scholarly journals KAI-1 and p53 expression in odontogenic cysts: An immunohistochemical (IHC) marker study

2017 ◽  
Vol 04 ◽  
pp. 1
Author(s):  
Namrata N. Patil ◽  
Vijay Wadhwan ◽  
Minal Chowdhary ◽  
Abhishek Singh Nayyar ◽  
◽  
...  
Keyword(s):  
P53 Protein ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Odontogenic Cysts ◽  
P53 Expression ◽  
Odontogenic Keratocysts ◽  
P53 Antibodies ◽  
Dentigerous Cysts ◽  
Protein Functions ◽  
Marker Study

Background: KAI-1/CD82 is a tumour suppressor gene; decreased gene expression is associated with the increased invasive ability of oral squamous cell carcinoma (OSCC), as hypothesised for various odontogenic cysts and tumours. p53 protein functions in the G1-S phase of the cell cycle to allow repair of the damaged DNA. In the present study, p53 and KAI-1 expression was investigated by using monoclonal antibodies in the various odontogenic cysts. Aims: To detect KAI-1 and p53 expression in radicular cysts, dentigerous cysts and odontogenic keratocysts (OKCs) and to assess the relation between p53 and KAI-1 expression in the aforementioned cysts. Materials and Methods: The present study included histopathologically diagnosed cases of radicular cysts, dentigerous cysts and OKCs for the expression of KAI-1 and p53 antibodies. Results: Amongst odontogenic cysts, radicular cysts expressed a maximum positivity of KAI-1 (20.92%) while p53 positive cells were maximum in odontogenic keratocysts (4.04%). The correlation between KAI-1 and p53 expression in the various odontogenic cysts was not found to be significant. Conclusion: The increased KAI-1 expression in the radicular cysts and its downregulation in OKCs may be indicative of aggressive clinical behaviour and the fact that OKCs are hypothesised as neoplastic rather than being developmental in origin.

scholarly journals Effect of Chromatographic Conditions on Supercoiled Plasmid DNA Stability and Bioactivity

2019 ◽  
Vol 9 (23) ◽  
pp. 5170 ◽  
Author(s):  
G.M. Azevedo ◽  
J.F.A. Valente ◽  
A. Sousa ◽  
A.Q. Pedro ◽  
P. Pereira ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Plasmid Dna ◽  
P53 Protein ◽  
Metabolic Stress ◽  
Suppressor Gene ◽  
Experimental Conditions ◽  
P53 Expression ◽  
Supercoiled Plasmid ◽  
Protein P53

The dysfunction of the tumor suppressor gene TP53 has been associated with the pathogenesis of the majority of the cases of cancer reported to date, leading the cell to acquire different features known as the cancer hallmarks. In normal situations, the protein p53 protects the cells against tumorigenesis. By detecting metabolic stress or DNA damage in response to stress, p53 can lead the cell to senescence, autophagy, cell cycle arrest, DNA repair, and apoptosis. Thus, in the case of p53 mutations, it is reasonable to assume that the reestablishment of its function, may restrain the proliferation of cancer cells. The concept of cancer gene therapy can be based on this assumption, and suitable biotechnological approaches must be explored to assure the preparation of gene-based biopharmaceuticals. Although numerous procedures have already been established to purify supercoiled plasmid DNA (sc pDNA), the therapeutic application is highly dependent on the biopharmaceutical’s activity, which can be affected by the chromatographic conditions used. Thus, the present work aims at comparing quality and in vitro activity of the supercoiled (sc) isoform of the p53 encoding plasmid purified by three different amino acids-based chromatographic strategies, involving histidine–agarose, arginine–macroporous, and histidine–monolith supports. The B-DNA topology was maintained in all purified pDNA samples, but their bioactivity, related to the induction of protein p53 expression and apoptosis in cancer cells, was higher with arginine–macroporous support, followed by histidine–monolith and histidine–agarose. Despite the purity degree of 92% and recovery yield of 43% obtained with arginine–macroporous, the sc pDNA sample led to a higher expression level of the therapeutic p53 protein (58%) and, consequently, induced a slightly higher apoptotic effect (27%) compared with sc pDNA samples obtained with histidine–monolithic support (26%) and histidine–agarose support (24%). This behavior can be related to the mild chromatographic conditions used with arginine–macroporous support, which includes the use of low salt concentrations, at neutral pH and lower temperatures, when compared to the high ionic strength of ammonium sulfate and acidic pH used with histidine-based supports. These results can contribute to field of biopharmaceutical preparation, emphasizing the need to control several experimental conditions while adapting and selecting the methodologies that enable the use of milder conditions as this can have a significant impact on pDNA stability and biological activity.

scholarly journals p53 Protein Detected By Immunohistochemical Staining is Not Always Mutant

1993 ◽  
Vol 11 (5-6) ◽  
pp. 239-250 ◽  
Author(s):  
Catriona Macgeoch ◽  
Diana M. Barnes ◽  
Julia A. Newton ◽  
Shehla Mohammed ◽  
Shirley V. Hodgson ◽  
...  
Keyword(s):  
Magnetic Beads ◽  
Direct Sequencing ◽  
P53 Protein ◽  
Pcr Amplification ◽  
P53 Gene ◽  
Tumour Suppressor Gene ◽  
Nuclear Staining ◽  
Breast Carcinomas ◽  
Direct Dna Sequencing ◽  
P53 Antibodies

The expression of the tumour suppressor gene p53 was analyzed in a variety of human solid tumours by immunohistochemistry and direct DNA sequencing. Positive nuclear staining using a panel of anti-p53 antibodies was used to select tumours for further genetic analysis. Using PCR amplification followed by immobilization onto magnetic beads and direct sequencing, we sequenced exons 5-9 of the p53 gene fro m 9 melanomas, 8 nasopharyngeal carcinomas, 16 sporadic breast carcinomas and 11 patients from familial breast cancer families. No sequence alterations of the p53 gene were detected in either the melanoma or nasopharyngeal tumours and only 19% of the primary breast carcinomas showed a variant band indicative of a mutation. Our results indicate firstly that p53 mutations are not generally involved in the tumour types studied and secondly the data emphasize the disparity encountered when attempting to correlate p53 immunohistochemical positivity with mutations within the p53 gene.

scholarly journals Isolation of a full-length mouse cDNA clone coding for an immunologically distinct p53 molecule.

1985 ◽  
Vol 5 (1) ◽  
pp. 127-132 ◽  
Author(s):  
D Wolf ◽  
N Harris ◽  
N Goldfinger ◽  
V Rotter
Keyword(s):  
Monoclonal Antibodies ◽  
Tumor Cells ◽  
Cdna Clone ◽  
P53 Protein ◽  
P53 Gene ◽  
Full Length ◽  
Antigenic Determinants ◽  
Entire Group ◽  
P53 Expression ◽  
P53 Antibodies

Transfection of a cloned p53 gene into a p53 nonproducer Abelson murine leukemia virus-transformed cell line, L12, reconstituted p53 expression. The protein expressed in these cells was indistinguishable from that naturally expressed in p53 producer tumor cells. Conversely, p53 protein expressed in L12-derived clones that were established by transfection with a full-length p53 cDNA clone (pM8) exhibited a discrete immunological form. Immunoprecipitation of p53 with a panel of monoclonal anti-p53 antibodies showed that L12-derived clones that were transfected with the genomic p53 clone contained the same antigenic determinants as those found in the p53 protein expressed in tumor cells. These p53 proteins bound all monoclonal antibody types as well as the polyclonal anti-p53 tested. However, L12-derived clones established by transfection of the p53 cDNA clone (pM8) expressed a p53 protein that bound the RA3-2C2 and PAb200.47 anti-p53 monoclonal antibodies as well as polyclonal anti-p53 serum but totally lacked the antigenic receptor for the PAb122 and PAb421 monoclonal antibodies. The p53 proteins expressed by either genomic or cDNA p53 clones exhibited the same apparent molecular sizes and identical partial peptide maps. We suggest that transfection of the p53 gene induced expression of the entire group of the possible mRNA species, whereas cloned p53 cDNA (pM8) represented a single mRNA molecule that codes for a discrete species of p53 protein.

scholarly journals Frequency of Different Odontogenic Cysts in Patients Visiting Oral Maxillofacial Department of Dental Hospitals in Peshawar

2015 ◽  
Vol 1 (2) ◽  
pp. 29-35
Author(s):  
Sofia Haider Durrani ◽  
Waqar -Ul- Nisa ◽  
Saira Afridi
Keyword(s):  
Relative Frequency ◽  
Odontogenic Cysts ◽  
Anterior Maxilla ◽  
Odontogenic Keratocysts ◽  
Posterior Maxilla ◽  
Dentigerous Cysts ◽  
History Of

Background and Objective:The aim of this study was to investigate the relative frequency of odontogenic cysts in two local dental college hospitals.Methodology:In this study 90 cysts from both jaws, treated at Khyber College of Dentistry and Sardar Begum Dental College from March 2008 to March 2013 were analyzed in order to evaluate the incidence of these cysts.Results:Case history of 52 males and 38 females were analyzed. The age of patients varied from 07 to 70 years, with a mean age of 26.4±13.89. In this 5-year study of odontogenic cysts, 48 were radicular cysts, 22 were odontogenic keratocysts and 20 were dentigerous cysts. Out of these 46 cysts were present in the maxilla and 44 in the mandible. In the maxilla 46.7%were present in the anterior maxilla and 4.4% in the posterior maxilla. In the mandible 35.6% were present in the posterior mandible and 13.3% in the anterior mandible.Conclusion:From the findings of this study we conclude that odontogenic cysts were mostly inflammatory in nature i.e. the radicular cysts and was followed by odontogenic keratocysts. Majority of the cysts were located in the anterior maxilla and posterior mandible regions. The male predilection was higher as compared to females.

Molecular analysis of different allelic variants of wild-type human p53

1992 ◽  
Vol 70 (10-11) ◽  
pp. 1014-1019 ◽  
Author(s):  
France Moreau ◽  
Greg Matlashewski
Keyword(s):  
Cultured Cells ◽  
Human Cancer ◽  
P53 Protein ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Allelic Variant ◽  
Wild Type ◽  
Allelic Variants ◽  
Wild Type P53

The p53 tumour suppressor gene is intensively studied because mutations in this gene are the most common genetic alteration so far identified in human cancer. Considerable emphasis has thus been placed on characterizing the biological differences between mutant and wild-type p53 protein. This has led to the realization that in cultured cells, mutant p53 behaves like an oncogene, whereas wild-type p53 is a tumour suppressor gene. The p53 protein is also a target for the tumour virus oncogene products SV40 large T, adenovirus E1B, and human papillomavirus type 16 E6, which are all capable of forming complexes to the p53 protein. Although p53 represents an extremely important cellular regulatory molecule which is well conserved, there exists two allelic variants of wild-type human p53 that differ both in primary and confirmational structure. One variant contains an arginine at amino acid 72 (p53Arg), whereas the other form contains a proline at this residue (p53Pro). The possible implications for more than one allelic variant of wild-type human p53 in the general population is unknown. The present study was undertaken to compare some of the biological features of the different wild-type p53 variants. We present data demonstrating that there was a post-transcriptional selection against accumulation of both variants of wild-type human p53 in 3T3-A31 cells, arguing that both forms are proliferation inhibitory in these cells. Both variants of human p53 were stabilized by SV40 large T, but did not displace mouse p53 from SV40 large T. Neither allelic variant of human p53 was able to reduce significantly SV40-mediated anchorage-independent growth of 3T3-A31 cells. Taken together, these data suggest that although there are structurally different variants of wild-type human p53, there is no difference in the biological activity of these molecules at the level of the biological assays performed here.Key words: human p53, large T, transformation, oncogenes, tumour suppressor.

KAI-1 ad p53 Expression in Odontogenic Cysts: An Immunohistochemical Marker Study

2018 ◽  
Vol 7 (2) ◽  
pp. 62 ◽  
Author(s):  
AbhishekSingh Nayyar ◽  
NamrataN Patil ◽  
Vijay Wadhwan ◽  
Minal Chaudhary ◽  
SanthoshD Reddy ◽  
...  
Keyword(s):  
Odontogenic Cysts ◽  
P53 Expression ◽  
Immunohistochemical Marker ◽  
Marker Study

DNA damage signalling recruits RREB-1 to the p53 tumour suppressor promoter

2009 ◽  
Vol 422 (3) ◽  
pp. 543-551 ◽  
Author(s):  
Hanshao Liu ◽  
Hoi Chin Hew ◽  
Zheng-Guang Lu ◽  
Tomoko Yamaguchi ◽  
Yoshio Miki ◽  
...  
Keyword(s):  
Dna Damage ◽  
Target Genes ◽  
Core Promoter ◽  
Genotoxic Stress ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Dependent Manner ◽  
P53 Expression ◽  
Protein Levels

Transcriptional regulation of the p53 tumour suppressor gene plays an important role in the control of the expression of various target genes involved in the DNA damage response. However, the molecular basis of this regulation remains obscure. In the present study we demonstrate that RREB-1 (Ras-responsive-element-binding protein-1) efficiently binds to the p53 promoter via the p53 core promoter element and transactivates p53 expression. Silencing of RREB-1 significantly reduces p53 expression at both the mRNA and the protein levels. Notably, disruption of RREB-1-mediated p53 transcription suppresses the expression of the p53 target genes. We also show that, upon exposure to genotoxic stress, RREB-1 controls apoptosis in a p53-dependent manner. These findings provide evidence that RREB-1 participates in modulating p53 transcription in response to DNA damage.

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