1999
DOI: 10.1002/(sici)1096-9896(199901)187:1<39::aid-path235>3.0.co;2-q
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Perspective: chromosomal translocations can affect genes controlling gene expression and differentiation—why are these functions targeted?

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Cited by 26 publications
(13 citation statements)
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“…Oncogene activation through gene aberration is thought to be a consequence of functional selection, especially when it reoccurs in multiple tumors (Rabbitts, 1994(Rabbitts, , 1999Sorensen and Triche, 1996;Bystritskiy and Razin, 2004). Previous studies have suggested that in cancer the chromosome 11q13 locus is subject to complex aberrations including deletions, rearrangement and amplifications (Koreth et al, 1999).…”
Section: Discussionmentioning
confidence: 99%
“…Oncogene activation through gene aberration is thought to be a consequence of functional selection, especially when it reoccurs in multiple tumors (Rabbitts, 1994(Rabbitts, , 1999Sorensen and Triche, 1996;Bystritskiy and Razin, 2004). Previous studies have suggested that in cancer the chromosome 11q13 locus is subject to complex aberrations including deletions, rearrangement and amplifications (Koreth et al, 1999).…”
Section: Discussionmentioning
confidence: 99%
“…Most spontaneous human acute leukemias exhibit specific chromosomal translocations that result in either the enforced expression of an oncogene or the fusion of genes normally involved in the control of hemopoietic differentiation. 1 Unlike the oncogenic gain-of-function genetic alterations observed in spontaneous leukemias, radiation-induced leukemias in mouse and humans exhibit chromosomal loss, [2][3][4][5][6][7][8][9][10][11] suggesting that tumor-suppressor gene loss of function has a role in maturation arrest in radiation-induced hemopoietic malignancies.…”
Section: Introductionmentioning
confidence: 99%
“…Chromosomal rearrangements are frequent in hematological malignancies and typically involve genes encoding proteins, transcription factors in particular, that regulate cell growth, differentiation, or survival (8,85). The TAL1 (or SCL) gene was initially identified as the transcriptional unit activated by a reciprocal (1;14) translocation in patients with T-cell acute lymphoblastic leukemia (T-ALL) (10,17,36).…”
mentioning
confidence: 99%