---
title: "Inflammatory Biomarkers and Risk of Postmenopausal ER-Positive Breast Cancer"
id: "british-journal-of-cancer-0-inflammatory-biomarkers-and-risk-of-postmenopausal-oestrogen-receptor-positive"
canonical_url: "https://medichelpline.com/clinical-feed/british-journal-of-cancer-0-inflammatory-biomarkers-and-risk-of-postmenopausal-oestrogen-receptor-positive"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "British Journal of Cancer"
source_url: "https://www.nature.com/articles/s41416-026-03624-6"
published_at: "2026-09-19T12:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Inflammatory Biomarkers and Risk of Postmenopausal ER-Positive Breast Cancer
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/british-journal-of-cancer-0-inflammatory-biomarkers-and-risk-of-postmenopausal-oestrogen-receptor-positive
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** British Journal of Cancer
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41416-026-03624-6)
- **Published At:** 2026-09-19T12:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- This case-cohort study within the Melbourne Collaborative Cohort Study evaluated circulating **inflammatory biomarkers** and the risk of postmenopausal **oestrogen receptor (ER)-positive breast cancer**. - The analysis included 1,223 postmenopausal females at blood collection, of whom 347 were cases. - Risk ratios (RRs) and 95% confidence intervals (CIs) were estimated per doubling of biomarker concentration and by quartiles, using weighted Poisson regression with a robust variance estimator. - Per doubling in concentration, higher **leptin** (RR 1.13, 95% CI 1.03–1.25) and **interleukin-10** (IL-10) (RR 1.14, 95% CI 1.01–1.29) were associated with increased risk. - Per doubling, **adiponectin** showed an RR of 1.10 (95% CI 0.90–1.34) and **tumour necrosis factor-alpha (TNF-α)** an RR of 1.27 (95% CI 0.96–1.68); both point estimates suggested increased risk but CIs included the null. - The leptin-to-adiponectin ratio had an RR per doubling of 1.07 (95% CI 0.99–1.16). - Other markers showed weaker or null associations per doubling: interferon-gamma RR 1.04 (0.93–1.17), interleukin-6 RR 1.01 (0.88–1.17), interleukin-8 RR 0.98 (0.83–1.16), and **C-reactive protein (CRP)** RR 1.03 (0.95–1.11). - The authors conclude that systemic inflammation may be relevant to the development of ER-positive breast cancer after menopause. - The source article discusses mechanistic links between obesity, adipose tissue dysfunction, adipokines, pro-inflammatory cytokines, aromatase activity and insulin resistance as plausible pathways connecting inflammation to postmenopausal breast carcinogenesis. - The published article date and full methodological details beyond the abstract (e.g., covariates, biomarker assay methods, follow-up time) are present in the original paper but are not reported in the provided source text.
## Clinical Analysis & Structured Key Points
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[nature](https://www.nature.com/) 2. [british journal of cancer](https://www.nature.com/bjc) 3. [articles](https://www.nature.com/bjc/articles?type=article) 4. article Inflammatory biomarkers and risk of postmenopausal oestrogen receptor-positive breast cancer: a case-cohort analysis [ Download PDF ](https://www.nature.com/articles/s41416-026-03624-6.pdf) [ Download PDF ](https://www.nature.com/articles/s41416-026-03624-6.pdf) * Article * [Open access](https://www.springernature.com/gp/open-science/about/the-fundamentals-of-open-access-and-open-research) * Published: 19 September 2026 Epidemiology # Inflammatory biomarkers and risk of postmenopausal oestrogen receptor-positive breast cancer: a case-cohort analysis * [Frances EM Albers](https://www.nature.com/articles/s41416-026-03624-6#auth-Frances_EM-Albers-Aff1-Aff2) [ORCID: orcid.org/0000-0002-7319-5182](https://orcid.org/0000-0002-7319-5182)[1](https://www.nature.com/articles/s41416-026-03624-6#Aff1),[2](https://www.nature.com/articles/s41416-026-03624-6#Aff2), * [Christopher TV Swain](https://www.nature.com/articles/s41416-026-03624-6#auth-Christopher_TV-Swain-Aff2-Aff3)[2](https://www.nature.com/articles/s41416-026-03624-6#Aff2),[3](https://www.nature.com/articles/s41416-026-03624-6#Aff3), * [S. Ghazaleh Dashti](https://www.nature.com/articles/s41416-026-03624-6#auth-S__Ghazaleh-Dashti-Aff4-Aff5)[4](https://www.nature.com/articles/s41416-026-03624-6#Aff4),[5](https://www.nature.com/articles/s41416-026-03624-6#Aff5), * [Sabina Rinaldi](https://www.nature.com/articles/s41416-026-03624-6#auth-Sabina-Rinaldi-Aff6)[6](https://www.nature.com/articles/s41416-026-03624-6#Aff6), * [Vivian Viallon](https://www.nature.com/articles/s41416-026-03624-6#auth-Vivian-Viallon-Aff6)[6](https://www.nature.com/articles/s41416-026-03624-6#Aff6), * [Amalia Karahalios](https://www.nature.com/articles/s41416-026-03624-6#auth-Amalia-Karahalios-Aff1)[1](https://www.nature.com/articles/s41416-026-03624-6#Aff1), * [Kristy A. Brown](https://www.nature.com/articles/s41416-026-03624-6#auth-Kristy_A_-Brown-Aff7) [ORCID: orcid.org/0000-0003-3382-5546](https://orcid.org/0000-0003-3382-5546)[7](https://www.nature.com/articles/s41416-026-03624-6#Aff7), * [Marc J. Gunter](https://www.nature.com/articles/s41416-026-03624-6#auth-Marc_J_-Gunter-Aff6-Aff8)[6](https://www.nature.com/articles/s41416-026-03624-6#Aff6),[8](https://www.nature.com/articles/s41416-026-03624-6#Aff8), * [Roger L. Milne](https://www.nature.com/articles/s41416-026-03624-6#auth-Roger_L_-Milne-Aff1-Aff2-Aff9)[1](https://www.nature.com/articles/s41416-026-03624-6#Aff1),[2](https://www.nature.com/articles/s41416-026-03624-6#Aff2),[9](https://www.nature.com/articles/s41416-026-03624-6#Aff9), * [Dallas R. English](https://www.nature.com/articles/s41416-026-03624-6#auth-Dallas_R_-English-Aff1-Aff2)[1](https://www.nature.com/articles/s41416-026-03624-6#Aff1),[2](https://www.nature.com/articles/s41416-026-03624-6#Aff2) & * … * [Brigid M. Lynch](https://www.nature.com/articles/s41416-026-03624-6#auth-Brigid_M_-Lynch-Aff1-Aff2) [ORCID: orcid.org/0000-0001-8060-547X](https://orcid.org/0000-0001-8060-547X)[1](https://www.nature.com/articles/s41416-026-03624-6#Aff1),[2](https://www.nature.com/articles/s41416-026-03624-6#Aff2) Show authors [_British Journal of Cancer_](https://www.nature.com/bjc) (2026) [Cite this article](https://www.nature.com/articles/s41416-026-03624-6#citeas) [ Save article ](https://www.nature.com/articles/s41416-026-03624-6/save-research?_csrf=nEfMBlYmxsiJUNVg4PxXyzARWwUfD-3a) [ View saved research ](https://www.nature.com/saved-research) ## Abstract ### Background The role of systemic inflammation in postmenopausal breast carcinogenesis remains unclear. Using a case-cohort study within the Melbourne Collaborative Cohort Study, we estimated the effects of circulating inflammatory biomarkers on the risk of postmenopausal oestrogen receptor (ER)-positive breast cancer. ### Methods We included 1223 females (347 cases) who were postmenopausal at blood collection. For each biomarker, risk ratios (RRs) and 95% confidence intervals (CIs) for ER-positive breast cancer were estimated (1) per-doubling in biomarker concentration and (2) for quartiles of concentration with the lowest category as the reference, using weighted Poisson regression with a robust variance estimator. ### Results The risk of postmenopausal ER-positive breast cancer increased per doubling in blood concentrations of leptin (RR: 1.13, 95% CI: 1.03, 1.25), adiponectin (RR: 1.10, 95% CI: 0.90, 1.34), tumour necrosis factor-alpha (RR: 1.27, 95% CI: 0.96, 1.68), and interleukin-10 (RR: 1.14, 95% CI: 1.01, 1.29). The RR for a doubling of the leptin-to-adiponectin ratio was 1.07 (0.99, 1.16). RRs for other biomarkers were 1.04 (0.93, 1.17) for interferon-gamma, 1.01 (0.88, 1.17) for interleukin-6, 0.98 (0.83, 1.16) for interleukin-8, and 1.03 (0.95, 1.11) for C-reactive protein. ### Conclusion Systemic inflammation may be important in the risk of developing ER-positive breast cancer for postmenopausal females. ![](https://media.springernature.com/lw685/springer-static/image/art%3A10.1038%2Fs41416-026-03624-6/MediaObjects/41416_2026_3624_Figa_HTML.png) ### Explore related subjects Discover the latest articles and news in related subjects. * [Breast cancer](https://www.nature.com/subjects/breast-cancer) * [Epidemiology](https://www.nature.com/subjects/epidemiology) * [Predictive markers](https://www.nature.com/subjects/predictive-markers) * [Risk factors](https://www.nature.com/subjects/risk-factors) ## Background Chronic inflammation promotes carcinogenesis by fostering an environment that facilitates the malignant transformation of pre-cancerous cells [[1](https://www.nature.com/articles/s41416-026-03624-6#ref-CR1 "Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144:646–74.")]. It may play a role in the development of breast cancer [[2](https://www.nature.com/articles/s41416-026-03624-6#ref-CR2 "Danforth DN. The role of chronic inflammation in the development of breast cancer. Cancers \(Basel\). 2021;13\(15\):3918.")], and is hypothesised to be one of the mechanisms by which obesity increases the risk of postmenopausal oestrogen receptor (ER)-positive breast cancer [[3](https://www.nature.com/articles/s41416-026-03624-6#ref-CR3 "Absence of Excess Body Fatness. Lyon, France: International Agency for Research on Cancer; 2018. Available from: http://publications.iarc.fr/570 .")]. The expansion of white adipose tissue in people with obesity leads to the increased production of leptin, a pro-inflammatory adipokine which activates intracellular signalling networks that may promote the proliferation, growth and survival of breast cancer cells [[4](https://www.nature.com/articles/s41416-026-03624-6#ref-CR4 "Gérard C, Brown KA. Obesity and breast cancer—role of estrogens and the molecular underpinnings of aromatase regulation in breast adipose tissue. Mol Cell Endocrinol. 2018;466:15–30."),[5](https://www.nature.com/articles/s41416-026-03624-6#ref-CR5 "Christodoulatos GS, Spyrou N, Kadillari J, Psallida S, Dalamaga M. The role of adipokines in breast cancer: current evidence and perspectives. Curr Obes Rep. 2019;8:413–33."),[6](https://www.nature.com/articles/s41416-026-03624-6#ref-CR6 "Miracle CE, McCallister CL, Egleton RD, Salisbury TB. Mechanisms by which obesity regulates inflammation and anti-tumor immunity in cancer. Biochem Biophys Res Commun. 2024;733:150437."),[7](https://www.nature.com/articles/s41416-026-03624-6#ref-CR7 "Jardé T, Perrier S, Vasson MP, Caldefie-Chézet F. Molecular mechanisms of leptin and adiponectin in breast cancer. Eur J Cancer \(Oxf, Engl 1990\). 2011;47:33–43.")]. The expansion of white adipose tissue also leads to hypoxia and cell death in adipocytes, triggering an inflammatory response that upregulates the secretion of pro-inflammatory cytokines – such as tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) – by adipocytes and macrophages [[4](https://www.nature.com/articles/s41416-026-03624-6#ref-CR4 "Gérard C, Brown KA. Obesity and breast cancer—role of estrogens and the molecular underpinnings of aromatase regulation in breast adipose tissue. Mol Cell Endocrinol. 2018;466:15–30."),[5](https://www.nature.com/articles/s41416-026-03624-6#ref-CR5 "Christodoulatos GS, Spyrou N, Kadillari J, Psallida S, Dalamaga M. The role of adipokines in breast cancer: current evidence and perspectives. Curr Obes Rep. 2019;8:413–33."),[6](https://www.nature.com/articles/s41416-026-03624-6#ref-CR6 "Miracle CE, McCallister CL, Egleton RD, Salisbury TB. Mechanisms by which obesity regulates inflammation and anti-tumor immunity in cancer. Biochem Biophys Res Commun. 2024;733:150437.")]. Higher levels of TNF-α and IL-6, in turn, increase the production of C-reactive protein (CRP)—a non-specific marker of inflammation [[8](https://www.nature.com/articles/s41416-026-03624-6#ref-CR8 "Sproston NR, Ashworth JJ. Role of C-reactive protein at sites of inflammation and infection. Front Immunol. 2018;9:754.")]. Higher levels of CRP have been associated with an increased risk of postmenopausal breast cancer in several systematic reviews and meta-analyses of prospective cohort studies [[9](https://www.nature.com/articles/s41416-026-03624-6#ref-CR9 "Guo L, Liu S, Zhang S, Chen Q, Zhang M, Quan P, et al. C-reactive protein and risk of breast cancer: a systematic review and meta-analysis. Sci Rep. 2015;5:10508."),[10](https://www.nature.com/articles/s41416-026-03624-6#ref-CR10 "Chan DS, Bandera EV, Greenwood DC, Norat T. Circulating C-reactive protein and breast cancer risk-systematic literature review and meta-analysis of prospective cohort studies. Cancer Epidemiol Biomark Prev. 2015;24:1439–49."),[11](https://www.nature.com/articles/s41416-026-03624-6#ref-CR11 "Lou MWC, Drummond AE, Swain CTV, Milne RL, English DR, Brown KA, et al. Linking physical activity to breast cancer via inflammation, part 2: the effect of inflammation on breast cancer risk. Cancer Epidemiol Biomark Prev. 2023;32:597–605.")]. Adiponectin, on the other hand, is an anti-inflammatory adipokine that is reduced with obesity and chronic inflammation [[4](https://www.nature.com/articles/s41416-026-03624-6#ref-CR4 "Gérard C, Brown KA. Obesity and breast cancer—role of estrogens and the molecular underpinnings of aromatase regulation in breast adipose tissue. Mol Cell Endocrinol. 2018;466:15–30."),[5](https://www.nature.com/articles/s41416-026-03624-6#ref-CR5 "Christodoulatos GS, Spyrou N, Kadillari J, Psallida S, Dalamaga M. The role of adipokines in breast cancer: current evidence and perspectives. Curr Obes Rep. 2019;8:413–33."),[6](https://www.nature.com/articles/s41416-026-03624-6#ref-CR6 "Miracle CE, McCallister CL, Egleton RD, Salisbury TB. Mechanisms by which obesity regulates inflammation and anti-tumor immunity in cancer. Biochem Biophys Res Commun. 2024;733:150437."),[7](https://www.nature.com/articles/s41416-026-03624-6#ref-CR7 "Jardé T, Perrier S, Vasson MP, Caldefie-Chézet F. Molecular mechanisms of leptin and adiponectin in breast cancer. Eur J Cancer \(Oxf, Engl 1990\). 2011;47:33–43.")]. In laboratory studies of cell lines and animal models, adiponectin exhibits anti-proliferative, anti-migratory and pro-apoptotic properties that may serve to reduce the risk of postmenopausal breast cancer [[4](https://www.nature.com/articles/s41416-026-03624-6#ref-CR4 "Gérard C, Brown KA. Obesity and breast cancer—role of estrogens and the molecular underpinnings of aromatase regulation in breast adipose tissue. Mol Cell Endocrinol. 2018;466:15–30."), [5](https://www.nature.com/articles/s41416-026-03624-6#ref-CR5 "Christodoulatos GS, Spyrou N, Kadillari J, Psallida S, Dalamaga M. The role of adipokines in breast cancer: current evidence and perspectives. Curr Obes Rep. 2019;8:413–33."), [7](https://www.nature.com/articles/s41416-026-03624-6#ref-CR7 "Jardé T, Perrier S, Vasson MP, Caldefie-Chézet F. Molecular mechanisms of leptin and adiponectin in breast cancer. Eur J Cancer \(Oxf, Engl 1990\). 2011;47:33–43.")]. The epidemiological evidence linking inflammation to risk of postmenopausal breast cancer is strongest for CRP [[9](https://www.nature.com/articles/s41416-026-03624-6#ref-CR9 "Guo L, Liu S, Zhang S, Chen Q, Zhang M, Quan P, et al. C-reactive protein and risk of breast cancer: a systematic review and meta-analysis. Sci Rep. 2015;5:10508."),[10](https://www.nature.com/articles/s41416-026-03624-6#ref-CR10 "Chan DS, Bandera EV, Greenwood DC, Norat T. Circulating C-reactive protein and breast cancer risk-systematic literature review and meta-analysis of prospective cohort studies. Cancer Epidemiol Biomark Prev. 2015;24:1439–49."),[11](https://www.nature.com/articles/s41416-026-03624-6#ref-CR11 "Lou MWC, Drummond AE, Swain CTV, Milne RL, English DR, Brown KA, et al. Linking physical activity to breast cancer via inflammation, part 2: the effect of inflammation on breast cancer risk. Cancer Epidemiol Biomark Prev. 2023;32:597–605.")]. There is also evidence that leptin is positively associated with risk, whereas adiponectin is inversely associated [[11](https://www.nature.com/articles/s41416-026-03624-6#ref-CR11 "Lou MWC, Drummond AE, Swain CTV, Milne RL, English DR, Brown KA, et al. Linking physical activity to breast cancer via inflammation, part 2: the effect of inflammation on breast cancer risk. Cancer Epidemiol Biomark Prev. 2023;32:597–605.")]. There is a paucity of epidemiological evidence for other markers of inflammation, and anti-inflammatory markers other than adiponectin have rarely been studied. Developing a more detailed understanding of the role of inflammatory biomarkers in postmenopausal breast carcinogenesis may help to inform prevention strategies e.g., by helping to identify biological targets for intervention in postmenopausal females with obesity or who are physically inactive. The inflammatory pathway may also influence other biological pathways involved in postmenopausal breast carcinogenesis, such as the insulin/insulin-like growth factor (IGF)-signalling and sex-steroid hormone pathways. For example, chronic inflammation in the context of obesity contributes to insulin resistance [[12](https://www.nature.com/articles/s41416-026-03624-6#ref-CR12 "Shoelson SE, Lee J, Goldfine AB. Inflammation and insulin resistance. J Clin Investig. 2006;116:1793–801."), [13](https://www.nature.com/articles/s41416-026-03624-6#ref-CR13 "Xourafa G, Korbmacher M, Roden M. Inter-organ crosstalk during development and progression of type 2 diabetes mellitus. Nat Rev Endocrinol. 2024;20:27–49.")]. Adiponectin has insulin-sensitising properties, and both leptin and adiponectin can influence oestrogen biosynthesis via aromatase [[4](https://www.nature.com/articles/s41416-026-03624-6#ref-CR4 "Gérard C, Brown KA. Obesity and breast cancer—role of estrogens and the molecular underpinnings of aromatase regulation in breast adipose tissue. Mol Cell Endocrinol. 2018;466:15–30."), [7](https://www.nature.com/articles/s41416-026-03624-6#ref-CR7 "Jardé T, Perrier S, Vasson MP, Caldefie-Chézet F. Molecular mechanisms of leptin and adiponectin in breast cancer. Eur J Cancer \(Oxf, Engl 1990\). 2011;47:33–43."), [14](https://www.nature.com/articles/s41416-026-03624-6#ref-CR14 "Panno ML, Naimo GD, Spina E, Andò S, Mauro L. Different molecular signaling sustaining adiponectin action in breast cancer. Curr Opin Pharmacol. 2016;31:1–7.")]. Pro-inflammatory cytokines, such as TNF-α and IL-6, can also stimulate aromatase activity [[4](https://www.nature.com/articles/s41416-026-03624-6#ref-CR4 "Gérard C, Brown KA. Obesity and breast cancer—role of estrogens and the molecular underpinnings of aromatase regulation in breast adipose tissue. Mol Cell Endocrinol. 2018;466:15–30.")]. Further, the inflammatory pathway may be implicated in the mechanisms of several protective factors for postmenopausal breast cancer. For example, physical activity may protect against postmenopausal breast
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