Factors associated with perceived personal risk for breast cancer among women with dense breasts.

PURPOSE: To determine what patient factors are associated with a high or an accurate perceived personal risk (PPR) for breast cancer. METHODS: An IRB-approved survey study of women with dense breasts presenting for annual screening mammography was previously conducted from March 2017 to February 2018. Patients were asked to estimate their personal risk for breast cancer and to answer questions about prior breast care-related medical interactions. Survey data were combined post hoc with demographic and clinical data, including breast cancer risk status, and socioeconomic data imputed for each patient from census data. Logistic regression was used to determine which patient factors were associated with a high or accurate PPR. RESULTS: Surveys were completed by 508 women with dense breasts (median age 59.0 years). A high PPR was independently associated with younger age (AOR, 1.71 [95% CI, 1.13, 2.60]), family history of breast cancer (AOR 4.27 [95% CI, 2.81-7.34]), having a clinical "high-risk" designation (AOR, 3.43 [95% CI, 1.13-10.39], and having been called back from screening (AOR, 1.94 [95% CI, 1.14-3.32]). A lower accuracy of PPR was independently associated with a family history of breast cancer (AOR, 0.25 [95% CI, 0.14-0.42]) and having been called back from screening (AOR, 0.58 [95% CI, 0.35-0.98]). CONCLUSION: Women with dense breasts who had a family history of breast cancer or who had been called back from screening had a higher but less accurate PPR. Women with a "high-risk" clinical designation had a higher PPR, even when controlling for family history.

GalNAc-Specific Soybean Lectin Inhibits HIV Infection of Macrophages through Induction of Antiviral Factors.

Although it has been shown that some mannose-binding lectins (MBLs) exhibit significant activity against HIV infection, little is known about whether N-acetylgalactosamine (GalNAc)-binding lectins have the ability to inhibit HIV infection. Here, we demonstrate that a soybean-derived lectin (SBL) with GalNAc-binding affinity could potently suppress HIV infection of macrophages in a dose-dependent fashion. Unlike the MBLs, which block HIV only through binding to the glycosylated envelope proteins (gp120 and gp41) of the virus, SBL inhibited HIV at multiple steps of the virus infection/replication cycle. SBL could activate the beta interferon (IFN-ß)-STAT signaling pathway, resulting in the upregulation of a number of antiviral interferon-stimulated genes (ISGs) in macrophages. In addition, SBL treatment of macrophages induced the production of C-C chemokines, which bind to HIV entry coreceptor CCR5. Deglycosylation of cell surface galactosyl moieties or presaturation of GalNAc-binding capacity could compromise SBL-mediated induction of the antiviral factors. Furthermore, SBL exerted its anti-HIV activity in the low nanomolar range with no mitogenic effect on CD4+ T cells, a major advantage in the development of SBL as a potential anti-HIV agent compared with MBLs. These data indicate a necessity to further investigate SBL as an alternative and cost-effective anti-HIV natural product.IMPORTANCE Mannose-binding lectins (MBLs) can block the attachment of HIV to target cells and have been suggested as anti-HIV microbicides. However, the mitogenic effect of MBLs on CD4+ T cells limits this potential in clinical settings. Lectins with galactose (Gal)- or N-acetylgalactosamine (GalNAc)-binding specificity are another important category of carbohydrate-binding proteins (CBP). Compared to high-mannose N-linked glycans, GalNAc-type glycans present much less in HIV gp120 or gp41 glycosylation. Here, we demonstrate that GalNAc-specific soybean lectin (SBL) triggers antiviral signaling via recognition of the cell surface galactosyl group of macrophages, which results in the suppression of HIV at multiple steps. More importantly, SBL has no mitogenic effect on the activation of CD4+ T cells, a major advantage in the development of Gal/GalNAc-specific lectins as naturopathic anti-HIV agents.