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Nutritional status is associated with prognosis in a variety of cancers. Studies analyzing the association between the measurements of skeletal muscle and adipose tissue obtained from Computerized Tomography (CT) images at the time of diagnosis of advanced non-small cell lung cancer (NSCLC) and overall survival (OS) are relatively few. Data from 425 patients diagnosed with advanced NSCLC between January 2016 and December 2017 were retrospectively analyzed, with an average follow-up of 15.3 months. To outline the patient's chest CT plain image at the time of diagnosis,skeletal muscle and subcutaneous fat at the level of both thoracic vertebrae were quantified in terms of mass and quantity by the pectoral muscle index (PMI), pectoral muscle density (PMD), subcutaneous fat index (SFI), subcutaneous fat density (SFD), paravertebral muscle index (PVMI), and paravertebral muscle density (PVMD). The SFI value in the female survival group is significantly lower than that in the death group (P = 0.049), and the PVMI value in the overall survival group is significantly lower than that in the death group (P < 0.001). After adjusting for clinical variables such as gender, smoking status, clinical staging, degree of differentiation, and radiotherapy history, the multivariable Cox regression analysis showed that an increase in SFI significantly improves the overall survival rate of patients (Hazard Ratio [HR] = 1.410, 95% Confidence Interval [CI]: 1.042–1.908, P = 0.026). Conversely, a decrease in PVMD is significantly associated with improved overall survival and prognosis (HR = 0.762, 95% CI: 0.579–0.982, P = 0.048). No association was found between body mass index (BMI) and chest muscle status indicators and overall survival (P > 0.05). CT-measured body composition parameters provide precise prognostic information and are superior to BMI; an increased OS rate in advanced NSCLC is associated with a greater SFI and a lower PVMD. [ABSTRACT FROM AUTHOR]

Purpose: Optical surgical navigation (OSN) will be a potent tool to help surgeons more accurately and efficiently remove tumors. The purpose of this study was to evaluate a novel humanized 3E8 antibody (3E8 MAb) fragment site-specifically conjugated with IR800, 3E8.scFv.Cys-IR800, as a potential OSN agent to target colorectal adenocarcinoma.Procedures: An engineered single-chain variable fragment of 3E8 MAb (targeted to TAG-72), appending a C-terminal cysteine residue (3E8.scFv.Cys), was created and reacted with IRDye800-maleimide. 3E8.scFv.Cys-IR800 identity and purity were verified by MALDI-TOF mass spectra and 800 nm detected size exclusion column HPLC. In vitro human colon adenocarcinoma LS-174 T cells binding and competition assay validated biological functionality. We further evaluated the imaging ability and receptor-specific binding of 3E8.scFv.Cys-IR800 in an orthotopic LS-174 T mouse model.Results: A 1:1 dye to protein conjugate was achieved at greater than 90 % HPLC purity. A 1 nmol dose of 3E8.scFv.Cys-IR800 via intraperitoneal injection administration was sufficient to produce high tumor to background fluorescence contrast. Blocking competition studies both in vitro and in vivo using a different blocking protein, 3E8ΔCH2, demonstrated 3E8.scFv.Cys-IR800 binding specificity for TAG-72 antigen.Conclusions: 3E8.scFv.Cys-IR800 shows properties useful in a clinically viable OSN agent for colorectal cancer. [ABSTRACT FROM AUTHOR]

Celecoxib is a potent nonsteroid antiinflammatory drug (NSAID) that has shown great promise in cancer chemoprevention and treatment. The tumor suppression activity of celecoxib and other NSAIDs have been related to the induction of apoptosis in many cancer cell lines and animal models. While celecoxib is a specific inhibitor of cyclooxygenase (COX)-2, recent data indicate that its apoptotic properties may also be mediated through COX-independent pathways. In our study, we evaluated second generation celecoxib derivatives, lacking COX-2 inhibitory activity, in a premalignant and malignant human oral cell culture model to determine their potential anticancer effect and mechanisms responsible for the COX-independent apoptotic activity. Celecoxib and its derivatives delayed the progression of cells through the G [ABSTRACT FROM AUTHOR]

Examines the performance of free nerve graft with vascular implantation of rats in China. Repair of nerve defect by vascularized nerve graft; Use of histochemical staining, electrophysiological and vascular morphology examination; Ratio of regenerated nerve fiber area and conduction velocity.

Background: Alterations in the vascular microenvironment of cancer have gradually gained widespread attention in oncology research, and early qualitative diagnosis using noninvasive examination techniques is crucial in clinical practice. This study aimed to explore the value of quantitative parameters of dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) in the assessment of vascular architecture of solid solitary pulmonary nodules (SSPNs)., Methods: DCE-MRI scan images of a total of 79 patients with SSPNs from November 2021 to December 2023 were prospectively analyzed. Quantitative permeability parameters K trans , K ep , and V e values of the lesions were measured, labeled immunohistochemically with CD31 microvessel density (CD31-MVD), smooth muscle actin microvessel density (SMA-MVD), and vascular endothelial growth factor (VEGF), and quantitative values of vascular architectural parameters were obtained using the image analysis software Image-J. The diagnostic efficacy of quantitative permeability parameters for the diagnosis of malignant SSPNs was analyzed by receiver operating characteristic (ROC) curves using surgical pathology findings as the gold standard for the diagnosis of malignant SSPNs. Spearman's correlation analysis was used to evaluate the relationship between quantitative permeability parameters and vascular construct parameters., Results: The study included 51 female patients (64.6%) with a mean age of 50.5±11.5 years. Only 21 patients (26.6%) had a smoking history, and 30 patients (38.0%) had a normal weight. Statistically significant differences were found between benign and malignant SSPNs subgroups in K trans and V e values in quantitative permeability parameters, and in SMA-MVD and microvascular perfusion index (MPI) in vascular conformation parameters (P<0.05). K trans and V e values showed high diagnostic value for malignant SSPNs [area under the curve (AUC), 0.813 and 0.759]. K trans , K ep , and V e were significantly positively correlated with CD31-MVD, with r-values of 0.857, 0.830, and 0.798 (P<0.05); they were also significantly positively correlated with VEGF, with r-values of 0.851, 0.859, and 0.764 (P<0.05); and K trans and K ep were significantly negatively correlated with MPI, with r-values were -0.779 and -0.864 (P<0.05)., Conclusions: The quantitative permeability parameters of DCE-MRI correlate with some of the vascular architectural parameters, and magnetic resonance image-based quantification of pulmonary nodal vascular architecture provides a noninvasive method for the differential diagnosis of SSPNs., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-24-1467/coif). The authors have no conflicts of interest to declare., (Copyright © 2025 AME Publishing Company. All rights reserved.)

DNA methylation in the promoter of certain genes is associated with transcriptional silencing. Methylation affects gene expression directly by interfering with transcription factor binding and/or indirectly by recruiting histone deacetylases through methyl-DNA-binding proteins. In this study, we demonstrate that the human lung cancer cell line H719 lacks p53-dependent and -independent p21(Cip1) expression. p53 response to treatment with gamma irradiation or etoposide is lost due to a mutation at codon 242 of p53 (C-->W). Treatment with depsipeptide, an inhibitor of histone deacetylase, was unable to induce p53-independent p21(Cip1) expression because the promoter of p21(Cip1) in these cells is hypermethylated. By analyzing luciferase activity of transfected p21(Cip1) promoter vectors, we demonstrate that depsipeptide functions on Sp1-binding sites to induce p21(Cip1) expression. We hypothesize that hypermethylation may interfere with Sp1/Sp3 binding. By using an electrophoretic mobility shift assay, we show that, although methylation within the consensus Sp1-binding site did not reduce Sp1/Sp3 binding, methylation outside of the consensus Sp1 element induced a significant decrease in Sp1/Sp3 binding. Depsipeptide induced p21(Cip1) expression was reconstituted when cells were pretreated with 5-aza-2'-deoxycytidine. Our data suggest, for the first time, that hypermethylation around the consensus Sp1-binding sites may directly reduce Sp1/Sp3 binding, therefore leading to a reduced p21(Cip1) expression in response to depsipeptide treatment.