Objective The efficacy of rapid on‐site evaluation (ROSE) combined with computed tomography‐guided transthoracic core needle biopsy (CT‐guided TCNB) is rarely investigated. This study aimed to evaluate the diagnostic efficiency and safety of ROSE combined with CT‐guided TCNB for suspected lung cancer patients. Materials and Methods Clinical data from 285 patients who received CT‐guided TCNB for suspected lung cancer in Huashan Hospital from 2015 to 2018 were retrospectively analysed. Of these 163 patients underwent CT‐guided TCNB combined with ROSE (ROSE group), while the remaining 122 patients underwent without ROSE (non‐ROSE group). The smears from TCNB were quickly processed with Diff‐Quick staining and analysed by a skilled cytologist on‐site. The consistency of ROSE with the final clinicopathological diagnosis and the diagnostic efficiency and safety of ROSE combined with CT‐guided TCNB in suspected lung cancer patients were evaluated. Results ROSE was highly concordant with pathological diagnosis (κ = 0.791; P < 0.001), with an accuracy of 95.7%. Diagnostic accuracy was significantly higher in the ROSE compared with the non‐ROSE group (96.3% vs 86.1%; P = 0.002), with overall incidences of complications of 36.8% and 23.8%, respectively. Minor pneumothorax without drainage was slightly greater in the ROSE compared with the non‐ROSE group (14.1% vs 6.6%; P = 0.046). However, there was no significant difference in serious complications between the two groups. Conclusion ROSE was highly consistent with the final clinicopathological diagnosis for suspected lung cancer. ROSE further improved the diagnostic efficiency of CT‐guided TCNB with no increased incidence of serious complications.
Background: As a member of the Ephrin protein family that elicits short distance cell-cell signaling, EphrinA3 has been shown to promote or inhibit tumorigenesis depending on tumor types, but its roles and the underlying mechanisms in lung adenocarcinoma (LUAD) have not been reported. Materials and Methods:The TCGA database and Kaplan-Meier Plotter database were used to analyze the differential expression of EphrinA3 between LUAD and para-carcinoma tissues, and its effect on overall survival of LUAD patients. CCK-8 assay, Edu assay, and flow cytometry were used to probe the effect of EphrinA3 on the proliferation of LUAD cells, and transwell assay was employed to examine its effect on migration and invasion. In addition, the effect of EphrinA3 on the growth of LUAD was further evaluated using a xenograft tumor model. Results: EphrinA3 was expressed highly in LUAD, and its expression level was negatively correlated with the prognosis of LUAD patients. In addition, EphrinA3 promoted proliferation, migration, and invasion of LUAD cells, and accelerated tumor growth in a xenograft LUAD model. The reported EphrinA3 receptors, EphA1 and EphA10, were expressed in clinical LUAD tissues and co-localized with EphrinA3 in LUAD cells. Mechanistically, EphrinA3/Eph signaling activated AKT, ERK, and p38MAPK, induced epithelial-mesenchymal transition (EMT), and upregulated matrix metalloproteases-2 and -9 (MMP-2/−9). Conclusion: EphrinA3 expression was negatively correlated with prognosis of patients with LUAD. EphrinA3 promoted proliferation, migration, and invasion of LUAD cells. EphrinA3 enhanced the phosphorylation of ERK and AKT, and potentiates EMT and MMP expression in LUAD cells.
Background: Hypoxic pulmonary hypertension (HPH) is a challenging lung arterial disorder with remarkably high incidence and mortality, and so far patients have failed to benefit from therapeutics clinically available. Max interacting protein 1–0 (Mxi1-0) is one of the functional isoforms of Mxi1. Although it also binds to Max, Mxi1-0, unlike other Mxi1 isoforms, cannot antagonize the oncoprotein c-Myc because of its unique proline rich domain (PRD). While Mxi1-0 was reported to promote cell proliferation via largely uncharacterized mechanisms, it is unknown whether and how it plays a role in the pathogenesis of HPH.Methods: GEO database was used to screen for genes involved in HPH development, and the candidate players were validated through examination of gene expression in clinical HPH specimens. The effect of candidate gene knockdown or overexpression on cultured pulmonary arterial cells, e.g., pulmonary arterial smooth muscle cells (PASMCs), was then investigated. The signal pathway(s) underlying the regulatory role of the candidate gene in HPH pathogenesis was probed, and the outcome of targeting the aforementioned signaling was evaluated using an HPH rat model.Results: Mxi1 was significantly upregulated in the PASMCs of HPH patients. As the main effector isoform responding to hypoxia, Mxi1-0 functions in HPH to promote PASMCs proliferation. Mechanistically, Mxi1-0 improved the expression of the proto-oncogene c-Myc via activation of the MEK/ERK pathway. Consistently, both a MEK inhibitor, PD98059, and a c-Myc inhibitor, 10058F4, could counteract Mxi1-0-induced PASMCs proliferation. In addition, targeting the MEK/ERK signaling significantly suppressed the development of HPH in rats.Conclusion: Mxi1-0 potentiates HPH pathogenesis through MEK/ERK/c-Myc-mediated proliferation of PASMCs, suggesting its applicability in targeted treatment and prognostic assessment of clinical HPH.
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