# The Inflammatory Footprint of Anti-Breast Cancer Treatments and Psychosocial Factors in Women Undergoing Chemotherapy

**Authors:** Magda A. Oliveira, Susana S. Almeida, Gabriela Martins, Inês Godinho, Carlos Palmeira, Maria Emília Sousa, Lia Fernandes, Rui Medeiros, Marina Prista Guerra

PMC · DOI: 10.3390/biomedicines13102563 · Biomedicines · 2025-10-21

## TL;DR

This study explores how breast cancer treatments and psychosocial factors affect inflammation in women undergoing chemotherapy.

## Contribution

The study identifies specific inflammatory and psychosocial markers affected by chemotherapy and coping strategies.

## Key findings

- Chemotherapy significantly reduced TNF-α, IL-17a, and IL-10 levels in breast cancer patients.
- Psychosocial factors like venting and emotional support correlated with inflammatory biomarker changes.
- The findings suggest a biopsychosocial approach could improve both survival and psychological outcomes.

## Abstract

Background/Objectives: Despite the well-recognized role of inflammation in breast cancer course, the biological mechanisms involved in its pathophysiology are complex, heterogeneous, and still unclear. However, evidence shows that cancer treatments and stress system responses impact the patient’s inflammatory status. We aim to analyze the inflammatory footprint of anti-breast cancer treatments and psychosocial factors by observing the evolution of inflammatory and psychosocial markers pre- and post-chemotherapy; to examine the associations between pro- and anti-inflammatory cytokines with psychosocial factors after chemotherapy; and to identify vulnerability/resilience variables that may improve patients’ referral for psycho-oncological interventions before/after chemotherapy. Methods: We performed a well-controlled cohort study of premenopausal women diagnosed with stage I to III breast cancer undergoing chemotherapy. Patients were longitudinally evaluated at pre-chemotherapy (post-surgery in the adjuvant cohort) and post-chemotherapy. Both evaluations included clinical, immunological, and psychosocial data. Results: A significant decrease in TNF-α (p = 0.001) was observed in the adjuvant cohort compared to the neoadjuvant cohort. After chemotherapy, we found a significant decline in IL-17a, TNF-α, and IL-10 (p = 0.000, 0.000, 0.020), reinforcing the influence of chemotherapy on immunocompetence. Significant relations (p < 0.01) were found between the inflammatory biomarkers that decreased post-chemotherapy and psychosocial factors. Venting and instrumental/emotional support coping played the greatest role in immunological–psychological interactions. Conclusions: The findings confirm an inflammatory footprint, linking the complex interplay between breast tumors, anti-breast cancer treatments, and psychosocial factors. By supporting the immunoregulatory role of biological and psychosocial factors in immunocompetence, our findings bring potential insights into a biopsychosocial approach that targets both survival and psychological adjustment outcomes.

## Linked entities

- **Proteins:** TNF (tumor necrosis factor), IL17A (interleukin 17A), IL10 (interleukin 10)
- **Diseases:** breast cancer (MONDO:0004989)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}
- **Diseases:** Inflammatory (MESH:D007249), Breast Cancer (MESH:D001943), cancer (MESH:D009369)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12561099/full.md

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12561099/full.md

## References

100 references — full list in the complete paper: https://tomesphere.com/paper/PMC12561099/full.md

---
Source: https://tomesphere.com/paper/PMC12561099