Open Access

Link between chronic inflammation and human papillomavirus-induced carcinogenesis (Review)

  • Authors:
    • José Veríssimo Fernandes
    • Thales Allyrio Araújo de Medeiros Fernandes
    • Jenner Chrystian Veríssimo de Azevedo
    • Ricardo Ney Oliveira Cobucci
    • Maria Goretti Freire de Carvalho
    • Vania Sousa Andrade
    • Josélio Maria Galvão de Araújo
  • View Affiliations

  • Published online on: January 16, 2015     https://doi.org/10.3892/ol.2015.2884
  • Pages: 1015-1026
  • Copyright: © Fernandes et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Inflammation is a defense strategy against invading agents and harmful molecules that is activated immediately following a stimulus, and involves the release of cytokines and chemokines, which activate the innate immune response. These mediators act together to increase blood flow and vascular permeability, facilitating recruitment of effector cells to the site of injury. Following resolution of the injury and removal of the stimulus, inflammation is disabled, but if the stimulus persists, inflammation becomes chronic and is strongly associated with cancer. This is likely to be due to the fact that the inflammation leads to a wound that does not heal, requiring a constant renewal of cells, which increases the risk of neoplastic transformation. Debris from phagocytosis, including the reactive species of oxygen and nitrogen that cause damage to DNA already damaged by the leukotrienes and prostaglandins, has an impact on inflammation and various carcinogenic routes. There is an association between chronic inflammation, persistent infection and cancer, where oncogenic action is mediated by autocrine and paracrine signals, causing changes in somatic cells under the influence of the microbial genome or of epigenetic factors. Among the infectious agents associated with cancer, certain genotypes of human papillomavirus (HPV) stand out. HPV is responsible for virtually all cases of cervical cancer and a lower proportion of cancers of the vagina, vulva, anus, penis and a number of extragenital cancers. In the present review, recent advances in the mechanisms involved in the inflammatory response are presented with their participation in the process of carcinogenesis, emphasizing the role of chronic inflammation in the development of HPV‑induced cervical cancer.
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March-2015
Volume 9 Issue 3

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Spandidos Publications style
Fernandes JV, Fernandes TA, de Azevedo JC, Cobucci RN, de Carvalho MG, Andrade VS and de Araújo JM: Link between chronic inflammation and human papillomavirus-induced carcinogenesis (Review). Oncol Lett 9: 1015-1026, 2015.
APA
Fernandes, J.V., Fernandes, T.A., de Azevedo, J.C., Cobucci, R.N., de Carvalho, M.G., Andrade, V.S., & de Araújo, J.M. (2015). Link between chronic inflammation and human papillomavirus-induced carcinogenesis (Review). Oncology Letters, 9, 1015-1026. https://doi.org/10.3892/ol.2015.2884
MLA
Fernandes, J. V., Fernandes, T. A., de Azevedo, J. C., Cobucci, R. N., de Carvalho, M. G., Andrade, V. S., de Araújo, J. M."Link between chronic inflammation and human papillomavirus-induced carcinogenesis (Review)". Oncology Letters 9.3 (2015): 1015-1026.
Chicago
Fernandes, J. V., Fernandes, T. A., de Azevedo, J. C., Cobucci, R. N., de Carvalho, M. G., Andrade, V. S., de Araújo, J. M."Link between chronic inflammation and human papillomavirus-induced carcinogenesis (Review)". Oncology Letters 9, no. 3 (2015): 1015-1026. https://doi.org/10.3892/ol.2015.2884