A Prospective Study of Intraprostatic Inflammation, Focal Atrophy, and Progression to Lethal Prostate Cancer.


Journal

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
ISSN: 1538-7755
Titre abrégé: Cancer Epidemiol Biomarkers Prev
Pays: United States
ID NLM: 9200608

Informations de publication

Date de publication:
12 2019
Historique:
received: 21 06 2019
revised: 15 08 2019
accepted: 11 09 2019
pubmed: 20 9 2019
medline: 12 9 2020
entrez: 20 9 2019
Statut: ppublish

Résumé

Inflammation and focal atrophy are common features adjacent to prostate tumors. Limited evidence exists on whether these features have prognostic significance. In the Health Professionals Follow-Up Study and Physicians' Health Study, we studied 1,035 men diagnosed with prostate cancer. A genitourinary pathologist centrally reviewed tumor and normal areas of hematoxylin and eosin slides from prostate cancer specimens for the presence of acute and chronic inflammation, and four subtypes of focal atrophy. Cox proportional hazards models adjusted for potential confounders were used to estimate HRs and 95% confidence intervals (CI) for the association of these features with lethal prostate cancer, defined as development of metastatic disease or death during follow-up. During a median of 12 years of follow-up, 153 men developed lethal prostate cancer. A total of 84% of men had histologic evidence of chronic inflammation and 30% had acute inflammation. Both chronic and acute inflammation were inversely associated with lethal prostate cancer in age- and lifestyle-adjusted models. Chronic inflammation remained inversely associated with lethal prostate cancer after additionally adjusting for prognostic clinical features (HR = 0.45; 95% CI, 0.30-0.69 for mild and HR = 0.51; 95% CI, 0.33-0.80 for moderate to severe). None of the atrophic lesions were associated with lethal prostate cancer. Our data suggest that the presence of inflammation, particularly chronic inflammation, in prostate cancer tissue is associated with better prognosis among patients with prostate cancer. This is the largest prospective cohort study to examine the association between inflammation, focal atrophy, and lethal prostate cancer.

Sections du résumé

BACKGROUND
Inflammation and focal atrophy are common features adjacent to prostate tumors. Limited evidence exists on whether these features have prognostic significance.
METHODS
In the Health Professionals Follow-Up Study and Physicians' Health Study, we studied 1,035 men diagnosed with prostate cancer. A genitourinary pathologist centrally reviewed tumor and normal areas of hematoxylin and eosin slides from prostate cancer specimens for the presence of acute and chronic inflammation, and four subtypes of focal atrophy. Cox proportional hazards models adjusted for potential confounders were used to estimate HRs and 95% confidence intervals (CI) for the association of these features with lethal prostate cancer, defined as development of metastatic disease or death during follow-up.
RESULTS
During a median of 12 years of follow-up, 153 men developed lethal prostate cancer. A total of 84% of men had histologic evidence of chronic inflammation and 30% had acute inflammation. Both chronic and acute inflammation were inversely associated with lethal prostate cancer in age- and lifestyle-adjusted models. Chronic inflammation remained inversely associated with lethal prostate cancer after additionally adjusting for prognostic clinical features (HR = 0.45; 95% CI, 0.30-0.69 for mild and HR = 0.51; 95% CI, 0.33-0.80 for moderate to severe). None of the atrophic lesions were associated with lethal prostate cancer.
CONCLUSIONS
Our data suggest that the presence of inflammation, particularly chronic inflammation, in prostate cancer tissue is associated with better prognosis among patients with prostate cancer.
IMPACT
This is the largest prospective cohort study to examine the association between inflammation, focal atrophy, and lethal prostate cancer.

Identifiants

pubmed: 31533941
pii: 1055-9965.EPI-19-0713
doi: 10.1158/1055-9965.EPI-19-0713
pmc: PMC6941930
mid: NIHMS1540350
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

2047-2054

Subventions

Organisme : NCI NIH HHS
ID : P30 CA006516
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA006973
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA113913
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA167552
Pays : United States

Informations de copyright

©2019 American Association for Cancer Research.

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Auteurs

Yiwen Zhang (Y)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.

Cindy Ke Zhou (CK)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.

Emily M Rencsok (EM)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.

Katja Fall (K)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Department of Clinical Epidemiology and Biostatistics, School of Health and Medical Sciences, Orebro University Hospital, Orebro, Sweden.

Tamara L Lotan (TL)

Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland.

Massimo Loda (M)

Department of Oncologic Pathology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, New York.

Francesca Giunchi (F)

Department of Pathology, Addarii Institute of Oncology, S.Orsola-Malpighi Teaching Hospital, University of Bologna, Bologna, Italy.

Elizabeth A Platz (EA)

Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.

Angelo M De Marzo (AM)

Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland.

Lorelei A Mucci (LA)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.

Michelangelo Fiorentino (M)

Department of Pathology, Addarii Institute of Oncology, S.Orsola-Malpighi Teaching Hospital, University of Bologna, Bologna, Italy.

Ericka M Ebot (EM)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. enoonan@hsph.harvard.edu.

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