Clinical Significance of BD Bactec FX Blood Culture Incubation Beyond 96 Hours (4 Days).

Blood cultures (BC) for bacteria and yeast have traditionally been incubated for 5 days using modern instruments. Many organisms may grow sooner, and the need for the full 5-day incubation period has been questioned. This study evaluated the clinical significance of isolates recovered beyond 96 h.

Activation of NF-κB and p300/CBP potentiates cancer chemoimmunotherapy through induction of MHC-I antigen presentation.

Many cancers evade immune rejection by suppressing major histocompatibility class I (MHC-I) antigen processing and presentation (AgPP). Such cancers do not respond to immune checkpoint inhibitor therapies (ICIT) such as PD-1/PD-L1 [PD-(L)1] blockade. Certain chemotherapeutic drugs augment tumor control by PD-(L)1 inhibitors through potentiation of T-cell priming but whether and how chemotherapy enhances MHC-I-dependent cancer cell recognition by cytotoxic T cells (CTLs) is not entirely clear.

Bi-allelic Loss of CDKN2A Initiates Melanoma Invasion via BRN2 Activation.

Loss of the CDKN2A tumor suppressor is associated with melanoma metastasis, but the mechanisms connecting the phenomena are unknown. Using CRISPR-Cas9 to engineer a cellular model of melanoma initiation from primary human melanocytes, we discovered that a lineage-restricted transcription factor, BRN2, is downstream of CDKN2A and directly regulated by E2F1. In a cohort of melanocytic tumors that capture distinct progression stages, we observed that CDKN2A loss coincides with both the onset of invasive behavior and increased BRN2 expression.

Author Correction: Inflammation-induced IgA cells dismantle anti-liver cancer immunity.

In this Article, the sentence: "After 7 months of HFD, MUP-uPA mice developed HCC, which contained numerous (usually 50-100 per tumour) non-recurrent coding mutations in pathways that are mutated in human HCC (Fig. 2d and Extended Data Fig. 6a).

Erratum: Inflammation-induced IgA cells dismantle anti-liver cancer immunity.

This corrects the article DOI: 10.1038/nature24302.

Inflammation-induced IgA+ cells dismantle anti-liver cancer immunity.

The role of adaptive immunity in early cancer development is controversial. Here we show that chronic inflammation and fibrosis in humans and mice with non-alcoholic fatty liver disease is accompanied by accumulation of liver-resident immunoglobulin-A-producing (IgA) cells. These cells also express programmed death ligand 1 (PD-L1) and interleukin-10, and directly suppress liver cytotoxic CD8 T lymphocytes, which prevent emergence of hepatocellular carcinoma and express a limited repertoire of T-cell receptors against tumour-associated antigens.