https://www.zora.uzh.ch/id/eprint/40126/4/Conter_V_et_al_Molecular_response_in_AIEOP-BFM_ALL_2000_V.pdf

Molecular response to treatment redefines all prognostic factors in children and adolescents with B-cell precursor acute lymphoblastic leukemia: results in 3184 patients of the AIEOP-BFM ALL 2000 study

Patients with acute leukemia in clinical remission may still have up to 10(10) residual malignant cells (the upper limit of detection by standard morphologic techniques). Sensitive techniques to detect minimal residual disease (MRD) may allow better estimates of the leukemia burden and help the selection of appropriate therapeutic strategies. Flow cytometry and polymerase chain reaction have emerged as the most promising methods for detecting submicrospopic levels of leukemia. Flowcytometric detection of MRD is based on the identification of immunophenotypic combinations expressed on leukemic cells but not on normal hematopoietic cells. It affords the detection of one leukemic cell among 10,000 normal bone marrow cells, and can be currently applied to at least two thirds of all patients with acute leukemia. Prospective studies in large series of patients have demonstrated a strong correlation between MRD levels during clinical remission and treatment outcome. Therefore, MRD assays can be reliably used to assess early response to treatment and predict relapse. In this review, we discuss methodologic aspects and clinical results of flowcytometric detection of MRD in patients with acute leukemia.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/%28SICI%291097-0320%2819990815%2938%3A4%3C139%3A%3AAID-CYTO1%3E3.0.CO%3B2-H

Detection of minimal residual disease in acute leukemia by flow cytometry.

NPM1-mutated acute myeloid leukemia: from bench to bedside.

Nucleophosmin (NPM1) is a highly conserved nucleo-cytoplasmic shuttling protein that shows a restricted nucleolar localization. Mutations of NPM1 gene leading to aberrant cytoplasmic dislocation of nucleophosmin (NPMc+) occurs in about one third of acute myeloid leukaemia (AML) patients that exhibit distinctive biological and clinical features. We discuss the latest advances in the molecular basis of nucleophosmin traffic under physiological conditions, describe the molecular abnormalities underlying altered transport of nucleophosmin in NPM1-mutated AML and present evidences supporting the view that cytoplasmic nucleophosmin is a critical event for leukaemogenesis. We then outline how a highly specific immunohistochemical assay can be exploited to diagnose NPM1-mutated AML and myeloid sarcoma in paraffin-embedded samples by looking at aberrant nucleophosmin accumulation in cytoplasm of leukaemic cells. This procedure is also suitable for detection of haemopoietic multilineage involvement in bone marrow trephines. Moreover, use of immunohistochemistry as surrogate for molecular analysis can serve as first-line screening in AML and should facilitate implementation of the 2008 World Health Organization classification of myeloid neoplasms that now incorporates AML with mutated NPM1 (synonym: NPMc+ AML) as a new provisional entity. Finally, we discuss the future therapeutic perspectives aimed at reversing the altered nucleophosmin transport in AML with mutated NPM1.

Altered nucleophosmin transport in acute myeloid leukaemia with mutated NPM1: molecular basis and clinical implications

The level of residual disease based on mutant NPM1 is an independent prognostic factor for relapse and survival in AML

Prophylactic treatment of the central nervous system (CNS) in childhood leukemia and non-Hodgkin lymphoma (NHL) has negative effects on intelligence. We investigated the clinical significance of this finding by comparing the effect of different types of CNS prophylaxis on the survivor’s learning capabilities. To isolate the effect of different types of CNS prophylaxis from other treatment and disease variables on learning problems, children treated for leukemia or NHL who received CNS prophylaxis with cranial irradiation (n = 30) or without cranial irradiation (n = 36) were compared with children treated for solid tumors who received systemic chemotherapy without any CNS treatment (n = 30) and with matched healthy controls (n = 265). The identification of learning problems was based on the school system’s assessment. Parents and teachers reported on the child’s educational status in a standardized way. Learning problems were found in 80% of children who received CNS prophylaxis with cranial irradiation. This was significantly higher than the 14% found in children treated with CNS prophylaxis without cranial irradiation (P < 0.000). the prevalence of learning problems in this latter group did not differ significantly from that in childhood cancer survivors without any form of cns prophylaxis (20%) and in healthy matched controls (17%). we conclude that the high prevalence of learning problems in survivors of childhood leukemia and nhl is directly related to cns prophylaxis with cranial irradiation and not to cns prophylaxis per se or to other treatment and disease variables.

Cranial irradiation is the major cause of learning problems in children treated for leukemia and lymphoma: a comparative study

Nucleophosmin leukaemic mutants contain C-terminus peptides that bind HLA class I molecules

Nucleophosmin leukaemic mutants contain C-terminus peptides that bind HLA class I molecules.

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Cranial irradiation is the major cause of learning problems in children treated for leukemia and lymphoma: a comparative study

Nucleophosmin leukaemic mutants contain C-terminus peptides that bind HLA class I molecules.