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Abstract
Oncogenes as the center of cancer research focused attention 30 years ago on signal transduction especially tyrosine phosphorylation. Discovery that the Jun oncoprotein was a site-specific DNA binding protein demanded a connection of signaling abnormalities with transcriptional control [1]. The cytokine responsive Jak-STAT pathway, discovered through studying α-interferon activation of STATs 1 and 2 by the Jak tyrosine kinases (Tyk2, Jak1, Jak2) was soon broadened to include the other five STATs [2]. The first description of STAT3 in 1994 [3] raised suspicion in the direction of cancer because IL-6 and EGF, already recognized to have cancer connections, were the originally recognized ligands that activated the STAT3 homodimer.
Highlights
Oncogenes as the center of cancer research focused attention 30 years ago on signal transduction especially tyrosine phosphorylation
Perhaps half or more of human tumors have long since been documented to contain persistently active STAT3 and human tumor cell lines depend on STAT3 for continued rapid growth and avoidance of apoptosis [7]
Valeria Poli and a host of colleagues [8] have published a synthesis of previously established results plus many new experiments to provide convincing evidence that STAT3 transcriptional activity has an important role in establishing the addiction of tumor cells to glycolytic energy derivation and attendant glucose dependence ---the Warburg effect [9, 10]
Summary
Oncogenes as the center of cancer research focused attention 30 years ago on signal transduction especially tyrosine phosphorylation. Src-transformed cell lines all had persistently active STAT3 that was found to be required for Src-dependent oncogenic transformation of cultured cells [5,6].
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