Marike Gabrielson

Senior research specialist

About me

I am a researcher in molecular cancer epidemiology at Karolinska Institutet at the Department of Medical Epidemiology and Biostatistics. I am also a scientific project leader in the unique, prospective mammography screening and breast cancer cohort KARMA, including over 70,000 participants [karmastudy.org] (Gabrielson et al. IJE 2017). The overarching goal of KARMA is to reduce the incidence and mortality of breast cancer by focusing on individualised screening and prevention.

I graduated with a PhD in Biomedicine from Örebro University in Sweden in 2013, specialising on breast cancer cell biology. I have an undergraduate degree in Biomedicine (combined BSc/MSc) from Örebro University.

Research description

My research focuses on the aetiology of breast cancer with an emphasis on the molecular epidemiology of breast cancer risk and mammographic density. 

Since 2014 I have focused on setting up and conducting research within three target areas: 

1) Understanding the biology of breast cancer risk, and identifying biomarkers of risk within the breast and tissue and by hormone and proteomic profiles

2) Understanding the mechanisms of action of the drug tamoxifen in preventing breast cancer, and identifying biomarkers for treatment effects by tamoxifen

3) Using biomarkers for tailoring individualised preventive and adjuvant therapy of breast cancer


Selected previous studies within my main topics:  

The effects of tamoxifen at different doses on the breast tissue. This is the first biopsy-paper within the KARISMA randomised dose-determination clinical trial. In KARISMA, we aimed to study the efficacy of lower doses of tamoxifen on the mammographic density change and reported side-effects in healthy women without breast cancer. By studying breast biopsies before and after tamoxifen at different doses, I found that tamoxifen extensively reorganises the breast tissue composition already after six months. Particularly, the glandular-epithelial tissue is reduced already at low doses of tamoxifen. Tamoxifen also changes the expression of hormone receptors and reduces the proliferation rate of epithelial cells. Interestingly, most effects were seen in premenopausal women only (Gabrielson et al. IJC 2023).

Breast tissue characteristics of the normal breast for understanding the mechanisms underlying mammographic density as a risk factor for breast cancer. By using breast biopsies, I have investigated associations between breast tissue characteristics with mammographic density, and established risk factors for breast cancer. These studies provide new insights in tissue composition regulation and demonstrate that early life events influence the tissue characteristics, which remain in later life. (Gabrielson et al. BCRT 2016 & Gabrielson et al. BCRT 2018)

Plasma hormones are associated with mammographic density and density change over time. This project identified that hormones from the progestogen, oestrogen and corticoid pathways influence the levels of mammographic density. In contrast, the density change over time is mainly driven by androgens. This study emphasises the complexity of risk factors for breast cancer and their mechanisms of action. (Gabrielson et al. BCR 2020)

Plasma proteomic approaches for basic research and biomarker discovery for risk prediction, early detection, and prevention of breast cancer. We showed plasma protein signatures associated with mammographic density among healthy women. The study gives new understandings to the mechanistic processes underlying mammographic density (Byström BCR 2018). We have also identified circulating markers of potential long-lasting molecular effects of menopausal hormonal therapy on the circulating proteome, even after women had ended their treatment (Thomas et al. Trasl Oncol 2022).

Plasma hormone concentrations for basic research and biomarker discovery for risk prediction, early detection, and prevention of breast cancer. I have identified plasma prolactin and DHEAS as risk factors for breast cancer in a manner independent of mammographic density (Gabrielson et al. JNCI CS 2018 & Gabrielson et al. Cancer EpiBiomarkers & Prev 2020). I have also identified an interaction between progesterone, calcifications, and breast cancer risk, further identifying endogenous hormones as regulators of breast tissue homeostasis and mammographic features. I am now leading the work to develop risk prediction models based on hormone signatures of breast cancers and controls.

I am also responsible for the biological material collected within KARMA and studies/clinical trials within KARMA [karmastudy.org].