High Mn twinning induced plasticity (TWIP) steel is a new type of structural steel, characterised by both high strength and superior formability. TWIP steel offers an extraordinary opportunity to adjust the mechanical properties of steel by modifying the strain hardening. The use of TWIP steel may therefore lead to a considerable lightweighting of steel components, a reduction of material use and an improved press forming behaviour. These key advantages will help implement current automotive vehicle design trends which emphasise a reduction of greenhouse gas emissions and lowering of fuel consumption. In addition, high strength TWIP steel will effectively contribute to weight containment in vehicles equipped with hybrid and electric motors, as these are considerably heavier than conventional motors. The present review addresses all aspects of the physical metallurgy of the high strength TWIP steel with a special emphasis on the properties and key advantages of TWIP sheet steel products relevant to automotive applications.

The secondary T790M mutation in epidermal growth factor receptor (EGFR) is the major mechanism of acquired resistance to EGFR tyrosine kinase inhibitors (TKI) in non-small cell lung cancer (NSCLC). Although irreversible EGFR TKIs, such as afatinib or dacomitinib, have been introduced to overcome the acquired resistance, they showed a limited efficacy in NSCLC with T790M. Herein, we identified the novel de novo resistance mechanism to irreversible EGFR TKIs in H1975 and PC9-GR cells, which are NSCLC cells with EGFR T790M. Afatinib activated interleukin-6 receptor (IL-6R)/JAK1/STAT3 signaling via autocrine IL-6 secretion in both cells. Inhibition of IL-6R/JAK1/STAT3 signaling pathway increased the sensitivity to afatinib. Cancer cells showed stronger STAT3 activation and enhanced resistance to afatinib in the presence of MRC5 lung fibroblasts. Blockade of IL-6R/JAK1 significantly increased the sensitivity to afatinib through inhibition of afatinib-induced STAT3 activation augmented by the interaction with fibroblasts, suggesting a critical role of paracrine IL-6R/JAK1/STAT3 loop between fibroblasts and cancer cells in the development of drug resistance.