AI Article Synopsis
- The study focused on 95 women with multiple breast fibroadenomas (MFAs) to investigate the potential role of germline variants of the prolactin receptor (PRLR) in breast tumor development.
- Research included a second MFA cohort of 71 women, 496 control subjects, and 119 women with breast cancer, examining the prevalence of PRLR variants across these groups.
- Findings showed no significant link between PRLR variants and increased risk of breast cancer or MFAs, though ongoing research may reveal complex interactions with oncogenic pathways.
Article Abstract
Context: In a cohort of 95 women with multiple breast fibroadenomas (MFAs), we recently identified patients harboring germline heterozygous variants of the prolactin receptor (PRLR) exhibiting constitutive activity (PRLR and PRLR).
Objective: This study sought to better delineate the potential role of PRLR gain-of-function variants in benign and malignant mammary tumorigenesis.
Design: This was an observational study and transgenic mouse model analysis.
Setting: The study took place at the Department of Endocrinology, Reproductive Disorders and Rare Gynecologic Diseases, Pitié Salpêtrière, Paris, and Inserm Unit 1151, Paris.
Patients Or Other Participants: We generated a second MFA cohort (n = 71) as well as a group of control subjects (n = 496) and a cohort of women with breast cancer (n = 119). We also generated two transgenic mouse models carrying the coding sequences of human PRLR or PRLR.
Intervention: We aimed to determine the prevalence of PRLR variants in these three populations and to uncover any association of the latter with specific tumor pattern, especially in patients with breast cancer.
Results: This study did not highlight a higher prevalence of PRLR variants in the MFA group and in the breast cancer group compared with control subjects. Transgenic mice expressing PRLR exhibited very mild histological mammary phenotype but tumors were never observed.
Conclusion: PRLR and PRLR variants are not associated with breast cancer or MFA risk. However, one cannot exclude that low but sustained PRLR signaling may facilitate or contribute to pathological development driven by oncogenic pathways. Long-term patient follow-up should help to address this issue.
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| http://dx.doi.org/10.1210/jc.2016-2372 | DOI Listing |
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