Home About us Contact
|
Home About us Contact | ||
|
|
||
Malignant Conversion (malignant + conversion)
Selected AbstractsAssociation of aberrant p53 and p21WAF1 immunoreactivity with the outcome of oral verrucous leukoplakia in TaiwanJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 2 2000Kuo-Wei Chang Abstract: The expression of p53 and p21WAF1 in 53 oral verrucous leukoplakias (OVLs), mostly non-dysplastic lesions, was investigated to ascertain the role of such events in malignant conversion. Immunohistochemical analysis revealed aberrant p53 and p21WAF1 immunoreactivity in 51% (27 cases) and 75% (40 cases), respectively. After an average follow-up period of three and a half years, histopathological examination revealed that 22 (42%) cases had developed oral squamous cell carcinoma (OSCC), 14 (26%) cases had undergone recurrence, and 17 (32%) cases were free of disease. The oncogenic potential of this subset of premalignant lesions warrants attention. A significant difference in the frequency of OSCC progression/recurrence was noted in lesions bearing aberrant immunoreactivity of either p53 (93% vs 42%; P=0.00008) or p21WAF1 (80% vs 32%; P=0.002) in comparison with lesions without immunoreactivity. This study suggested that the aberrant immunoreactivity of p53 and p21WAF1 may represent important alterations of OVL and could affect the outcome of this lesion. [source] Malignant transformation of mature cystic teratoma to squamous cell carcinoma involves altered expression of p53- and p16/Rb-dependent cell cycle regulator proteinsPATHOLOGY INTERNATIONAL, Issue 12 2008Atsuko Iwasa Ovarian mature cystic teratomas (MCT) uncommonly undergo malignant transformation to squamous cell carcinoma (SCC). While alterations in the p53 tumor suppressor gene and protein have been shown, few studies have analyzed other molecular changes leading to this malignant conversion. The purpose of the present study was to investigate 21 samples of SCC arising in MCT for altered expression in known p53- and p16/Rb-dependent cell cycle regulatory proteins, and the association between their expression and cellular proliferation and histological features. Overexpression of the p53 protein was observed in 14 SCC (67%), while four (19%) had point mutations in the p53 gene. Reduced expression of the p16 protein was observed in 18 SCC (86%), while p16 gene alterations (hypermethylation (29%) and point mutation (33%)) were found in 11 (52%). Furthermore, a statistically significant correlation was observed between p53 and Rb overexpression (P = 0.0010), and the overexpression of both p53 and Rb was respectively significantly correlated with increased cellular proliferation. The results indicate that alterations in both the p53 and p16-Rb pathways are associated with SCC arising in MCT. [source] S-phase fraction and DNA ploidy in oral leukoplakiaANZ JOURNAL OF SURGERY, Issue 7-8 2010Rahul Khanna Abstract Background:, The risk of malignant conversion in oral leukoplakia is well documented. Histological findings are often unreliable and it is difficult to predict on the basis of clinical and histopathological changes which leukoplakic lesion will turn malignant. Methods:, We used the technique of flow cytometry to evaluate the ploidy status, DNA index and S-phase fraction in leukoplakia, oral cancer and normal oral mucosal biopsies and compared it with histological findings. The study was carried out on 30 patients with oral cancer, 60 with leukoplakia and 30 with normal oral mucosal biopsies. Results:, The aneuploidy rate in oral cancers was 64%, for leukoplakia 20%, while all normal mucosal biopsies were diploid. Aneuploid lesions also had a greater S-phase fraction (SPF). The DNA Index (DI) of aneuploid oral cancers was 1.72 and aneuploid leukoplakias was 1.24. Leukoplakia specimens which showed histological evidence of dysplasia had aneuploidy rate of 38%, DI of 1.19 and SPF of 6.2%. The corresponding values for leukoplakia specimens without dysplasia were 14%, 1.09 and 4.1%, respectively. Conclusion:, The method of flow cytometry can be used to identify the subset of leukoplakia patients who are at a higher risk of malignant conversion. These patients could undergo more rigid surveillance or undergo excision biopsy of their lesions. [source] Protection against Malignant Progression of Spontaneously Developing Liver Tumors in Transgenic Mice Expressing O6 -Methylguanine-DNA MethyltransferaseCANCER SCIENCE, Issue 11 2000Xiusheng Qin To study the effect of O6 -methylguanine-DNA methyltransferase (MGMT) on carcinogenesis, we have previously generated MGMT transgenic mice overexpressing the bacterial MGMT gene, ada, and demonstrated that high MGMT levels in the liver suppress induction of liver tumors after treatment with an alkylating hepatocarcinogen. To examine the effects of life-long elevation of MGMT activity on mouse spontaneous liver tumor development, ada-transgenic and control nontransgenic mice were compared. We also examined mutations at codon 61 of the H-ras oncogene, reported as a hot spot in mouse liver tumors, using a direct DNA sequencing method. The results revealed no significant difference in tumor incidence or mutation spectrum, but interestingly, ada-transgenic mice were found to have fewer malignant tumors and survived longer, indicating a possible protective role of MGMT against malignant conversion. [source] | ||||||||||