Risk factors and histological outcome of abnormal cervix with human papilloma infection in northeastern Thai-women.

This study aimed to investigate the histological outcome of cervix with human papillomavirus (HPV) infection and the association of risk factors with cervical intraepithelial neoplasia (CIN) and invasive cervical carcinoma (ICC) development in Northeast Thai women. The study population (n=210) comprised 71 cases of normal cervix, 71 cases of CIN and 68 cases of ICC. The histological outcome of HPV infection was determined for 9.5% of the study population. Increased risk factors for CIN were observed for more than one partner (odds ratio (OR)=3.75, p<0.05), history of sexually transmitted disease (STD) (OR=2.28, p<0.05), menarche under 14 years of age (OR=0.31, p<0.05) and partners' smoking history (OR=3.98, p<0.01). Increased risk for ICC was observed for those with a history of STDs (OR=0.14, p<0.01) and multiparity (OR=2.53, p<0.01). Age at first sexual intercourse was not a risk factor in this study population. Further studies with HPV-DNA tests should more precisely quantify the risks.

Chromosome 3p alterations in northeastern Thai women with cervical carcinoma.

The purpose of this study was to determine the incidence of the loss of heterozygosity (LOH) among normal cervixes, cervical intraepithelial neoplasias (CINs) and invasive cervical cancers (ICCs). DNA samples (136) were obtained from 31 normal cervixes, 49 CINs and 56 ICCs. Four polymorphic microsatellite markers (D3S1300, D3S1351, D3S1478 and D3S4103) covering the chromosome 3p arm, were employed. LOH at one or more loci were identified in: 9/31 (8.1%) normal cervixes, 17/49 (14.6%) CINs and 26/56 (22.1%) invasive cancers. The incidence of the LOH at 3p varied for each locus and ranged from 5.6% for D3S1351 to the highest rate of 16.6% for D3S1300. We thus found that LOH of chromosome 3p can occur in normal cervixes and that incidences increase in CINs and ICCs. Deletion in the 3p14.2 (D3S1300) and 3p21.2 (D3S1478) regions might be an early event and, in fact, necessary for cervical cancer progression. The loss of function of tumor suppressor genes (TSGs) located in these regions may have a sequential effect in cervical cancer carcinogenesis.