Characterizing the molecular immune subtype and micro-environment of lung cancer is necessary to understand immunogenic interactions between infiltrating immune and stromal cells, and how tumor cells overcome immune checkpoint blockades. This study seeks to identify computational methodologies for subtyping gene expression-based tumor-immune micro-environment interactions, which differentiate non-small cell lung cancer (NSCLC) into immune-defective and immune-competent subtypes. Here, 101 lung squamous cell carcinomas (LUSCs) and 87 lung adenocarcinomas (LUADs) tumor samples have been analyzed. Several micro-environmental factors differentially induce LUAD or LUSC immune subtypes, as well as immune checkpoint expression. In particular, tumor-associated macrophages (TAMs) are key immune cells play a vital role in inflammation and cancer micro-environments of LUSCs; whereas, regulatory B cells are immunosuppressive and tumorigenic in LUADs. Additionally, cytolytic activity upon CD8⁺ T cell activation is decreased by the abundance of B cells and macrophages in immune-competent subtypes. Therefore, identifying immune subtypes in lung cancer and their impact on tumor micro-environment will lead to clinical tools for assessing LUADs and LUSCs in patients, as well as maximize the efficacy of immune checkpoint inhibitors.

Rheumatoid arthritis (RA) includes musculoskeletal symptoms that lead to disuse atrophy of muscles and changes in body composition. Musculoskeletal symptoms and loss of physical function may be associated with sarcopenia, which is characterized by muscle loss. This study aimed to investigate the prevalence of sarcopenia and its association with RA in a Korean population. We analyzed nationwide data from the Korea National Health and Nutrition Examination Survey of 7389 men and 9798 women. Binomial logistic regression models were used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) for sarcopenia prevalence in participants with RA. The prevalence of sarcopenia was 23.0% in men, 25.0% in women, 61.5% in men with RA, 32.3% in women with RA, 22.8% in men without RA, and 24.9% in women without RA. After adjusting for potential confounding variables, the prevalence of sarcopenia was higher in men with RA than in men without RA (OR, 3.11; 95% CI, 1.29–7.46), but this difference was not observed in women. In subgroup analysis which was stratified by age (age under 40, age between 40 and 59, age over 60), the OR for sarcopenia was higher in men with age over 60 years (OR, 4.12; 95% CI, 1.48–11.44) and women with age between 40 and 59 (OR, 2.29; 95% CI, 1.05–5.00). The prevalence of sarcopenia was higher in Korean men with RA and women with RA in middle age, suggesting the management of muscle loss will be needed, especially in Koreans with RA.

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DHFR gene amplification is present in methotrexate (MTX)-resistant colon cancer cells and acute lymphoblastic leukemia. However, little is known about DHFR gene amplification due to difficulties in quantifying amplification size and recognizing the repetitive rearrangements involved in the process. In this study, we have proposed an integrative framework to characterize the amplified region by using a combination of single-molecule real time sequencing, next-generation optical mapping, and chromosome conformation capture (Hi-C). Amplification of the DHFR gene was optimized to generate homogenously amplified patterns. The amplification units of 11 genes, from the DHFR gene to the ATP6AP1L gene position on chromosome 5 (~2.2Mbp), and a twenty-fold tandemly amplified region were verified using long-range genome and RNA sequencing data. In doing so, a novel inversion at the start and end positions of the amplified region as well as frameshift insertions in most of the MSH and MLH genes were detected. These might stimulate chromosomal breakage and cause the dysregulation of mismatch repair pathways. Using Hi-C technology, high adjusted interaction frequencies were detected on the amplified unit and unsuspected position on 5q, which could have a complex network of spatial contacts to harbor gene amplification. Characterizing the tandem gene-amplified unit and genomic variants as well as chromosomal interactions on intra-chromosome 5 can be critical in identifying the mechanisms behind genomic rearrangements. These findings may give new insight into the mechanisms underlying the amplification process and evolution of drug resistance.