Guilian Niu

TL;DR: It is shown that VEGF expression correlates with Stat3 activity in diverse human cancer cell lines and indicates that Stat3 represents a common molecular target for blocking angiogenesis induced by multiple signaling pathways in human cancers.

TL;DR: It is proposed that tumor Stat-3 activity can mediate immune evasion by blocking both the production and sensing of inflammatory signals by multiple components of the immune system.

TL;DR: It is shown that Stat3 is constitutively activated in diverse tumor-infiltrating immune cells, and ablating Stat3 in hematopoietic cells triggers an intrinsic immune-surveillance system that inhibits tumor growth and metastasis.

TL;DR: It is shown that Src and JAK family tyrosine kinases cooperate to mediate constitutive Stat3 activation in the absence of EGF stimulation in model human breast cancer cell lines, suggesting that tyrosINE kinases transduce signals through Stat3 protein that contribute to the growth and survival of human breast cancers cells in culture and potentially in vivo.

TL;DR: It is shown here that maintenance of NF-kappaB activity in tumors requires Stat3, which is also frequently constitutively activated in cancer, and is central to both the transformed and nontransformed elements in tumors.