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ne does not appear to be a sufficient predictor of taselisib activity. Comprehensive genomic profiling has defined key oncogenic drivers and distinct molecular subtypes in esophagogastric cancer; however, the number of clinically actionable alterations remains limited. To establish preclinical models for testing genomically driven therapeutic strategies, we generated and characterized a large collection of esophagogastric cancer patient-derived xenografts (PDXs). We established a biobank of 98 esophagogastric cancer PDX models derived fro