Is stat3 a positive regulator of gap junctional intercellular communication in cultured , human lung carcinoma cells?
Our findings demonstrate that although Stat3 is generally growth promoting and in an activated form it can act as an oncogene, it is actually required for gap junctional communication both in nontransformed lung epithelial cells and in certain lung cancer lines that retain extensive GJIC.
The risk for biochemical failure after adjuvant radiotherapy in post-operative patients presenting with minimal residual disease is significantly influenced by the Roach formula. These findings are considered to provide a rationale for the decision on the volume of post-operative radiotherapy.