Sizhi Paul Gao

TL;DR: In this article, the authors found that persistently activated or tyrosine-phosphorylated STAT3 (pSTAT3) is found in 50% of lung adenocarcinomas.

TL;DR: A statistical algorithm is developed to identify recurrently mutated residues in tumor samples and finds that half of all human tumors possess one or more mutational hotspots with widespread lineage-, position- and mutant allele–specific differences, many of which are likely functional.

TL;DR: The data reported here suggest that broader, early testing for molecular alterations that have not yet been recognized as standard-of-care predictive biomarkers of drug response could accelerate the development of targeted agents for rare mutational events and could result in improved clinical outcomes.

TL;DR: This study provides the first evidence for IL-6 expression at the leading edge of invasive human breast tumors and demonstrates mechanistically that IL- 6/JAK/Stat3 signaling plays a critical and pharmacologically targetable role in orchestrating the composition of the tumor microenvironment that promotes growth, invasion, and metastasis.

TL;DR: A principal mechanism of Stat3 activation in breast cancer is through the IL-6/gp130/Jak pathway, and a positive correlation between pStat3 and IL- 6 expression is found.