Detection of Ras Gene-Mutations and HPV in Lesions of the Human Female Reproductive-Tract

Koffa, Maria; Koumantakis, E.; Ergazaki, M.; Malamou‐Mitsi, Vassiliki; Spandidos, Demetrios Α.

doi:10.3892/ijo.5.2.189

Cited by 19 publications

(22 citation statements)

References 20 publications

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“…Although in several studies point mutations at codon 12 of the H-ras gene in endometrial carcinomas have not been frequently detected [23], the present study revealed such point mutations in 7.3% of cases, while in a previous study of ours 14% was detected [24],…”

Section: Discussioncontrasting

confidence: 48%

ras Gene Mutations in Human Endometrial Carcinoma

Varras

Koffa²,

Koumantakis³

et al. 1996

Oncology

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The purpose of this study was to assess the extent of involvement of the ras oncogene activation by point mutations in endometrial carcinoma in the Greek population. The PCR technique was employed, followed by RFLP analysis to identify the point mutations in codon 12 of the K-ras, H-ras and N-ras genes. K-ras gene point mutations were detected in 8 of the 55 cases (15%) of primary endometrial carcinoma, H-ras in 4 (7.3%), while no mutations were found for the N-ras gene. No correlation was found between the presence of ras gene mutations and the clinicopathological parameters, or patient survival. The only association found was between H-ras mutations and the FIGO stage of the tumor (Fisher’s exact test, p = 0.011). These results indicate a possible role of ras gene activation in a small subset of endometrial carcinomas.

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Section: Discussioncontrasting

confidence: 48%

ras Gene Mutations in Human Endometrial Carcinoma

Varras

Koffa²,

Koumantakis³

et al. 1996

Oncology

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“…HPV status was determined by PCR using general primers GP5-GP6 (Snijders et al, 1990) as well as primers specific for HPV11, HPV16, HPV18 and HPV33 (Arends et al, 1991). PCR reaction conditions have been described (Koffa et al, 1994).…”

Section: Cells and Tissuementioning

confidence: 99%

Deregulation of RNA polymerase III transcription in cervical epithelium in response to high-risk human papillomavirus

et al. 2004

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RNA polymerase (pol) III transcription is a major determinant of biosynthetic capacity, providing essential products such as tRNA and 5S rRNA. It is controlled directly by the tumour suppressors RB and p53. High-risk types of human papillomavirus (HPV), such as HPV16, express the oncoproteins E6 and E7 that can inactivate p53 and RB, respectively. Accordingly, both E6 and E7 stimulate pol III transcription in cultured cells. HPV16-positive cervical biopsies express elevated levels of tRNA and 5S rRNA when compared to biopsies that test negative for HPV or are infected with the lower risk HPV11. Integration of viral DNA into the host cell genome stimulates expression of E6 and E7 and correlates with induction of tRNA and 5S rRNA. Expression of mRNA encoding the pol III-specific transcription factor Brf1 also correlates with the presence of integrated HPV16. Brf1 levels are limiting for tRNA and 5S rRNA synthesis in cervical cells. Furthermore, pol III-transcribed genes that do not use Brf1 are not induced in HPV16-positive biopsies. Three complementary mechanisms may therefore allow high-risk HPV to stimulate production of tRNA and 5S rRNA: E6-mediated removal of p53; E7-mediated neutralization of RB; and induction of Brf1. The resultant increase in biosynthetic capacity may contribute to deregulated cell growth.

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“…The oligonucleotides used for K-ras, H-ras and N-ras codon 12 have been previously described [27][28][29]. Taq polymerase was purchased form Gibco BRL.…”

Section: Oligonucleotide Primers and Pcr Amplificationmentioning

confidence: 99%

Detection and Clinical Correlations of ras Gene Mutations in Human Ovarian Tumors

Varras

Sourvinos²,

Diakomanolis

et al. 1999

Oncology

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In epithelial ovarian neoplasms K-ras codon 12 gene mutations show a wide variation fluctuating between 4–39% in invasive carcinomas and 20–48% in borderline malignant tumors. In this study, we showed the pattern of point mutations in codon 12 of the K-ras, H-ras and N-ras genes, using polymerase chain reaction restriction fragment length polymorphism analysis in 74 tissue specimens of Greek patients with epithelial ovarian tumors. K-ras and H-ras gene mutations were detected in 11/48 (23%) and 3/48 (6%) cases with primary invasive ovarian carcinomas, respectively, while N-ras gene mutations were not found. No mutation of K-, H- and N-ras genes was detected in 23 ovarian cystadenomas. In 1 out of 3 borderline ovarian tumors (33%) we found an H-ras gene mutation. The prevalence of mutations in K-ras gene was 1/8 (13%) in mucinous, 7/29 (24%) in serous, 1/3 (33%) in endometrioid and 2/8 (25%) in clear-cell adenocarcinomas and in H-ras gene 1/8 (13%) in mucinous and 2/29 (7%) in serous adenocarcinomas. Analysis of the results revealed no significant correlation between ras gene mutations and clinicopathological parameters or clinical outcome of this primary invasive ovarian carcinoma population. Our present data suggest that ras gene mutations in invasive ovarian carcinomas occur in 29% of Greek patients and are not associated with the differentiation of the epithelial cells or the response of patients to adjuvant platinum-based chemotherapy.

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Detection of Ras Gene-Mutations and HPV in Lesions of the Human Female Reproductive-Tract

Cited by 19 publications

References 20 publications

<i>ras</i> Gene Mutations in Human Endometrial Carcinoma

<i>ras</i> Gene Mutations in Human Endometrial Carcinoma

Deregulation of RNA polymerase III transcription in cervical epithelium in response to high-risk human papillomavirus

Detection and Clinical Correlations of <i>ras</i> Gene Mutations in Human Ovarian Tumors

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