Expression of p53 protein in melanoma progression

Kanoko, Mpu; Ueda, Masato; Nagano, Tohru; Ichihashi, Masamitsu

doi:10.1016/0923-1811(95)00465-3

Cited by 16 publications

(17 citation statements)

References 27 publications

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“…In contrast to studies reporting that an elevated rate of p53 expression could be observed in metastatic MM (Saylors et al, 1991;Kanoko et al, 1995;Poremba et al, 1995), which may indirectly reflect p53 gene mutations, we could not confirm this phenomenon. However, we frequently detected cytogenetic loss of the 17p11-13 region.…”

Section: Discussioncontrasting

confidence: 99%

“…Loss of function of p53 has been reported for colon, oesophageal squamous cell, pancreatic and hepatic carcinoma and other malignant tumours of the brain, lung, breast and ovary (Levine, 1993). Despite numerous studies, no clear information on the role of p53 in MM is available to date (Stretch et al, 1991;Akslen et al, 1992;Catresana et al, 1993;Piepkorn, 1994;Kanoko et al, 1995;Poremba et al, 1995;Saez-Santamaría et al, 1995;Talve et al, 1996). The majority of cultured MM cell lines is described to express p53 protein as assessed by monoclonal antibody binding.…”

Section: Malignant Melanoma (Mm) Is a Common Cancer Amongmentioning

confidence: 99%

“…Only specimens with nuclear labelling and staining of more than 1% of the cells examined were considered to be positive for p53 (Kanoko et al, 1995). A minimum of 1000 cells per specimen was evaluated.…”

Section: Immunohistochemistrymentioning

confidence: 99%

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Deletions of the region 17p11-13 in advanced melanoma revealed by cytogenetic analysis and fluorescence in situ hybridization

et al. 1998

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Malignant melanoma (MM) is a common cancer amongCaucasians and has shown a deplorable increase in incidence rates during recent decades. Early diagnosis -and consequently early surgical excision -has been greatly improved, leading to an average 5-year survival rate of up to 80%. Therefore, stable incident death rates of MM could be observed. However, the prognosis of metastatic MM still remains poor, with a long-term survival rate of about 20% in stage III patients (Balch et al, 1992;Johnson et al, 1995).Cytogenetic analyses of cell lines derived from MM have been reported for more than 20 years (Chen et al, 1973). The data obtained are quite complex and not always unambiguous. However, the non-random involvement of chromosomes 1, 6, 7 and 9 has been published repeatedly (Chen et al, 1973;Koprowski et al, 1985;Heim et al, 1988;Trent at al, 1990;Balch et al, 1992). Deletions or loss of function of the p53 tumour-suppressor gene (p53-TSG) have been found in roughly 50% of all malignant tumours . Mutations of the p53-TSG have been found to be characteristic for carcinogenes and biochemical mechanisms responsible for genetic lesions in DNA that cause cancer (Harris et al, 1993). Loss of function of p53 has been reported for colon, oesophageal squamous cell, pancreatic and hepatic carcinoma and other malignant tumours of the brain, lung, breast and ovary (Levine, 1993). Despite numerous studies, no clear information on the role of p53 in MM is available to date (Stretch et al, 1991;Akslen et al, 1992;Catresana et al, 1993;Piepkorn, 1994;Kanoko et al, 1995;Poremba et al, 1995;Saez-Santamaría et al, 1995;Talve et al, 1996). The majority of cultured MM cell lines is described to express p53 protein as assessed by monoclonal antibody binding. Point mutations in the p53 coding sequence (usually cytosine to thymidine) have been found in 30% of cases (Piepkorn, 1994). Stretch et al report that 73% of primary and 93% of metastatic melanomas express mutant p53 protein (Stretch et al, 1991). However, there are also reports describing a reduced p53 expression in metastatic MM compared with primary lesions (Catresana et al, 1993).To investigate the role of p53-TSG in metastatic MM, we analysed 11 metastatic MM derived from 11 patients cytogenetically by chromosome banding techniques and FISH after shortterm culture. In addition, paraffin-embedded tissues of 9 of the 11 MM were examined immunohistochemically using DO-7, an antibody reacting with both wild-type and mutant p53 protein. MATERIAL AND METHODS MaterialEleven surgically removed, histologically confirmed metastatic MM (ME 1 to ME 11) from 11 patients were minced with scissors and prepared for short-term culture by standard methods (Pederson et al, 1986). Patients' data are briefly described in Table 1. For preparing MM specimens for cytogenetic investigation, collagenase (Worthington Biochemical Corporation, NJ, USA) 200 U ml -1 was used over night.The next day, cells were washed three times to start cultivation in a collagenase-free medium with RPMI-1640 medium (Sera-l...

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Section: Discussioncontrasting

confidence: 99%

Section: Malignant Melanoma (Mm) Is a Common Cancer Amongmentioning

confidence: 99%

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Deletions of the region 17p11-13 in advanced melanoma revealed by cytogenetic analysis and fluorescence in situ hybridization

et al. 1998

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“…The cytoplasmic accumulation of p53 in the cell lines and tumor samples was not a feature of the antibody or the conditions used or an artifact of tissue culture; p53 was localized almost exclusively in the nuclear compartment of Cf2Th cells, 55 and seven tumor samples contained abundant nuclear p53. In human melanomas, mutations of the p53 gene or abnormalities that result in accumulation of p53 protein that is functionally excluded from the nucleus occur frequently, 9,28,31,57,70,71 and melanomas with mutant p53 gene carry a worse prognosis than those without p53 mutations. 17,34 However, numerous events may affect the stability and subcellular localization of p53, 36 and overexpression of p53 protein in tumor cells does not necessarily imply mutation or loss of function of the p53 gene.…”

Section: Discussionmentioning

confidence: 99%

Expression and Significance of p53, Rb, p21/waf-1, p16/ink-4a, and PTEN Tumor Suppressors in Canine Melanoma

et al. 2002

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Abstract. The role of tumor suppressor genes in the pathogenesis of canine melanoma is incompletely understood. The genes encoding the tumor suppressors p53, Rb, p21 (waf-1), p16 (ink-4a), and PTEN have been postulated to contribute to the pathogenesis of melanoma in humans and experimental animal models. To assess whether inactivation of these genes similarly contributes to the origin and progression of canine melanoma, we examined their expression in seven distinct canine melanoma cell lines and in 31 retrospective samples (representing 29 dogs) of spontaneous canine melanoma. Various patterns suggestive of loss of tumor suppressor function emerged in these cell lines. The most frequently observed abnormality was loss or significant reduction of p16 expression in six of seven cell lines and in 21 of 26 tumor samples. Loss or significant reduction of PTEN expression was seen in four of seven cell lines and in 13 of 27 tumor samples. Although p53 was detectable in all the cell lines and in 24 of 30 tumors, exclusion of p53 from the nuclear compartment was observed in each of the cell lines and in 18 of 25 tumor samples. These results indicate that loss of function of these tumor suppressor proteins is a common occurrence that may contribute to the origin of canine melanoma. In our sample population, abnormalities in the expression or localization of one or more tumor suppressor proteins occurred with similar frequency in malignant and benign tumors; thus, additional work is necessary to determine how these proteins may impact disease progression and response to therapy.

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“…The erythematous plaque on the dorsum of her hand exhibited hyperkeratosis, papillomatosis and acanthotic epidermis but no atypical keratinocytes. Immunohistochemical staining of SCC and SCC in situ using the monoclonal mouse anti-p53 antibody DO-7 (Dako, Kyoto, Japan) at a dilution of 1:100 was performed as described [18], resulting in positive nuclear staining of atypical keratinocytes in both lesions but not in peripheral nontumorous skin ( fig. 2).…”

mentioning

confidence: 99%

A Nonfamilial Japanese Case of Huriez Syndrome: p53 Expression in Squamous Cell Carcinoma

Watanabe¹,

Takai²,

Ichihashi³

et al. 2003

Dermatology

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Expression of p53 protein in melanoma progression

Cited by 16 publications

References 27 publications

Deletions of the region 17p11-13 in advanced melanoma revealed by cytogenetic analysis and fluorescence in situ hybridization

Deletions of the region 17p11-13 in advanced melanoma revealed by cytogenetic analysis and fluorescence in situ hybridization

Expression and Significance of p53, Rb, p21/waf-1, p16/ink-4a, and PTEN Tumor Suppressors in Canine Melanoma

A Nonfamilial Japanese Case of Huriez Syndrome: p53 Expression in Squamous Cell Carcinoma

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