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Conference Paper: The adipokines TNF-alpha and IL6 predicted incident cancer development in a Chnese community-based cohort

TitleThe adipokines TNF-alpha and IL6 predicted incident cancer development in a Chnese community-based cohort
Authors
Issue Date2012
PublisherBioScientifica.
Citation
The 15th International and 14th European Congress of Endocrinology (ICE/ECE 2012), Florence, Italy, 5-9 May 2012. In Endocrine Abstracts, 2012, v. 29, p. 1210 How to Cite?
AbstractAdipose tissue is recognized as an active endocrine organ. Cytokines released from adipocytes induce chronic low-grade inflammation, which is linked to the development of cardiovascular diseases and malignancy.In this study, we examined the relationship between baseline adipokines level and incident cancer risk in a community-based cohort of Chinese subjects. Subjects were recruited from the Hong Kong Cardiovascular Risk Factors Prevalence Study 2(CRISPS 2) cohort. Those with known malignancy were excluded. Fasting blood forglucose, insulin, lipids, the adipokines interleukin-6 (IL6), soluble tumor necrosis factor receptor 2 (sTNFR2, as a surrogate marker of tumor necrosis factor-alpha), adiponectin and adipocyte-fatty acid binding protein (A-FABP) levels was collected at baseline. Incident cancer cases were identified after a median follow up of 9.6 years. 1897 subjects were included in the final analysis. During the study period, 94 subjects developed cancers. Compared to subjects with no cancer, subjects who developed cancer were older at baseline (61.0±11.5 vs 51.9±11.8, P<0.001), had a higher proportion of males (59.6 vs 45.9%, P=0.009), central obesity (38.3 vs 29.6%, P=0.008), diabetes (27.7 vs 14.8%, P=0.036), hypertension (36.2 vs 26.7%, P=0.045) and dyslipidemia (71.9 vs 60.6%, P=0.013). They had a higher serum level of IL6 (0.78 vs 0.58 pg/ml in male, 0.65 vs 0.54 pg/ml in female, P<0.001), sTNFR2 (2419.2 vs 1991.7 ng/ml in male, 2051.7 vs 1816.0 ng/ml in female, P<0.001) and A-FABP (21.0 vs 19.0 ng/ml in male, 24.2 vs 27.9 ng/ml in female, P=0.02). Adiponectin level between the two groups was not significantly different. After adjustment for conventional risk factors, only baseline IL6 (HR 1.51, 95% CI 1.16–1.97) and sTNFR2 (HR 2.36, 95%CI 1.16–4.81) predicted incident cancer development. Our data supported the hypothesis that chronic low grade inflammation caused by obesity could increase the risk of malignancy.
Persistent Identifierhttp://hdl.handle.net/10722/196397
ISSN

 

DC FieldValueLanguage
dc.contributor.authorYeung, CYen_US
dc.contributor.authorTso, AWKen_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorLam, THen_US
dc.contributor.authorLo, SVen_US
dc.contributor.authorFong, Cen_US
dc.contributor.authorWat, Nen_US
dc.contributor.authorWoo, Jen_US
dc.contributor.authorCheung, BMYen_US
dc.contributor.authorLam, KSL-
dc.date.accessioned2014-04-07T03:24:27Z-
dc.date.available2014-04-07T03:24:27Z-
dc.date.issued2012en_US
dc.identifier.citationThe 15th International and 14th European Congress of Endocrinology (ICE/ECE 2012), Florence, Italy, 5-9 May 2012. In Endocrine Abstracts, 2012, v. 29, p. 1210en_US
dc.identifier.issn1470-3947-
dc.identifier.urihttp://hdl.handle.net/10722/196397-
dc.description.abstractAdipose tissue is recognized as an active endocrine organ. Cytokines released from adipocytes induce chronic low-grade inflammation, which is linked to the development of cardiovascular diseases and malignancy.In this study, we examined the relationship between baseline adipokines level and incident cancer risk in a community-based cohort of Chinese subjects. Subjects were recruited from the Hong Kong Cardiovascular Risk Factors Prevalence Study 2(CRISPS 2) cohort. Those with known malignancy were excluded. Fasting blood forglucose, insulin, lipids, the adipokines interleukin-6 (IL6), soluble tumor necrosis factor receptor 2 (sTNFR2, as a surrogate marker of tumor necrosis factor-alpha), adiponectin and adipocyte-fatty acid binding protein (A-FABP) levels was collected at baseline. Incident cancer cases were identified after a median follow up of 9.6 years. 1897 subjects were included in the final analysis. During the study period, 94 subjects developed cancers. Compared to subjects with no cancer, subjects who developed cancer were older at baseline (61.0±11.5 vs 51.9±11.8, P<0.001), had a higher proportion of males (59.6 vs 45.9%, P=0.009), central obesity (38.3 vs 29.6%, P=0.008), diabetes (27.7 vs 14.8%, P=0.036), hypertension (36.2 vs 26.7%, P=0.045) and dyslipidemia (71.9 vs 60.6%, P=0.013). They had a higher serum level of IL6 (0.78 vs 0.58 pg/ml in male, 0.65 vs 0.54 pg/ml in female, P<0.001), sTNFR2 (2419.2 vs 1991.7 ng/ml in male, 2051.7 vs 1816.0 ng/ml in female, P<0.001) and A-FABP (21.0 vs 19.0 ng/ml in male, 24.2 vs 27.9 ng/ml in female, P=0.02). Adiponectin level between the two groups was not significantly different. After adjustment for conventional risk factors, only baseline IL6 (HR 1.51, 95% CI 1.16–1.97) and sTNFR2 (HR 2.36, 95%CI 1.16–4.81) predicted incident cancer development. Our data supported the hypothesis that chronic low grade inflammation caused by obesity could increase the risk of malignancy.-
dc.languageengen_US
dc.publisherBioScientifica.-
dc.relation.ispartofEndocrine Abstracts-
dc.titleThe adipokines TNF-alpha and IL6 predicted incident cancer development in a Chnese community-based cohorten_US
dc.typeConference_Paperen_US
dc.identifier.emailYeung, CY: ycy167@hku.hken_US
dc.identifier.emailTso, AWK: awktso@hku.hken_US
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_US
dc.identifier.emailLam, TH: hrmrlth@hkucc.hku.hken_US
dc.identifier.emailLo, SV: losv@hkucc.hku.hken_US
dc.identifier.emailCheung, BMY: mycheung@hku.hken_US
dc.identifier.emailLam, KSL: ksllam@hku.hken_US
dc.identifier.authorityTso, AWK=rp00535en_US
dc.identifier.authorityXu, A=rp00485en_US
dc.identifier.authorityLam, TH=rp00326en_US
dc.identifier.authorityCheung, BMY=rp01321en_US
dc.identifier.authorityLam, KSL=rp00343en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros228525en_US
dc.identifier.volume29en_US
dc.identifier.spage1210en_US
dc.identifier.epage1210en_US
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl1470-3947-

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