Absence ofp53 mutations in benign and pre-malignant male genital lesions with over-expressed p53 protein

Castrén, Katariina; Vähäkangas, Kirsi; Heikkinen, E; Ranki, Annamari

doi:10.1002/(sici)1097-0215(19980831)77:5<674::aid-ijc2>3.0.co;2-s

Cited by 34 publications

(18 citation statements)

References 21 publications

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“…It was later recognized, however, that there are cases and tumour types that express high levels of p53 protein in the absence of mutations of the p53 gene (Peng et al, 1993;Castren et al, 1998; for review, see Hall and Lane, 1994). The present results show that AML also belongs to this category of malignancies.…”

Section: Cell Line Number Of Positive Cells (%) Asupporting

confidence: 53%

p53 status of newly established acute myeloid leukaemia cell lines

et al. 1999

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SummaryWe analysed the status of the p53 gene and protein in eight newly established acute myeloid leukaemia (AML) cell lines representing blast cells of either de novo leukaemia patients in first remission or patients with relapsed and chemotherapy-resistant disease causing their death. There were no mutations in the p53 gene in any of the cell lines as analysed by single-strand conformation polymorphism of amplified exons 5-8. However, the p53 protein was clearly and consistently expressed in all of these cell lines, as shown by immunohistochemistry, Western blotting and flow cytometry. The consistently expressed p53 protein was located in both the nucleus and the cytoplasm of all the cell lines and, as shown by flow cytometry, it was mostly in a conformation typical of the mutated protein. These AML cell lines offer a tool for studying the production and function of the p53 protein and its possible role in cell cycle regulation and chemoresistance as well as in the regulation of apoptosis in AML.

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Section: Cell Line Number Of Positive Cells (%) Asupporting

confidence: 53%

p53 status of newly established acute myeloid leukaemia cell lines

et al. 1999

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“…Soufir et al [25] suggested a mutation of p53 gene to have been observed in three of three cases (100%), Levi et al [15] in seven of 21 cases (33%), but both Castern et al [3] and Suzuki et al [27] suggested no mutation of p53 gene was observed. Alves et al [1] presented deletions in 13q21-22 and 4q21-32 on chromosome region and Poetsch et al [20] presented deletions in 2q,6p,8q, 9p, 21q, and 17p13 on chromosome region.…”

Section: Discussionmentioning

confidence: 99%

Frequent epigenetic silencing of the FHIT gene in penile squamous cell carcinomas

et al. 2008

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Methylation of normally unmethylated CpG-rich islands in or near the promoter region has been associated with transcriptional inactivation of tumor-suppressor and tumor-related genes in human cancers. However, so far, only a few studies have searched for DNA methylation in penile carcinoma (PC). On the other hand, human papillomavirus (HPV) has been reported to be associated with the pathogenesis of PC. To elucidate the methylation status of PC and HPV infection, the methylation status of eight genes (DAPK, FHIT, MGMT, p14, p16, RAR-beta, RASSF1A, and RUNX3), the incidences of the HPV status, and the expression of Fhit protein were examined in 25 PCs. The frequencies of methylation were: 28% for DAPK, 92% for FHIT, 20% for MGMT, 4% for p14, 24% for p16, 24% for RAR-beta, 12% for RASSF1A, and 44% for RUNX3. Negative expression of Fhit protein was observed in 22 of the 25 cancers (88%). Among those 22, 20 showed methylation of the FHIT gene. HPV-DNA was detected in three of the 25 cancers (12%). Methylation of FHIT gene was frequently found than HPV infection, therefore methylation of the FHIT gene is suggested to play an important role in the pathogenesis of penile squamous cell carcinoma.

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“…Enhancement of the oncogenic properties of these low-risk viruses by genomic alterations has also been suggested on the basis of several observations (rearrangements of the noncoding region in DNA sequences, subtle aminoacid changes in the HPV 6 E7 protein, etc.). [185][186][187][188] A p53 tumor suppressor gene mutation may be the critical biologic event in the shifting of this low-risk HPV-related neoplasm to its locally aggressive behavior, 189 although this hypothesis is still controversial 190 and deserves further evaluation. Altered p53 expression has been demonstrated in 2 tumors associated with invasive SCC (1 positive for HPV 6, the other for HPV 11).…”

Section: Lack Of Circumcision and Related Factorsmentioning

confidence: 99%