PMC:4307189 / 2874-4015 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4307189","sourcedb":"PMC","sourceid":"4307189","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4307189","text":"Cancer development involves a series of events, ranging from tumorigenesis to metastasis, each of which may be caused by perturbations in crucial signal transduction pathways. Recently, drugs (inhibitors) specifically targeting critical components of signaling pathways known to be up-regulated in specific cancers have been used in the clinic. However, success of these inhibitors is limited by the intrinsic potential of cancer cells to acquire drug resistance. Recent advances in both clinical and laboratory research have reported that cancer cells may adopt several mechanisms against particular treatments including adjusting the signaling circuitry, activation of alternative pathways and cross-talks among various pathways to overcome the effects of inhibitors [1,2]. Resistance to a particular drug such as EGFR (Epidermal Growth Factor Receptor) tyrosine kinase inhibitors, may occur not only due to cross-talks among EGFR-mediated pathways, but also due to cross-talks with pathways triggered by other receptors. Therefore, targeting signaling cross-talks may have the potential to sensitize cancer cells to particular inhibitors.","tracks":[{"project":"2_test","denotations":[{"id":"25599599-23542173-14868090","span":{"begin":770,"end":771},"obj":"23542173"},{"id":"25599599-22474259-14868091","span":{"begin":772,"end":773},"obj":"22474259"}],"attributes":[{"subj":"25599599-23542173-14868090","pred":"source","obj":"2_test"},{"subj":"25599599-22474259-14868091","pred":"source","obj":"2_test"}]}],"config":{"attribute types":[{"pred":"source","value type":"selection","values":[{"id":"2_test","color":"#ecec93","default":true}]}]}}