The latest medical research on Lung Cancer

The research magnet gathers the latest research from around the web, based on your specialty area. Below you will find a sample of some of the most recent articles from reputable medical journals about lung cancer gathered by our medical AI research bot.

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CircRNA circ_0008037 facilitates tumor growth and the Warburg effect via upregulating NUCKS1 by binding to miR-433-3p in non-small cell lung cancer.

Thoracic Cancer

Circular RNAs (circRNAs) participate in the genesis and progression of tumors, including non-small cell lung cancer (NSCLC). At present, the role and regulatory mechanisms of circRNAs in NSCLC have not been fully elucidated. The aim of this study was to explore the role and regulatory mechanism of circRNA hsa_circ_0008037 (circ_0008037) in NSCLC.

Expression of circ_0008037 in NSCLC tissues and cells was detected by quantitative real-time polymerase chain reaction (RT-qPCR). Loss-of-function experiments were performed to analyze the influence of circ_0008037 knockdown on proliferation, migration, invasion, and the Warburg effect of NSCLC cells. Western blotting was utilized for protein analysis. The regulatory mechanism of circ_0008037 was surveyed by bioinformatics analysis, RNA pulldown assay, and dual-luciferase reporter assay. Xenograft assay was used to validate the oncogenicity of circ_0008037 in NSCLC in vivo.

Circ_0008037 was upregulated in NSCLC tissues and cells. Circ_0008037 downregulation reduced tumor growth in vivo and repressed proliferation, migration, invasion, and decreased the Warburg effect of NSCLC cells in vitro. Mechanically, circ_0008037 regulated nuclear ubiquitous casein kinase and cyclin-dependent kinase substrate 1 (NUCKS1) expression via sponging miR-433-3p. Furthermore, MiR-433-3p inhibitor reversed the inhibiting influence of circ_0008037 silencing on proliferation, migration, invasion, and the Warburg effect of NSCLC cells. Also, NUCKS1 elevation overturned the repressive influence of miR-433-3p mimic on proliferation, migration, invasion, and the Warburg effect of NSCLC cells.

Circ_0008037 accelerated tumor growth and elevated the Warburg effect via regulating NUCKS1 expression by adsorbing miR-433-3p, providing an underlying target for NSCLC treatment.

Clinical outcome, long-term survival and tolerability of sequential therapy of first-line crizotinib followed by alectinib in advanced ALK+NSCLC: A multicenter retrospective analysis in China.

Thoracic Cancer

There is limited data on the clinical outcome, long-term survival and tolerability of sequential therapy of first-line crizotinib followed by alectinib in a real-world setting for Chinese patients with advanced ALK+ NSCLC.

The medical records of patients who received sequential therapy with first-line crizotinib followed by alectinib (no intermittent systemic therapy was allowed between the two ALK-TKIs) were collected from six centers in China. Combined time treatment to failure (C-TTF) was defined as the period from the start of crizotinib to the complete discontinuation of alectinib due to any cause.

A total of 61 patients were included in our study. Fifty-two patients were switched to alectinib due to disease progression, seven as a result of toxicity, and two due to patient preference. At the time of data cutoff, alectinib treatment was discontinued in 31 patients on account of disease progression while severe adverse events resulted in cessation of alectinib in another two patients. Rebiopsy was conducted in 21 patients following disease progression on alectinib in whom ALK secondary mutation was found in 13 patients. Patients with ALK secondary mutation demonstrated better PFS during treatment with subsequent ALK-TKIs compared with those without (10.4 vs. 3.1 m, p = 0.0018, HR = 0.08). With a median follow-up of 34.3 months, C-TTF was 39.2 months and estimated 5-year OS was 68.6% in the overall population.

Sequential therapy with first-line crizotinib followed by alectinib demonstrated long-term benefits. Different efficacy in subsequent ALK-TKI between patients with or without ALK secondary mutation further emphasized the importance of rebiopsy to guide targeted therapy more precisely.

Mig-6 could inhibit cell proliferation and induce apoptosis in esophageal squamous cell carcinoma.

Thoracic Cancer

To investigate the expression and biological functions of mitogen-induced gene 6 (Mig-6) in esophageal squamous cell carcinoma (ESCC).

The expression of Mig-6 in ESCC tissues and normal esophageal epithelial tissues were measured by immunohistochemistry (IHC) assay. MTT test was applied to detect the proliferative ability of ESCC cells after Mig-6 was upregulated by transfection. A fluid cytology assay was used to detect apoptosis of ESCC cells. Agilent whole human genome oligo microarray was used to screen different expressed genes and the possible signaling pathways which might be involved.

The expression of Mig-6 protein was lower in ESCC tissues compared to normal esophageal epithelial tissues. Mig-6 could restrain the ESCC cell growth and induce cell apoptosis. PPAR, CAMs and MAPK signaling pathways might be involved.

Mig-6 might be a new tumor suppressor gene and a possible target for the specific therapy of ESCC.

Comprehensive analysis of PD-L1 in non-small cell lung cancer with emphasis on survival benefit, impact of driver mutation and histological types, and archival tissue.

Thoracic Cancer

The aim of the study was to assess programmed death-ligand-1 (PD-L1) expression in different histological types and gene mutation status of patients with non-small cell lung cancer (NSCLC).

A total of 4062 pathology-confirmed lung cancer patients were retrospectively screened at Kaohsiung Chang Gung Memorial Hospital from November 2010 to June 2017. There were 699 NSCLC patients with confirmed PD-L1 expression level retrospectively enrolled for analysis.

There was a trend of higher PD-L1 expression in squamous cell carcinoma and adenosquamous cell carcinoma than in adenocarcinoma (p = 063). Significant higher PD-L1 expression in EGFR wild-type was noted (p < 0.001). No significant differences in PD-L1 expression were found between ALK wild- and mutant types, but there seem was a trend of high PD-L1 level noted in ALK mutation patients (p = 0.069). In EGFR mutation patients, a higher time to treatment failure (TTF) duration was observed in no PD-L1 expression (p = 0.011). Longer tumor tissue storage time correlated with lower PD-L1 expression in lung cancer (p < 0.001 for linear trend).

There were a trend or significant differences in PD-L1 expression between different histological types in NSCLC, different EGFR and ALK status, and different tumor tissue storage time. A higher survival benefit was observed in no PD-L1 expression than with PD-L1 expression in adenocarcinoma, EGFR and ALK mutation patients. We recommend that PD-L1 assay should be performed as early as possible if tissue is available.

MicroRNA-21 was a promising biomarker for lung carcinoma diagnosis: An update meta-analysis.

Thoracic Cancer

To investigate the diagnostic performance of microRNA-21 detected in serum or sputum as a biomarker for lung carcinoma identification through pooling the open published data.

Clinical diagnostic studies related to microRNA-21 as a biomarker for lung carcinoma identification were electronically searched in the databases of Pubmed, EMBASE, Cochrane Library, Chinese National Knowledge Infrastructure, Wanfang, and Google Scholar. The data of the included studies was extracted and made pooling of diagnostic sensitivity, specificity, diagnostic odds ratio (DOR), area under the summary receiver operating characteristic curve (ROC) (AUC) for microRNA-21 expression in serum or sputum as a biomarker for lung carcinoma identification. The publication bias was evaluated by Deek's funnel plot.

Seventeen diagnostic studies were finally included and made data pooling. For the included 17 studies, 4 investigated the microRNA-21 expression in sputum and 13 studies in serum. The pooled diagnostic sensitivity and specificity were 0.73 (95% CI, 0.67-0.78) and 0.81 (95% CI, 0.75-0.85), respectively, under random effect model. The combined DOR was 9.65 (95% CI, 6.64-14.03) with the AUC of 0.84 (95% CI, 0.80-0.87). Given a pre-test probability of 50%, the post-test positive probability and post-test negative probability were 79% and 25%, respectively, by using microRNA-21 as a biomarker for lung carcinoma diagnosis. Deek's funnel was obviously asymmetry and indicated significant publication bias (p < 0.05).

MicroRNA-21 in serum or sputum was a promising biomarker for lung cancer identification with relative high diagnostic sensitivity and specificity.

Icaritin alleviates docetaxel-induced skin injury by suppressing reactive oxygen species via estrogen receptors.

Thoracic Cancer

Docetaxel (DTX) exhibits antitumor effects against breast cancer by stabilizing microtubules and increasing the accumulation of reactive oxygen species (ROS). DTX extravasation during infusion often causes skin injury. The present study aimed to investigate the effects and mechanisms of icaritin (ICT) on DTX-induced skin injury.

The effects of ICT on the viability and apoptosis of HaCaT cells were measured by SRB assay and flow cytometry, respectively. Endogenous LC3 puncta and microtubules were determined by immunofluorescence. The number of mitochondria was measured by MitoTracker orange staining. ROS were determined by dihydroethidium staining. The expression of markers of ROS and autophagy were measured by western blotting. Chloroquine, compound D, and tamoxifen were employed as the inhibitor for autophagy and AMPK, estrogen receptors (ERs) modulator, respectively.

DTX inhibited the viability and decreased apoptosis of HaCaT cells, which can be rescued by ICT. ICT decreased microtubule bundles, increased the number of mitochondria, and attenuated ROS of HaCaT cells induced by DTX. ICT blocks autophagy and the autophagic flux. Compound C or tamoxifen diminished the protection effects of ICT on DTX-treated HaCaT cells.

ICT alleviates DTX-induced skin injury by suppressing ROS, reducing microtubule bundles, and blocking autophagy via ERs. Our study indicated that ICT may be a potential candidate for DTX-induced skin injury.

Circulating cytokines associated with clinical outcomes in advanced non-small cell lung cancer patients who received chemoimmunotherapy.

Thoracic Cancer

Pretreatment and on-treatment plasma cytokine levels in predicting clinical benefit in patients with advanced non-small cell lung cancer (NSCLC) treated with anti-programmed death-1 (PD-1)-based chemotherapy is still a matter of debate.

We measured 12 kind of plasma cytokines in patients with stage III/IV NSCLC before and during treatment with anti-PD-1 based chemotherapy. Associations with best overall response, and survival including progression-free survival (PFS) and overall survival (OS) were assessed using Chi-square test and Kaplan-Meier plots with log-rank test, respectively. Logistic regression and Cox regression were used to determine independent risk factors.

Of a total of 60 patients, high-level of pretreatment interleukin-2 was associated with longer PFS (log rank p = 0.049), while high-level of pretreatment interleukin-8 was associated with shorter OS (log rank p = 0.006). Increased on-treatment interleukin-1β (IL-1β) was associated with both better response (odds ratio [OR] 6.233, 95% confidential interval [CI]: 1.451-26.344, p = 0.013) and longer PFS (hazard ratio [HR] 0.305, 95% CI: 0.127-0.730, p = 0.008). On the contrary, increased on-treatment interleukin-6 (IL-6) was associated with a worse response (OR 0.015, 95% CI: 0.001-0.400, p = 0.012), worse PFS (HR 2.639, 95% CI: 1.163-5.991, p = 0.020) and worse OS (HR 2.742, 95% CI: 1.063-7.074, p = 0.037). Increased interferon-γ (IFN-γ) was found to be associated with better PFS (HR 0.336, 95% CI: 0.153-0.745, p = 0.007).

In patients with advanced NSCLC who received chemoimmunotherapy, on-treatment increased IL-1β and IFN-γ may serve as positive indicator of efficacy, while on-treatment increased IL-6 might play a predictive role of worse clinical outcome.

Onset of pulmonary Epstein-Barr virus-positive diffuse large B-cell lymphoma in a patient with silicosis.

Thoracic Cancer

How Epstein-Barr virus (EBV)-positive diffuse large B-cell lymphoma (DLBCL) occasionally occurs following chronic inflammation remains to be elucid...

LncRNA LINC00460: Function and mechanism in human cancer.

Thoracic Cancer

Long non-coding RNAs (LncRNAs), which are more than 200 nucleotides in length and with limited protein-coding potential, play vital roles in the pa...

Solid histological component of adenocarcinoma might play an important role in PD-L1 expression of lung adenocarcinoma.

Thoracic Cancer

In this study we aimed to clarify the PD-L1 positive expression in lung adenocarcinoma, including various adenocarcinoma subtypes paying particular attention to its component.

A total of 307 lung adenocarcinoma patients who underwent lobectomy or segmentectomy, as well as systematic lymph node dissection (ND2a), from February 2008 to March 2020 at our hospital, were enrolled into the study. A final diagnosis of adenocarcinoma was obtained from the resected lung specimens of all 307 patients to determine the histological type, adenocarcinoma subtype, and component of adenocarcinoma by ethics of 5%. PD-L1 was immunohistochemically stained using the murine monoclonal antibody clone 22C3.

When PD-L1 expression-positive was defined by tumor proportion score (TPS) ≥1%, the positive cases were 6/33 in adenocarcinoma (Ad) in situ (AIS), 2/26 in minimally invasive Ad (MIA), 12/60 in lepidic predominant Ad (LPA), 44/91 in papillary predominant Ad (PPA), 24/49 in acinar predominant Ad (APA), 23/28 in solid predominant Ad (SPA), 4/7 in micropapillary predominant Ad (MPA), and 0/13 in invasive mucinous Ad (IMA). In the high proportion group (APA, PPA, SPA, and MPA) of PD-L1 expression, SPA was the only subtype which was statistically significant when both PD-L1 expression-positive was defined by TPS ≥ 1% (p < 0.0001) and TPS ≧ 50% (p < 0.0001). We then considered the solid component. We investigated 279 cases of the other subtype group excluding SPA. The group containing a solid component (≥5%) tended to be PD-L1 expression-positive both when defined by TPS ≥1% (p < 0.0001) and TPS ≧50% (p = 0.0049).

The PD-L1 expression tended to be positive when a solid component was confirmed (≥5%) in specimens of lung adenocarcinoma patients.

Utility of mass spectrometry and artificial intelligence for differentiating primary lung adenocarcinoma and colorectal metastatic pulmonary tumor.

Thoracic Cancer

Rapid intraoperative diagnosis for unconfirmed pulmonary tumor is extremely important for determining the optimal surgical procedure (lobectomy or sublobar resection). Attempts to diagnose malignant tumors using mass spectrometry (MS) have recently been described. This study evaluated the usefulness of MS and artificial intelligence (AI) for differentiating primary lung adenocarcinoma (PLAC) and colorectal metastatic pulmonary tumor.

Pulmonary samples from 40 patients who underwent pulmonary resection for PLAC (20 tumors, 20 normal lungs) or pulmonary metastases originating from colorectal metastatic pulmonary tumor (CRMPT) (20 tumors, 20 normal lungs) were collected and analyzed retrospectively by probe electrospray ionization-MS. AI using random forest (RF) algorithms was employed to evaluate the accuracy of each combination.

The accuracy of the machine learning algorithm applied using RF to distinguish malignant tumor (PLAC or CRMPT) from normal lung was 100%. The algorithms offered 97.2% accuracy in differentiating PLAC and CRMPT.

MS combined with an AI system demonstrated high accuracy not only for differentiating cancer from normal tissue, but also for differentiating between PLAC and CRMPT with a short working time. This method shows potential for application as a support tool facilitating rapid intraoperative diagnosis to determine the surgical procedure for pulmonary resection.

Construction of a circular RNA-microRNA-messenger RNA regulatory network of hsa_circ_0043256 in lung cancer by integrated analysis.

Thoracic Cancer

Patients with non-small cell lung cancer (NSCLC) are diagnosed in advanced stages and with a poor 5-year survival rate. There is a critical need to identify novel biomarkers to improve the therapy and overall prognosis of this disease.

Differentially expressed genes (DEGs) were identified from three profiles of GSE101586, GSE101684 and GSE112214 using Venn diagrams. hsa_circ_0043256 were validated using quantitative real-time polymerase chain reaction (RT-qPCR). The circular RNA-microRNA-messenger RNA (circRNA-miRNA-mRNA) regulatory network was constructed with Cytoscape 3.7.0. Hub genes were identified with protein interaction (PPI) and validated with the Gene Expression Profiling Interactive Analysis (GEPIA), Human Protein Atlas (HPA) databases, and immunohistochemistry. Survival analyses were also performed using a Kaplan-Meier (KM) plotter. The effects of hsa_circ_0043256 on cell proliferation and cell cycles were evaluated by EdU staining and flow cytometry, respectively.

hsa_circ_0043256, hsa_circ_0029426 and hsa_circ_0049271 were obtained. Following RT-qPCR validation, hsa_circ_0043256 was selected for further analysis. In addition, functional experiment results indicated that hsa_circ_0043256 could inhibit cell proliferation and cell-cycle progression of NSCLC cells in vitro. Prediction by three online databases and combining with DEGs identified from The Cancer Genome Atlas (TCGA), a network containing one circRNAs, three miRNAs, and 209 mRNAs was developed. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated DEGs might be associated with lung cancer onset and progression. A PPI network based on the 209 genes was established, and five hub genes (BIRC5, SHCBP1, CCNA2, SKA3, and GINS1) were determined. Following verification of five hub genes using GEPIA database, HPA database, and immunohistochemistry. High expression of all five hub genes led to poor overall survival.

Our study constructed a circRNA-miRNA-mRNA network of hsa_circ_0043256. hsa_circ_0043256 may be a potential therapeutic target for lung cancer.