ABSTRACT
Objective To investigate the relationship between the amplification of human telomerase reverse tran-scriptase (hTERT) gene and high-risk human papillomavirus (HR-HPV) infections in cervical intraepithelial neoplasia (CIN) and cervical carcinoma. Methods The cervical epithelial cells were collected from 34 samples of normal cervical epithelium, 31 samples of CIN (gradeⅠ), 33 samples of CIN (gradeⅡ), 34 samples of CIN (gradeⅢ) and 20 samples of cer-vical carcinoma. HPV DNA was detected by polymerase chain reaction-reverse dot blot hybridization (PCR-RDB) and the amplification of hTERT gene was detected by fluorescence in situ hybridization (FISH). Results Twenty subtypes of HR-HPV were detected including HPV16, 18, 26, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66, 67, 68, 69, 73 and 82. The inci-dence of HR-HPV infection was higher in CINⅡgroup (72.73%), CINⅢgroup (85.29%) and cervical carcinoma group (90.00%) than that of normal cervical epithelium group (20.59%). There was no significant difference in the positive rate of HR-HPV DNA between CINⅠ group (54.84%) and normal cervical epithelium group (P < 0.005). The positive rate of hTERT gene amplification was higher in cervical carcinoma group (80.00%) than that of normal cervical epithelium group (0). There were no significant differences in the positive rates of hTERT gene amplification between CINⅠgroup ( 3.22%), CIN Ⅱ group (18.18%), cervical carcinoma group and CIN Ⅲ group (41.18%). There was positive correlation between hTERT gene amplification and HR-HPV infection (r=0.238, P<0.05). Conclusion The incidence of HR-HPV infection was positively correlated with hTERT gene amplification in cervical lesions. HR-HPV infection may be an early event of ab-normal amplification of hTERT gene. The detection of HPV-DNA and hTERT gene can be used in the clinical diagnosis of early cervical lesions.
ABSTRACT
Nobel Prize 2009 in Physiology or Medicine is awarded to three American scientists, Elizabeth H.Blackburn, Carol W.Greider and Jack W.Szostak, for the discovery of"how the chromosomes are protected by telomeres and the enzyme telomerase".Telomere is the specific structure at the ends of the chromosomes and protects it from fusion and degradation.Telomerase synthesizes telomere DNA to maintain the telomere length.Studies suggest that telomere length and telomerase activity is directly associated with cell life and the genesis of many diseases.With the progress of study, how to control the telomere length and telomerase activity is helpful to shed light on the studies in"cancer, inherited diseases and senescence", and will stimulate the development of potential new therapies.
ABSTRACT
Telomere is the end structure of chromosome and it will be shortened during replication． Telomerase is a reverse transcripatse consisting of both RNA and protein components and synthesizes telomeric DNA by copying the template sequence of its own RNA components to maintain telomere length for function．Telomerase activity in germline cells，immortal and neoplastic cells was detected，but not in mostly normal cells．The telomere-telomerase hypothesis was brung out to explain this phenomenon．According to this hypothesis，re-actived telomerase will maintain telomere's length for protecting chromosome to make the cell immortal．The aging procedure will be explained by this hypothesis too．This hypothesis provides a new concepts of cancer and cancer's treatment．