How long can pulmonary resection surgery be performed after SARS-CoV-2 infection? A multicenter retrospective study.

BACKGROUND: No studies to date have focused on the timing of pulmonary resection in patients with previous severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. In the present study, the authors analyzed the surgical outcomes and evaluated the optimal time point of pulmonary resection surgery following SARS-CoV-2 infection. MATERIALS AND METHODS: In this multicenter retrospective cohort study, patients were divided into different groups according to the time interval between SARS-CoV-2 diagnosis and pulmonary resection. The primary outcome measure was postoperative complications within 30 days after surgery, which was investigated to determine the optimal time point of pulmonary resection. Logistic regression models were used to calculate the risk factors for postoperative complications. RESULTS: In total, 400 patients were enrolled, and the postoperative pathologic examination of 322 (80.5%) patients showed lung cancer. As the interval between SARS-CoV-2 infection and pulmonary resection increased, the incidence of complications gradually decreased in each group. The incidence of grade ≥II complications was higher in the ≤2-week and 2-week to 4-week groups than in the 4-week to 6-week, 6-week to 8-week and >8-week groups [3 (21.4%), 17 (20.2%), 10 (10.6%), 13 (7.9%), and 3 (6.5%), respectively] ( P <0.05). Multiclassification regression analysis showed that the risk of grade ≥II complications in the ≤2-week and 2-week to 4-week groups was significantly higher than that in the >8-week group [odds ratio (95% CI), 3.937 (1.072-14.459), P =0.039 and 3.069 (1.232-6.863), P =0.015]. The logistic regression analysis suggested that underlying disease, persistent SARS-CoV-2 symptoms, and surgical timing (≤4 weeks) were independent risk factors for complications of pulmonary resection after SARS-CoV-2 infection. CONCLUSION: Pulmonary resection should be delayed for at least 4 weeks following SARS-CoV-2 infection to reduce the risk of postoperative complications.

Components of the JNK-MAPK pathway play distinct roles in hepatocellular carcinoma.

PURPOSE: Mitogen-activated protein kinases (MAPK), specifically the c-Jun N-terminal kinase (JNK)-MAPK subfamily, play a crucial role in the development of various cancers, including hepatocellular carcinoma (HCC). However, the specific roles of JNK1/2 and their upstream regulators, MKK4/7, in HCC carcinogenesis remain unclear. METHODS: In this study, we performed differential expression analysis of JNK-MAPK components at both the transcriptome and protein levels using TCGA and HPA databases. We utilized Kaplan-Meier survival plots and receiver operating characteristic (ROC) curve analysis to evaluate the prognostic performance of a risk scoring model based on these components in the TCGA-HCC cohort. Additionally, we conducted immunoblotting, apoptosis analysis with FACS and soft agar assays to investigate the response of JNK-MAPK pathway components to various death stimuli (TRAIL, TNF-α, anisomycin, and etoposide) in HCC cell lines. RESULTS: JNK1/2 and MKK7 levels were significantly upregulated in HCC samples compared to paracarcinoma tissues, whereas MKK4 was downregulated. ROC analyses suggested that JNK2 and MKK7 may serve as suitable diagnostic genes for HCC, and high JNK2 expression correlated with significantly poorer overall survival. Knockdown of JNK1 enhanced TRAIL-induced apoptosis in hepatoma cells, while JNK2 knockdown reduced TNF-α/cycloheximide (CHX)-and anisomycin-induced apoptosis. Neither JNK1 nor JNK2 knockdown affected etoposide-induced apoptosis. Furthermore, MKK7 knockdown augmented TNF-α/CHX- and TRAIL-induced apoptosis and inhibited colony formation in hepatoma cells. CONCLUSION: Targeting MKK7, rather than JNK1/2 or MKK4, may be a promising therapeutic strategy to inhibit the JNK-MAPK pathway in HCC therapy.

Circulating tumor DNA minimal residual disease in clinical practice of non-small cell lung cancer.

INTRODUCTION: The advance of diagnostics and treatments has greatly improved the prognosis of non-small cell lung cancer (NSCLC) patients. However, relapse and metastasis are still common problems encountered by NSCLC patients who have achieved complete remission. Therefore, overcoming the challenge of relapse and metastasis is particularly important for improving the prognosis of NSCLC patients. Research has shown that minimal residual disease (MRD) was a potential source of tumor relapse and metastasis, and circulating tumor DNA (ctDNA) MRD has obvious advantages in predicting the relapse and metastasis of NSCLC and evaluating treatment effectiveness. Therefore, dynamic monitoring of MRD is of great significance for NSCLC patient management strategies. AREAS COVERED: We have reviewed articles related to NSCLC MRD included in PubMed and describes the biological significance and historical context of MRD research, reasons for using ctDNA to evaluate MRD, and potential value and challenges of ctDNA MRD in assessing relapse and metastasis of NSCLC, ultimately guiding clinical therapeutic strategies and management. EXPERT OPINION: The standardized scope of ctDNA MRD detection for NSCLC requires more clinical research evidence to minimize study differences, making it possible to include in the clinical staging as a reliable indicator.

Experimental mouse models for translational human cancer research.

The development and growth of tumors remains an important and ongoing threat to human life around the world. While advanced therapeutic strategies such as immune checkpoint therapy and CAR-T have achieved astonishing progress in the treatment of both solid and hematological malignancies, the malignant initiation and progression of cancer remains a controversial issue, and further research is urgently required. The experimental animal model not only has great advantages in simulating the occurrence, development, and malignant transformation mechanisms of tumors, but also can be used to evaluate the therapeutic effects of a diverse array of clinical interventions, gradually becoming an indispensable method for cancer research. In this paper, we have reviewed recent research progress in relation to mouse and rat models, focusing on spontaneous, induced, transgenic, and transplantable tumor models, to help guide the future study of malignant mechanisms and tumor prevention.

Clinical Efficacy of Single-Port Thoracoscopic Lobectomy versus Three-Port Thoracoscopic Lobectomy for Lung Cancer.

Objective: To evaluate the clinical efficacy of single-port thoracoscopic lobectomy versus three-port thoracoscopic lobectomy for lung cancer. Methods: From February 2020 to February 2021, 200 lung cancer patients treated in our institution assessed for eligibility were enrolled and randomly assigned (1 : 1) to either the experimental group (single-port thoracoscopic lobectomy) or the control group (three-port thoracoscopic lobectomy). The outcomes were the eligible patients' surgical indices, pain stress indexes, and postoperative complications. Results: The experimental group outperformed the control group in terms of incision length, postoperative drainage time, extubation time, time to get out of bed, time to analgesics administration, and postoperative pain score (P < 0.001). Compared with the control group, the experimental group reduced the intraoperative bleeding (161.98 ± 10.65 versus 179.65 ± 14.20, P < 0.001) and length of hospital stay (7.98 ± 0.56 versus 10.46 ± 1.23, P < 0.001). The operative time of the single-port thoracoscopic lobectomy was longer than that of the three-port thoracoscopic lobectomy (P < 0.001). There was no statistical difference between the two groups in the intraoperative conversion to thoracotomy and the number of lymph node dissections (P > 0.05). Postoperative pain stress indices and complication rates of the experimental group were significantly lower than those of the control group (P < 0.001). Conclusion: Single-port thoracoscopic lobectomy can improve the perioperative indices of lung cancer patients, reduce their pain stress response, and accelerate postoperative recovery. However, its operation is difficult and time-consuming, requiring experienced surgeons for improved surgical outcomes in practice.

ZNF3 regulates proliferation, migration and invasion through MMP1 and TWIST in colorectal cancer.

Colorectal cancer (CRC) is a malignant tumor with a high incidence and mortality worldwide. Currently, the underlying molecular mechanisms of CRC are still unclear. Zinc finger protein 3 (ZNF3) is a zinc-finger transcription factor that has been reported as a candidate for breast cancer prognosis, suggesting its involvement in the regulation of tumorigenesis. However, the association between ZNF3 and CRC remains unknown. To investigate the role of ZNF3 in CRC, we first analyze the correlation between ZNF3 expression and CRC, and the results demonstrate that ZNF3 is highly expressed in CRC tissue and cells, which is associated with the age of CRC patients. In vitro studies show that ZNF3 overexpression promotes CRC cell migration. Compared to control cells, knockdown of ZNF3 markedly suppresses CRC cell proliferation, migration and invasion and promotes G0/G1 phase cell cycle arrest. The expressions of the EMT-related markers TWIST and MMP1 are significantly decreased when ZNF3 is silenced. Additionally, overexpression of MMP1 and TWIST exacerbates CRC cell proliferation, accelerates the S phase cell cycle in ZNF3-knockdown SW480 cells, and increases cell migration and invasion through Transwell chambers. These data suggest that ZNF3 is involved in cellular proliferation, migration and invasion by regulating MMP1 and TWIST in CRC cells.

Immune Response-Related Genes - STAT4, IL8RA and CCR7 Polymorphisms in Lung Cancer: A Case-Control Study in China.

PURPOSE: This study aimed to evaluate the associations between immune response-related genes - STAT4, IL8RA and CCR7 polymorphisms and risk of lung cancer. METHODS: Seven polymorphisms of STAT4, IL8RA and CCR7 were genotyped in 350 cases and 350 controls using a MassARRAY platform. RESULTS: The STAT4 rs1400656-G and rs7574865-T alleles may decrease the susceptibility to lung cancer (p rs1400656= 0.020; p rs7574865= 0.014); while IL8RA rs1008562-C and CCR7 rs3136685-T alleles may increase the risk of disease (p rs1008562< 0.001; p rs3136685= 0.018). The STAT4 rs1400656-GA and rs7574865-GT genotypes were determined as protective genotypes against lung cancer risk (p rs1400656= 0.048; p rs7574865= 0.042). However, IL8RA rs1008562-CG/GG and CCR7 rs3136685-TT genotypes were significantly associated with an elevated risk of disease (p rs1008562< 0.0001; p rs3136685= 0.020). Genetic model analysis revealed that STAT4 rs1400656 and rs7574865 were relate to a declining risk of disease under dominant and log-additive models (rs1400656: p dominant = 0.014, p log-additive= 0.016; rs7574865: p dominant = 0.013, p log-additive= 0.013). In contrast, IL8RA rs1008562 exhibited a strong correlation with an elevated risk of lung cancer under all three models (p dominant < 0.0001, p recessive = 0.011, p log-additive< 0.0001). Moreover, CCR7 rs3136685 was correlated with an increased risk of disease under recessive and log-additive models (p recessive = 0.007, p log-additive= 0.019); and CCR7 rs17708087 was also identified as a risk factor in the dominant model (p = 0.038). CONCLUSION: These results widen the scope of knowledge about the association between STAT4, IL8RA and CCR7 polymorphisms and risk of lung cancer.

Selective phenol hydrogenation to cyclohexanone over a dual supported Pd-Lewis acid catalyst.

Cyclohexanone is an industrially important intermediate in the synthesis of materials such as nylon, but preparing it efficiently through direct hydrogenation of phenol is hindered by over-reduction to cyclohexanol. Here we report that a previously unappreciated combination of two common commercial catalysts-nanoparticulate palladium (supported on carbon, alumina, or NaY zeolite) and a Lewis acid such as AlCl3-synergistically promotes this reaction. Conversion exceeding 99.9% was achieved with >99.9% selectivity within 7 hours at 1.0-megapascal hydrogen pressure and 50 degrees C. The reaction was accelerated at higher temperature or in a compressed CO(2) solvent medium. Preliminary kinetic and spectroscopic studies suggest that the Lewis acid sequentially enhances the hydrogenation of phenol to cyclohexanone and then inhibits further hydrogenation of the ketone.

Effect of pressure on the selectivity for the esterification of ethylene glycol with propionic acid in supercritical CO2.

The esterification of ethylene glycol with propionic acid was investigated in supercritical CO2 at 50.0 degrees C. The effect of pressure on equilibrium conversion and selectivity of ethylene glycol monopropionate (monoester) and ethylene glycol dipropinonate (diester) was studied systematically. It was shown that the equilibrium conversion and selectivity was nearly independent of pressure as pressure was lower than 9 MPa. At higher pressure, however, the yield and selectivity of the diester increased considerably, while those of the monoester decreased with increasing pressure. The main reason was that reactants and products distributed between the vapor phase and liquid phase at higher pressures. The solvent power of CO2 for the diester is stronger than that for the monoester. More diester molecules in the liquid phase were extracted into the vapor at higher pressures, which shifted equilibrium of the consecutive reversible reactions.