Loss of imprinting and allele switching of p73 in renal cell carcinoma

Mai, Ming; Qian, Chiping; Yokomizo, Akira; Tindall, Donald J.; Bostwick, David G.; Polychronakos, Constantin; Smith, Jeremy C.; Liu, Wanguo

doi:10.1038/sj.onc.1202099

Cited by 80 publications

(59 citation statements)

References 11 publications

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“…Overexpression of p73 in p53-null human cancer cells or in baby hamster kidney cells induced apoptosis, similar to overexpression of p53 (Jost et al, 1997). Unlike p53, however, p73 was found not to be induced by genotoxic damage (Mai et al, 1998). No mutations were found in p73 among a number of lung cancers examined, although overexpression of p73 was noted in 24% of tumors compared to their normal tissue controls (Mai et al, 1998).…”

Section: Non-transcriptional Roles For P53 In Apoptosismentioning

confidence: 77%

Roles for p53 in growth arrest and apoptosis: putting on the brakes after genotoxic stress

1998

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The tumor suppressor gene p53 plays a major role in regulation of the mammalian cellular stress response, in part through the transcriptional activation of genes involved in cell cycle control, DNA repair, and apoptosis. Many factors contribute to control of the activation of p53, and the downstream response to its activation may also vary depending on the cellular enviroment or other modifying factors in the cell. The complexity of the p53 response makes this an ideal system for application of newly emerging rapid throughput analysis techniques and informatics analysis

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Section: Non-transcriptional Roles For P53 In Apoptosismentioning

confidence: 77%

Roles for p53 in growth arrest and apoptosis: putting on the brakes after genotoxic stress

1998

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“…In addition, p73 expression has been found to increase in lung cancer rather than decrease (Mai et al, 1998;Tokuchi et al, 1999), and no spontaneous tumor has been observed in p73-deficient mice (Yang et al, 2000). All these suggest the presence of other unidentified tumor-suppressor genes in 1p36.…”

Section: Discussionmentioning

confidence: 94%

Evidence that MIG-6 is a tumor-suppressor gene

et al. 2006

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“…In contrast to p53, mutational analysis of the p73 gene in several human solid tumors did not reveal loss of p73 expression or mutations in the p73 gene (Mai et al, 1998;Sunahara et al, 1998;Kroiss et al, 1998). On the other hand, transcriptional silencing of the p73 gene in acute lymphoblastic leukemia and Burkitt's lymphoma was reported, suggesting that silencing of the p73 gene by hypermethylation may contribute to development of lymphoid neoplasms (Corn et al, 1999;Kawano et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Expression of the vascular endothelial growth factor gene is inhibited by p73

2000

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Recently, p73, a new member of the p53 family, has been cloned and mapped to chromosome 1p36, a region that is frequently deleted in a variety of human cancers. p73 can activate p53-responsive promoters and induce apoptosis when overexpressed in certain p53-de®cient tumor cells. In contrast to p53, analysis of the p73 gene in several human solid tumors did not reveal loss of p73 expression or mutations in the p73 gene. However, transcriptional silencing of the p73 gene by hypermethylation of a CpG island was observed in several leukemias and lymphomas. These lymphoid neoplasms also show increased expression of vascular endothelial growth factor (VEGF), an endothelial cell-speci®c mitogen and a key mediator of angiogenesis. To evaluate a possible relationship between p73 status and VEGF expression, we have studied the e ect of ectopically expressed p73 on the regulation of the VEGF gene. Our results demonstrate that p73 can down-regulate endogenous VEGF gene expression on mRNA and protein level. This e ect is mediated by transcriptional repression of the VEGF promoter and involves the promoter region 785 to 750 bp, containing a cluster of Sp 1 binding sites. Our results suggest a regulatory role for p73 in tumor angiogenesis. Oncogene (2000) 19, 3470 ± 3476.

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Loss of imprinting and allele switching of p73 in renal cell carcinoma

Cited by 80 publications

References 11 publications

Roles for p53 in growth arrest and apoptosis: putting on the brakes after genotoxic stress

Roles for p53 in growth arrest and apoptosis: putting on the brakes after genotoxic stress

Evidence that MIG-6 is a tumor-suppressor gene

Expression of the vascular endothelial growth factor gene is inhibited by p73

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