We analyzed background data including birth year, lung cancer status, and interferon-gamma release assay (IGRA) data of lung cancer patients who were admitted to National Hospital Organization Tokyo National Hospital from 2010 to 2016.
Overall, the odds ratio to develop lung cancer was almost three times greater for women than for men, DNA adduct levels were higher among females than in males and mutations in the tumor suppressor gene p53 and the proto-oncogene K-RAS were more frequently found in women than in men.
The evaluation of Programmed cell Death Ligand 1 (PD-L1) expression in the tumor cells with immunohistochemistry is a mandatory diagnostic step in the treatment of lung cancer.
Most importantly, further experiments demonstrated that decreased the expression of KLF20A significantly downregulated expression of p-JNK and MMP7, which indicated that knockdown of KIF20A alters lung cancer cell phenotype and regulates JNK pathways.
This study was investigated the production of IL-8 from cancer cells induced by X-rays may involve in the radiation-induced inflammation.<i>Materials and methods:</i> We analyzed IL-8 in human lung cancer cell lines after expose to X-rays, and we also detect IL-8 in HUVEC cells and THP1 cells as endothelial cell and macrophage model to identify the change in normal cells after expose.
Multiplex fluorescence in situ hybridisation to detect anaplastic lymphoma kinase and ROS proto-oncogene 1 receptor tyrosine kinase rearrangements in lung cancer cytological samples.
In a blinded study, we detected ALK fusion from formalin-fixed paraffin-embedded lung cancer samples with a 100% 47) and genotyping /47) and genotyping (7/7).
The role of serum tumor markers (STMs) in the modern management of epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) mutations in lung cancer remains poorly described.
We aimed to characterize the mechanisms of resistance to lorlatinib occurring in patients with <i>ALK</i>-rearranged lung cancer and design new therapeutic strategies in this setting.
Higher healthcare system delay was observed among patients with extra-pulmonary TB (2.067, 1.885-2.268) and pulmonary comorbidities - lung cancer (2.391, 1.656-3.452), sarcoidosis (3.316, 1.370-8.022) and COPD (1.295, 1.059-1.584) - and in patients residing further from a healthcare service (1.040, 1.018-1.062).
Besides being a predictive biomarker of response to immunotherapy in lung cancer in general, programmed death-ligand 1 (PD-L1) is not so well correlated with treatment outcomes of lung adenocarcinoma (ADC) harbouring epidermal growth factor receptor (EGFR) mutations, as reported studies are inconclusive and seldom addressed the issues of response to treatment and resistance.
Besides being a predictive biomarker of response to immunotherapy in lung cancer in general, programmed death-ligand 1 (PD-L1) is not so well correlated with treatment outcomes of lung adenocarcinoma (ADC) harbouring epidermal growth factor receptor (EGFR) mutations, as reported studies are inconclusive and seldom addressed the issues of response to treatment and resistance.
We investigated whether A2B receptor is involved in EGFR translocation and DNA damage response (γH2AX/53BP1 focus formation) of lung cancer cells by means of immunofluorescence studies.
Several growth related genes such as EGFR and VEGF as well as tumour suppressor genes such as p53 have been implicated in LC pathogenesis and progression.
Mechanistically, we uncovered that autophagy was induced upon loss of <i>circHIPK3</i> via the <i>MIR124-3p</i>-STAT3-PRKAA/AMPKa axis in STK11 mutant lung cancer cell lines (A549 and H838).
These results demonstrated that tumor-infiltrating TAMs are extrinsic regulators of tumor PD-L1 expression, indicating that combination therapy targeting both tumor PD-L1 and stromal TAMs might be a possible strategy for effective treatment of lung cancer.