Home About us Contact
|
Home About us Contact | ||
|
|
||
Childhood Acute Myeloid Leukemia (childhood + acute_myeloid_leukemia)
Selected AbstractsCharacterization of 6q abnormalities in childhood acute myeloid leukemia and identification of a novel t(6;11)(q24.1;p15.5) resulting in a NUP98,C6orf80 fusion in a case of acute megakaryoblastic leukemiaGENES, CHROMOSOMES AND CANCER, Issue 3 2005Sabrina Tosi Chromosome abnormalities of 6q are not frequently observed in myeloid disorders. In this article, we report the incidence of these chromosome changes in childhood myeloid leukemia as 2%,4% based on the cytogenetic database of a single institution. We applied fluorescence in situ hybridization (FISH) to characterize precisely the types of 6q abnormalities in seven patients (six with acute myeloid leukemia and one with myelodysplastic syndrome). They carried various translocations involving different breakpoints in 6q, as confirmed by FISH using a whole-chromosome-6 paint. Four cases were reported as t(6;11), although the breakpoints varied. Among these, we identified a novel translocation, t(6;11)(q24.1;p15.5), in a patient with acute megakaryoblastic leukemia. Molecular cytogenetic studies using the PAC clone RP5-1173K1 localized the genomic breakpoint on chromosome 11 to within the NUP98 gene. The breakpoint on chromosome 6 was narrowed down to a 500-kb region between BAC clones RP11-721P14 and RP11-39H10. Reverse-transcription PCR was performed using a forward primer specific for NUP98 and a reverse primer for the candidate gene in the 500-kb interval in 6q. This experiment resulted in the identification of a new fusion between NUP98 and C6orf80. Further studies will aim to fully characterize C6orf80 and will elucidate the role of this new NUP98 fusion in myeloid leukemia. © 2005 Wiley-Liss, Inc. [source] MDM2 polymorphism increases susceptibility to childhood acute myeloid leukemia: A report from the Children's Oncology Group,PEDIATRIC BLOOD & CANCER, Issue 2 2010Christine L. Phillips MD Abstract Background The variant polymorphism in the gene MDM2, SNP309, leads to increased level of mdm2 protein and subsequent downregulation of p53 tumor suppressor pathway. Presence of this single nucleotide polymorphism (SNP) has been associated with earlier tumorigenesis in patients with Li,Fraumeni syndrome, as well as decreased survival in patients with CLL. In addition, cells homozygous (G/G) for SNP 309 were found to have 10-fold increase resistance to topoisomerase II inhibitors in vitro. Procedure We genotyped children (n,=,575) with de novo acute myeloid leukemia (AML) treated on three Children's Oncology Group protocols (CCG 2941/2961/AAML 03P1) for the presence of SNP309. Healthy blood donors were genotyped as control population. Results The variant G/G genotype was associated with an increased susceptibility to AML (OR 1.5; P,=,0.049). However, the presence of the variant allele at SNP309 did not modify disease response or toxicity in children treated on CCG protocols 2941/2961. Conclusions The variant SNP 309 influences susceptibility to pediatric AML, but does not impact overall response to therapy. Pediatr Blood Cancer. 2010;55:248,253. © 2010 Wiley,Liss, Inc. [source] Health and risk behaviors in survivors of childhood acute myeloid leukemia: A report from the Children's Oncology Group,PEDIATRIC BLOOD & CANCER, Issue 1 2010Kris Ann P. Schultz MD Abstract Background Survivors of childhood acute myeloid leukemia (AML) face increased risks of chronic disease and secondary malignancies. Substance exposure may compound these risks. Procedures Participants were diagnosed with AML at <21 years of age and survived ,5 years following diagnosis. All underwent chemotherapy alone or followed by autologous BMT (chemo,±,autoBMT) or underwent allogeneic BMT (alloBMT) if an HLA-matched related donor was available. Survivors completed a health questionnaire and a Youth Risk Behavior Survey (YRBS). Results Of eligible survivors, 117 were ,18 years of age and completed a YRBS. Survivors were a mean age of 10 years at diagnosis and 24 years at interview. Of the substance exposures assessed by YRBS, tobacco, alcohol, and marijuana were most common. Twenty-two percent (22%) had smoked cigarettes in the last 30 days. One-quarter (25%) reported binge drinking in the last month. None of these exposures varied by treatment group. Less than 10% of survivors reported cocaine, heroin, or methamphetamine use. Men were more likely to report high substance exposure (P,=,0.004). Sadness/suicidality score was associated with cancer-related anxiety (P,=,0.006) and multiple health conditions (P,=,0.006). Conclusions This analysis reveals exposure to tobacco, alcohol, and marijuana in young adults with few differences based on treatment received. Survivors with cancer-related anxiety or multiple health conditions were more likely to report sadness/hopelessness. Pediatr Blood Cancer 2010;55:157,164. © 2010 Wiley-Liss, Inc. [source] Late-appearing Philadelphia chromosome in childhood acute myeloid leukemiaPEDIATRIC BLOOD & CANCER, Issue 5 2008Niketa Shah MD Abstract A 3-year-old female was diagnosed with acute myeloid leukemia (AML-M2). The disease was refractory to various chemotherapeutic agents. Cytogenetic analysis revealed a clone with trisomy 8 at diagnosis that was replaced by a clone containing a t(11;15) and del(20q) by the end of the second induction. A new clone, characterized by a Philadelphia chromosome, with the minor BCR/ABL p190 transcript, emerged 14 months after diagnosis and remained to the end of disease course. The late occurrence of the Philadelphia chromosome in AML has been documented rarely in adults. Pediatr Blood Cancer 2008;50:1052,1053. © 2008 Wiley-Liss, Inc. [source] Prognostic factors and outcome of recurrence in childhood acute myeloid leukemia,CANCER, Issue 1 2007Jeffrey E. Rubnitz MD Abstract BACKGROUND. Outcome after recurrence of childhood acute myeloid leukemia (AML) is poor. We performed this study to identify prognostic factors for recurrence and for survival after recurrence of AML. METHODS. The clinical characteristics, biological features, treatment modalities, and outcomes of children with de novo AML who were enrolled on 3 consecutive clinical protocols from 1987 to 2002 at St. Jude Children's Research Hospital were studied. Regression modeling was used to identify prognostic factors for recurrence and for survival after recurrence. RESULTS. The outcome after recurrence was poor, with a 5-year survival estimate of only 23.3% ± 5.7%. Multivariable analysis indicated that male sex (P = .005), autologous stem cell transplant before recurrence (P = .097), each additional month from diagnosis to recurrence (P = .041), and stem cell transplant after recurrence (P < .001) were associated with a better survival after recurrence, whereas M5 or M7 morphology (P = .001) were significantly predictive of a lower survival estimate after recurrence. CONCLUSIONS. Survival after recurrence was poor in children with AML. Novel therapies are urgently needed to prevent or to treat recurring AML. Cancer 2007. © 2006 American Cancer Society. [source] | ||||||||||