scholarly journals Role of the tumor suppressor gene Brca1 in genetic stability and mammary gland tumor formation

Oncogene ◽  
2000 ◽  
Vol 19 (8) ◽  
pp. 1059-1064 ◽  
Author(s):  
Chu-Xia Deng ◽  
Frank Scott
1998 ◽  
Vol 8 (3) ◽  
pp. 157-161 ◽  
Author(s):  
C. Onur ◽  
D. Orhan ◽  
M. Orhan ◽  
S. Dizbay Sak ◽  
Ö. Tulunay ◽  
...  

Purpose The pathogenesis of pterygium is still not completely understood and many environmental factors, including ultraviolet (UV) radiation, play an important role in its etiology. Chronic exposure to UV radiation causes mutations in the p53 tumor suppressor gene, eventually leading to tumor formation. We analyzed the immunohistochemical expression of p53 proteins in pterygial tissues to determine the role of the p53 tumor suppressor gene in the development of pterygium. Methods Pterygial specimens were studied immunohistochemically using antibodies against p53 protein. Results Out of 38 specimens studied, 35 (92.1%) had conjunctival epithelial cells without p53 specific nuclear staining. Only three specimens (7.9%) had a few p53 stained cells. The role of UV radiation in the pathogenesis of pterygium is supported by epidemiological, geographical and microscopic findings. However, our results are not consistent with these data on a genetic basis. Conclusions We conclude that defective p53 tumor suppressor gene function seems to have no role in the pathogenesis of pterygium.


1998 ◽  
Vol 16 (3) ◽  
pp. 1197-1206 ◽  
Author(s):  
W H Liggett ◽  
D Sidransky

Since its discovery as a CDKI (cyclin-dependent kinase inhibitor) in 1993, the tumor suppressor p16 (INK4A/MTS-1/CDKN2A) has gained widespread importance in cancer. The frequent mutations and deletions of p16 in human cancer cell lines first suggested an important role for p16 in carcinogenesis. This genetic evidence for a causal role was significantly strengthened by the observation that p16 was frequently inactivated in familial melanoma kindreds. Since then, a high frequency of p16 gene alterations were observed in many primary tumors. In human neoplasms, p16 is silenced in at least three ways: homozygous deletion, methylation of the promoter, and point mutation. The first two mechanisms comprise the majority of inactivation events in most primary tumors. Additionally, the loss of p16 may be an early event in cancer progression, because deletion of at least one copy is quite high in some premalignant lesions. p16 is a major target in carcinogenesis, rivaled in frequency only by the p53 tumor-suppressor gene. Its mechanism of action as a CDKI has been elegantly elucidated and involves binding to and inactivating the cyclin D-cyclin-dependent kinase 4 (or 6) complex, and thus renders the retinoblastoma protein inactive. This effect blocks the transcription of important cell-cycle regulatory proteins and results in cell-cycle arrest. Although p16 may be involved in cell senescence, the physiologic role of p16 is still unclear. Future work will focus on studies of the upstream events that lead to p16 expression and its mechanism of regulation, and perhaps lead to better therapeutic strategies that can improve the clinical course of many lethal cancers.


Author(s):  
Laura D. Hover ◽  
Michael W. Pickup ◽  
Agnieszka E. Gorska ◽  
Anna Chytil ◽  
Yan Guo ◽  
...  

2016 ◽  
Author(s):  
Pratima Basak ◽  
Pratima Basak ◽  
Heather Leslie ◽  
Heather Leslie ◽  
Afshin Raouf ◽  
...  

2004 ◽  
Vol 200 (4) ◽  
pp. 326
Author(s):  
C. Boltze ◽  
C. Hoang-Vu ◽  
R. Schneider-Stock ◽  
H. Lehnert ◽  
A. Roessner

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