Example sentences for: carcinogenesis

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

  • The cyclooxygenase pathway and NSAIDs have been implicated in pancreatic carcinogenesis, as elevated levels of COX-2 mRNA and protein have been detected in pancreatic carcinomas relative to histologically normal cells [ 14 15 16 17 18 19 ] . Further, both aspirin [ 20 21 22 ] and other NSAIDs [ 19 ] have been shown to inhibit pancreatic cancer cell proliferation and induce apoptosis in vitro . Recent studies have also reported an association between oncogenic ras and COX-2 expression [ 23 24 ] . Since pancreatic tumors tend to exhibit a high frequency of K- ras mutations [ 25 ] , the relationship between the K- ras oncogene and COX-2 should be explored further in vivo.

  • 3% of invasive CC, and 11% and 29% of low- and high-grade CIN lesions, respectively [ 12 ] . These authors suggest that RARB methylation is an early event in multistage cervical carcinogenesis.

  • [ 9 ] , but employed far greater doses of aspirin (45 and 90 mg/kg/day) and reported no dose-response relationship and a maximal suppression of 55% [ 7 ] . Furthermore, in the rat model of azoxymethane-induced colon carcinogenesis, aspirin has also only been found to inhibit aberrant crypt foci and tumour development by no more than 65% [ 4 39 ] . Coincidentally, epidemiological data also report reductions in the 40-50% range [ 13 14 15 32 ] . However, whether this can be used as an argument to support the notion that aspirin is only able to suppress tumour formation by 50% is difficult to extrapolate because two different end points are being examined (i.e.

  • Wnt-1 TG mice have been used to assess the functions of a number of genetic lesions in breast carcinogenesis because tumors appear with predictable kinetics.

  • 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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