When mutant p53 plays hide and seek: a new challenge for diagnosis and therapy?

Soussi, Thierry; Hjortsberg, Linn

doi:10.1016/j.molmed.2008.11.002

Cited by 2 publications

(2 citation statements)

References 20 publications

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“…On the contrary, BCPAP, a cell line which harbors a mutant copy of p53, did not show any changes in the parameters measured at the low dose of irradiation. Evidence of cross-talk between the p53-p21 and p16-pRb pathways has existed for some time (34,35). However, the exact nature of this cross-talk is not entirely clear.…”

Section: Discussionmentioning

confidence: 99%

Response to low-dose X-irradiation is p53-dependent in a papillary thyroid carcinoma model system

et al. 2011

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Abstract. The link between high doses of radiation and thyroid cancer has been well established in various studies, as opposed to the effects of low doses. In this study, we investigated the effects of low-dose X-ray irradiation in a papillary thyroid carcinoma model with wild-type and mutated p53. A low dose of 62.5 mGy was enough to cause an upregulation of p16 and a decrease in the number of TPC-1 cells in the S phase, but not in the number of BCPAP p53-mutant cells. At a dose of 0.5 Gy, visible signs of senescence appeared only in the TPC-1 cells. We conclude that low doses of X-rays are enough to cause a change in cell cycle distribution, possibly p53-dependent p16 activation, but no significant apoptosis. Senescence requires higher doses of X-irradiation via a mechanism involving both p16 and p21.

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Section: Discussionmentioning

confidence: 99%

Response to low-dose X-irradiation is p53-dependent in a papillary thyroid carcinoma model system

et al. 2011

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“…Considering the intrinsic instability of p53 even when enhanced by a pathogenic mutation we would expect very low levels of p53 in the cell. On the contrary, p53 and especially the mutated forms are over-represented in cancer cells through a mechanism that has long challenged cancer biologists [16]. In pathologic cells, the mutated and misfolded p53 forms multiple chaperon complexes.…”

Section: P53 Misfolding and Cancermentioning

confidence: 99%

Protein Misfolding Diseases

Bellotti¹,

Stoppini²

2009

TOBIOJ

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Diseases caused by protein misfolding are an emerging pathologic category that are thought to share some basic common mechanisms and display impressive heterogeneity in terms of tissue involvement, age of onset and clinical features. The growing recognition of the impact that protein misfolding has on human diseases is certainly related to the phenomenon of population aging and the expansion of the population in which these diseases are more frequent, but it is also based on a scientific revolution that looks at protein dynamics and relates these data to their potential pathologic implications. The multidisciplinary exchange of knowledge between experts in apparently unrelated diseases, such as sickle cell anemia and Alzheimer's disease, has helped clarify the pathogenesis of these and many other diseases. The quick expansion of knowledge on the mechanisms of these diseases is priming pharmaceutical research that is now providing the first prototype drugs.

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When mutant p53 plays hide and seek: a new challenge for diagnosis and therapy?

Cited by 2 publications

References 20 publications

Response to low-dose X-irradiation is p53-dependent in a papillary thyroid carcinoma model system

Response to low-dose X-irradiation is p53-dependent in a papillary thyroid carcinoma model system

Protein Misfolding Diseases

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