, seizures, cardiac arrhythmia, or sudden death. An expert TLS pane...

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Acute myeloid leukemia

Johansson

Harrison

2015

Cancer Cytogenetics

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Cytogenetic profile of patients with acute myeloid leukemia and central nervous system disease

Cited by 70 publications

References 23 publications

Outcome of Allogeneic Hematopoietic Stem Cell Transplantation for Acute Myeloid Leukemia Patients with Central Nervous System Involvement

Outcome of Allogeneic Hematopoietic Stem Cell Transplantation for Acute Myeloid Leukemia Patients with Central Nervous System Involvement

How I treat hematologic emergencies in adults with acute leukemia

Acute myeloid leukemia

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