Example sentences for: papillomavirus

How can you use “papillomavirus” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • sunlight, human papillomavirus infection).

  • Recently, it has been shown that the hTERT amplification and over expression is common in CC [ 19 ] . TRIP13 , thyroid receptor interacting protein 13, is a transcription factor that regulates expression of a variety of specific target genes including the human papillomavirus type 16 (HPV16) E1 protein [ 13 ] . Similar to TERT , the TRIP13 also showed very low expression in normal cervix and highly elevated levels of expression in CC cell lines (Fig.

  • Formalin-fixed paraffin-embedded (FFPE) human papillomavirus (HPV) positive cell-lines (SiHa, HeLa and CaSki,) as well as FFPE cervical lesions (pre-invasive and invasive) infected with HPV have been used as model systems.

  • These include, PDCD6 , a protein that plays a role in T cell receptor-, FAS-, and glucocorticoid-induced cell death [ 11 ] ; TERT , a gene that encodes a reverse transcriptase component of telomerase, dysfunction of which promotes chromosomal instability [ 12 ] ; and TRIP13 , a thyroid hormone receptor interacting protein that binds with the human papillomavirus type 16 (HPV16) E1 protein [ 13 ] . We have identified POLS gene that encodes a DNA polymerase sigma, and plays a role in DNA replication and sister chromatid cohesion at the proximal minimal deleted region [ 14 ] . We performed a semi-quantitative RT-PCR analysis of all four genes ( PDCD6 , TERT , TRIP13 , and POLS ) in eight CC cell lines and did not find evidence for lack of or down regulated expression compared to normal cervix (Fig.

  • Converging evidence from epidemiological and molecular studies suggests that infection of genital human papillomavirus (HPV) is causally linked to the development of CC [ 4 ] . Since only a small fraction of HPV-infected cervical intra-epithelial neoplastic (CIN) lesions progress to invasive cancer, these studies further suggest that in addition to HPV, other host genetic factors play a role in cervical carcinogenesis [ 5 ] . A number of molecular studies have identified genetic alterations in these two histologic types of CC and at various stages of precursor lesions [ 6 7 8 ] . Despite this molecular characterization, the genetic basis of CC initiation and progression is still very poorly understood.


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