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.
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.
In this study, on the basis of the crystal structure of K-Ras, 21 analogues (TKR01-TKR21) containing urea or thiourea were rationally designed, which can effectively inhibit the lung cancer cell A549 growth.
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.
However, patients lacking EGFR mutations are not sensitive to EGFR-TKI treatment and the emergence of secondary resistance poses new challenges for the targeted therapy of lung cancer.
PET/CT images of lung cancer patients were obtained from public databases and used to establish two datasets, respectively to classify histological subtypes (156 adenocarcinomas and 32 squamous cell carcinomas) and EGFR mutation status (38 mutant and 100 wild-type samples).
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).
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.
BRAF- and MEK-targeted therapies are effective in BRAFV600E/K metastatic melanoma and lung cancers; however, responses are short-lived due to emergence of 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.
<b>Conclusions:</b> In conclusion, metformin may potentially enhance the therapeutic effect and increase survival in type 2 DM patients with lung cancer receiving EGFR-TKI therapy.
Gene polymorphisms of CHRNA3 (rs578776) and CHRNA4 (rs1044396 and rs2229959) were associated with the success of smoking cessation after the diagnosis of lung cancer, which should be considered in the management of smoking cessation after patients are diagnosed with lung cancer.
BRAF- and MEK-targeted therapies are effective in BRAF V600E/K metastatic melanoma and lung cancers; however, responses are short-lived due to emergence of resistance.
Taken together, our results reveal a novel mitophagic mechanism in lung cancer, suggesting that lung cancer-linked mutations in PARK2 are associated with impaired mitophagy and identifying DFP as a novel therapeutic agent for PARK2-linked lung cancer and possibly other types of cancers driven by mitophagic dysregulation.
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.
Sub-group analysis revealed that high expression of cyclin D1 was related to worse OS of head and neck cancers (HR=2.08, 95% CI: 1.75-2.47; P<0.001), but not in breast (HR=1.033, 95% CI: 0.873-1.223, P= 0.702), gastrointestinal (HR = 1.025, 95% CI:0.824-1.275; P=0.825), bladder (HR=0.937, CI: 0.844-1.041; P=0.225) and in lung cancer patients (HR=1.092, CI: 0.819-1.455; P=0.549).