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Cigarette, non-small-cell lung cancer patients with elevated IDO1 levels and low Trp/kynurenine ratios were reported clinically. In NSCLC patients, smokers with lower IDO1 sensitivity responded more to anti-PD1 antibody therapy than those with higher IDO1. These results reveal that tobacco smoking causes IDO1 to catabolize Trp metabolism and immune suppression to promote carcinogenesis, and lower IDO1 could be a potential anti-PD1 biomarker in smoker patients, while IDO1-high smoker patients could benefit from IDO1 inhibitors in combination with anti-PD1 antibodies.
Source link: https://doi.org/10.1038/s41392-022-01127-3
Oral cancer tumor cell characteristics include Epidermal Growth Factor Receptor Overexpression and dysregulation of its downstream effector pathways. The present research explores the chemopreventive use of polymeric black tea polyphenols/thearubigins in the hamster model of oral carcinogenesis, as well as the effect of PBPs on EGFR and the molecular participants in the EGFR pathway. Pre and concurrent PBPs reduced the number and number of macroscopic tumors, as well as the number and location of microscopic lesions in a dose-dependent manner.
Source link: https://doi.org/10.1038/s41598-022-18680-0
LKB1's loss of function is the first oncogenic event in lung cancer. LKB1 loss of function is related to patients'u2019 smoking status, according to clinical results. In an LKB1-dependent manner, NNAL exposure has also resulted in increased lung cancer cell migration and chemoresistance. Nevertheless, even in the absence of NNAL, a 120-day NNAL exposure in lung cancer cells resulted in more prominent LKB1 phosphorylation, cell migration, and chemoresistance, suggesting the long-lasting LKB1 loss of function even in the absence of NNAL, although such an effect faded after NNAL was suspended for two months. In comparison to matched normal lung tissues, human lung cancer tissue samples demonstrated elevated LKB1 phosphorylation in comparison to paired normal lung tissues. These findings indicate that LKB1's loss of function in human lung cancer may have been extended to its phosphorylation, which may be mediated by nicotine smoke in a dose-dependent manner via the u03b2-AR/PKA signaling pathway.
Source link: https://doi.org/10.1038/s41388-022-02410-x
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