p53 Protein expression in laryngeal squamous cell carcinomas bearing wild-type and mutated p53 gene

1996 ◽  
Vol 28 (6) ◽  
pp. 513-519 ◽  
Author(s):  
G. PRUNERI ◽  
L. PIGNATARO ◽  
N.S. FRACCHIOLLA ◽  
S. FERRERO ◽  
P. CAPACCIO ◽  
...  
Keyword(s):  
Protein Expression ◽  
Squamous Cell ◽  
P53 Protein ◽  
P53 Gene ◽  
Squamous Cell Carcinomas ◽  
Wild Type ◽  
P53 Protein Expression

scholarly journals p53 protein expression in conjunctival squamous cell carcinomas of domestic animals

1999 ◽  
Vol 2 (4) ◽  
pp. 227-231 ◽  
Author(s):  
Giuseppe Sironi ◽  
Pietro Riccaboni ◽  
Luca Mertel ◽  
Giorgio Cammarata ◽  
Dennis E. Brooks
Keyword(s):  
Protein Expression ◽  
Squamous Cell ◽  
P53 Protein ◽  
Domestic Animals ◽  
Squamous Cell Carcinomas ◽  
P53 Protein Expression

Regulation of p53 protein expression in human breast cancer cell lines

1993 ◽  
Vol 105 (3) ◽  
pp. 607-612 ◽  
Author(s):  
B. Vojtesek ◽  
D.P. Lane
Keyword(s):  
Protein Expression ◽  
Cell Lines ◽  
P53 Protein ◽  
Critical Role ◽  
P53 Gene ◽  
Breast Cancer Cell Lines ◽  
Breast Cancers ◽  
Human Breast ◽  
Wild Type ◽  
P53 Protein Expression

Mutation of the p53 gene is a common occurrence in human breast cancers but is by no means universal. However, even in tumours where the gene is not mutated altered levels of p53 protein are often detected. This is also observed in cell lines derived from human breast cancers. By transfecting such cell lines containing either wild type or mutant p53 genes with a temperature-sensitive mutant mouse p53 gene we have established that the cellular environment plays a critical role in the regulation of p53 protein expression. The results suggest that tumours that aberrantly express wild-type p53 may have lost the normal growth regulatory response to the protein and thus be functionally similar to those expressing the mutant protein.

scholarly journals p53 Protein expression in squamous cell carcinoma of the vulva

Cancer ◽  
1999 ◽  
Vol 85 (5) ◽  
pp. 1133-1138 ◽  
Author(s):  
Marit Scheistr�en ◽  
Claes Trop� ◽  
Erik O. Pettersen ◽  
Jahn M. Nesland
Keyword(s):  
Squamous Cell Carcinoma ◽  
Protein Expression ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
P53 Protein ◽  
P53 Protein Expression

Effect of the specific P53 stabilizer CBS9106 on multiple myeloma (MM)

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 8601-8601
Author(s):  
H. Ikeda ◽  
T. Hideshima ◽  
G. Perrone ◽  
Y. Okawa ◽  
N. Raje ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Multiple Myeloma ◽  
Protein Expression ◽  
Tumor Cells ◽  
Cell Lines ◽  
Primary Tumor ◽  
P53 Protein ◽  
Wild Type ◽  
Cycle Arrest ◽  
P53 Protein Expression

8601 Background: The mutations of P53 tumor suppressor protein are associated with progressive in Multiple Myeloma (MM), conversely, stabilization of P53 leads to cell cycle arrest and apoptosis. In this study, we examined p53 protein expression and demonstrated the effect of P53 stabilization using a novel specific P53 stabilizer CBS9106 in MM. Method: We examined P53 protein expression using Immunoblot analysis, as well as the growth inhibitory effect of CBS9106 in MM cell lines and primary tumor cells from MM patients. We also defined whether CBS9106 can overcome the growth promoting effect of exogenous cytokines and bone marrow stroma cells (BMSCs) using [3H]-thymidine uptake assay. Results: Expression of P53 protein was observed in 3/3 primary tumor cells from MM patients and 6/6 MM cell lines. CBS9106 at low nM levels triggered cytotoxicity against p53 wild type MM cell lines and primary tumor cells from MM patients, associated with phosphorylation of P53 (serine15 and 20). In contrast, CBS9106 did not affect the survival of normal peripheral blood mononuclear cells from healthy volunteers at concentrations as high as 10 μM. This agent also induced G1 cell cycle arrest, followed by apoptosis associated with cleavage of caspase-3, -8, -9 and PARP. Neither growth stimulating cytokines (IL-6 and IGF-1) nor BMSCs protected against apoptotic effect of CBS9106. Moreover, we demonstrate that combination of CBS9106 with MDM2 inhibitor Nutrin3 or proteasome inhibitor bortezomib induces synergistic anti-MM activity in both P53 wild type MM cell lines and primary tumor cells from MM patients. Conclusions: Stabilizing P53 by CBS9106 represents a novel promising p53-based therapy in MM. These results provide the preclinical framework supporting evaluation of CBS9106 in clinical trials to improve patient outcome in MM. No significant financial relationships to disclose.

scholarly journals p53 protein expression in non-Hodgkin's lymphoma. Comparative study with the wild type p53 induced proteins mdm2 and p21/waf1

1996 ◽  
Vol 49 (5) ◽  
pp. M278-M282 ◽  
Author(s):  
M Tzardi ◽  
C. Kouvidou ◽  
I Panayiotides ◽  
K Stefanaki ◽  
D Rontogianni ◽  
...  
Keyword(s):  
Protein Expression ◽  
Comparative Study ◽  
P53 Protein ◽  
Hodgkin's Lymphoma ◽  
Wild Type ◽  
P53 Protein Expression ◽  
Non Hodgkin's Lymphoma ◽  
Wild Type P53 ◽  
P21 Waf1 ◽  
Induced Proteins

Radiation Enhances the Anti-tumor Effects of Vaccinia-p53 Gene Therapy in Glioma

2003 ◽  
Vol 2 (3) ◽  
pp. 223-235 ◽  
Author(s):  
Tatyana M. Timiryasova ◽  
Daila S. Gridley ◽  
Bing Chen ◽  
Melba L. Andres ◽  
Radha Dutta-Roy ◽  
...  
Keyword(s):  
Protein Expression ◽  
P53 Protein ◽  
P53 Gene ◽  
Immunohistochemical Analysis ◽  
Live Cells ◽  
C6 Cells ◽  
Rat Glioma ◽  
Combination Treatments ◽  
P53 Protein Expression ◽  
Single Modality

The overall goal of this study was to analyze the effect and mechanism of radiation in combination with vaccinia viruses (VV) carrying the p53 gene against glioma. Comparison of two alternative treatments of cultured C6 (p53+) and 9L (p53−) rat glioma cells showed significantly reduced survival for both cell lines, especially 9L, when radiation was applied prior to virus versus radiation alone. High p53 protein expression mediated by VV-TK-p53 was measured in infected cells. Single modality treatment of C6 cells with psoralen and UV (PUV)-inactivated VV-TK-p53 (PUV-VV-TK-53) or radiation significantly decreased survival compared with PUV-inactivated L-15 (PUV-L-15) control virus. However, no difference was observed between radiation and combination treatments of C6 cells. In contrast, radiation followed by PUV-VV-TK-53 resulted in dramatic reduction of 9L cell viability, compared to single modality treatment. Flow cytometry analysis of Annexin-V-stained 9L cells showed that radiation and PUV-VV-TK-53 caused a significant decrease in live cells (17.2%) as compared to other treatments and control (61.6–98.3%). Apoptosis was observed in 37.2% of cells, while the range was 0.7–7.8% in other treatment groups; maximal p53 level was measured on day 7 post-infection. In athymic mice bearing C6 tumors, VV-TK-53 plus radiation in both single and multiple therapies resulted in significantly smaller tumors by day 30 compared to the agents given only once. Immunohistochemical analysis of tumor sections demonstrated p53 protein expression over 20 days after VV-TK-53 treatment. Analysis of blood and spleen cells of mice given multiple combination treatments showed significant splenomegaly, leukocytosis, and increased DNA synthesis and response to mitogen. Multiple combination treatments were also associated with significantly elevated natural killer and B cells in the spleen. There were no overt toxicities, although depression in red blood cell and thrombocyte parameters was noted. Collectively, the data demonstrate that radiation significantly improves the efficacy of VV-mediated tumor suppressor p53 therapy and may be a promising strategy for glioma treatment. Furthermore, the results support the conclusion that the mechanisms underlying the enhanced anti-tumor effect of combination treatment include apoptosis/necrosis and upregulation of innate immune defenses.

P53 expression as a predictor of recurrence in cervical squamous cell carcinoma

2002 ◽  
Vol 12 (3) ◽  
pp. 299-303 ◽  
Author(s):  
S. M. F Brenna ◽  
L. C Zeferino ◽  
G. A Pinto ◽  
R. A Souza ◽  
L. A. L Andrade ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Protein Expression ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
P53 Protein ◽  
Figo Stage ◽  
Cervical Squamous Cell Carcinoma ◽  
Stage Ii ◽  
P53 Expression ◽  
P53 Protein Expression

Abstract.Brenna SMF, Zeferino LC, Pinto GA, Souza RA, Andrade LAL, Vassalo J, Martinez EZ, Syrjänen KJ. P53 expression as a predictor of recurrence in cervical squamous cell carcinoma.P53 protein function is frequently down-regulated in cervical cancer by complexing with human papillomavirus (HPV) E6 protein, leading to degradation of p53, genomic instability, and mutations. Results are controversial, however, on the prognostic value of p53 protein expression in cervical cancer. In this study, a cohort of 220 Brazilian women with FIGO stage IB-III cervical squamous cell carcinoma (SCC), followed for 5 years, was analyzed for p53 protein expression using immunohistochemistry. The disease-free survival (DFS) and relapse rate were analyzed using univariate (Kaplan-Meier) and multivariable (Cox's proportional hazards model) survival analyses. P53 protein expression was detected in 35% of the patients, including 21% in stage I, 28% in stage II and 51% in stage III of disease. Of 220 women, only 116 completed one of the treatment options standardized by FIGO within 120 days. There was a higher risk of relapse in stage II and III disease, that was not modified by p53 positivity; HR 3.0 (1.3–6.5) to stage II and HR 4.0 (1.9–8.5) to stage III. The multivariate analysis evidenced that p53 expression is not an independent factor exceeding the power of FIGO stage as the single most important determinant of the hazards for disease relapse.

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