ArticleCancer research2019
Lulling the Cancer Cell into an Eternal Sleep.
Article in Cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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2 authors at 2 institutions in 1 country.
Funding
Abstract
A hallmark of metastasis is the ability of cancer cells to undergo the epithelial-to-mesenchymal transition to invade and disseminate to distal sites. More recently, the case has been made that the critical last step in metastasis is dependent on the ability to undergo reversion to an epithelial phenotype in a process known as the mesenchymal-to-epithelial transition (MET). It is this transition in the metastatic cascade that researchers are focusing on clinically to treat disseminated disease. Shinde and colleagues identified spleen tyrosine kinase (SYK) as a critical mediator of MET that facilitated the removal of P-bodies during autophagy. Remarkably, pharmacologic inhibition of SYK inhibited the clearance of P-bodies and autophagy in preclinical models of metastasis, arresting cancer cells in an indefinite dormant state and preventing tumor cell colonization and thus the establishment of aggressive metastatic disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.