Cigarette smoke induces endoplasmic reticulum stress and the unfolded protein response in normal and malignant human lung cells.

Although our data support the conclusion that modulators of the UPR pathway are chronically impacted in this tumor type, aside from a modestly significant increase in BiP in the NSCLC diagnostic group with increasing age (p = 0.0187), we found no obvious correlation with any histopathological criteria such as gender, pathologic stage, histological type, or TMN-status and the increased expression of eIF2α, phospho-eIF2α, and BiP.

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