The odds ratio (OR) and its 95% confidence interval (95% CI) were used to evaluate the correlation between TGF-β1 gene polymorphism and lung tumor risk.
Finally, PTBP1 was found to be negatively correlated with AXL expression in lung tumor tissues in Oncomine datasets and in tissue micro-array (TMA) analysis.
Finally, PTBP1 was found to be negatively correlated with AXL expression in lung tumor tissues in Oncomine datasets and in tissue micro-array (TMA) analysis.
The expression levels of IL-17A gene and miR-9 was assessed in 26 NSCLC tissue samples and 26 unchanged lung tissue adjacent to lung tumors (control tissue), using qPCR.
The epidermal growth factor receptor (EGFR), when carrying an activating mutation like del19 or L858R, acts as an oncogenic driver in a subset of lung tumors.
<b>Results:</b> LM-Dox exhibited tumor tropism in response to CCL2 produced by A549 lung tumor cells and lung tumor tissues resulting in a remarkably higher amount of tumor accumulation than the case of Lipo-Dox (~ 4-fold).
PSAT1 silencing also reduced the number of lung tumor nodules in a model of experimental metastasis; yet did not decrease anchorage-independent growth.
Levels of secreted SOCS3 were diminished in lungs of patients with non-small cell lung cancer and in a mouse model of lung cancer, and the impaired ability of murine AMs to secrete SOCS3 within EVs preceded the development of lung tumors.
To explore the molecular mechanism/s by which PRMT6 promotes lung tumor growth, we used proteomics-based approaches and identified interleukin-enhancer binding protein 2 (ILF2) as a novel PRMT6-associated protein.
We show this association of PRPRT methylation with upregulation of the STAT3 target genes <i>Cyclin D1</i> and <i>Bcl-X<sub>L</sub></i> in patient derived lung tumour samples.
We show this association of PRPRT methylation with upregulation of the STAT3 target genes <i>Cyclin D1</i> and <i>Bcl-X<sub>L</sub></i> in patient derived lung tumour samples.
Here we report interferon regulatory factor 8 (<i>IRF8</i>), a member of the <i>IRF</i> family of transcription factors, as a potent lung tumor suppressor gene.
Using NU5455, a newly identified highly selective oral inhibitor of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) activity, we found that it was indeed possible to preferentially augment the effect of targeted radiotherapy on human orthotopic lung tumors without influencing acute DNA damage or a late radiation-induced toxicity (fibrosis) to normal mouse lung.
Diplatin's mode of action was characterized to be through cell cycle arrest in the G2/M phase and induction of lung tumor apoptosis <i>via</i> ROS/JNK/p53-mediated pathways.
We demonstrate that Keap1-deficient Kras<sup>G12D</sup> lung tumors arise from a bronchiolar cell-of-origin, lacking pro-tumorigenic macrophages observed in tumors originating from alveolar cells.