Acute and Chronic Effects of Adjuvant Therapy on Inflammatory Markers in Breast Cancer Patients.


Journal

JNCI cancer spectrum
ISSN: 2515-5091
Titre abrégé: JNCI Cancer Spectr
Pays: England
ID NLM: 101721827

Informations de publication

Date de publication:
01 07 2022
Historique:
accepted: 18 05 2022
received: 24 02 2022
revised: 20 04 2022
pubmed: 29 7 2022
medline: 31 8 2022
entrez: 28 7 2022
Statut: ppublish

Résumé

Inflammation contributes to poor behavioral, functional, and clinical outcomes in cancer survivors. We examined whether standard cancer treatments-radiation and chemotherapy-led to acute and persistent changes in circulating markers of inflammation in breast cancer patients. A total of 192 women diagnosed with early stage breast cancer provided blood samples before and after completion of radiation and/or chemotherapy and at 6-, 12-, and 18-month posttreatment follow-ups. Samples were assayed for circulating inflammatory markers, including tumor necrosis factor-α (TNF-α) and interleukin (IL)-6, downstream markers of their activity (soluble TNF receptor type II [sTNF-RII], C reactive protein), and other inflammatory mediators (IL-8, interferon-γ [IFN-γ]). Analyses evaluated within-group changes in inflammatory markers in 4 treatment groups: no radiation or chemotherapy (n = 39), radiation only (n = 77), chemotherapy only (n = 18), and chemotherapy with radiation (n = 58). Patients treated with chemotherapy showed statistically significant increases in circulating concentrations of TNF-α, sTNF-RII, IL-6, and IFN-γ from pre- to posttreatment, with parameter estimates in standard deviation units ranging from 0.55 to 1.20. Those who received chemotherapy with radiation also showed statistically significant increases in IL-8 over this period. Statistically significant increases in TNF-α, sTNF-RII, IL-6, IFN-γ, and IL-8 persisted at 6, 12, and 18 months posttreatment among patients treated with chemotherapy and radiation (all P < .05). Patients treated with radiation only showed a statistically significant increase in IL-8 at 18 months posttreatment; no increases in any markers were observed in patients treated with surgery only. Chemotherapy is associated with acute increases in systemic inflammation that persist for months after treatment completion in patients who also receive radiation therapy. These increases may contribute to common behavioral symptoms and other comorbidities in cancer survivors.

Sections du résumé

BACKGROUND
Inflammation contributes to poor behavioral, functional, and clinical outcomes in cancer survivors. We examined whether standard cancer treatments-radiation and chemotherapy-led to acute and persistent changes in circulating markers of inflammation in breast cancer patients.
METHODS
A total of 192 women diagnosed with early stage breast cancer provided blood samples before and after completion of radiation and/or chemotherapy and at 6-, 12-, and 18-month posttreatment follow-ups. Samples were assayed for circulating inflammatory markers, including tumor necrosis factor-α (TNF-α) and interleukin (IL)-6, downstream markers of their activity (soluble TNF receptor type II [sTNF-RII], C reactive protein), and other inflammatory mediators (IL-8, interferon-γ [IFN-γ]). Analyses evaluated within-group changes in inflammatory markers in 4 treatment groups: no radiation or chemotherapy (n = 39), radiation only (n = 77), chemotherapy only (n = 18), and chemotherapy with radiation (n = 58).
RESULTS
Patients treated with chemotherapy showed statistically significant increases in circulating concentrations of TNF-α, sTNF-RII, IL-6, and IFN-γ from pre- to posttreatment, with parameter estimates in standard deviation units ranging from 0.55 to 1.20. Those who received chemotherapy with radiation also showed statistically significant increases in IL-8 over this period. Statistically significant increases in TNF-α, sTNF-RII, IL-6, IFN-γ, and IL-8 persisted at 6, 12, and 18 months posttreatment among patients treated with chemotherapy and radiation (all P < .05). Patients treated with radiation only showed a statistically significant increase in IL-8 at 18 months posttreatment; no increases in any markers were observed in patients treated with surgery only.
CONCLUSIONS
Chemotherapy is associated with acute increases in systemic inflammation that persist for months after treatment completion in patients who also receive radiation therapy. These increases may contribute to common behavioral symptoms and other comorbidities in cancer survivors.

Identifiants

pubmed: 35900175
pii: 6651075
doi: 10.1093/jncics/pkac052
pmc: PMC9420043
pii:
doi:

Substances chimiques

Biomarkers 0
Interleukin-6 0
Interleukin-8 0
Receptors, Tumor Necrosis Factor 0
Tumor Necrosis Factor-alpha 0
Interferon-gamma 82115-62-6

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NCI NIH HHS
ID : P30 CA016042
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA160427
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

© The Author(s) 2022. Published by Oxford University Press.

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Auteurs

Julienne E Bower (JE)

Department of Psychology, University of California, Los Angeles, CA, USA.
Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA, USA.
Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, USA.
Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA, USA.

Patricia A Ganz (PA)

Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA, USA.
Schools of Medicine and Public Health, University of California, Los Angeles, CA, USA.

Michael R Irwin (MR)

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA, USA.
Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, USA.

Steve W Cole (SW)

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA, USA.
Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, USA.
Department of Medicine, University of California, Los Angeles, CA, USA.

Judith Carroll (J)

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA, USA.
Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, USA.

Kate R Kuhlman (KR)

Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, USA.
Department of Psychological Science of California, University of California, Irvine, CA, USA.

Laura Petersen (L)

Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA, USA.

Deborah Garet (D)

Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, USA.

Arash Asher (A)

Cedars-Sinai Medical Center, Samuel Oschin Comprehensive Cancer Institute, Los Angeles, CA, USA.

Sara A Hurvitz (SA)

Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA, USA.
Department of Medicine, University of California, Los Angeles, CA, USA.

Catherine M Crespi (CM)

Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA, USA.
Department of Biostatistics, University of California, Los Angeles, CA, USA.

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Classifications MeSH