Prediction of prognosis and immune response in lung adenocarcinoma based on mitophagy and lactate-related gene signatures.

Background: Lung adenocarcinoma (LUAD) causes leading death worldwide. Mitophagy and lactate metabolism accumulation are distinctive features of LUAD. We aimed to identify lactate-related genes (LRGs) signatures based on mitophagy for predicting prognosis and immune response in LUAD.

Neoadjuvant Camrelizumab Plus Platinum-Based Chemotherapy vs Chemotherapy Alone for Chinese Patients With Resectable Stage IIIA or IIIB (T3N2) Non-Small Cell Lung Cancer: The TD-FOREKNOW Randomized Clinical Trial.

Importance: The benefit of neoadjuvant camrelizumab plus chemotherapy for resectable stage IIIA or IIIB non-small cell lung cancer (NSCLC) remains unknown.

Objective: To assess the efficacy and safety of neoadjuvant camrelizumab plus chemotherapy vs chemotherapy alone for patients with resectable stage IIIA or IIIB NSCLC.

Design, Setting, And Participants: In this randomized phase 2 clinical trial conducted at 2 hospitals in China, patients aged 18 to 70 years with resectable stage IIIA or IIIB (T3N2) NSCLC were enrolled between April 7, 2020, and January 12, 2022.

Regulation of CD18 stability by SIGIRR-modulated ubiquitination: new insights into the relationship between innate immune response and acute lung injury.

Inappropriate accumulation of alveolar macrophages (AMs) and subsequent excessive production of immune responses play critical roles in the pathogenesis of acute lung injury (ALI), but the core negative regulators governing innate signalling in AMs are ill defined. We have previously shown that single immunoglobin IL-1 receptor-related protein (SIGIRR), a negative regulator of IL-1 receptor and Toll-like receptor signalling, inhibits lipopolysaccharide (LPS)-induced inflammatory responses in AMs. To address the biological relevance of SIGIRR in vivo, we generated a murine ALI model via intratracheal instillation of LPS.

Heterogeneity and Clinical Effect of Epidermal Growth Factor Receptor in Primary Lung and Brain Metastases of Nonsmall Cell Lung Cancer.

Introduction: This study aimed to analyze the heterogeneity in epidermal growth factor receptor (EGFR) gene mutation and its impact on clinical outcomes in primary tumor and corresponding brain metastasis (BM) in nonsmall cell lung cancer (NSCLC).

Materials And Methods: Primary pulmonary tumors and paired BMs of 27 NSCLC patients were surgically removed. All brain lesions were histologically confirmed as metastatic NSCLC.

Wandering rod: form lumbar spine into left pleural cavity with nerve irritated symptoms.

Spinal instrumented rod migrating from the surgical site to another remote site in the body is rare. Some cases result in organ or blood vessel injury. Most reported cases were asymptomatic until the finally injuries were generated.

Negative Effects of SIGIRR on TRAF6 Ubiquitination in Acute Lung Injury In Vitro.

In this study, the effects of single immunoglobin IL-1 receptor-related protein (SIGIRR) on tumor necrosis factor- (TNF-) receptor-associated factor 6 (TRAF6) ubiquitination in acute lung injury (ALI) were evaluated in both alveolar epithelial cells and alveolar macrophage cells in vitro. Our results found that SIGIRR negatively regulated TRAF6 ubiquitination and such SIGIRR inhibition could enhance the TRAF6 expression in both alveolar epithelial cells (AECs) and alveolar macrophage cells (AMCs). SIGIRR knockdown may increase NF-B activity via TRAF6 regulation by the classical but not the nonclassical NF-B signaling pathway.

Three-Dimensional Printing PEEK Implant: A Novel Choice for the Reconstruction of Chest Wall Defect.

Background: The purpose of this study is to use 3-dimensional printing (3DP) polyetheretherketone (PEEK) implants for skeletal reconstructions after wide excision of chest wall. 3DP PEEK implants were expected to provide a better physiological simulation than traditional ones because of a closer elastic modulus to cortical bone and similar biomechanical properties.

Methods: Eighteen patients (mean age 44.

[Research Status of the Skeletalre Construction of Chest Wall].

Chest wall defect may be caused by many factors such as the resection of tumor and trauma, and the reconstruction of bone-defection is still the key point of thoracic surgery. With the development of material science, more and more new materials have been used in medical practice, which makes huge progress in the surgery of chest wall. However, none of these materials satisfy all the practical needs of the reconstruction.

Tracheal suspension by using 3-dimensional printed personalized scaffold in a patient with tracheomalacia.

The major methods are used to fix or stabilize the central airways and major bronchi with either anterior suspension and/or posterior fixation for severe tracheomalacia (TM). Many support biomaterials, like mesh and sternal plate, can be used in the surgery. But there are no specialized biomaterials for TM which must be casually fabricated by the doctors in operation.

The chimeric ubiquitin ligase SH2-U-box inhibits the growth of imatinib-sensitive and resistant CML by targeting the native and T315I-mutant BCR-ABL.

Chronic myeloid leukemia (CML) is characterized by constitutively active fusion protein tyrosine kinase BCR-ABL. Although the tyrosine kinase inhibitor (TKI) against BCR-ABL, imatinib, is the first-line therapy for CML, acquired resistance almost inevitably emerges. The underlying mechanism are point mutations within the BCR-ABL gene, among which T315I is notorious because it resists to almost all currently available inhibitors.

Upregulation of microrna-451 increases the sensitivity of A549 cells to radiotherapy through enhancement of apoptosis.

Background: As radioresistance of non-small cell lung cancers (NSCLC) is one of the main causes of failure in radiotherapy, we examined whether micro ribonucleic acid (miR-451) could function as a potential radiosensitizer of NSCLC and the related mechanism.

Methods: Radioresistant NSCLC cell line A549 was transfected with pre-miR-451 or a scrambled control. The miR-451 messenger RNA level, colony-forming ability, apoptosis, and phosphatase and tensin homolog (PTEN) protein level of 549 cells were examined by real-time polymerase chain reaction, clonogenic assay, flow cytometry analysis, and Western blot.

Pulmonary resident neutrophils regulate the production of GM-CSF and alveolar macrophages.

Alveolar macrophages exist in the lung airspaces, and their differentiation and function are considerably regulated by the microenvironment. In this study, we examine the important role of resident neutrophil/IL-23/granulocyte/macrophage colony-stimulating factor (GM-CSF) axis in the development and preferential phenotype of alveolar macrophages under physiological conditions. Using CD18-deficient (CD18(-/-) ) mice, we show a correlation between increased granulopoiesis and enhanced alveolar macrophage development in an IL-23- and GM-CSF-dependent manner.

Chimeric ubiquitin ligases inhibit non-small cell lung cancer via negative modulation of EGFR signaling.

Targeting epidermal growth factor receptor (EGFR) represents a promising therapeutic strategy for non-small cell lung cancers (NSCLC). The ubiquitin-proteasome system (UPS) is a major pathway that mediates protein degradation. To target the degradation of EGFR, we generated two artificial ubiquitin ligases, which are composed of an EGFR-binding domain, i.

Sea-urchin-like Au nanocluster with surface-enhanced raman scattering in detecting epidermal growth factor receptor (EGFR) mutation status of malignant pleural effusion.

Somatic mutations in the epidermal growth factor receptor (EGFR) gene are common in patients with lung adenocarcinomas and are associated with sensitivity to the small-molecule tyrosine kinase inhibitors (TKIs). For 10%-50% of the patients who experienced malignant pleural effusion (MPE), pathological diagnosis might rely exclusively on finding lung cancer cells in the MPE. Current methods based on polymerase chain reaction were utilized to test EGFR mutation status of MPE samples, but the accuracy of the test data was very low, resulting in many patients losing the chance of TKIs treatment.

Potassium channel ether à go-go1 is aberrantly expressed in human liposarcoma and promotes tumorigenesis.

The ether à go-go1 (Eag1) channel is overexpressed in a variety of cancers. However, the expression and function of Eag1 in liposarcoma are poorly understood. In the present study, the mRNA expression of Eag1 in different adipose tissue samples was examined by real-time PCR.

Engineered ubiquitin ligase PTB-U-box targets insulin/insulin-like growth factor receptor for degradation and coordinately inhibits cancer malignancy.

The type 1 insulin-like growth factor receptor (IGF-1R) is a promising target for cancer therapy with antibodies and small molecule tyrosine kinase inhibitors (TKIs) which have been actively tested clinically. Evidences have demonstrated that insulin receptor (IR), which is implicated in tumorigenesis, conveys resistance to IGF-1R targeted therapy. This provided the compelling rationale for co-targeting IGF-1R and IR.

TC-1 overexpression promotes cell proliferation in human non-small cell lung cancer that can be inhibited by PD173074.

Thyroid cancer-1 (TC-1), a natively disordered protein, is widely expressed in vertebrates and overexpressed in many kinds of tumors. However, its exact role and regulation mechanism in human non-small cell lung cancer (NSCLC) are still unclear. In the present study, we found that TC-1 is highly expressed in NSCLC and that its aberrant expression is strongly associated with NSCLC cell proliferation.

Silencing of Ether à go-go 1 by shRNA inhibits osteosarcoma growth and cell cycle progression.

Recently, a member of the voltage-dependent potassium channel (Kv) family, the Ether à go-go 1 (Eag1) channel was found to be necessary for cell proliferation, cycle progression and tumorigenesis. However, the therapeutic potential of the Eag1 channel in osteosarcoma remains elusive. In the present study, a recombinant adenovirus harboring shRNA against Eag1 was constructed to silence Eag1 expression in human osteosarcoma MG-63 cells.

Voltage-gated potassium channel Kv1.3 is highly expressed in human osteosarcoma and promotes osteosarcoma growth.

Deregulation of voltage-gated potassium channel subunit Kv1.3 has been reported in many tumors. Kv1.

MicroRNA-34a inhibits human osteosarcoma proliferation by downregulating ether à go-go 1 expression.

Aberrant expression of MicroRNAs (miRNAs) has been implicated in several types of cancer. As a direct target gene of p53, miR-34a has been suggested to mediate the tumor suppressor function of p53. Ether à go-go 1 (Eag1) channel is overexpressed in a variety of cancers and plays important roles in cancer progression.

p38 MAPK regulates the expression of ether à go-go potassium channel in human osteosarcoma cells.

Background: The ether à go-go (Eag) channel has been shown to be overexpressed in a variety of cancers. However, the expression and function of Eag in osteosarcoma are poorly understood. In addition, the molecular mechanisms responsible for Eag overexpression in cancer cells remain unclear.

Short Hairpin RNA (shRNA) Ether à go-go 1 (Eag1) inhibition of human osteosarcoma angiogenesis via VEGF/PI3K/AKT signaling.

Ether à go-go 1 (Eag1) channel is overexpressed in a variety of cancers but the therapeutic potential of Eag1 in osteosarcoma remains elusive. In this study, we constructed an Ad5-Eag1-shRNA vector and evaluated its efficiency for Eag1 knockdown and its effects on osteosarcoma. Our results showed that Ad5-Eag1-shRNA had high interference efficiency of Eag1 expression and suppressed osteosarcoma growth both in vitro and in vivo.