Breast imaging in transgender women: a review.

Transgender women are increasingly evaluated in breast imaging centers. Radiologists should be familiar with a range of imaging findings related to feminizing hormone therapy and breast augmentations as well as benign and malignant lesions seen in this population. A growing body of literature has suggested that feminizing hormone therapy may increase the risk of breast cancer, prompting professional organizations to develop screening guidelines. The aim of this paper is to review common breast imaging findings in transgender women, recent data on the association between feminizing hormone therapy and breast cancer, and guidelines for breast cancer screening. Knowing these unique imaging features in transgender women is essential for providing competent care and reducing health care disparities.

Breast cancer in transgender women: A case report.

The risk of breast cancer in transgender women continues to be a topic of debate in the medical literature. Studies have theorized an increased risk in transgender women taking feminizing hormone therapy on the basis of established risk factors and histological characteristics in cisgender men and established increased risk in cisgender women on hormone replacement therapy. Historically, testing this theory has been challenging due to a relative lack of cases and large-scale, long-term studies reported in the literature. Studies to date have been contradictory, and a lack of medical consensus has led to inconsistencies in establishing universally accepted standards of care, including guidelines for screening. We hope to contribute to the ongoing discussion by presenting a case report of a transgender woman who had taken feminizing hormone therapy intermittently over 40 years and was subsequently diagnosed with breast cancer.

Sirtuin 2-mediated deacetylation of cyclin-dependent kinase 9 promotes STAT1 signaling in type I interferon responses.

Type I interferons (IFNs) induce expression of multiple genes that control innate immune responses to invoke both antiviral and antineoplastic activities. Transcription of these interferon-stimulated genes (ISGs) occurs upon activation of the canonical Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathways. Phosphorylation and acetylation are both events crucial to tightly regulate expression of ISGs. Here, using mouse embryonic fibroblasts and an array of biochemical methods including immunoblotting and kinase assays, we show that sirtuin 2 (SIRT2), a member of the NAD-dependent protein deacetylase family, is involved in type I IFN signaling. We found that SIRT2 deacetylates cyclin-dependent kinase 9 (CDK9) in a type I IFN-dependent manner and that the CDK9 deacetylation is essential for STAT1 phosphorylation at Ser-727. We also found that SIRT2 is subsequently required for the transcription of ISGs and for IFN-driven antiproliferative responses in both normal and malignant cells. These findings establish the existence of a previously unreported signaling pathway whose function is essential for the control of JAK-STAT signaling and the regulation of IFN responses. Our findings suggest that targeting sirtuin activities may offer an avenue in the development of therapies for managing immune-related diseases and cancer.