No abstract available.
Female ; Humans

No abstract available.

No abstract available.
Cell Culture Techniques* ; Chorionic Gonadotropin* ; Epidermal Growth Factor* ; Humans* ; Trophoblasts*

Although squamous cell carcinomas compose the majority of invasive cervical cancers, adenocarcinomas account for 10-20% of cervical cancers. Human papillomavirus (HPV) types 16 and 18 are strongly involved in the development of cervical neoplastic lesions squamous cell type. However, little is known about the association of HPV with adenocarcinoma because of its rarity, The p53 gene acts as a tumor suppressor and has been implicated in controlling cell cycle progression at the Gl-S transition, and absence or mutant of p53 gene is related to tumor progression. The present study was undertaken to identify clinical profiles, to characterize HPV infection status and p53 overexpression in the cervical adenocarcinoma and to investigate the prognostic significance of these findings. Thirty-six paraffin-embedded tumor tissues were obtained and patients clinical records were reviewed from tumor registry. Tissues were analyzed for the detection of HPV 16/1S by multiplex PCR and for the expression of p53 protein by immunohistochemical staining. Eighty-four percent of the cases were positive for HPV 16 and/or 18. HPV 16 positive rate was 36.1%, HPV 18 was 72.2%. The rate of double infection with HPV 16 and 18 was 25.0%. The p53 overexpression was detected in 11.1%. The overall 5 year-survival rate (YSR) was 72.2%. There were no significant difference in survival rate between HPV 18-positive and HPV 18-negative groups. The 5 YSR of the p53-positive group was 25.0% and that of p53-negative group was 78.1% (p=0.174). Inverse relationship between p53 overexpression and HPV DNA positivity was not found. In cervical adenocarcinoma, HPV type 18 was detected as the predo#minant type and may play a role in the carcinogenic process.
Adenocarcinoma ; Carcinoma, Squamous Cell ; Cell Cycle ; Cervix Uteri* ; DNA ; Female ; Genes, p53 ; Human papillomavirus 16 ; Human papillomavirus 18 ; Humans* ; Multiplex Polymerase Chain Reaction ; Polymerase Chain Reaction ; Survival Rate

Human papillomavirus (HPV)infection are now generally accepted as the most important factor for development of uterine cervical cancer and its precursor lesions. With increasing evidences that the HPV E7 encodes for oncoproteins critical for viral replication, host cell immortalization and transformation. Based on the previous reports that the high risk HPV type 16 DNA is frequently detected in specimens from Korean women with cervical cancer and that there is the sequence variation and geographical dependence of HPV 16 E7 gene in preinvasive and invasive cervical lesions, it is crucial to determine the prevalence of HPV 16 variants in uterine cervical lesions of Korean women. This study was performed to identify sequence variations of HPV 16 E7 gene and an association between HPV 16 E7 variants and uterine cervical cancer. The author has determined nucleotide sequences of the E7 gene of HPV 16 isolated from uterine cervical tissues in Korean women. HPV 16 DNAs were detected by the nested PCR in 112 (24.5%) of a total of 457 samples. By direct sequencing of PCR-HPV 16 E7 positive cases, 79 samples (70.5%) showed variant sequences, while the prototype sequence was found in only 33 samples (29.5%). Twenty-three cases (57.5%) of 40 normal cervical samples showed sequence variation. Forty-eight (77.4%) of 62 cervical cancer cases showed sequence diversity from prototype HPV 16 E7 gene. There were four types of sequence variations. A single nucleotide change at position 647 (A-->G) was found in 52 cases (65.8%) of 79 HPV 16 E7 variants. Predicted amino acid change (Asn -->Ser) was found in the HPV 16 E7 oncoproteins at amino acid position at 29. And this KE7-1 variant was commonly detected in the uterine cervical cancer compared to the normal cervix. The second most common variant, detected in 16 cases (20.3%), had three silent mutations at nucleotide positions 732 (T-->C), 789 (T-->C) and 795 (T-->G). The third variant had a single nucleotide change at position 666 (G-->A), and the fourth had a change at position 796 (T-->C). Furthermore, PCR-SSCP clearly showed distinct bands compatible with HPV 16 E7 variants as with the direct-sequencing method. PCR-SSCP was also an effective and reliable tool in detecting HPV 16 E7 variants. This study showed that there were four variant types of HPV 16 E7 in uterine cervical tissues and KE7-1 with corresponding amino acid change was the most commonly detected type in E7 variants of HPV 16 isolated from uterine cervical cancer in Korean women.
Base Sequence ; Cervix Uteri ; DNA ; Female ; Human papillomavirus 16 ; Humans* ; Oncogene Proteins ; Polymerase Chain Reaction ; Polymorphism, Genetic* ; Prevalence ; Uterine Cervical Neoplasms*

No abstract available.
Epidermal Growth Factor* ; Receptor, Epidermal Growth Factor* ; Uterine Cervical Neoplasms*

No abstract available.
Epidermal Growth Factor* ; Receptor, Epidermal Growth Factor* ; Uterine Cervical Neoplasms*

bcl-2 prevents cell death from a wide variety of stimuli and provides survival of cells with accumulated genetic alterations and c-myc can promote both cell proliferation and cell death through the transcriptional regulation of target genes. Although several studies have been reported on the expression of bcl-2 or c-myc separately, little has been known about the role of coexpression of bcl-2 and c-myc to cell proliferation and apoptosis, as well as the frequency of these coexpression in cervical cancer specimens. In this study, we have examined the expression of bcl-2 and c-myc in cervical cancer specimens and cervical intraepithelial neoplasia(CIN) to determine the role of coexpression of bcl-2 and c-myc during progression into cervical cancer. Proteins and transcripts of bcl-2 and c-myc were evaluated by immunohistochemistry in 60 clinical specimens(20 cervical cancer, 30 CIN, and 10 normal cervix). In addtion, we evaluated kinetic indices of cell proliferation and apoptosis simultaneously. The cell proliferation index was determined by detection of the Ki- 67 in immunohistochemistry. Apoptotic index was determined by the detection of apoptotic cells with TUNEL staining. Medical records including pathologic reports were reviewed. Overexpression of bcl-2 and c-myc was identified in 7(35%) and 10(50%) of 20 cervical cancer specimens respectively, but none in normal cervix and CIN samples. In addition, coexpression of bcl-2 and c-myc was found in 5(25%) of 20 cervical cancer specimens. The cell proliferation index increased with progression from normal to CIN and invasive cancer(normal cervix, 10.2; CIN 1, 24.1; CIN 2/3 59.7; cervical cancer, 71.2; p <0.01). The apoptotic index also increased with grade of lesions(normal cervix, 0; CIN 1, 0.33; CIN 2/3, 1.85; cervical cancer, 3.89; p <0.01) and showed a significant correlation with proliferation index(r=0.7451, p=0.0002). However, there was no significant difference in apoptotic index between bcl-2 positive and bcl-2 negative group in cervical cancer(p=0.4765). In addition, there was also no significant difference in cell proliferation between c-myc positive and c-myc negative group(p=0.6891). Furthermore, there was no significant difference in cell proliferation and apoptosis between bcl-2 and c-myc positive group and others in cervical cancer(p=0.6311 and p=0.7600 respectively). The well-known clinicopathologic parameters, including tumor diameter, FIGO clinical stage, lymph node metastasis, did not correlate with simultanuos positive immunoreactivity for bcl-2 and c-myc proteins in cervical cancer. In conclusion, the cell proliferation and apoptosis increase with increasing lesion grade of cervical neoplasia and apoptosis correlates with cell proliferation. In addition, overexpression of bcl-2 and/or c-myc may be genetic alteration found only in cervical cancer and may not play a role in the development and progression of CIN. However, neither bcl-2 nor c-myc immunoreactivity correlated with the proliferation index or apoptotic index. These results suggest that other factors may also play a role in controlling the cell proliferation and apoptosis of cervical cancer.
Apoptosis* ; Cell Death ; Cell Proliferation ; Cervical Intraepithelial Neoplasia* ; Cervix Uteri ; Female ; Immunohistochemistry ; In Situ Nick-End Labeling ; Lymph Nodes ; Medical Records ; Neoplasm Metastasis ; Proto-Oncogene Proteins c-myc ; Uterine Cervical Neoplasms

Carcinoma of the uterine cervix has been considered to be a sexually transmitted disease(STD) and at present time, particullary human papillomavirus (HPV) is considered as the most likely infectious causative agents of uterine cervical cancer. But less is known about the sexual transmission of HPV and the status of HPV infection of male partner. Therefore, screenng of couples for HPV is very important for understanding HPV infection as a sexually transmitted disease and prevention of cervical carcinoma. The polymerase chain reaction(PCR) was employed to detect HPV 16 and 18 in cytological samples from the uterine cervix of the patients with cervical carcinoma(4 CIS and 34 invasive cervical carcinoma) and from urethral metatus and glans sulcus of their male consorts. The results are as follows; 1. HPV 16 or 18 were detected in 31(81.6%) of 38 patients with cervical cancer(HPV 16; 78.9%(30/38), HPV 1S; 28.9%(11/38), HPV 16 and 18; 26.3%(10/38)), 2. HPV 16 was detected in 27(90,0%) of 30 males whose wives were positive for HPV 16. But HPV 18 was detected in only 3(27.3%) of 11 male consorts whose wives were positive for HPV 18. And HPV 1S was detected in all male consorts whose wives were positive for HPV 16. In addition, HPV 16 or 18 were positive in 3 of 7(42.9%) male consorts whose wives were negative for HPV 16 and 18. Conclusively, these results suggest that HPV might be transmitted by sexual contacts in heterosexual couples.
Cervix Uteri ; Family Characteristics* ; Female ; Heterosexuality* ; Human papillomavirus 16 ; Human papillomavirus 18 ; Humans* ; Male ; Polymerase Chain Reaction ; Sexually Transmitted Diseases ; Spouses ; Uterine Cervical Neoplasms

No abstract available.
DNA* ; Uterine Cervical Neoplasms*