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The transcription factor, interferon regulatory factor 4 (IRF4), serves an essential role in the regulation of immune responses, and has been reported to act as a diagnostic and prognostic marker for various hematological malignancies. The present study aimed to investigate whether IRF4 could exert effects on human non‑small cell lung cancer (NSCLC) and to explore the underlying mechanism. The mRNA and protein expression of IRF4 was detected in NSCLC tissues using reverse‑transcription quantitative polymerase chain reaction and western blotting, respectively. In the in vitro experiment, IRF4 expression was knocked down or overexpressed using lentivirus in human lung adenocarcinoma A549 and lung squamous cell carcinoma LC‑AI cell lines. Cell proliferation and colony number were analyzed using MTT and colony formation assays, respectively. The expression levels of IRF4 mRNA and protein were significantly higher in NSCLC tissues (n=54) compared with that in adjacent non‑tumor tissues. Similarly, the expression levels of Notch1 and Notch2 mRNA were significantly higher in NSCLC tissues. Furthermore, the expression level of IRF4 mRNA was positively correlated with the levels of Notch1 and Notch2 mRNA in NSCLC tissues. Consequently, using NSCLC cell lines, it was demonstrated that the knockdown of IRF4 expression significantly reduced the cell proliferation rate and colony formation, whereas IRF4‑overexpression significantly increased them. Notably, the IRF4 knockdown significantly decreased the expression levels of Notch1 and Notch2 mRNA, and phosphorylated protein kinase B (AKT), whereas IRF4 overexpression resulted in the opposite. The results of the present study indicate that IRF4 is overexpressed and serves as a tumor promoter in human NSCLC, at least partially, through activating the Notch‑Akt signaling pathway.

The aim was to compare the efficacy and toxicity of gemcitabine plus docetaxel (GD) with platinum-based regimens in patients with untreated advanced non-small cell lung cancer (NSCLC). We searched PubMed, Embase and the Cochrane Central Register of Controlled Trials databases for relevant trials. Reference lists of original articles and review articles were also examined. Abstracts presented at the ASCO and ESMO meetings were also searched. Studies were evaluated for eligibility and quality, and then, the data were extracted and analyzed. Statistical analyses were conducted by using RevMan 5.1. The primary end point was overall survival (OS). Secondary end points included 1-year survival, time to progression (TTP), overall response rate (ORR) and grade 3–4 toxicity. Nine randomized controlled trials were identified ultimately. The meta-analysis demonstrated that the survival between GD and platinum-based regimens was comparable according to the pooled HR for overall survival (1.04, 95% CI = 0.96–1.12, p = 0.39) and RR for one-year survival (0.94, 95% CI = 0.84–1.06, p = 0.33). Platinum-based regimens had an advantage in TTP (HR = 1.12, 95% CI = 1.02–1.24, p = 0.02) and ORR (RR = 0.86, 95% CI = 0.74–0.99, p = 0.03). However, GD induced less grade 3–4 nausea/vomiting, anemia, neutropenia and febrile neutropenia (RR = 0.36, 95% CI = 0.15–0.86, p = 0.02; RR = 0.35, 95% CI = 0.23–0.53, p = 0.00; RR = 0.68, 95% CI = 0.52–0.88, p = 0.003; RR = 0.53, 95% CI = 0.34–0.82, p = 0.004, respectively). Grade 3–4 diarrhea, sensory neuropathy, fatigue and thrombocytopenia were comparable between the two groups. GD acquired similar survival with platinum-based regimens in first-line treatment of advanced NSCLC. Platinum-based regimens had an advantage in TTP and ORR with more grade 3–4 nausea/vomiting, anemia, neutropenia and febrile neutropenia compared with GD.

Aims: Pleiotrophin (PTN), an angiogenic factor, is associated with various types of cancer, including lung cancer. Our aim was to investigate the possibility of using serum PTN as an early indicator regarding disease diagnosis, classification and prognosis, for patients with non-small cell lung cancer (NSCLC). Methods: Significant differences among PTN levels in patients with small cell lung cancer (SCLC, n=40), NSCLC (n=136), and control subjects with benign pulmonary lesions (n=21), as well as patients with different pathological subtypes of NSCLC were observed. Results: A serum level of PTN of 300.1 ng/ml, was determined as the cutoff value differentiating lung cancer patients and controls, with a sensitivity and specificity of 78.4% and 66.7%, respectively. Negative correlations between serum PTN level and pathological differentiation level, stage, and survival time were observed in our cohort of patients with NSCLC. In addition, specific elevation of PTN levels in pulmonary tissue in and around NSCLC lesions in comparison to normal pulmonary tissue obtained from the same subjects was also observed (n=2). Conclusion: This study suggests that the serum PTN level of patients with NSCLC could be an early indicator for diagnosis and prognosis. This conclusion should be further assessed in randomized clinical trials.