Tumor suppressor gene p16/INK4A/CDKN2A-dependent regulation into and out of the cell cycle in a spontaneous canine model of breast cancer

2013 ◽  
Vol 114 (6) ◽  
pp. 1355-1363 ◽  
Author(s):  
Payal Agarwal ◽  
Maninder Sandey ◽  
Patricia DeInnocentes ◽  
R. Curtis Bird
2012 ◽  
Vol 114 (1) ◽  
pp. 56-66 ◽  
Author(s):  
Farruk M. Lutful Kabir ◽  
Payal Agarwal ◽  
Patricia DeInnocentes ◽  
Jishan Zaman ◽  
Allison Church Bird ◽  
...  

2015 ◽  
Vol 149 (3) ◽  
pp. 693-703 ◽  
Author(s):  
Marleen Ansems ◽  
Jonas Nørskov Søndergaard ◽  
Anieta M. Sieuwerts ◽  
Maaike W. G. Looman ◽  
Marcel Smid ◽  
...  

2021 ◽  
pp. 2833-2838
Author(s):  
Marwa Mohammed Ali Jassim ◽  
Khetam Habeeb Rasool ◽  
Majid Mohammed Mahmood

Background and Aim: The mutation in the wild-type tumor suppressor gene p53 is the most common genetic change in human tumors. In addition, the normal function of p21, which is both antiproliferative and an inhibitor of the cell cycle, is disrupted in some types of cancer. Meanwhile, cyclin D1 is a member of the cyclin protein family that is involved in regulating cell cycle progression. This study aimed to assess the expressions of the cell cycle inhibitory proteins p21, cyclin D1, and tumor suppressor gene p53, as well as their influence on the expressed histopathological changes in breast cancer tissues. Materials and Methods: Overall, 40 breast tissue specimens were investigated in this study, 30 of which were cancerous, while 10 were healthy tissues. p53, p21, and cyclin D1 expression patterns were detected using an immunohistochemistry (IHC) system. Results: The IHC reactions for p53 were positively observed in 27/30 (90%) cancerous tissues, compared with 2/10 (20%) normal breast tissues. For p21, reactions were observed in 28/30 (93.33%) cancerous tissues and 3/10 (30%) control tissues. For cyclin D1, reactions were observed in 25/30 (83.33%) cancerous tissues and 1/10 (10%) control tissues. The differences between the breast cancer tissues and the control tissues were statistically highly significant (p<0.01). Conclusion: The high expression rates of p21, cyclin D1, and p53 in malignant breast cancer cells with little or no regulatory role might imply mutational events in these proteins operating in concert with a variety of other genetic mutations in these tissues, which may play a molecular role in the development and/or progression of breast carcinogenesis.


Neurographics ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 228-235
Author(s):  
S. Naganawa ◽  
T. Donohue ◽  
A. Capizzano ◽  
Y. Ota ◽  
J. Kim ◽  
...  

Li-Fraumeni syndrome is a familial cancer predisposition syndrome associated with germline mutation of the tumor suppressor gene 53, which encodes the tumor suppressor p53 protein. Affected patients are predisposed to an increased risk of cancer development, including soft-tissue sarcomas, breast cancer, brain tumors, and adrenocortical carcinoma, among other malignancies. The tumor suppressor gene TP53 plays an important, complex role in regulating the cell cycle, collaborating with transcription factors and other proteins. The disruption of appropriate cell cycle regulation by mutated TP53 is considered to be the cause of tumorigenesis in Li-Fraumeni syndrome. Appropriate surveillance, predominantly by using MR imaging, is used for early malignancy screening in an effort to improve the survival rate among individuals who are affected. Patients with Li-Fraumeni syndrome are also at increased risk for neoplasm development after radiation exposure, and, therefore, avoiding unnecessary radiation in both the diagnostic and therapeutic settings is paramount. Here, we review the epidemiology, genetics, imaging findings, and the current standard surveillance protocol for Li-Fraumeni syndrome from the National Comprehensive Cancer Network as well as potential treatment options.Learning Objective: Describe the cause of second primary malignancy among patients with Li-Fraumeni syndrome.


Leukemia ◽  
2000 ◽  
Vol 14 (1) ◽  
pp. 183-187 ◽  
Author(s):  
M González ◽  
MV Mateos ◽  
R García-Sanz ◽  
A Balanzategui ◽  
R López-Pérez ◽  
...  

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