Surveillance of SARS-CoV-2 transmission in educational institutions, August to December 2020, Germany.

This study aims at providing estimates on the transmission risk of SARS-CoV-2 in schools and day-care centres. We calculated secondary attack rates (SARs) using individual-level data from state-wide mandatory notification of index cases in educational institutions, followed by contact tracing and PCR-testing of high-risk contacts. From August to December 2020, every sixth of overall 784 independent index cases was associated with secondary cases in educational institutions. Monitoring of 14 594 institutional high-risk contacts (89% PCR-tested) of 441 index cases during quarantine revealed 196 secondary cases (SAR 1.34%, 0.99-1.78). SARS-CoV-2 infection among high-risk contacts was more likely around teacher-indexes compared to student-/child-indexes (incidence rate ratio (IRR) 3.17, 1.79-5.59), and in day-care centres compared to secondary schools (IRR 3.23, 1.76-5.91), mainly due to clusters around teacher-indexes in day-care containing a higher mean number of secondary cases per index case (142/113 = 1.26) than clusters around student-indexes in schools (82/474 = 0.17). In 2020, SARS-CoV-2 transmission risk in educational settings was low overall, but varied strongly between setting and role of the index case, indicating the chance for targeted intervention. Surveillance of SARS-CoV-2 transmission in educational institutions can powerfully inform public health policy and improve educational justice during the pandemic.

Expression of the adhesion molecule CEACAM1 (CD66a, BGP, C-CAM) in breast cancer is associated with the expression of the tumor-suppressor genes Rb, Rb2, and p27.

The adhesion molecule CEACAM1 (CD66a, BGP, C-CAM) is not only involved in maintaining normal tissue architecture, but also acts as a tumor suppressor in several experimental systems where loss of CEACAM1 expression results in enhanced tumor-cell growth and tumorigenicity. In order to further analyze the role of CEACAM1 in the development of breast cancer, we performed Western-blot analysis and immunohistochemistry with highly specific monoclonal antibodies in a cohort of 68 mammary carcinomas which had also been analyzed for expression of cell-cycle regulatory proteins cyclin D1, cyclin E, p16, p21, p27, Rb, and Rb2, as well as for steroid hormone receptor status, Ki67, and HER2/neu immunoreactivity. High CEACAM1 protein expression as found using both methods correlated significantly with expression of the retinoblastoma proteins Rb (P=0.004 and 0.013) and Rb2/p130 (P=0.003 and 0.007). In addition, we found a weak association of CEACAM1 expression with p27 protein levels (P=0.087 and 0.039), but with none of the other analyzed parameters. These results indicate the possibility of a functional link between cell-adhesion molecules and cell-cycle regulation that might play an important role in the development of mammary carcinomas.

FosB is highly expressed in normal mammary epithelia, but down-regulated in poorly differentiated breast carcinomas.

FosB is a member of the AP-1 family of transcription factors which represent important regulators of cell proliferation and differentiation. Based on prior results which indicated a role of FosB in breast cancer, we studied FosB protein and mRNA expression by immunohistochemistry and, partly, in situ hybridization in 68 mammary carcinomas and normal breast tissues. We found strong nuclear FosB immunoreactivity in epithelial cells of normal lobules and ducts, whereas carcinomas frequently showed loss of FosB expression (n = 8) or weak immunostaining (n = 24). Reduced FosB protein expression in tumors correlated with high grading (p = 0.005), negative estrogen and progesterone receptor status (p < 0.001), and strong HER2/neu expression (p = 0.025). Comparison with expression of seven cell-cycle regulators revealed an association of low/absent FosB staining with p16MTS1 overexpression (p = 0.005). RT-PCR showed expression of full-length FosB and the smaller splice variant FosB2 in most carcinomas and cell lines with and without FosB protein expression, indicating that both proteins are differentially regulated mainly at a post-transcriptional level. By sequence analysis of the coding region in four cell lines and 17 carcinomas we detected a mutation in HBL-100 cells. Our results indicate that high FosB expression might be necessary for normal proliferation and differentiation of mammary epithelial cells, and reduced FosB protein levels might be involved in dedifferentiation during breast tumorigenesis.