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Inflammation, prostatitis, proliferative inflammatory atrophy: 'Fertile ground' for prostate cancer development?

G Perletti, E Montanari, Anne Vral UGent, G Gazzano, E Marras, Sylvia Mione UGent and V Magri (2010) MOLECULAR MEDICINE REPORTS. 3(1). p.3-12
abstract
Inflammatory processes caused by chemical, physical or biological agents are known to be important cofactors in the pathogenesis of human cancer. In the prostate, epithelial tissue damage followed by cell regeneration in the presence of inflammation is believed to be a key event in neoplastic transformation. According to the 'injury and regeneration' model, inflammatory cells infiltrating the prostate release reactive species in response to bacterial/viral infection, uric acid, or dietary prostate carcinogens. Besides inducing inflammation, tissue injury by these and other agents would promote the appearance of proliferative inflammatory atrophy (PIA). A subset of proliferating atrophic cells - possibly showing stem-cell features - may be exposed to the genotoxic insult of free radicals and to an increased rate of mutations and chromosomal aberrations. ultimately leading to neoplastic initiation, promotion and progression. In the last decade, the link between inflammation and cancer and the hypothesis pointing to PIA as a risk lesion for prostate cancer have been extensively investigated at the pre-clinical, clinical, morphological, cellular and molecular levels. In this article., recent reports describing Supportive or negative evidence on the link between prostate inflammation, atrophy and cancer are schematically reviewed.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
BASAL-CELL HYPERPLASIA, SEQUENCE VARIANTS, EXPRESSION, NONSTEROIDAL ANTIINFLAMMATORY DRUGS, DNA ADDUCT FORMATION, INTRAEPITHELIAL-NEOPLASIA, ANDROGEN RECEPTOR, C-MYC, NEEDLE BIOPSIES, POSTATROPHIC HYPERPLASIA
journal title
MOLECULAR MEDICINE REPORTS
Mol. Med. Rep.
volume
3
issue
1
pages
10 pages
publisher
SPANDIDOS PUBL LTD
place of publication
ATHENS
Web of Science type
Article
Web of Science id
000272753700001
JCR category
MEDICINE, RESEARCH & EXPERIMENTAL
JCR impact factor
0.307 (2010)
JCR rank
99/105 (2010)
JCR quartile
4 (2010)
ISSN
1791-2997
DOI
10.3892/mmr_00000211
language
English
UGent publication?
yes
classification
A1
copyright statement
I don't know the status of the copyright for this publication
id
844016
handle
http://hdl.handle.net/1854/LU-844016
date created
2010-01-28 11:53:33
date last changed
2010-02-05 14:55:47
@article{844016,
  abstract     = {Inflammatory processes caused by chemical, physical or biological agents are known to be important cofactors in the pathogenesis of human cancer. In the prostate, epithelial tissue damage followed by cell regeneration in the presence of inflammation is believed to be a key event in neoplastic transformation. According to the 'injury and regeneration' model, inflammatory cells infiltrating the prostate release reactive species in response to bacterial/viral infection, uric acid, or dietary prostate carcinogens. Besides inducing inflammation, tissue injury by these and other agents would promote the appearance of proliferative inflammatory atrophy (PIA). A subset of proliferating atrophic cells - possibly showing stem-cell features - may be exposed to the genotoxic insult of free radicals and to an increased rate of mutations and chromosomal aberrations. ultimately leading to neoplastic initiation, promotion and progression. In the last decade, the link between inflammation and cancer and the hypothesis pointing to PIA as a risk lesion for prostate cancer have been extensively investigated at the pre-clinical, clinical, morphological, cellular and molecular levels. In this article., recent reports describing Supportive or negative evidence on the link between prostate inflammation, atrophy and cancer are schematically reviewed.},
  author       = {Perletti, G and Montanari, E and Vral, Anne and Gazzano, G and Marras, E and Mione, Sylvia and Magri, V},
  issn         = {1791-2997},
  journal      = {MOLECULAR MEDICINE REPORTS},
  keyword      = {BASAL-CELL HYPERPLASIA,SEQUENCE VARIANTS,EXPRESSION,NONSTEROIDAL ANTIINFLAMMATORY DRUGS,DNA ADDUCT FORMATION,INTRAEPITHELIAL-NEOPLASIA,ANDROGEN RECEPTOR,C-MYC,NEEDLE BIOPSIES,POSTATROPHIC HYPERPLASIA},
  language     = {eng},
  number       = {1},
  pages        = {3--12},
  publisher    = {SPANDIDOS PUBL LTD},
  title        = {Inflammation, prostatitis, proliferative inflammatory atrophy: 'Fertile ground' for prostate cancer development?},
  url          = {http://dx.doi.org/10.3892/mmr\_00000211},
  volume       = {3},
  year         = {2010},
}

Chicago
Perletti, G, E Montanari, Anne Vral, G Gazzano, E Marras, Sylvia Mione, and V Magri. 2010. “Inflammation, Prostatitis, Proliferative Inflammatory Atrophy: ‘Fertile Ground’ for Prostate Cancer Development?” Molecular Medicine Reports 3 (1): 3–12.
APA
Perletti, G, Montanari, E., Vral, A., Gazzano, G., Marras, E., Mione, S., & Magri, V. (2010). Inflammation, prostatitis, proliferative inflammatory atrophy: “Fertile ground” for prostate cancer development? MOLECULAR MEDICINE REPORTS, 3(1), 3–12.
Vancouver
1.
Perletti G, Montanari E, Vral A, Gazzano G, Marras E, Mione S, et al. Inflammation, prostatitis, proliferative inflammatory atrophy: “Fertile ground” for prostate cancer development? MOLECULAR MEDICINE REPORTS. ATHENS: SPANDIDOS PUBL LTD; 2010;3(1):3–12.
MLA
Perletti, G, E Montanari, Anne Vral, et al. “Inflammation, Prostatitis, Proliferative Inflammatory Atrophy: ‘Fertile Ground’ for Prostate Cancer Development?” MOLECULAR MEDICINE REPORTS 3.1 (2010): 3–12. Print.