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

The p53 expression in various skin tumors was immunohistologically evaluated using two mouse monoclonal anti-p53 antibodies, PAb421 and PAb1801. The p53 expression was not detected in the normal epidermal cells. Nuclear staining suggested that the p53 expression was observed in 10 of 26 squamous cell carcinomas (SCCs) from 24 patients, in one undifferentiated carcinoma, one proliferating trichilemmal cyst, one malignant proliferating trichilemmal tumor and in one metastatic carcinoma of breast cancer. None off four cases of Bowen's disease (SCC in situ) showed nuclear staining. In the SCCs, five of 20 primary lesions, three of four recurrent lesions and both of two metastatic lesions had positive nuclei. There was one case of SCC in which a primary lesion was negative but a recurrent lesion was positive. Thus, p53 expression was more frequently observed in SCCs at more clinically advanced stages. This may suggest that p53 has some relevance to progression of SCC. Nuclear staining was not detected in any of the following cases: two cases of seborrheic keratosis, one eccrine poroma, one keratoacanthoma, 11 basal cell epitheliomas, two mammary Paget's disease, three genital Paget's disease, one sebaceous carcinoma, four malignant melanomas, six lymphomas, two leukemia cutis and two angiosarcomas.
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PMID:Immunohistological analysis of P53 expression in human skin tumors. 830 55

Expression of the cellular p53 tumour-suppressor protein was examined in 78 epidermal tumours, including basal and squamous cell carcinomas, keratoacanthomas, solar keratoses, Bowen's disease and viral warts. An immunohistochemical study was employed using the antibody CM-1, raised against recombinant human p53 protein. Positive staining for p53, not detectable in normal cells because wild-type p53 is rapidly degraded, reflects abnormal stabilization of p53 protein, and in many cases suggests p53 gene mutation. p53 immunoreactivity was not observed in normal skin or in viral warts. In contrast, positive staining for CM-1 was seen throughout the tumour in the majority of basal and squamous cell carcinomas and in Bowen's disease. Immunoreactivity to p53 was also observed in the majority of keratoacanthomas and solar keratoses, but was confirmed to areas of dysplastic basal epithelium. This study demonstrates that accumulation of p53 protein, suggestive in many cases of p53 gene mutation and hence loss of tumour-suppressor function, may occur as an important early step in the development of diverse epidermal cancers.
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PMID:Aberrant expression of p53 tumour-suppressor protein in non-melanoma skin cancer. 146 84

Using three antibodies (JG8, CM-1 and 1081) directed to the p53 protein, strong positivity was found in 16/47 (34.0%) of mucosal squamous cell carcinomas of the head and neck and in two squamous carcinoma cell lines (LICR-LON- HN5 and HN6Rr). The presence of the mutant p53 was confirmed in the cell lines as substitutions in exon 7 (codon 238, TGT greater than AGT) and exon 5 (codon 152, CCG greater than CTG) respectively. Positive staining was seen only in the undifferentiated cells and progressively lost as the cells keratinized, both in the tumour specimens and in the cell lines. Similar results were seen in areas of dysplasia, well removed from the site of the primary tumour. Staining of epidermal lesions showed positivity in 2/12 (16.6%) cases of Bowen's disease, 0/12 (0.0%) cases of solar keratosis, 0/10 (0.0%) basal cell carcinomas and in 3/20 (15.0%) squamous cell carcinomas. These results are discussed in relation to the multifocal origin of squamous cell carcinomas, the role of p53 mutations in squamous cell carcinomas from different sites and the significance of the 'basal' distribution of p53 as a normal growth regulator. The possible significance of the distribution of p53 in squamous epithelium as it relates to papilloma virus infection is also considered.
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PMID:Expression of p53 in premalignant and malignant squamous epithelium. 171 23

p53 is a tumor suppressor gene whose protein product is overexpressed in several human tumors. In this study we used a monoclonal antibody (DO7) direct against p53 and a previously described antigen retrieval methodology to examine p53 expression in 27 cases of microinvasive squamous cell carcinoma of the skin and in 10 cases of Bowen's disease. Immunohistochemical studies were performed on formalin-fixed, paraffin-embedded tissue sections that had been microwave-heated to improve antigenicity. Positive nuclear staining for p53 was observed in 23 of 27 (85%) cases of microinvasive squamous cell carcinoma and in five of 10 (50%) cases Bowen's disease. With the exception of occasional focal positive staining of basal layer cells, no p53 immunoreactivity was observed in normal skin. Our results demonstrate that increased expression of the p53 protein is a common finding in both in situ and microinvasive squamous cell carcinoma of the skin, and they suggest that loss of normal p53 tumor suppressor activity may be an important mechanism of oncogenesis in these neoplasms.
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PMID:p53 expression in Bowen's disease and in microinvasive squamous cell carcinoma of the skin. 767 72

Aberrant p53 immunoreactivity has been found in skin pre-malignancies and dysplasias such as Bowen's disease and actinic keratoses. Vulval lichen sclerosus (LS) has been reported to be pre-malignant, with an association of vulval carcinoma in 3% to 6% of patients. In contrast, non-genital LS appears to have no malignant potential. In this immunocytochemical study, we investigated p53 expression in 10 cases of histologically proven vulval LS and 9 cases of non-genital LS using the murine monoclonal antibody Do-1 raised against recombinant human p53 which reacts with both wild-type and mutant p53. None of the vulval specimens had epithelial dysplasia or malignancy. Normal vulval (7 cases) and non-genital skin (5 cases) were used as tissue controls, respectively. The cell proliferation index was also studied using the MIB 1 monoclonal antibody which detects the cell-cycle associated Ki-67 antigen. The technique of microwave irradiation for antigen unmasking was employed on formalin-fixed and paraffin-embedded tissues. There was a significant increase in p53 immunoreactivity in vulval LS (32.13 +/- 15.11 epidermal cells per 100 basal cells) compared to normal vulval skin (7.52 +/- 5.04 epidermal cells per 100 basal cells) (p < 0.001), whereas the MIB 1 labelling index was lower in vulval LS (39.45 +/- 15.88 epidermal cells per 100 basal cells) than in normal controls (86.26 +/- 32.31 epidermal cells per 100 basal cells) (0.001 < p < 0.01). In contrast, there was no significant difference in p53 immunoreactivity or MIB 1 labelling index between non-genital LS and normal controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered p53 expression and epidermal cell proliferation is seen in vulval lichen sclerosus. 779 88

The product of the p53 tumour suppressor gene is a sequence-specific DNA-binding protein that acts as a transcription factor and can inhibit transformation in vitro. Mutational inactivation of p53 is the most frequent genetic alteration found in human cancer. Point mutations of the p53 gene have been detected in about 50% of squamous cell carcinomas, basaliomas and cases of Bowen's disease. A significant portion of these mutations were CC-->TT or C-->T transitions suggestive of UV involvement in mutagenesis. Increased concentrations of p53 protein were immunohistochemically detected in cutaneous malignant melanomas, but p53 mutations are rare in this tumour.
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PMID:[The tumor suppressor gene p53 and its significance for dermatology]. 782 96

Bowen's disease is a premalignant dermatosis comprised of a clonal proliferation of atypical keratinocytes in the full thickness of the epidermis. To elucidate the relationship between the alteration of the p53 tumor suppressor protein and cell proliferation rate, we immunohistochemically examined the expression of proliferating cell nuclear antigen (PCNA) and p53 protein in 30 cases of Bowen's disease. All the cases exhibited the full-thickness distribution of PCNA-positive cycling cells in the lesional epidermis. Quantitation of PCNA staining by image cytometry revealed a mean labeling index (LI) of 75.1 +/- 20.3. p53 expression was detected in 13 cases (43%). Expression was diffuse (p53 LI > 50) in 9 cases, but focal (p53 LI < 30) in the other four. The mean PCNA LI of p53 diffusely positive cases was significantly greater than that of both p53 focally positive and p53 negative cases (89.3 +/- 10.1 vs 62.7 +/- 21.2, and 70.5 +/- 21.6; p < 0.01, respectively). These findings suggest that a high-level accumulation of p53 protein results in a more increased cell proliferation in Bowen's disease.
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PMID:Proliferating cell nuclear antigen (PCNA) and p53 protein expression in Bowen's disease. 786 67

The monoclonal Ki-67-specific MIB-1 and p53 protein-specific DO-1 antibodies were used to identify proliferating cell fractions on microwave-pretreated paraffin sections of 7 cutaneous Bowen's disease specimens. A high Ki-67 score was characteristic of all cases examined, and significant p53-positivity was seen in 4 cases. In the peritumoral, histologically normal epidermis, Ki-67- and p53-positive cells were frequently present, in one case with very high scores (89% as well as 82%, respectively). These findings indicate an increase in the proliferative activity of the Bowen cells (high Ki-67 score) and that p53 mutations are frequently found in this disease. The p53 expression was not related to the Ki-67 score. The expression of Ki-67 and p53 in morphologically normal epidermal cells is also discussed. The histologically normal epidermal cells expressing p53 and Ki-67 antigens may correspond to pre-malignant clones.
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PMID:Ki-67 and p53 expression in cutaneous Bowen's disease: an immunohistochemical study of fixed-embedded tissue sections. 791 36

We have investigated point mutations of codons 12, 13, and 61 in H-, K-, and N-ras oncogenes as well as p53 tumour suppressor gene exon 5 through exon 9 by PCR-SSCP analysis in 26 skin biopsy tissues from 16 arsenic-related Bowen's disease patients and 6 skin samples from 4 paraquat manufacturing workers. No mutation was found. These results are different from findings with UV associated skin cancers. Interestingly, a silent change at codon 27 of H-ras in one allele was detected in all 4 paraquat manufacturing workers and in 2 of 16 arsenic-related Bowen's disease patients. It is likely that the molecular mechanisms involved in arsenic and paraquat induced skin cancers differ from sunlight-related skin malignancies.
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PMID:Arsenic-related Bowen's disease and paraquat-related skin cancerous lesions show no detectable ras and p53 gene alterations. 795 56

Mutations of exons 3 through 9 of the p53 gene in skin lesions were screened in 23 cases of squamous cell carcinoma (SCC), 25 cases of basal cell carcinoma (BCC), two cases of Bowen's disease, 10 cases of solar keratosis, and five cases of keratoacanthoma by polymerase chain reaction--single strand conformation polymorphism analysis. Mutations of the p53 gene were detected in seven of 23 SCCs (30%), three of 25 BCCs (12%), and none in all cases of Bowen's disease, solar keratosis, or keratoacanthoma. Of 23 cases of SCC, mutations were detected in four of 15 SCCs (27%) that originated in the sunlight-exposed skin region, in two of three SCCs (67%) that originated in the scar tissue, and in one of three SCCs (33%) that originated in radiation dermatitis. Mutations of C-->T transition predominated in SCC and BCC that originated in the sunlight-exposed skin region. Mutations of C-->A or CC-->AT observed in tumors that originated in the predisposed conditions, presumably unrelated to UV light, are different from those found in UV light-related SCC or BCC. Twelve cases of SCC were comparatively analyzed with the immunohistochemical staining with anti-p53 antibody. Two of four cases with positive staining had missense mutations, and three of eight cases with negative staining had nonsense mutations. Based on these findings, immunohistochemical results do not necessarily mean the presence or absence of p53 gene mutations in skin tumors, and sequence analysis is essential for determining whether the gene is mutated.
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PMID:p53 gene mutations in human skin cancers and precancerous lesions: comparison with immunohistochemical analysis. 815 Nov 21


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