MLL Genomic Breakpoint Distribution Within the Breakpoint Cluster Region in De Novo Leukemia in Children

Felix, Carolyn A.; Hosler, Matthew R.; Slater, Diana J.; Parker, Robert I.; Masterson, Margaret; Whitlock, James A.; Rebbeck, Timothy R.; Nowell̀, Peter C.; Lange, Beverly J.

doi:10.1097/00043426-199807000-00004

Cited by 38 publications

(28 citation statements)

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“…51 This allelic variant is associated with increased risk of prostate cancer in men and with decreased risk of treatment-related leukemia with MLL gene translocations. 51,52 CYP3A4 activity is also two times higher in females. 53 Among recent CCG studies, the biggest differences in outcome by race were in CCG-1891 for standard risk ALL.…”

Section: Prognostic Factors In Allmentioning

confidence: 88%

Pediatric Acute Lymphoblastic Leukemia: Challenges and Controversies in 2000

Felix¹

2000

Hematology

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This article discusses ways in which pediatric patients with acute lymphoblastic leukemia (ALL) can be stratified to receive intensive and less intensive therapies in order to decrease morbidity and mortality. Specifically, the focus may shift away from current intensive therapies for ultra low-risk patients and away from transplantation for certain patients at relapse. In contrast, infants with ALL comprise an ultra high-risk population in need of specialized approaches.In Section I Dr. Lange describes the need to identify ultra low-risk children. Groups around the world have improved the outcome of children with ALL by identifying the basic "total therapy" model of the 1970s and stratifying treatment according to risk of relapse. Current first-line treatment cures about 85% of children with standard-risk ALL and 70% of children with high-risk disease. However, all children receive anthracyclines, alkylating agents, or moderate-to high-dose antimetabolite infusions. While randomized clinical trials prove that these intensifications reduce relapses, they also show that half of all children with ALL can be cured with the modest therapy of the 1970s and early 1980s. The patients curable with lesser therapy may be considered an ultra low-risk group. Attempts to use age, gender, white count, morphology, and karyotype to identify the ultra low-risk group of patients with a 90-95% cure rate with minimal therapy have failed. An expanded repertoire of tools such as pharmacogenetic profiling, PCR measurement of minimal residual disease and microarray technology may make this goal achievable in this decade.In section II Dr. Chessells addresses the management of children with relapsed ALL. The chance of successful re-treatment with conventional chemotherapy for relapse depends on the duration of first remission and the site of relapse. Bone marrow transplantation from a histocompatible sibling or other suitable donor, which is widely accepted as the treatment of choice for children with a first remission of < 24 months, is associated with a high risk of relapse. Bone marrow transplantation for later bone marrow relapse improves leukemia-free survival but has significant shortterm and long-term toxicities. The challenges are to develop more effective treatment for early relapse and to identify those children with relapsed ALL who are curable with chemotherapy or, failing this, those children who would be candidates for bone marrow transplantation in third remission.In Section III Dr. Felix addresses the problem of infant ALL. ALL of infancy is clinically aggressive, and infants continue to have the worst prognosis of all pediatric patients with ALL. High white blood cell count, younger age, bulky extramedullary disease, and CNS disease at diagnosis are unfavorable characteristics. These features occur with MLL gene translocations. The probability of an MLL gene translocation and the probability of poor outcome both are greatest in younger infants. Specialized intensive chemotherapy approaches and bone marrow transplantation...

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Section: Prognostic Factors In Allmentioning

confidence: 88%

Pediatric Acute Lymphoblastic Leukemia: Challenges and Controversies in 2000

Felix¹

2000

Hematology

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“…Genomic DNAs were prepared from bone marrow or peripheral blood leukemic cells as previously described. [13][14][15] For cytogenetic studies, the cells were cultured for 24 hours without mitogen and karyotypes were prepared by standard methods. 16 There were 39 patients diagnosed with de novo leukemia characterized by translocation of the MLL gene at chromosome band 11q23, and 18 with treatment-related leukemia with MLL translocations.…”

Section: Study Subjects and Biologic Samplesmentioning

confidence: 99%

“…The karyotypes were previously described. 13,17,18 There were 19 ALL cases, including one case of T-cell ALL; 17 AML cases; and 3 biphenotypic cases. The morphology was French-American-British (FAB) M4 (myelomonocytic) or FAB M5 (monoblastic) in 13 cases of AML and in one of the biphenotypic cases.…”

Section: Study Subjects and Biologic Samplesmentioning

confidence: 99%

Low NAD(P)H:quinone oxidoreductase activity is associated with increased risk of leukemia with MLL translocations in infants and children

Smith

Wang

Skibola

et al. 2002

Blood

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131

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“…Note 36 cases are available to date (Kaneko et al,1986;Gregoire et al, 1987;Selypes and Laszlo, 1987;Hagemeijer et al, 1987;Hayashi et al, 1989;Raimondi et al, 1989;Shippey et al, 1989;Pui et al, 1990;Lampert et al, 1991;Abshire et al, 1992;Bernard et al, 1994;Felix et al, 1995;Felix et al, 1998;Harrison et al, 1998;Laughlin et al, 1998;Pinto et al, 1998;Secker-Walker et al, 1998;Nakamura et al, 2000;von Bergh et al, 2000;Chessells et al, 2002;Kim et al, 2002;Tsujioka et al, 2003;Douet-Guilbert et al, 2005;Sagawa et al, 2006;Jeon and Yi, 2009;de Braekeleer et al, 2010;Shinohara et al, 2010); we have excluded from this review a case of t(1;6;11)(p32;q21;q23) in a T-cell lymphoma referred as "T-CLL", as it probably represents another entity (Mecucci et al, 1988). We must also keep in mind that some of the t(1;11)(p32;q23) above harvested may not all share the common genetic event 5' MLL -3' EPS15: a case of t(1;11)(p32;q23), del(5q), +8 in a patient with therapyrelated leukaemia has recently been described without MLL rearrangement (Yamamoto et al, 2010).…”

Section: Diseasementioning

confidence: 99%

t(1;11)(p32;q23)

Huret¹

2011

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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MLL Genomic Breakpoint Distribution Within the Breakpoint Cluster Region in De Novo Leukemia in Children

Cited by 38 publications

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Pediatric Acute Lymphoblastic Leukemia: Challenges and Controversies in 2000

Pediatric Acute Lymphoblastic Leukemia: Challenges and Controversies in 2000

Low NAD(P)H:quinone oxidoreductase activity is associated with increased risk of leukemia with MLL translocations in infants and children

t(1;11)(p32;q23)

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