122 publications were included.In 39 (32.0%) publications, QoL was not listed among endpoints: in 10/17 (58.8%) early stage/locally advanced NSCLC, in 15/54 (27.8%) first-line of advanced NSCLC; in 10/41 (24.4%) second and further lines of advanced NSCLC, in 4/10 (40.0%) SCLC.
To provide evidence-based recommendations to practicing clinicians on radiographic imaging and biomarker surveillance strategies after definitive curative-intent therapy in patients with stage I-III non-small-cell lung cancer (NSCLC) and SCLC.
The impact of oncologic treatment for (non)-small-cell lung cancer (NSCLC and SCLC, respectively) on cognition is relevant when deciding which treatment is the most preferable option, especially when curation is not possible.
After adjustment for potential confounders, multivariable analyses demonstrated lower odds of SAEs in NSCLC (odds ratio [OR] 0.52, 95% CI 0.40-0.69, P < 0.001) and SCLC (OR 0.41, 95% CI 0.31-0.54, P < 0.001) compared with melanoma.
The triple-mutant population had a higher incidence of whole-genome doubling compared to NSCLC and SCLC at large (80% versus 34%, p < 5 × 10<sup>-9</sup> versus 51%, p < 0.002, respectively) and further enrichment in triple-mutant cancers with eventual small cell histology (seven of seven pre-transformed plus four of four baseline SCLC versus 23 of 32 never transformed, respectively, p = 0.05).
Besides, patients with high PD-L1 expression had shorter OS in NSCLC (P=0.000), ADC (P=0.000), SCC (P=0.353) and LELC (P=0.810), while no significant difference was observed in SCLC (P=0.000).
In addition, our results suggest that there could be histological differences in the biological activity of bone metastatic lesions in lung cancer, especially between SCLC and NSCLC.
There was no statistically significant survival difference between different types of primary lung cancer: NSCLC (8.3 months, SD 13.8, SEM 0.91) and SCLC (7.0 months, SD 4.6, SEM 0.46; p = 0.36).
There was no association between HGF, cMET, EGF, EGFR (both protein and gene) expression levels with age, gender, smoking habit, COPD, pathological types or tumor size, stage, metastatic-non metastatic adenocarcinoma-squamous carcinoma, SCLC-NSCLC.
PA and BA enhancement distributed to different histologies: n = 42 adenocarcinomas (18 PA, 24 BA), n = 30 squamous cell carcinomas (4 PA, 26 BA), n = 13 other types of NSCLC (3 PA, 10 BA), and n = 4 SCLC (0 PA, 4 BA) (p = 0.016).
Individual level data analysis was performed on 25,430 patients with NSCLC and 2787 patients with SCLC from 16 studies of the International Lung Cancer Consortium evaluating the association between various BMI variables and lung cancer overall survival, reported as adjusted hazard ratios (aHRs) from Cox proportional hazards models and adjusted penalized smoothing spline plots.
We compared IOV in the pre- and mid-treatment setting using expert primary gross tumour volume (GTV) and clinical target volume (CTV) delineations in locoregionally advanced head-and-neck squamous cell carcinoma (HNSCC) and (non-)small cell lung cancer [(N)SCLC].
The objectives were to analyze survival data and to define epidemiologic, clinical, treatment and histomolecular characteristics at both the time of diagnosis of NSCLC and of SCLC.
Especially, the predictive value of SII was significant in the multivariable model for NSCLC (HR: 1.97, 95% CI: 1.69-2.25, P < .001; 5 studies, 1746 patients), and SCLC (HR: 1.38, 95% CI: 1.02-1.85, P < .001; 1 study, 919 patients).
The majority of data published to date, including the results of almost all large cohorts, are strongly supportive of the value of CTC enumeration as a predictor of survival, mainly in advanced/metastatic non-small and small cell lung cancer (NSCLC and SCLC, respectively).
In the case of LCNECs, which present with a high mutation burden, two major molecular subtypes have been identified: one with biallelic inactivation of tumor protein p53 gene (TP53) and retinoblastoma gene (RB1), a hallmark of SCLC; and the other one with biallelic inactivation of TP53 and serine/threonine kinase 11 gene (STK11)/kelch like ECH associated protein 1 gene (KEAP1), genes that are frequently mutated in NSCLC.
Next-generation sequencing (NGS) for <i>TP53, RB1, STK11,</i> and <i>KEAP1</i> genes, as well as IHC for RB1 and P16 was performed on 79 and 109 cases, respectively, and correlated with overall survival (OS) and progression-free survival (PFS), stratifying for non-small cell lung cancer type chemotherapy including platinum + gemcitabine or taxanes (NSCLC-GEM/TAX) and platinum-etoposide (SCLC-PE).<b>Results:</b><i>RB1</i> mutation and protein loss were detected in 47% (<i>n</i> = 37) and 72% (<i>n</i> = 78) of the cases, respectively.
We harvested a heart-lung block from a rat and placed it in a bioreactor after cannulating the pulmonary artery, trachea and tying the right main bronchus for 10-15 days without any tumor cells as a control group or with NSCLC (A549, H1299 or H460), SCLC (H69, H446 or SHP77) or breast cancer cell lines (MCF7 or MDAMB231) through the trachea.
A total of 150 serum samples were collected, including 91 from patients with SCLC or NSCLC, 22 from patients with benign lung diseases, and 37 from healthy subjects.