Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the case of a 50-year-old male homosexual suffering from AIDS, who developed diffuse annular hyperkeratotic lesions on the arms and legs. Histopathological examination revealed typical features of porokeratosis, which clinically was of the disseminated superficial type. Ultrastructural examination showed a paucity of keratohyalin granules and lamellar bodies. Immunohistochemical studies showed an almost complete absence of Langerhans cells in lesional epidermis. Involucrin and filaggrin expression were altered in areas of cornoid lamella formation, whereas basal keratinocytes in these areas expressed PCNA/cyclin and, to a lesser degree, p53 protein. Porokeratosis may affect immunocompetent patients, but has also been reported in the setting of immunosuppression following organ transplantation. As far as we are aware, the development of porokeratosis during the course of HIV infection has not been reported previously.
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PMID:Disseminated superficial porokeratosis in a patient with AIDS. 791 97

We examined 9 Japanese cases of porokeratosis (4 of the plaque type, 2 of disseminated superficial actinic porokeratosis, 2 of disseminated superficial porokeratosis, and one of giant porokeratosis) for the expression of p53 tumor suppressor protein immunohistochemically, using two anti-p53 antibodies, CM1 and DO1. The same results were obtained with both antibodies. The epidermis central to the cornoid lamellae was positive in 8 of 9 specimens. On the other hand, the peripheral epidermis was positive in 2 of the 9 cases. The epidermis beneath the cornoid lamellae was positive in 3 of the 9 cases. The frequency of p53 positivity was significantly higher in the epidermis central to cornoid lamellae over that beneath or peripheral to them (Fisher's exact probability test, p < 0.05). The majority of squamous cell carcinoma cells arising on giant porokeratosis stained with CM1 and DO1. These data may suggest that the abnormal p53 expression has some relevance to the skin carcinogenesis of porokeratosis.
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PMID:Immunohistochemical detection of p53 tumor suppressor protein in porokeratosis. 867 31

In this and previous studies, we have shown p53 overexpression immunohistochemically in 14 of 17 porokeratotic specimens obtained from 14 lesions of nine cases, and in all six specimens of squamous cell carcinoma (SCC) arising on porokeratotic lesions of two cases. We screened mutations in exons 5 to 10 of the p53 gene in all these specimens by polymerase chain reaction-single strand conformation polymorphism analysis. Mutations of the p53 gene were detected in two of the six SCCs but not in any of the 17 porokeratotic specimens. These two mutations were C to T transitions at codons 146 and 175 in exon 5, which were a nonsense mutation at a dipyrimidine site and a missense mutation at a CG site, respectively. To our knowledge, neither of these mutations has been identified in skin cancers before. Our observations indicate that mutations of the p53 gene are not the major molecular etiology for porokeratosis, but are related to its skin carcinogenesis, and that p53 overexpression in porokeratosis is not due to p53 gene mutations.
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PMID:p53 gene mutation analysis in porokeratosis and porokeratosis-associated squamous cell carcinoma. 913 74

A 40-year-old man developed squamous cell carcinoma on a perianal lesion of linear porokeratosis after renal transplantation. The tumor metastasized to the left inguinal lymph node 25 months after the primary tumor was excised. p53 overexpression was observed in the tumor cells, but not in the porokeratotic lesion. Interestingly, continuous subcutaneous infusion of peplomycin for the lymph node metastasis significantly improved the warty lesions of porokeratosis. In this patient, immunosuppressive agents might have accelerated the development of carcinoma on a skin area with malignant potential.
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PMID:Squamous cell carcinoma in a renal transplant recipient with linear porokeratosis. 1034 71

The etiology of the porokeratoses is unknown. Overexpression of the p53 tumor suppressor protein and disregulated cell cycle control have been pathogenically implicated. The p53 tumor suppressor gene product is regulated by mdm2 and both gene products influence cell cycle progression through the cyclin-dependent kinase inhibitor p21. Thirty-three cases of the various types of porokeratosis were immunohistochemically studied for p53, mdm2, and p21 proteins. Each of the cases showed increased p53 and decreased mdm2 and p21 expression within keratinocytes underlying cornoid lamella. This study confirms the previous findings of increased p53 staining and expands the potential roles of mdm2 and p21 in the pathogenesis of the porokeratoses.
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PMID:p53, mdm-2, and p21 waf-1 in the porokeratoses. 1053 69

Disseminated superficial porokeratosis (DSP) consists of multiple small lesions of porokeratosis. Although the pathogenesis of DSP remains unclear, localized cloning of abnormal epidermis has been hypothesized. Malignant cutaneous neoplasms, especially Bowen's disease, have been frequently reported in DSP. Immunopositive p53 has been demonstrated in a variety of human malignant tumours, and its role in oncogenesis and tumour progression is thought to be important. p21Waf1/Cip1 is thought to mediate the signal of p53 induced by DNA damaging agents to arrest the cell cycle. To clarify the role of p53 and p21Waf1/Cip1 in Bowen's disease and DSP, we analysed 12 cases of Bowen's disease and eight cases of DSP by immunohistochemistry. In five of the 12 Bowen's disease patients and two of the eight DSP patients, positive p53 staining was detected. In contrast, whereas p21Waf1/Cip1 overexpression was detected in all Bowen's disease patients, it was not seen in DSP. The present data suggest that p53 immunostaining provides relevant information concerning the pathogenesis of Bowen's disease and DSP. Furthermore, high p21Waf1/Cip1 expression appears to be a useful indicator of tumour activity in Bowen's disease.
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PMID:Overexpression of p2lWaf1/Cip1 immunohistochemical staining in Bowen's disease, but not in disseminated superficial porokeratosis. 1058 11

Immunosuppression and transplantation have been reported to induce porokeratosis (PK), especially its variant, disseminated superficial PK (DSP). On the other hand, there is ample evidence of a relationship between hepatitis C virus (HCV) infection, liver cirrhosis (LC), and hepatocellular carcinoma (HCC). We report 3 cases of DSP in which the outbreak of DSP was suspected to have occurred during the development of HCC in patients with HCV-positive LC. The patients had undergone ultrasonographic study regularly, and no signs of malignancy had been found before the development of DSP. Their outbreaks of DSP were very acute, and the period between the development of DSP and diagnosis of HCC ranged from 2 to 6 months. The association of HCV-related HCC and DSP has never been previously reported. HCV-induced immunomodulation or its effect on the p53 system may be the basis for this type of association. It is necessary to consider development of HCC whenever DSP is found in HCV-positive patients. DSP may be a new paraneoplastic dermadrome.
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PMID:Synchronous development of disseminated superficial porokeratosis and hepatitis C virus-related hepatocellular carcinoma. 1104 35

A 73-year-old man with porokeratosis palmaris, plantaris et disseminata is presented. He had punctate, guttate and annular hyperkeratotic papular lesions widespread on his body with thorn-like hyperkeratosis on the palms and soles. Lesional skin did not show mutations of TP53 exons 5-6, 7, 8.
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PMID:Lack of TP53 mutations in a case of porokeratosis palmaris, plantaris et disseminata. 1105 22

We report on a patient with a disseminated form of porokeratosis in whom bowenoid lesions and squamous cell carcinoma developed in an apparent sequential progression. Local and disseminated metastases ensued, resulting in the death of the patient. Furthermore, we found an overexpression of the p53 protein in the keratinocytes beneath and adjacent to the cornoid lamella in the porokeratotic lesion and throughout the epidermis in a bowenoid lesion. Although malignancy has been reported previously in various types of porokeratosis, the development of fatal metastatic squamous cell carcinoma in the setting of this disease is a rare event. The histopathologic findings of this case document the association of porokeratotic lesions with bowenoid dysplasia and aggressive squamous cell carcinoma and confirm that a p53 functional aberration can be important in a malignant outcome such as this.
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PMID:Disseminated porokeratosis with fatal metastatic squamous cell carcinoma: an additional case of "malignant disseminated porokeratosis". 1197 75

Overexpression of cyclooxygenase-2 (COX-2) has been demonstrated in various cancers, including experimentally promoted tumors, gastrointestinal cancers, breast tumors and skin tumors. The mechanism that controls COX-2 expression is not yet clear. Currently, it is reported that COX-2 expression is frequently associated with mutated p53 genes. The goal of this study was to evaluate the expression patterns of COX-2 and p53 in several skin tumors and their correlation. An immunohistochemical method was used to investigate the expression of COX-2 and p53 proteins on formalin-fixed, paraffin-embedded tissue specimens of squamous cell carcinomas (SCC), basal cell carcinomas (BCC), Bowen's disease (BD), actinic keratosis (AK) and porokeratosis. The expression of COX-2 increased in 50% (5/10) of SCC, 80% (8/10) of BCC, 40% (4/10) of BD, 50% (5/10) of AK, and 20% (2/10) of porokeratosis cases. The expression of p53 increased in 90% (9/10) of SCC, 70% (7/10) of BCC, 70% (7/10) of BD, 50% (5/10) of AK, and 40% (4/10) of porokeratosis cases. COX-2 positivity rates of the p53-positive skin tumors were 56%, 100%, 57%, 80% and 25% in SCC, BCC, BD, AK and porokeratosis, respectively. However, the correlation between p53 and COX-2 expression in skin tumors was not statistically significant (P > 0.05). Our results indicate that skin COX-2 and p53 may play roles in skin tumors, but that there is no apparent correlation between the two markers.
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PMID:Immunohistochemical study of cyclooxygenase-2 and p53 expression in skin tumors. 1670 Jun 63


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