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Background: Esophageal cancer (EC), a common and fatal disease, includes two histological subtypes; esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (ECA). To aid policymakers in the allocation of resources for the prevention and treatment of EC, updated data on EC deaths and disability‐adjusted life years (DALYs) attributable to high body mass index (BMI) are necessary. The objective of this study was to identify trends in EC associated with high BMI between 1990 and 2019 using 2019 Global Burden of Disease data. Methods: In this observational population‐based study, epidemiological data on the association between high BMI and EC were obtained from GBD 2019. The age‐standardized mortality rate (ASMRs) and disability‐adjusted life year rate (ASDRs) attributable to high BMI‐related EC were stratified by year, age, country, and sociodemographic index (SDI). The estimated annual percentage change (EAPC) was calculated to evaluate the temporal trends of the ASMRs and ASDRs between 1990 and 2019. Results: In 2019, the proportion of EC deaths and DALYs attributed to high BMI was 18.1% and 18.9%, respectively, resulting in 89 904 (95% confidence interval [CI]: 27 879–171 255) deaths and 2 202 314 (95% CI: 681 901–4 173 080) DALYs. High BMI‐related deaths and DALYs showed a strong upward trend, increasing by more than two‐fold since 1990. East Asia and Western Europe showed the highest risk of EC mortality and DALYs attributable to high BMI; China and the USA bear the greatest burden. The ASMR and ASDR increased in five SDI regions. Conclusions: The incidence of EC is increasing, particularly in developing nations, which may be attributed to the prevalence of high BMI. To mitigate the impact of high BMI on the incidence of EC, it is important to increase awareness of its deleterious effects, which may alleviate the burden of this disease. [ABSTRACT FROM AUTHOR]

Abstract Lung cancer is the most frequent cause of cancer-related deaths worldwide, but its molecular pathogenesis is poorly understood. The tumor suppressor candidate 3 (TUSC3) gene is located on chromosome 8p22 and is universally acknowledged as a cancer suppressor. However, our research has demonstrated that TUSC3 expression is significantly upregulated in non-small-cell lung cancer compared to benign controls. In this study, we analyzed the consequences of TUSC3 knockdown or overexpression on the biological functions of non-small-cell lung cancer cell lines. To identify the molecules and signaling pathways with which TUSC3 might interact, we completed immunoblotting, quantitative polymerase chain reaction, microarray, co-immunoprecipitation, and immunofluorescence assays. We demonstrated that TUSC3 knockdown leads to decreased proliferation, migration, and invasion, and reduced xenograft tumor growth of non-small-cell lung cancer cell lines, whereas opposite results were observed with overexpression of TUSC3. In addition, TUSC3 knockdown suppressed epithelial-mesenchymal transition by downregulating the expression of claudin-1, which plays an indispensable role in EMT progress. On the contrary, overexpression of TUSC3 significantly enhanced EMT progress by upregulating claudin-1 expression. Overall, our observations suggest that TUSC3 accelerates cancer growth and induces the epithelial-mesenchymal transition in non-small-cell lung cancer cells; we also identified claudin-1 as a target of TUSC3. [ABSTRACT FROM AUTHOR]

Background: The identification of targeted intersegmental planes and resection with adequate surgical margins are among the crucial steps in anatomical pulmonary segmentectomy, and technical improvements are still needed.Case Presentation: We reported three cases of intersegmental plane identification using highly selective independent segmental ventilation during segmentectomy. All cases required cooperation with an anesthesiologist who was able to perform segmental ventilation and double confirmation of segmental bronchus branches by the surgeon. The surgical procedure provides a direct visualization of spare segment inflation and saves time in deflation over the conventional residual segment inflation method.Conclusions: Highly selective independent segmental ventilation could be considered a suitable option for pulmonary intersegmental plane identification and could be universally used for lung segmentectomy. [ABSTRACT FROM AUTHOR]

Background: Whether prognosis differs between lung acinar predominant adenocarcinoma (ACN) and papillary predominant adenocarcinoma (PAP) patients remains controversial. Furthermore, the appropriate surgical plan for each subtype is undetermined. Methods: Data of stage I ACN or PAP patients from 2004 to 2015 were retrospectively reviewed by SEER*Stat 8.3.5. The primary outcome was overall survival (OS) and lung cancer specific survival (LCSS). Results: 1531 patients (PAP, 484; ACN, 1047) were included. ACN patients had better OS (P =.001) and LCSS (P =.003) than PAP patients. Among stage I ACN patients, lobectomy with mediastinal lymph node dissection (Lob) (P =.001) or segmentectomy (Seg) (P =.003) provided a better OS than wedge resection (Wed). And ACN patients who received Lob had a equivalent LCSS, compared to those who received Seg (P =.895). For patients with PAP in stage I, those who received Lob tended to have a better prognosis than that received Seg (HR of OS, 0.605, 95% CI: 0.263‐1.393; HR of LCSS, 0.541, 95% CI: 0.194‐1.504) or Wed (HR of OS, 0.735, 95% CI: 0.481‐1.123; HR of LCSS, 0.688, 95% CI: 0.402‐1.180). Conclusions: Among patients with lung adenocarcinoma in stage I, those with ACN have a better OS and LCSS than that with PAP. For patients with stage I ACN, Seg and Lob, rather than Wed, seem to be an equivalent treatment choice; however, Seg is the prior option because it could preserve more lung function than Lob. For patients with PAP, Lob tends to be a better choice than Wed and Seg, although the prognostic difference between them is nonsignificant. [ABSTRACT FROM AUTHOR]

Programmed cell death protein 1 (PD-1) and its ligand PD-L1 have attracted wide attention from researchers in the field of immunotherapy. PD-1/PD-L1 have been shown to exist in many types of cells in addition to T lymphocytes, and studies have accordingly extended from their suppressive effect on T cell activation and function to examining their role in other cells. In this review, we summarize recent research on PD-1/PD-L1 in macrophages, with the aim of furthering our understanding of PD-1/PD-L1 and their detailed roles in macrophages. This information may provide additional insights for researchers, enrich the basic theory of anti-PD-1/PD-L1 immunotherapy, and thus ultimately benefit more patients. [ABSTRACT FROM AUTHOR]

Micropapillary or solid pattern predicts recurrence free survival benefit from adjuvant chemotherapy in patients with stage IB lung adenocarcinoma. Some concerns were raised related to our study in the comments, which was published earlier in Cancer Medicine "Clinicopathological features, survival outcomes, and appropriate surgical approaches for stage I acinar and papillary predominant lung adenocarcinoma" (Article ID: CAM43012, Article DOI: 10.1002/cam4.3012, Internal Article ID: 16708831). Adjuvant chemotherapy improves the probability of freedom from recurrence in patients with resected stage IB lung adenocarcinoma. [Extracted from the article]

Cystic fibrosis (CF) and cystic fibrosis transmembrane conductance regulator (CFTR) mutations have been shown to be associated with the risk of a variety of cancers. However, the clinical significance of aberrant CFTR gene expression in human tumors remains unknown. The expression profiles and prognostic landscapes of CFTR in human cancers were identified from the PubMed, OVID, CNKI, TCGA, ONCOMINE, PrognoScan, and GEPIA databases. Over 11, 000 cancer samples from the literature, GEPIA database, and PrognoScan database were included in this study. In general, CFTR has various expression and prognostic profiles in cancers, but the results from cross-database and meta-analyses revealed that CFTR is a robust biomarker for LUAD prognosis. Collectively, this study suggests that CFTR is an important prognostic biomarker for LUAD survival, implying that it could be used as a prognostic biomarker and therapeutic target for LUAD. • An integrative cross-database bioinformatic approach to study potential targets for cancer diagnosis and prognosis. • The role of CFTR expression in over 11, 000 cancer samples from multiple datasets were analyzed; • CFTR has various expression profiles in cancers; • CFTR is a promising biomarker for lung adenocarcinoma prognosis. [ABSTRACT FROM AUTHOR]