Space applications have evolved to play a significant role in disaster relief by providing services including remote sensing imagery for mitigation and disaster damage assessments; satellite communication to provide access to medical services; positioning, navigation, and timing services; and data sharing. Common issues identified in past disaster response and relief efforts include lack of communication, delayed ordering of actions (eg, evacuations), and low levels of preparedness by authorities during and after disasters. We briefly summarize the Space for Health (S4H) Team Project, which was prepared during the Space Studies Program 2014 within the International Space University. The S4H Project aimed to improve the way space assets and experiences are used in support of public health during disaster relief efforts. We recommend an integrated solution based on nano-satellites or a balloon communication system, mobile self-contained relief units, portable medical scanning devices, and micro-unmanned vehicles that could revolutionize disaster relief and disrupt different markets. The recommended new system of coordination and communication using space assets to support public health during disaster relief efforts is feasible. Nevertheless, further actions should be taken by governments and organizations in collaboration with the private sector to design, test, and implement this system.

Background: Identification of cancer testis antigens (CTA) provides new tools for cancer diagnosis and therapy. Results: Expression of the spermatogenic protein FerT recurred in colon carcinoma (CC) cells via DNA demethylation and activation of an intronic promoter. Conclusion: FerT is a new CTA whose expression is regulated by a novel mechanism. Significance: FerT may serve as a new target for CC diagnosis and therapy.

Disruption of the reprogrammed energy management system of malignant cells is a prioritized goal of targeted cancer therapy. Two regulators of this system are the Fer kinase, and its cancer cell specific variant, FerT, both residing in subcellular compartments including the mitochondrial electron transport chain. Here, we show that a newly developed inhibitor of Fer and FerT, E260, selectively evokes metabolic stress in cancer cells by imposing mitochondrial dysfunction and deformation, and onset of energy-consuming autophagy which decreases the cellular ATP level. Notably, Fer was also found to associate with PARP-1 and E260 disrupted this association thereby leading to PARP-1 activation. The cooperative intervention with these metabolic pathways leads to energy crisis and necrotic death in malignant, but not in normal human cells, and to the suppression of tumors growth in vivo. Thus, E260 is a new anti-cancer agent which imposes metabolic stress and cellular death in cancer cells.

The kinase Fer and its spermatogenic meiotic variant, FerT, are coexpressed in normal testes and cancerous tumors, but whether they exert related roles in spermatogenic or malignant cells has not been known. Here, we show that Fer and FerT reside in the mitochondria of spermatogenic cells and are harnessed to the reprogrammed mitochondria of colon carcinoma cells. Both kinases bound complex I of the mitochondrial electron transport chain (ETC) in spermatogenic and in colon carcinoma cells, and silencing of either Fer or FerT was sufficient to impair the activity of this complex. Directed mitochondrial accumulation of FerT in nonmalignant NIH3T3 cells increased their ETC complex I activity, ATP production, and survival, contingent upon stress conditions caused by nutrient and oxygen deprivation. Strikingly, directed mitochondrial accumulation of FerT endowed nonmalignant cells with tumor-forming ability. Thus, recruitment of a meiotic mitochondrial component to cancer cell mitochondria highlights a pivotal role for reprogrammed mitochondria in tumorigenesis. Cancer Res; 74(22);

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