IMPORTANCE Establishment of the infant microbiome has lifelong implications on health and immunity. Gut microbiota of breastfed compared with nonbreastfed individuals differ during infancy as well as into adulthood. Breast milk contains a diverse population of bacteria, but little is known about the vertical transfer of bacteria from mother to infant by breastfeeding. OBJECTIVE To determine the association between the maternal breast milk and areolar skin and infant gut bacterial communities. DESIGN, SETTING, AND PARTICIPANTS In a prospective, longitudinal study, bacterial composition was identified with sequencing of the 16S ribosomal RNA gene in breast milk, areolar skin, and infant stool samples of 107 healthy mother-infant pairs. The study was conducted in

More than one million HIV-exposed, uninfected infants are born annually to HIV-positive mothers worldwide. This growing population of infants experiences twice the mortality of HIV-unexposed infants. We found that although there were very few differences seen in the microbiomes of mothers with and without HIV infection, maternal HIV infection was associated with changes in the microbiome of HIV-exposed, uninfected infants. Furthermore, we observed that human breast milk oligosaccharides were associated with the bacterial species in the infant microbiome. The disruption of the infant’s microbiome associated with maternal HIV infection may contribute to the increased morbidity and mortality of HIV-exposed, uninfected infants.

We demonstrate that the VEGF receptor, neuropilin-2 (NRP2) is associated with high-grade, PTEN-null prostate cancer and that its expression in tumor cells is induced by PTEN loss as a consequence of c-Jun activation. VEGF/NRP2 signaling represses IGF-1R expression and signaling and the mechanism involves Bmi-1-mediated transcriptional repression of the IGF-1R. This mechanism has significant functional and therapeutic implications that were evaluated. IGF-1R expression correlates with PTEN and inversely with NRP2 in prostate tumors. NRP2 is a robust biomarker for predicting response to IGF-1R therapy because prostate carcinomas that express NRP2 exhibit low levels of IGF-1R. Conversely, targeting NRP2 is only modestly effective because NRP2 inhibition induces compensatory IGF-1R signaling. Inhibition of both NRP2 and IGF-1R, however, completely blocks tumor growth in vivo.