Plasma Fibrinogen and sP-Selectin are Associated with the Risk of Lung Cancer in a Prospective Study.


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:
07 2019
Historique:
received: 29 11 2018
revised: 08 03 2019
accepted: 11 04 2019
pubmed: 25 4 2019
medline: 10 9 2020
entrez: 25 4 2019
Statut: ppublish

Résumé

While enhanced platelet activation and a procoagulant state may drive lung cancer progression and metastases, less is known about their role in earlier phases of cancer development. Thus, we evaluated whether prediagnostic biomarkers of platelet activation and coagulation are related to the risk of lung cancer in the prospective EPIC-Heidelberg Study using a case-cohort design. Levels of fibrinogen, soluble glycoprotein (sGP) IIb/IIIa, soluble P-selectin (sP-selectin), soluble thrombomodulin (sTM), and thrombopoietin (TPO) were measured in baseline plasma samples of a random subcohort ( Fibrinogen [HR highest vs. lowest quartile: 1.91 (95% confidence interval: 1.09-3.34)] and sP-Selectin [HR: 2.51 (1.39-4.52)] were significantly associated with lung cancer risk in multivariable adjusted Cox regression models. Adding both biomarkers to the established PLCO Our findings indicate that enhanced platelet activation and a procoagulative state contribute to lung carcinogenesis. The current prospective study supports the hypothesis of increased coagulation being a possible driver of lung carcinogenesis, as strong positive associations were found between two procoagulative markers, sP-Selectin and fibrinogen, with lung cancer risk. Both biomarkers could improve lung cancer risk prediction, but external validation of the results is needed.

Sections du résumé

BACKGROUND
While enhanced platelet activation and a procoagulant state may drive lung cancer progression and metastases, less is known about their role in earlier phases of cancer development. Thus, we evaluated whether prediagnostic biomarkers of platelet activation and coagulation are related to the risk of lung cancer in the prospective EPIC-Heidelberg Study using a case-cohort design.
METHODS
Levels of fibrinogen, soluble glycoprotein (sGP) IIb/IIIa, soluble P-selectin (sP-selectin), soluble thrombomodulin (sTM), and thrombopoietin (TPO) were measured in baseline plasma samples of a random subcohort (
RESULTS
Fibrinogen [HR highest vs. lowest quartile: 1.91 (95% confidence interval: 1.09-3.34)] and sP-Selectin [HR: 2.51 (1.39-4.52)] were significantly associated with lung cancer risk in multivariable adjusted Cox regression models. Adding both biomarkers to the established PLCO
CONCLUSION
Our findings indicate that enhanced platelet activation and a procoagulative state contribute to lung carcinogenesis.
IMPACT
The current prospective study supports the hypothesis of increased coagulation being a possible driver of lung carcinogenesis, as strong positive associations were found between two procoagulative markers, sP-Selectin and fibrinogen, with lung cancer risk. Both biomarkers could improve lung cancer risk prediction, but external validation of the results is needed.

Identifiants

pubmed: 31015200
pii: 1055-9965.EPI-18-1285
doi: 10.1158/1055-9965.EPI-18-1285
doi:

Substances chimiques

Selectins 0
Fibrinogen 9001-32-5

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1221-1227

Informations de copyright

©2019 American Association for Cancer Research.

Auteurs

Mirja Grafetstätter (M)

Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Anika Hüsing (A)

Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Member of the German Center for Lung Research (DZL), Translational Lung Research Center (TLRC), Heidelberg, Germany.

Sandra González Maldonado (S)

Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Disorn Sookthai (D)

Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Theron Johnson (T)

Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Laura Pletsch-Borba (L)

Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Verena A Katzke (VA)

Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Michael Hoffmeister (M)

Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Peter Bugert (P)

Institute of Transfusion Medicine and Immunology, Heidelberg University, Medical Faculty Mannheim, and German Red Cross Blood Service Baden-Württemberg-Hessen, Mannheim, Germany.

Rudolf Kaaks (R)

Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Member of the German Center for Lung Research (DZL), Translational Lung Research Center (TLRC), Heidelberg, Germany.

Tilman Kühn (T)

Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. t.kuehn@dkfz.de.

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