Developments in cytogenetics and oncogenes in acute leukemia

Current Opinion in Oncology

Volumn 9, Issue 1, 1997, Pages 8-17

  Strout, Matthew P ^a   Caligiuri, Michael A ^a  

^a ROSWELL PARK CANCER INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ACUTE LEUKEMIA; CHROMOSOME INVERSION; CYTOGENETICS; ENHANCER REGION; GENE ACTIVATION; GENE DELETION; GENE FUSION; HUMAN; LEUKEMOGENESIS; MOLECULAR BIOLOGY; NUMERICAL CHROMOSOME ABERRATION; ONCOGENE; PRIORITY JOURNAL; PROTO ONCOGENE; REVIEW;

EID: 0030939047     PISSN: 10408746     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001622-199701000-00003     Document Type: Review

References (77)

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67. Yu BD, Hess JL, Horning SE, Brown GAJ, Korsmeyer SJ: Altered Hox expression and segmental identity in M11-mutant mice. Nature 1995, 378:505-508. The ALL1 knockout mouse shows that ALL1 is an essential regulator of homeobox gene expression in embryonic development.
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73. Caligiuri MA, Schichman SA, Strout MP, Mrozek K, Baer MR, Frankel SR, Barcos M, Herzig GP, Croce CM, Bloomfield CD: Molecular rearrangement of the ALL-1 gene in acute myeloid leukemia without cytogenetic evidence of 11q23 chromosomal translocations. Cancer Res 1994, 54:370-373.
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75. Caligiuri MA, Strout MP, Schichman SA, Mrózek K, Arthur DC, Herzig GP, Baer MR, Schiffer CA, Heinonen K, Knuutila S, Nousiainen T, Ruutu T, Block AW, Schulman P, Pedersen-Bjergaard J, Croce CM, Bloomfield CD: Partial tandem duplication of ALL1 as a recurrent molecular defect in acute myeloid leukemia with trisomy 11. Cancer Res 1996, 56:1418-1425. This study reports the first specific gene rearrangement associated with recurrent trisomy in human cancer.
76. Caligiuri MA, Strout MP, Arthur DC, Baer MR, Shah D, Block AW, Mrózek K, Yu F, Oberkircher AR, Lawrence D, Knuutila S, Ruutu T, Herzig GP, Schiffer CA, Bloomfield CD: Rearrangement of ALL1 is a recurrent molecular defect in adult acute myeloid leukemia with normal cytogenetics that predicts a short complete remission duration [abstract]. Proc Am Soc Clin Oncol 1996, 15:360. The partial duplication of ALL1 is the first consistent molecular defect discovered in AML patients with normal cytogenetics.
77. Corral J, Lavenir I, Impey H, Warren AJ, Forster A, Larson TA, Bell S, McKenzie ANJ, King G, Rabbitts TH: An M11-AF9 fusion gene made by homologous recombination causes acute leukemia in chimeric mice: a method to create fusion oncogenes. Cell 1996, 85:853-861. In addition to reporting a novel knockin technique for functionally studying chimeric genes, the results of this study identify the ALL1-AF9 gene fusion as being directly responsible for leukemogenesis in t(9;11)(p22;q23)-associated AML.