How dying tumor cells get noticed: Besides killing tumor cells directly, some chemotherapies, such as anthracyclines, also activate the immune system to kill tumors. Vacchelli et al. discovered that in mice, anthracycline-induced antitumor immunity requires immune cells to express the protein formyl peptide receptor 1 (FPR1). Dendritic cells (DCs) near tumors expressed especially high amounts of FPR1. DCs normally capture fragments of dying tumor cells and use them to activate nearby T cells to kill tumors, but DCs lacking FPR1 failed to do this effectively. Individuals with breast or colon cancer expressing a variant of FPR1 and treated with anthracyclines showed poor metastasis-free and overall survival. Thus, FPR1 may affect anti-tumor immunity in people, too. Science , this issue p. 972

The reconstitution of a complex microenvironment on microfluidic chips is one of the cornerstones to demonstrate the improved flexibility of these devices with respect to macroscale in vitro approaches. In this work, we realised an on-chip model to investigate the interactions between cancer and immune system. To this end, we exploited mice deficient (Knock Out, KO) for interferon regulatory factor 8 (IRF-8), a transcription factor essential for the induction of competent immune responses, to investigate how IRF-8 gene expression contributes to regulate immune and melanoma cells crosstalk. In vivo, IRF-8 KO mice are highly permissive to B16 melanoma growth due to failure of immune cells to properly exert immunosurveillance. B16 cells and immune cells isolated from the spleen of wild type (WT) and IRF-8 KO mice were co-cultured for one week in a PDMS platform and monitored by fluorescence microscopy and time-lapse recordings. We observed that WT spleen cells migrated through microchannels connecting the culturing chambers towards B16 cells and tightly interacted with tumor cells, forming clusters of activation. In contrast, IRF-8 KO immune cells poorly interacted with melanoma cells. In parallel, B16 cells were more attracted towards microchannels, acquiring a more invasive behaviour in the presence of IRF-8 KO spleen cells, with respect to WT cells. Our results strongly confirm the in vivo observations and highlight the value of on-chip co-culture systems as a useful in vitro tool to elucidate the reciprocal interactions between cancer cells and host immune system, with relevant impact in the development of more effective anti-tumor therapeutic strategies.

We present time integrated and time-resolved photoluminescence (PL) measurements on a single InAs∕GaAs quantum dot (QD), embedded in a planar microcavity, emitting in the 1300nm telecom band. The results of both measurements clearly identify the exciton and biexciton transitions from a single QD. By optimizing the extraction efficiency of the QD PL into the single mode fibers and carefully tuning two InGaAs avalanche photodiodes, we were able to measure the second order correlation function with integration times comparable to those made with silicon based technology. These measurements demonstrate that our single QDs are efficient sources of triggered single photons for quantum key distribution in the O band.

RF deep hyperthermia systems make use of phased arrays of applicators in order to heat tumors selectively while maintaining healthy tissue at normal temperatures. A new method for the array synthesis is proposed based on the identification of targets to be heated (tumors) and targets to be prevented from excess electromagnetic radiation. The best array feed for each target is found from the solution of the eigenvector problem for a positive definite Hermitian matrix defined for that target. The optimal feed in a global sense then results from a trade-off of the best feeds of individual targets enforced through minimization of an objective function aimed at weighting the distances of the globally optimal feed from the feed vectors optimized for each target separately. An application to the heating of a pelvis is provided as an example.