Baseline breast tissue characteristics determine the effect of tamoxifen on mammographic density change.

breast cancer primary prevention mammographic breast density mammographic breast density change progesterone receptor proliferation tamoxifen

Journal

International journal of cancer
ISSN: 1097-0215
Titre abrégé: Int J Cancer
Pays: United States
ID NLM: 0042124

Informations de publication

Date de publication:
30 Mar 2024
Historique:
revised: 25 02 2024
received: 20 11 2023
accepted: 29 02 2024
medline: 30 3 2024
pubmed: 30 3 2024
entrez: 30 3 2024
Statut: aheadofprint

Résumé

Tamoxifen prevents recurrence of breast cancer and is also approved for preventive, risk-reducing, therapy. Tamoxifen alters the breast tissue composition and decreases the mammographic density. We aimed to test if baseline breast tissue composition influences tamoxifen-associated density change. This biopsy-based study included 83 participants randomised to 6 months daily intake of placebo, 20, 10, 5, 2.5, or 1 mg tamoxifen. The study is nested within the double-blinded tamoxifen dose-determination trial Karolinska Mammography Project for Risk Prediction of Breast Cancer Intervention (KARISMA) Study. Ultrasound-guided core-needle breast biopsies were collected at baseline before starting treatment. Biopsies were quantified for epithelial, stromal, and adipose distributions, and epithelial and stromal expression of proliferation marker Ki67, oestrogen receptor (ER) and progesterone receptor (PR). Mammographic density was measured using STRATUS. We found that greater mammographic density at baseline was positively associated with stromal area and inversely associated with adipose area and stromal expression of ER. Premenopausal women had greater mammographic density and epithelial tissue, and expressed more epithelial Ki67, PR, and stromal PR, compared to postmenopausal women. In women treated with tamoxifen (1-20 mg), greater density decrease was associated with higher baseline density, epithelial Ki67, and stromal PR. Women who responded to tamoxifen with a density decrease had on average 17% higher baseline density and a 2.2-fold higher PR expression compared to non-responders. Our results indicate that features in the normal breast tissue before tamoxifen exposure influences the tamoxifen-associated density decrease, and that the age-associated difference in density change may be related to age-dependant differences in expression of Ki67 and PR.

Identifiants

pubmed: 38554131
doi: 10.1002/ijc.34939
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Stockholm läns landsting
ID : 4-2645/2015
Organisme : Vetenskapsrådet
ID : E0718301
Organisme : Cancerfonden
ID : CAN 2015/649
Organisme : Cancerfonden
ID : CAN 21-0454 FE
Organisme : Cancerfonden
ID : CAN 21-1660
Organisme : Märit and Hans Rausing's Initiative Against Breast Cancer
Organisme : The Kamprad Foundation
ID : 20150052

Informations de copyright

© 2024 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.

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Auteurs

Marike Gabrielson (M)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

Mattias Hammarström (M)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

Jenny Bergqvist (J)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Breast Centre, Department of Surgery, Capio St Görans Hospital, Stockholm, Sweden.

Kristina Lång (K)

Department of Translational Medicine, Diagnostic Radiology, Lund University, Lund, Sweden.

Ann H Rosendahl (AH)

Department of Clinical Sciences Lund, Oncology, Lund University and Skåne University Hospital, Lund, Sweden.

Signe Borgquist (S)

Department of Clinical Sciences Lund, Oncology, Lund University and Skåne University Hospital, Lund, Sweden.
Department of Oncology, Aarhus University Hospital and Aarhus University, Aarhus, Denmark.

Roxanna Hellgren (R)

Department of Radiology, Södersjukhuset, Stockholm, Sweden.

Kamila Czene (K)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

Per Hall (P)

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Department of Oncology, South General Hospital, Stockholm, Sweden.

Classifications MeSH