Rearrangement of the p53 gene in human osteogenic sarcomas.

Masuda, Hatisaburo; Miller, Carl W.; Koeffler, H. Phillip; Battifora, Hector; Cline, Martin J.

doi:10.1073/pnas.84.21.7716

Cited by 427 publications

(267 citation statements)

References 21 publications

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“…Similar large genomic deletions have also been described in other tumour suppressor genes e.g. p53 (Masuda et al, 1987;Ruggeri et al, 1992), hMLH1 (Nystrom-Lahti et al, 1995), hMSH2 (Wijnen et al, 1998) and Rb-1 (Ruggeri et al, 1992). Thus, we wanted to investigate whether similar genomic deletions occur in BRCA2 which may have escaped detection using PCR-based techniques.…”

supporting

confidence: 56%

Absence of rearrangements in the BRCA2 gene in human cancers

et al. 2001

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Summary Mutations of BRCA2 in sporadic breast and ovarian carcinomas are exceedingly rare. This led to the suggestion that large genomic rearrangements could be involved. We performed Southern blots in genomic DNA from 130 primary breast cancers and 83 cancer cell lines (breast, ovarian, pancreatic and small cell lung carcinomas) and found no genomic rearrangements. These results suggest that a gene other than BRCA2 is the target of the frequent 13q12.3 allelic deletions in human cancers.

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supporting

confidence: 56%

Absence of rearrangements in the BRCA2 gene in human cancers

et al. 2001

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“…Alternatively, wild-type p53 may in¯uence the physiology of the cell in such a way that the a-actin promoter may become transcriptionally active. In order to see if changes in a-actin mRNA level seen under these conditions are due to a direct e ect of p53, we used Saos-2 human osteogenic sarcoma cell line (Masuda et al, 1987) and the (10)1 spontaneously arising, immortalized mouse ®broblast cell line (Harvey and , both of which have no endogenous p53 protein expressed. These two cell lines are devoid of p53 protein because of major deletions in the 5' region of the p53 gene.…”

Section: Resultsmentioning

confidence: 99%

Human smooth muscle α-actin gene is a transcriptional target of the p53 tumor suppressor protein

Comer¹,

Dennis²,

Armstrong³

et al. 1998

Oncogene

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Smooth muscle (sm) a-actin is expressed in vascular smooth muscle cells and ®broblast cells. Its expression is regulated by cell proliferation and repressed during oncogenic transformation. In this study, we demonstrate that p53 activation is associated with a dramatic increase in organized micro®lament bundles and an increase in sm a-actin mRNA level. Wild-type p53, but not mutant p53, strongly stimulated human sm a-actin promoter activity in p53 null cell lines. The sequences homologous to the p53 consensus sequence and to the p53 binding sequence from the muscle creatine kinase, were found within a speci®c region of the sm a-actin promoter. This sequence was su cient to confer p53-dependent activation to a heterologous promoter and p53 was capable of binding to this sequence as assessed by gel shift analysis. Ionizing irradiation of colorectal tumor cells caused an increase in a-actin mRNA level in a p53-dependent manner. Taken together, these results demonstrate that human sm aactin gene is a transcriptional target for p53 tumor suppressor protein and represents the ®rst example of a cytoskeletal gene with a functionally de®ned p53 response element.

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“…Saos-2 cells were derived from an osteosarcoma and are null for p53 (Masuda et al, 1987). The cells were routinely cultured in DMEM supplemented with 20% foetal bovine serum.…”

Section: Cell Culturementioning

confidence: 99%