Circulating inflammatory cytokines and risk of five cancers: a Mendelian randomization analysis

PRACTICAL Consortium; Emmanouil Bouras; Ville Karhunen; Dipender  Gill; Jian Huang; Philip C Haycock; Marc J.  Gunter; Mattias J Johansson; Paul Brennan; Tim J Key; Sarah J Lewis; Richard M Martin; Neil Murphy; Elizabeth A. Platz; Ruth C.  Travis; James Yarmolinsky; Verena Zuber; Paul B Martin; Michail Katsoulis; Heinz Freisling; Therese Haugdahl Nøst; Matthias B. Schulze; Laure Dossus; Rayjean J. Hung; Christopher I. Amos; Ari V Ahola-Olli; Saranya Palaniswamy; Minna Männikkö; Juha Auvinen; Karl-Heinz Herzig; Sirkka Keinänen-Kiukaanniemi; Terho Lehtimäki; Veikko Salomaa; Olli Raitakari; Marko Salmi; Sirpa Jalkanen; Marjo-Riitta  Jarvelin; Abbas  Dehghan; Konstantinos K.  Tsilidis

doi:10.1186/s12916-021-02193-0

Circulating inflammatory cytokines and risk of five cancers: a Mendelian randomization analysis

PRACTICAL Consortium, Emmanouil Bouras, Ville Karhunen, Dipender Gill, Jian Huang, Philip C Haycock, Marc J. Gunter , Mattias J Johansson, Paul Brennan, Tim J Key, Sarah J Lewis, Richard M Martin, Neil Murphy, Elizabeth A. Platz, Ruth C. Travis , James Yarmolinsky, Verena Zuber, Paul B Martin, Michail Katsoulis, Heinz FreislingTherese Haugdahl Nøst, Matthias B. Schulze, Laure Dossus, Rayjean J. Hung, Christopher I. Amos, Ari V Ahola-Olli, Saranya Palaniswamy, Minna Männikkö, Juha Auvinen, Karl-Heinz Herzig, Sirkka Keinänen-Kiukaanniemi, Terho Lehtimäki, Veikko Salomaa, Olli Raitakari, Marko Salmi, Sirpa Jalkanen, Marjo-Riitta Jarvelin, Abbas Dehghan, Konstantinos K. Tsilidis

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Abstract

Background
Epidemiological and experimental evidence has linked chronic inflammation to cancer aetiology. It is unclear whether associations for specific inflammatory biomarkers are causal or due to bias. In order to examine whether altered genetically predicted concentration of circulating cytokines are associated with cancer development, we performed a two-sample Mendelian randomisation (MR) analysis.

Methods
Up to 31,112 individuals of European descent were included in genome-wide association study (GWAS) meta-analyses of 47 circulating cytokines. Single nucleotide polymorphisms (SNPs) robustly associated with the cytokines, located in or close to their coding gene (cis), were used as instrumental variables. Inverse-variance weighted MR was used as the primary analysis, and the MR assumptions were evaluated in sensitivity and colocalization analyses and a false discovery rate (FDR) correction for multiple comparisons was applied. Corresponding germline GWAS summary data for five cancer outcomes (breast, endometrial, lung, ovarian, and prostate), and their subtypes were selected from the largest cancer-specific GWASs available (cases ranging from 12,906 for endometrial to 133,384 for breast cancer).

Results
There was evidence of inverse associations of macrophage migration inhibitory factor with breast cancer (OR per SD = 0.88, 95% CI 0.83 to 0.94), interleukin-1 receptor antagonist with endometrial cancer (0.86, 0.80 to 0.93), interleukin-18 with lung cancer (0.87, 0.81 to 0.93), and beta-chemokine-RANTES with ovarian cancer (0.70, 0.57 to 0.85) and positive associations of monokine induced by gamma interferon with endometrial cancer (3.73, 1.86 to 7.47) and cutaneous T-cell attracting chemokine with lung cancer (1.51, 1.22 to 1.87). These associations were similar in sensitivity analyses and supported in colocalization analyses.

Conclusions
Our study adds to current knowledge on the role of specific inflammatory biomarker pathways in cancer aetiology. Further validation is needed to assess the potential of these cytokines as pharmacological or lifestyle targets for cancer prevention.

Original language	English
Article number	3 (2022)
Number of pages	15
Journal	BMC Medicine
Volume	20
Issue number	1
DOIs	https://doi.org/10.1186/s12916-021-02193-0
Publication status	Published - 11 Jan 2022

Bibliographical note

Funding Information:
This work was supported by a Cancer Research UK Programme Grant (C18281/A29019). DG was supported by the British Heart Foundation Centre of Research Excellence (RE/18/4/34215) at Imperial College and a National Institute for Health Research Clinical Lectureship (CL-2020-16-001) at St. George’s, University of London. VK has received funding from the European Union’s Horizon 2020 research and innovation program under the Marie Sklodowska-Curie grant 721567 (CAPICE project) and grant 848158 (EarlyCause), and the Academy of Finland [Project 312123]. This project has received funding from the European Union’s Horizon 2020 research and innovation programme (666881), SVDs@target (to MD; 667375), CoSTREAM (to MD); the DFG as part of the Munich Cluster for Systems Neurology (SyNergy, EXC EXC 2145 SyNergy – ID 390857198 ), the CRC 1123 (B3; to MD) and project DI 722/13-1; the Corona Foundation (to MD); the LMUexcellent fond (to MD); the e:Med program (e:AtheroSysMed; to MD) and the FP7/2007-2103 European Union project CVgenes@target (grant agreement number Health-F2-2013-601456; to MD). NFBC1966 received financial support from University of Oulu Grant no. 65354, Oulu University Hospital Grant no. 2/97, 8/97, Ministry of Health and Social Affairs Grant no. 23/251/97, 160/97, 190/97, National Institute for Health and Welfare, Helsinki Grant no. 54121, Regional Institute of Occupational Health, Oulu, Finland Grant no. 50621, 54231. SJL and RMM were supported by the NIHR Biomedical Research Centre at University Hospitals Bristol and Weston NHS Foundation Trust and the University of Bristol. The views expressed are those of the author(s) and not necessarily those of the NIHR or the Department of Health and Social Care. JY is supported by a Cancer Research UK Population Research Postdoctoral Fellowship (C68933/A28534). TK and RT were supported by Cancer Research UK (grants C8221/A29017) and the Medical Research Council (grant MR/M012190/1). CIA and RH are supported by U19CA203654. CIA is a Research Scholar of the Cancer Prevention Research Institute of Texas and supported by CPRIT RR170048. VS was supported by the Finnish Foundation for Cardiovascular Research. SJ and MS were supported by the Finnish Academy. PCH was supported by Cancer Research UK (C52724/A20138 & C18281/A29019). MRJ was supported by the Academy of Finland grant numbers 24300796, 24302031, 285547 (EGEA); the Medical Research Council (MRC) UK (grant number G0601653); Medical Research Council Biotechnology and Biological Sciences Research Council PREcisE (Nutrition & Epigenome, The Joint Programming Initiative a Healthy Diet for a Healthy Life (JPI HDHL/EU-H2020)); SP and MRJ are supported by the European Union's Horizon 2020 programme EDCMET (grant number 825762). Funding sources of the PRACTICAL, CRUK, BPC3, CAPS and PEGASUS consortia are described in the Additional file .

Funding Information:
Members from the PRACTICAL Consortium, CRUK, BPC3, CAPS and PEGASUS are provided in the Additional file 1. Where authors are identified as personnel of the International Agency for Research on Cancer/World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy or views of the International Agency for Research on Cancer/World Health Organization.

Publisher Copyright:
© 2021, The Author(s).

Research Groups and Themes

ICEP

Keywords

cytokines
cancer
inflammation
Mendelian randomization

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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8074 (C18281/A29019) ICEP2 - Programme Award: Towards improved casual evidence and enhanced prediction of cancer risk and survival
Martin, R. M. (Principal Investigator)
1/10/20 → 30/09/25
Project: Research

Cite this

PRACTICAL Consortium, Bouras, E., Karhunen, V., Gill, D., Huang, J., Haycock, P. C., Gunter , M. J., Johansson, M. J., Brennan, P., Key, T. J., Lewis, S. J., Martin, R. M., Murphy, N., Platz, E. A., Travis , R. C., Yarmolinsky, J., Zuber, V., Martin, P. B., Katsoulis, M., ... Tsilidis , K. K. (2022). Circulating inflammatory cytokines and risk of five cancers: a Mendelian randomization analysis. BMC Medicine, 20(1), Article 3 (2022) . https://doi.org/10.1186/s12916-021-02193-0

@article{46a9f185db2c4035bf1f9734800137e7,

title = "Circulating inflammatory cytokines and risk of five cancers: a Mendelian randomization analysis",

abstract = "BackgroundEpidemiological and experimental evidence has linked chronic inflammation to cancer aetiology. It is unclear whether associations for specific inflammatory biomarkers are causal or due to bias. In order to examine whether altered genetically predicted concentration of circulating cytokines are associated with cancer development, we performed a two-sample Mendelian randomisation (MR) analysis.MethodsUp to 31,112 individuals of European descent were included in genome-wide association study (GWAS) meta-analyses of 47 circulating cytokines. Single nucleotide polymorphisms (SNPs) robustly associated with the cytokines, located in or close to their coding gene (cis), were used as instrumental variables. Inverse-variance weighted MR was used as the primary analysis, and the MR assumptions were evaluated in sensitivity and colocalization analyses and a false discovery rate (FDR) correction for multiple comparisons was applied. Corresponding germline GWAS summary data for five cancer outcomes (breast, endometrial, lung, ovarian, and prostate), and their subtypes were selected from the largest cancer-specific GWASs available (cases ranging from 12,906 for endometrial to 133,384 for breast cancer).ResultsThere was evidence of inverse associations of macrophage migration inhibitory factor with breast cancer (OR per SD = 0.88, 95% CI 0.83 to 0.94), interleukin-1 receptor antagonist with endometrial cancer (0.86, 0.80 to 0.93), interleukin-18 with lung cancer (0.87, 0.81 to 0.93), and beta-chemokine-RANTES with ovarian cancer (0.70, 0.57 to 0.85) and positive associations of monokine induced by gamma interferon with endometrial cancer (3.73, 1.86 to 7.47) and cutaneous T-cell attracting chemokine with lung cancer (1.51, 1.22 to 1.87). These associations were similar in sensitivity analyses and supported in colocalization analyses.ConclusionsOur study adds to current knowledge on the role of specific inflammatory biomarker pathways in cancer aetiology. Further validation is needed to assess the potential of these cytokines as pharmacological or lifestyle targets for cancer prevention.",

keywords = "cytokines, cancer, inflammation, Mendelian randomization",

author = "{PRACTICAL Consortium} and Emmanouil Bouras and Ville Karhunen and Dipender Gill and Jian Huang and Haycock, {Philip C} and Gunter, {Marc J.} and Johansson, {Mattias J} and Paul Brennan and Key, {Tim J} and Lewis, {Sarah J} and Martin, {Richard M} and Neil Murphy and Platz, {Elizabeth A.} and Travis, {Ruth C.} and James Yarmolinsky and Verena Zuber and Martin, {Paul B} and Michail Katsoulis and Heinz Freisling and N{\o}st, {Therese Haugdahl} and Schulze, {Matthias B.} and Laure Dossus and Hung, {Rayjean J.} and Amos, {Christopher I.} and Ahola-Olli, {Ari V} and Saranya Palaniswamy and Minna M{\"a}nnikk{\"o} and Juha Auvinen and Karl-Heinz Herzig and Sirkka Kein{\"a}nen-Kiukaanniemi and Terho Lehtim{\"a}ki and Veikko Salomaa and Olli Raitakari and Marko Salmi and Sirpa Jalkanen and Marjo-Riitta Jarvelin and Abbas Dehghan and Tsilidis, {Konstantinos K.}",

note = "Funding Information: This work was supported by a Cancer Research UK Programme Grant (C18281/A29019). DG was supported by the British Heart Foundation Centre of Research Excellence (RE/18/4/34215) at Imperial College and a National Institute for Health Research Clinical Lectureship (CL-2020-16-001) at St. George{\textquoteright}s, University of London. VK has received funding from the European Union{\textquoteright}s Horizon 2020 research and innovation program under the Marie Sklodowska-Curie grant 721567 (CAPICE project) and grant 848158 (EarlyCause), and the Academy of Finland [Project 312123]. This project has received funding from the European Union{\textquoteright}s Horizon 2020 research and innovation programme (666881), SVDs@target (to MD; 667375), CoSTREAM (to MD); the DFG as part of the Munich Cluster for Systems Neurology (SyNergy, EXC EXC 2145 SyNergy – ID 390857198 ), the CRC 1123 (B3; to MD) and project DI 722/13-1; the Corona Foundation (to MD); the LMUexcellent fond (to MD); the e:Med program (e:AtheroSysMed; to MD) and the FP7/2007-2103 European Union project CVgenes@target (grant agreement number Health-F2-2013-601456; to MD). NFBC1966 received financial support from University of Oulu Grant no. 65354, Oulu University Hospital Grant no. 2/97, 8/97, Ministry of Health and Social Affairs Grant no. 23/251/97, 160/97, 190/97, National Institute for Health and Welfare, Helsinki Grant no. 54121, Regional Institute of Occupational Health, Oulu, Finland Grant no. 50621, 54231. SJL and RMM were supported by the NIHR Biomedical Research Centre at University Hospitals Bristol and Weston NHS Foundation Trust and the University of Bristol. The views expressed are those of the author(s) and not necessarily those of the NIHR or the Department of Health and Social Care. JY is supported by a Cancer Research UK Population Research Postdoctoral Fellowship (C68933/A28534). TK and RT were supported by Cancer Research UK (grants C8221/A29017) and the Medical Research Council (grant MR/M012190/1). CIA and RH are supported by U19CA203654. CIA is a Research Scholar of the Cancer Prevention Research Institute of Texas and supported by CPRIT RR170048. VS was supported by the Finnish Foundation for Cardiovascular Research. SJ and MS were supported by the Finnish Academy. PCH was supported by Cancer Research UK (C52724/A20138 & C18281/A29019). MRJ was supported by the Academy of Finland grant numbers 24300796, 24302031, 285547 (EGEA); the Medical Research Council (MRC) UK (grant number G0601653); Medical Research Council Biotechnology and Biological Sciences Research Council PREcisE (Nutrition & Epigenome, The Joint Programming Initiative a Healthy Diet for a Healthy Life (JPI HDHL/EU-H2020)); SP and MRJ are supported by the European Union's Horizon 2020 programme EDCMET (grant number 825762). Funding sources of the PRACTICAL, CRUK, BPC3, CAPS and PEGASUS consortia are described in the Additional file . Funding Information: Members from the PRACTICAL Consortium, CRUK, BPC3, CAPS and PEGASUS are provided in the Additional file 1. Where authors are identified as personnel of the International Agency for Research on Cancer/World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy or views of the International Agency for Research on Cancer/World Health Organization. Publisher Copyright: {\textcopyright} 2021, The Author(s).",

year = "2022",

month = jan,

day = "11",

doi = "10.1186/s12916-021-02193-0",

language = "English",

volume = "20",

journal = "BMC Medicine",

issn = "1741-7015",

publisher = "BioMed Central",

number = "1",

}

PRACTICAL Consortium, Bouras, E, Karhunen, V, Gill, D, Huang, J, Haycock, PC, Gunter , MJ, Johansson, MJ, Brennan, P, Key, TJ, Lewis, SJ , Martin, RM, Murphy, N, Platz, EA, Travis , RC, Yarmolinsky, J, Zuber, V, Martin, PB, Katsoulis, M, Freisling, H, Nøst, TH, Schulze, MB, Dossus, L, Hung, RJ, Amos, CI, Ahola-Olli, AV, Palaniswamy, S, Männikkö, M, Auvinen, J, Herzig, K-H, Keinänen-Kiukaanniemi, S, Lehtimäki, T, Salomaa, V, Raitakari, O, Salmi, M, Jalkanen, S, Jarvelin, M-R, Dehghan, A & Tsilidis , KK 2022, 'Circulating inflammatory cytokines and risk of five cancers: a Mendelian randomization analysis', BMC Medicine, vol. 20, no. 1, 3 (2022) . https://doi.org/10.1186/s12916-021-02193-0

TY - JOUR

T1 - Circulating inflammatory cytokines and risk of five cancers

T2 - a Mendelian randomization analysis

AU - PRACTICAL Consortium

AU - Bouras, Emmanouil

AU - Karhunen, Ville

AU - Gill, Dipender

AU - Huang, Jian

AU - Haycock, Philip C

AU - Gunter , Marc J.

AU - Johansson, Mattias J

AU - Brennan, Paul

AU - Key, Tim J

AU - Lewis, Sarah J

AU - Martin, Richard M

AU - Murphy, Neil

AU - Platz, Elizabeth A.

AU - Travis , Ruth C.

AU - Yarmolinsky, James

AU - Zuber, Verena

AU - Martin, Paul B

AU - Katsoulis, Michail

AU - Freisling, Heinz

AU - Nøst, Therese Haugdahl

AU - Schulze, Matthias B.

AU - Dossus, Laure

AU - Hung, Rayjean J.

AU - Amos, Christopher I.

AU - Ahola-Olli, Ari V

AU - Palaniswamy, Saranya

AU - Männikkö, Minna

AU - Auvinen, Juha

AU - Herzig, Karl-Heinz

AU - Keinänen-Kiukaanniemi, Sirkka

AU - Lehtimäki, Terho

AU - Salomaa, Veikko

AU - Raitakari, Olli

AU - Salmi, Marko

AU - Jalkanen, Sirpa

AU - Jarvelin, Marjo-Riitta

AU - Dehghan, Abbas

AU - Tsilidis , Konstantinos K.

N1 - Funding Information: This work was supported by a Cancer Research UK Programme Grant (C18281/A29019). DG was supported by the British Heart Foundation Centre of Research Excellence (RE/18/4/34215) at Imperial College and a National Institute for Health Research Clinical Lectureship (CL-2020-16-001) at St. George’s, University of London. VK has received funding from the European Union’s Horizon 2020 research and innovation program under the Marie Sklodowska-Curie grant 721567 (CAPICE project) and grant 848158 (EarlyCause), and the Academy of Finland [Project 312123]. This project has received funding from the European Union’s Horizon 2020 research and innovation programme (666881), SVDs@target (to MD; 667375), CoSTREAM (to MD); the DFG as part of the Munich Cluster for Systems Neurology (SyNergy, EXC EXC 2145 SyNergy – ID 390857198 ), the CRC 1123 (B3; to MD) and project DI 722/13-1; the Corona Foundation (to MD); the LMUexcellent fond (to MD); the e:Med program (e:AtheroSysMed; to MD) and the FP7/2007-2103 European Union project CVgenes@target (grant agreement number Health-F2-2013-601456; to MD). NFBC1966 received financial support from University of Oulu Grant no. 65354, Oulu University Hospital Grant no. 2/97, 8/97, Ministry of Health and Social Affairs Grant no. 23/251/97, 160/97, 190/97, National Institute for Health and Welfare, Helsinki Grant no. 54121, Regional Institute of Occupational Health, Oulu, Finland Grant no. 50621, 54231. SJL and RMM were supported by the NIHR Biomedical Research Centre at University Hospitals Bristol and Weston NHS Foundation Trust and the University of Bristol. The views expressed are those of the author(s) and not necessarily those of the NIHR or the Department of Health and Social Care. JY is supported by a Cancer Research UK Population Research Postdoctoral Fellowship (C68933/A28534). TK and RT were supported by Cancer Research UK (grants C8221/A29017) and the Medical Research Council (grant MR/M012190/1). CIA and RH are supported by U19CA203654. CIA is a Research Scholar of the Cancer Prevention Research Institute of Texas and supported by CPRIT RR170048. VS was supported by the Finnish Foundation for Cardiovascular Research. SJ and MS were supported by the Finnish Academy. PCH was supported by Cancer Research UK (C52724/A20138 & C18281/A29019). MRJ was supported by the Academy of Finland grant numbers 24300796, 24302031, 285547 (EGEA); the Medical Research Council (MRC) UK (grant number G0601653); Medical Research Council Biotechnology and Biological Sciences Research Council PREcisE (Nutrition & Epigenome, The Joint Programming Initiative a Healthy Diet for a Healthy Life (JPI HDHL/EU-H2020)); SP and MRJ are supported by the European Union's Horizon 2020 programme EDCMET (grant number 825762). Funding sources of the PRACTICAL, CRUK, BPC3, CAPS and PEGASUS consortia are described in the Additional file . Funding Information: Members from the PRACTICAL Consortium, CRUK, BPC3, CAPS and PEGASUS are provided in the Additional file 1. Where authors are identified as personnel of the International Agency for Research on Cancer/World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy or views of the International Agency for Research on Cancer/World Health Organization. Publisher Copyright: © 2021, The Author(s).

PY - 2022/1/11

Y1 - 2022/1/11

N2 - BackgroundEpidemiological and experimental evidence has linked chronic inflammation to cancer aetiology. It is unclear whether associations for specific inflammatory biomarkers are causal or due to bias. In order to examine whether altered genetically predicted concentration of circulating cytokines are associated with cancer development, we performed a two-sample Mendelian randomisation (MR) analysis.MethodsUp to 31,112 individuals of European descent were included in genome-wide association study (GWAS) meta-analyses of 47 circulating cytokines. Single nucleotide polymorphisms (SNPs) robustly associated with the cytokines, located in or close to their coding gene (cis), were used as instrumental variables. Inverse-variance weighted MR was used as the primary analysis, and the MR assumptions were evaluated in sensitivity and colocalization analyses and a false discovery rate (FDR) correction for multiple comparisons was applied. Corresponding germline GWAS summary data for five cancer outcomes (breast, endometrial, lung, ovarian, and prostate), and their subtypes were selected from the largest cancer-specific GWASs available (cases ranging from 12,906 for endometrial to 133,384 for breast cancer).ResultsThere was evidence of inverse associations of macrophage migration inhibitory factor with breast cancer (OR per SD = 0.88, 95% CI 0.83 to 0.94), interleukin-1 receptor antagonist with endometrial cancer (0.86, 0.80 to 0.93), interleukin-18 with lung cancer (0.87, 0.81 to 0.93), and beta-chemokine-RANTES with ovarian cancer (0.70, 0.57 to 0.85) and positive associations of monokine induced by gamma interferon with endometrial cancer (3.73, 1.86 to 7.47) and cutaneous T-cell attracting chemokine with lung cancer (1.51, 1.22 to 1.87). These associations were similar in sensitivity analyses and supported in colocalization analyses.ConclusionsOur study adds to current knowledge on the role of specific inflammatory biomarker pathways in cancer aetiology. Further validation is needed to assess the potential of these cytokines as pharmacological or lifestyle targets for cancer prevention.

AB - BackgroundEpidemiological and experimental evidence has linked chronic inflammation to cancer aetiology. It is unclear whether associations for specific inflammatory biomarkers are causal or due to bias. In order to examine whether altered genetically predicted concentration of circulating cytokines are associated with cancer development, we performed a two-sample Mendelian randomisation (MR) analysis.MethodsUp to 31,112 individuals of European descent were included in genome-wide association study (GWAS) meta-analyses of 47 circulating cytokines. Single nucleotide polymorphisms (SNPs) robustly associated with the cytokines, located in or close to their coding gene (cis), were used as instrumental variables. Inverse-variance weighted MR was used as the primary analysis, and the MR assumptions were evaluated in sensitivity and colocalization analyses and a false discovery rate (FDR) correction for multiple comparisons was applied. Corresponding germline GWAS summary data for five cancer outcomes (breast, endometrial, lung, ovarian, and prostate), and their subtypes were selected from the largest cancer-specific GWASs available (cases ranging from 12,906 for endometrial to 133,384 for breast cancer).ResultsThere was evidence of inverse associations of macrophage migration inhibitory factor with breast cancer (OR per SD = 0.88, 95% CI 0.83 to 0.94), interleukin-1 receptor antagonist with endometrial cancer (0.86, 0.80 to 0.93), interleukin-18 with lung cancer (0.87, 0.81 to 0.93), and beta-chemokine-RANTES with ovarian cancer (0.70, 0.57 to 0.85) and positive associations of monokine induced by gamma interferon with endometrial cancer (3.73, 1.86 to 7.47) and cutaneous T-cell attracting chemokine with lung cancer (1.51, 1.22 to 1.87). These associations were similar in sensitivity analyses and supported in colocalization analyses.ConclusionsOur study adds to current knowledge on the role of specific inflammatory biomarker pathways in cancer aetiology. Further validation is needed to assess the potential of these cytokines as pharmacological or lifestyle targets for cancer prevention.

KW - cytokines

KW - cancer

KW - inflammation

KW - Mendelian randomization

U2 - 10.1186/s12916-021-02193-0

DO - 10.1186/s12916-021-02193-0

M3 - Article (Academic Journal)

C2 - 35012533

SN - 1741-7015

VL - 20

JO - BMC Medicine

JF - BMC Medicine

IS - 1

M1 - 3 (2022)

ER -

Circulating inflammatory cytokines and risk of five cancers: a Mendelian randomization analysis

Abstract

Bibliographical note

Research Groups and Themes

Keywords

UN SDGs

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8074 (C18281/A29019) ICEP2 - Programme Award: Towards improved casual evidence and enhanced prediction of cancer risk and survival

Cite this