Structural alterations of the RB1 gene in human soft tissue tumours

Stratton, M. R.; Williams, Susan E.; Fisher, Cindy L.; Ball, Amy Oberhauser; Westbury, G; Gusterson, B A; Fletcher, C. D. M.; Knight, JC; Fung, Y-K; Reeves, BR; Cooper, CS

doi:10.1038/bjc.1989.251

Cited by 84 publications

(40 citation statements)

References 25 publications

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“…Although ras mutations are less common, they do occur in human rhabdomyosarcomas (Stratton et al, 1989) and ®brosarcomas (Tanaka et al, 1986;Maillet et al, 1992;Andeol et al, 1988) where mutant N-ras can be essential for the maintenance of transformation (Paterson et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

Sequential development of an angiogenic phenotype by human fibroblasts progressing to tumorigenicity

1997

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Section: Discussionmentioning

confidence: 99%

Sequential development of an angiogenic phenotype by human fibroblasts progressing to tumorigenicity

1997

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“…40,41 Analyses of the genes and proteins in the Rb-cyclin D pathway have revealed frequent abnormalities in leiomyosarcoma. 23,42,43 Standard cytogenetic methods have rarely revealed rearrangements of 10q in leiomyosarcoma. 16 By CGH, we observed recurrent losses at 10q with the highest rate at 35% in the most frequent minimal common region of 10q23.q25.…”

Section: Similarities and Differences In Dna Sequence Copy Number Chamentioning

confidence: 99%

Do DNA copy number changes differentiate uterine from non-uterine leiomyosarcomas and predict metastasis?

et al. 2006

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DNA copy number changes were investigated in 51 (19 uterine and 32 nonuterine) primary leiomyosarcomas by comparative genomic hybridization. The aim was to evaluate whether true biological differences exist between uterine and nonuterine leiomyosarcoma and whether changes revealed by comparative genomic hybridization have prognostic value. Genomic imbalances were found in 48 (94%) cases. The most frequent DNA copy number changes were losses in 10q (35%), 13q (57%), and 16q (41%), gains in 1q (41%), and gains and high-level amplifications in 17p (39%). Gains were nearly as frequent as losses in both uterine and nonuterine leiomyosarcoma. Correlation-based tree modeling revealed two clusters that segregated significantly a group of uterine (gains at 1q11-q24) and a group of nonuterine (losses at 13q14-q34, 16q11.1-q24, and 10q21-q26) cases. The nonuterine cluster was associated with subcutaneous origin and a trend toward increased metastasis-free survival. Further explorative analyses identified aberrations associated with shorter metastasisfree survival time, including losses at 2q32.1-q37 and gains at 8q24.1-q24.3, whereas the cases with losses at 6cen-p25 showed longer metastasis-free survival time.

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“…This LOI can lead to a twofold gene dosage e ect, and may contribute to the characteristic overexpression of IGF2 observed in these tumors (Zhan et al, 1994). LOH studies have Barr et al, 1993;Galili et al, 1993Davis et al, 1994Besnard-GueÂ rin et al, 1996Visser et al, 1997Stratton et al, 1990Mulligan et al, 1990;Felix et al, 1992El-Badry et al, 1990Zhan et al, 1994Meddeb et al, 1996Keleti et al, 1996;Fiddler et al, 1996Khatib et al, 1993Knudsen et al, 1998Ferracini et al, 1996Garson et al, 1986Mitani et al, 1986;Bayani et al, 1995Weber-Hall et al, 1996Smith et al, 1998Iolascon et al, 1996Schweigerer et al, 1987De Giovanni et al, 1995Chardin et al, 1985Stratton et al, 1989 *Denotes alterations seen commonly in both RMS cell lines and tumor tissue; other lesions occur occasionally, and/or have been infrequently reported. LOH, loss of heterozygosity; LOI, loss of imprinting also suggested the existence of putative RMSassociated tumor suppressor genes residing at 11q and 16q (Loh et al, 1992;Visser et al, 1997).…”

Section: Cytogenetic De®nition Of Rhabdomyosarcomamentioning

confidence: 99%

“…Activated forms of N-ras and K-ras are among the most frequent oncogene abnormalities observed in RMS tumors (see review by Dias et al, 1994). In one study, 35% of embryonal tumors carried activating mutations of either N-or K-ras (Stratton et al, 1989;Wexler and Helman, 1994). Activated ras has been shown to block myogenic di erentiation by down-regulating myogenic factors such as MyoD and myogenin (Lassar et al, 1989;Konieczny et al, 1989).…”

Section: Cytogenetic De®nition Of Rhabdomyosarcomamentioning

confidence: 99%

“…A major problem in this regard is the relative dearth of human RMS tissue samples available for molecular analysis. In those RMS samples that have been analysed, the structure and expression of the RB gene itself appear to be normal (Stratton et al, 1989;De Chiara et al, 1993). Moreover, the occurrence of RMS as a secondary malignancy following retinoblastoma remains controversial (Dickman et al, 1997).…”

Section: Digging Deeper ± Prb and P53 At The Crossroadsmentioning

confidence: 99%

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Rhabdomyosarcoma – working out the pathways

1999

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Rhabdomyosarcomas constitute a collection of childhood malignancies thought to arise as a consequence of regulatory disruption of skeletal muscle progenitor cell growth and di erentiation. Our understanding of the pathogenesis of this neoplasm has recently bene®ted from the study of normal and malignant myogenic cells in vitro, facilitating the identi®cation of diagnostic cytogenetic markers and the elucidation of mechanisms by which myogenesis is regulated. It is now appreciated that the delicate balance between proliferation and di erentiation, mutually exclusive yet intimately associated processes, is normally controlled in large part through the action of a multitude of growth factors, whose signals are interpreted by members of the MyoD family of helix ± loop ± helix proteins, and key regulatory cell cycle factors. The latter have proven to be frequent targets of mutational events that subvert myogenesis and promote the development of rhabdomyosarcoma. Although signi®cant progress has been made in the treatment of rhabdomyosarcoma, patients presenting with metastatic disease or certain high risk features are still faced with a dismal prognosis. Only now are genetically engineered mouse models becoming available that are certain to provide fresh insights into the molecular/genetic pathways by which rhabdomyosarcomas arise and progress, and to suggest novel avenues of therapeutic opportunity.

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Structural alterations of the RB1 gene in human soft tissue tumours

Cited by 84 publications

References 25 publications

Sequential development of an angiogenic phenotype by human fibroblasts progressing to tumorigenicity

Sequential development of an angiogenic phenotype by human fibroblasts progressing to tumorigenicity

Do DNA copy number changes differentiate uterine from non-uterine leiomyosarcomas and predict metastasis?

Rhabdomyosarcoma – working out the pathways

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