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Query: UMLS:C0016632 (Fox)
 1,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In his best known contribution to the field of psychooncology, the late Dr Bernard H. Fox applied his breadth of scholarship in biopsychosocial cancer epidemiology to address the question of whether and to what extent stress and other psychosocial factors may contribute to cancer risk. Less well known but equally important to the field is his incisive critique of the 1989 study by Spiegel et al. on survival time of patients with metastatic breast cancer following a psychosocial intervention. This essay represents an attempt to take Fox's line of thought to the next logical level of rethinking research on psychosocial interventions in biopsychosocial oncology. Following an analysis of the inadequacy of randomized clinical trials (RCT) to evaluate the causal effects of psychosocial interventions on cancer outcomes and distinguish these from mere prediction, an integrated RCT design is suggested to take into account the psychogenicity of a given intervention, potential mediating mechanisms, and individual differences that could help illuminate hypothesized causal processes linking an experimental intervention and cancer outcomes.
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PMID:Rethinking research on psychosocial interventions in biopsychosocial oncology: an essay written in honor of the scholarly contributions of Bernard H. Fox. 1522 15

Sphingolipids are bioactive lipids that participate in a wide variety of biological mechanisms, including cell death and proliferation. The myriad of pro-death and pro-survival cellular pathways involving sphingolipids provide a plethora of opportunities for dysregulation in cancers. In recent years, modulation of these sphingolipid metabolic pathways has been in the forefront of drug discovery for cancer therapeutics. About two decades ago, researchers first showed that standard of care treatments, e.g., chemotherapeutics and radiation, modulate sphingolipid metabolism to increase endogenous ceramides, which kill cancer cells. Strikingly, resistance to these treatments has also been linked to altered sphingolipid metabolism, favoring lipid species that ultimately lead to cell survival. To this end, many inhibitors of sphingolipid metabolism have been developed to further define not only our understanding of these pathways but also to potentially serve as therapeutic interventions. Therefore, understanding how to better use these new drugs that target sphingolipid metabolism, either alone or in combination with current cancer treatments, holds great potential for cancer control. While sphingolipids in cancer have been reviewed previously (Hannun & Obeid, 2018; Lee & Kolesnick, 2017; Morad & Cabot, 2013; Newton, Lima, Maceyka, & Spiegel, 2015; Ogretmen, 2018; Ryland, Fox, Liu, Loughran, & Kester, 2011) in this chapter, we present a comprehensive review on how standard of care therapeutics affects sphingolipid metabolism, the current landscape of sphingolipid inhibitors, and the clinical utility of sphingolipid-based cancer therapeutics.
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PMID:Novel Sphingolipid-Based Cancer Therapeutics in the Personalized Medicine Era. 3006 Aug 15