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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the article is a review of own cytogenic studies on laryngeal cancer confronted with the literature data. Spontaneous and bleomycin-induced chromosome instability was analysed in peripheral blood lymphocytes in relation to genetic risk of cancer incidence and progression. Comparative genome hybridization (CGH) was applied to demonstrate gains and losses of DNA copy number in tumour and non-tumour laryngeal mucosa. The profiles of imbalances of DNA copy number were shown to differ between metastazing and non-metastazing tumours. Preliminary data indicate a frequent loss of Y chromosome in tumour cells. The loss of heterozygosity at chromosome p53 locus (17p) has been shown to be more frequent than at chromosome locus coding 16 gene (9p). Altogether, the experiments have proven that a dynamics of chromosome aberrations is highest at the stage of metastasis.
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PMID:[Chromosome damage in the course of laryngeal squamous cell carcinoma]. 1068 7

The prognostic value of the expression of the cyclin-dependent kinase inhibitor p21 and the p53 tumour suppressor gene was examined using immunohistochemistry in 60 patients with laryngeal cancer. Multivariate analysis using Cox's proportional hazard method, showed that p21 expression (P = 0.02) and advanced T stage (P = 0.003) significantly predicted survival. It was concluded that p21 expression may be a useful prognostic indicator in laryngeal cancer.
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PMID:Expression of cyclin-dependent kinase inhibitor p21(WAF1) and p53 tumour suppressor gene in laryngeal cancer. 1076 33

Possible differences were analyzed between histopathological and molecular biological findings in laryngeal cancer tissue and its adjacent normal tissues. p53 gene mutations were detected in histopathologically normal tissue both within 0.5 cm of and more than 0.5 cm distant from the nearest cancerous tissue. Since the p53 mutation was common in both cancer tissue and adjacent normal tissue, the gene mutation may play an important role in laryngeal carcinogenesis. Radical excision of the tumor is defined by histopathological limits, but 'normal' tissue may nevertheless contain the gene mutation, giving rise to the danger of further cancer development. We suggest that the determination of the surgical margin should be based on a combination of histopathology and molecular biological findings.
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PMID:Mutants of p53 gene presence in laryngeal carcinoma and adjacent histopathologically normal tissue. 1081 Feb 58

Mutations in the p53 gene--which codifies anuclear phosphoprotein that acts as a tumor suppressor gene--is the most common genetic alteration in head and neck cancers. The aim of the present study was to investigate the prognostic significance of p53 protein over expression in squamous cell laryngeal carcinoma. To do so we analyzed 31 patients affected by precancerous lesions of the larynx who had undergone multiple biopsy between 1980 and 1995. Twenty-five of these patients later developed laryngeal carcinoma. In this group of patients, 51 biopsies were performed for precancerous lesions (17 hyperplasia, 3 light dysplasia, 23 moderate dysplasia, 8 severe dysplasia) prior to evidence of laryngeal cancer (2.04 biopsies/patient). In the group of patients who did not develop laryngeal cancer, 18 biopsy were performed (2.2 biopsies/patient) and histology revealed: 5 keratosis, 5 light dysplasia, 4 moderate dysplasia and 4 grave dysplasia. Using the immunohistopathological staining technique, 69 formalin-fixed, paraffin-embedded precancerous samples and 25 laryngeal carcinomas were examined for p53 over expression. The monoclonal antibody Pab 1801 was used with the avidinbiotin immunoperoxidase technique; p53 intensity of expression was assessed and correlated with clinical-pathological parameters. Over expression of the p53 protein was found in 56.8% of the precancerous lesions (41% of the hyperplastic lesions, 66% of light dysplastic lesions, 60% of moderate dysplastic lesions and 75% of severe dysplastic lesions) in the group patients who did develop laryngeal cancer and in 22.2% of the precancerous lesions in the group of patients that did not. The transformed lesions showed a strong correlation between intensity of positivity and grade of cellular atypia. Further in 93.3% of the patients with p53 positive precancerous lesions which later developed into laryngeal cancer, p53 over expression was present in the cancerous lesions. There was no significant correlation between p53 immuno reactivity and such clinico pathological tumor parameters as TNM staging and tumorrecurrence. On the other hand, there was a correlation between p53 overexpression and differentiation grading: p53 overexpression was found in 75% of the poorly differentiated tumors, 58.3% of moderately differentiated and 44.4% of well differentiated tumors. The fact that p53 is detected in preneoplastic lesions suggests that p53 gene alteration takes place very early in laryngeal carcinoma and moderate-to-high p53 expression constitutes a high risk of transformation into cancer; on the other hand low expression may reflect reversible changes that can be attributed to the genotoxic effects of tobacco smoking. In conclusion the present data suggest that p53 over expression could be a good prognostic marker in predicting which precancerous laryngeal lesions will progress into cancer.
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PMID:[The role of p53 tumor suppressor gene as prognostic factor in laryngeal squamous cell carcinoma]. 1087 57

p53 gene mutations are a common genetic alteration in human cancer and codon 72/exon 4 polymorphism of the p53 gene has been implicated in cancer risk. Therefore in this study the p53 gene status of 32 shock-frozen tumor specimens from larynx carcinomas was analyzed by PCR and sequencing of exon 4 through 9. Four mutations (12.5%) in exon 5, 7, 8 and 9 were detected in the carcinoma specimen. Analysis of codon 72 revealed in eight cases a homozygosity for proline (CCC) and in 24 cases heterozygosity or homozygosity for arginine (CGC). The group with the proline/proline genotype had a median age 10.3 years lower than the remaining patients and included the only two non-smokers. Firstly, these results confirm the p53 mutational status of laryngeal cancer without any clinical correlation and secondly may suggest an oncogenic potential for the proline/proline genotype of codon 72 for laryngeal cancer as has already been assumed for lung cancer.
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PMID:p53 analysis of laryngeal cancer in exon 4 to 9. 1095 33

The authors estimated PCNA and P53 in subjects with laryngeal cancer in whom local or nodal recurrences were observed. The study included 54 patients from Upper Silesia in age 37-79 years (mean 57 +/- 8.8). The mean value of the PCNA index in subjects with local recurrence (LR) was 24.2% +/- 12.1 while in subjects without LR 22.1% +/- 9.4 (p > 0.05). Additionally, 21 subjects were separated from the investigated group in whom no lymph node metastases were found during laryngectomy. Among these subjects in 16 LR was observed (PCNA index was 30.9% +/- 12.5) while in remaining 5 subjects, in whom LR did not develop, PCNA index was 21.7% +/- 11.2. Analysis of the P53 index in subjects with LR revealed significantly higher values (19.2% +/- 9.1) in comparison to cases without LR (13.2% +/- 6.3). Our study revealed usefulness of the P53 and PCNA as markers which could support the histological diagnostic process describing biology of the cancer cells. The demonstrated increase of PCNA and P53 index in patients with LR might be useful in prediction of LR.
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PMID:[Assessment of usefulness of PCNA and protein p53 in subjects with laryngeal cancer with local recurrence]. 1097 77

The authors estimated PCNA and P53 in subjects with laryngeal cancer with local or nodal recurrences. The study concerned 54 patients from Upper Silesia aged 37-79 (mean 57 +/- 8.8). The mean value of the PCNA index in subjects with local recurrence (LR) was 24.2% +/- 12.1 while in subjects without LR 22.1% +/- 9.4 (p > 0.05). Additionally, 21 subjects in whom no lymph node metastases were found during laryngectomy were separated from the investigated group. In 16 of them local recurrences were observed and the mean value of PCNA index was 30.9% +/- 12.5. In remaining 5 subjects in whom local recurrences were not developed the mean value of PCNA index was 21.7% +/- 11.2. The analysis of the P53 index in subjects with LR revealed significantly higher values (19.2% +/- 9.1) in comparison with cases without LR (13.2% +/- 6.3). The assessment of the mean values of PCNA and P53 index depending on T, N or stage as well as nodal recurrence did not reveal any statistical significance. Our study revealed usefulness of the P53 and PCNA as markers which could support the histological diagnostic process describing biology of the cancer cells. The demonstrated increase of PCNA and P53 index in patients with LR might be useful in prediction of LR.
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PMID:[Assessment of usefulness of PCNA and oncoprotein p53 staining in prediction of the recurrences in subjects operated on for laryngeal carcinoma]. 1107 Jun 93

Evaluation of the biology of laryngeal cancer cell is connected either with many process inside the cell or reactions between cancer cell itself and extracellular matrix. The main purpose in this paper was the evaluation of p53 protein, bcl-2 protein, Ki-67 antigen and CD44 adhesive molecule expressions in comparison to clinical and histopathological features in patients with laryngeal cancer. Paraffin-embedded tissue sections from 89 patients with laryngeal cancer were stained with a monoclonal antibody raised against p53 and bcl-2 proteins, Ki-67 and CD44 antigens using a peroxidase-labelled streptavidin-biotin kit. There were statistically significant relationships between p-53 protein over-expression and pT, histological grading, survival and Ki-67 and CD44 antigens expressions. There were no correlation between bcl-2 protein expression and clinical and histopathological features. We observed statistically significant correlation between Ki-67 expression and pT, histological grading, recurrences and survival. Expression of CD44 statistically significant correlated only with tumour size. We conclude that comparison of data covering mentioned tumour markers expression gives valuable evaluation of biological activity of cancer cells and may allow to create the immunological panel of tumour markers which simplify the prognosis about nodal metastases, recurrences and survival in patients with laryngeal cancer.
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PMID:[Expression of selected markers for apoptosis, proliferation and metastasis in evaluation of laryngeal cancer invasiveness dynamics]. 1126 75

The role of p53 overexpression in the development of stomal recurrence was studied in patients with T1 glottic cancer who had undergone salvage laryngectomy after primary radiotherapy failure (first recurrence). The role of subglottic extension of the recurrent tumor in the development of stomal recurrence was also studied. One hundred fourteen patients with T1 squamous cell carcinoma of the glottic larynx were irradiated with curative intent. A local recurrence (first recurrence) developed in 23 patients (20%), and salvage laryngectomy was performed for 20 of these patients. No postlaryngectomy radiation therapy was included in the treatment of recurrences. Several risk factors thought to be significant in the development of stomal recurrence were analyzed in these 20 patients. Prognostic factors analyzed include: p53 overexpression in the preradiation biopsy specimen, subglottic extension of the first recurrence, thyroid cartilage and lymph node involvement at the time of first recurrence, emergency tracheostomy performed before salvage laryngectomy, and the laryngectomy procedure performed for first recurrence. Presence of p53 protein in the preradiation biopsy specimen of laryngeal cancer did not show any adverse effect on the development of stomal recurrence. Stomal recurrence developed in 27% of patients with positive biopsies and in 20% of patients with negative biopsies (p = 1.00). Subglottic extension of the first recurrence was associated with an increased incidence of stomal recurrence. Rates of stomal recurrence were 6% in patients without subglottic extension and 100% in patients with subglottic extension (p = 0.001). All other risk factors studied showed no effect on stomal recurrence. In this study, p53 overexpression showed no effect on the development of stomal recurrence after salvage laryngectomy in patients with T1 glottic cancer. Conversely, subglottic extension of the recurrence was found to be strongly associated with stomal recurrence. All other factors analyzed showed no effect on stomal recurrence.
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PMID:Stomal recurrence in patients with T1 glottic cancer after salvage laryngectomy for radiotherapy failures: role of p53 overexpression and subglottic extension. 1131 83

Co-transfer of immunomodulatory and anti-proliferative genes may be the basis for new strategies to enhance tumor regression. The purpose of this study was to develop a combination gene therapy strategy for the treatment of laryngeal cancer. Human wild-type p53 and granulocyte-macrophage colony-stimulating factor (GM-CSF) genes were transferred into human laryngeal cancer cells mediated by adenovirus type 5 vector co-expressing human wild-type p53 and GM-CSF (Ad-p53/GM-CSF). By the introduction of the wild-type p53 gene, the growth of human laryngeal cancer Hep-2 cells was inhibited and their apoptosis was induced. By the introduction of the GM-CSF gene, the immunogenicity of cancer cells was enhanced. Significant proliferation of tumor infiltrating lymphocytes and tumor-specific cytotoxicity of cytotoxic T lymphocytes were induced by Ad-p53/GM-CSF-infected cancer cells in vitro. The results suggest that the co-transfer of human wild-type p53 and GM-CSF genes into tumor cells via recombinant adenovirus may be further developed into an effective and practical combination gene therapy strategy for laryngeal cancer.
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PMID:Co-transfer of human wild-type p53 and granulocyte-macrophage colony-stimulating factor genes via recombinant adenovirus induces apoptosis and enhances immunogenicity in laryngeal cancer cells. 1132 95


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