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This novel report presents the first known case, to our knowledge, of a 16-year-old male patient who experienced intraventricular thrombosis and pulmonary embolism after a Nuss procedure for pectus excavatum, attributed to chronic bar displacement. Two years after the operation, the patient experienced post-exercise cough and hemoptysis, which led to his admission. Imaging revealed pulmonary embolism, thrombosis in the right ventricular outflow tract, and lung infiltrative lesions. We hypothesize that the chronic bar displacement led to its embedment in the right ventricle, resulting in thrombus formation, which subsequently contributed to partial pulmonary embolism. Surgery revealed the bars' intrusion into the right ventricle and lung. This case highlights the risk of severe complications from bar displacement in the Nuss procedure, which necessitates long-term follow-up evaluation, caution against strenuous activities after surgery, and use of thoracoscopic guidance during bar implantation and removal. It underscores the importance of vigilant evaluation for late-stage complications in patients with respiratory distress or thrombosis after a Nuss procedure.
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Tórax en Embudo , Embolia Pulmonar , Trombosis , Humanos , Embolia Pulmonar/etiología , Embolia Pulmonar/diagnóstico , Masculino , Adolescente , Tórax en Embudo/cirugía , Trombosis/etiología , Trombosis/diagnóstico por imagen , Trombosis/diagnóstico , Ventrículos Cardíacos/diagnóstico por imagen , Complicaciones Posoperatorias/etiología , Complicaciones Posoperatorias/diagnóstico , Tomografía Computarizada por Rayos XRESUMEN
Lung adenocarcinoma (LUAD) presents a significant global health challenge owing to its poor prognosis and high mortality rates. Despite its involvement in the initiation and progression of a number of cancer types, the understanding of the precise impact of MIS18 kinetochore protein A (MIS18A) on LUAD remains incomplete. In the present study, the role of MIS18A in LUAD was investigated by analyzing the genomic and clinical data from multiple public datasets. The expression of MIS18A was validated using reverse transcription-quantitative polymerase chain reaction, and in vitro experiments involving small interfering RNA-induced downregulation of MIS18A in lung cancer cells were conducted to further explore its impact. These findings revealed that elevated MIS18A expression in LUAD was associated with advanced clinical features and poor prognosis. Functional analysis also revealed the role of MIS18A in regulating the cell cycle and immune-related pathways. Moreover, MIS18A altered the immune microenvironment in LUAD, influencing its response to immunotherapy and drug sensitivity. The results of the in vitro experiments indicated that suppression of MIS18A expression reduced the proliferative and migratory capacities of LUAD cells. In summary, MIS18A possesses potential as a biomarker and may serve as a possible therapeutic target for LUAD, with significant implications for tumor progression by influencing both cell cycle dynamics and immune infiltration.
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Background: Shugoshin 2 (SGO2), a component of the cell division cohesion complex, is involved in both mitotic and meiotic processes. Despite being overexpressed in various malignant tumors and is associated with poor prognosis, its exact role in lung adenocarcinoma (LUAD) and its biological effects on lung cancer cells are not well understood. Methods: The transcriptomics data and clinical information for LUAD were obtained from TCGA and GEO, and DEGs associated with prognostic risk factors were screened using Cox regression analysis and chi-square testing. Identify these gene functions using correlation heatmaps, protein interaction networks (PPIs), and KEGG enrichment assays. The expression of SGO2 in tissues was verified by PCR and IHC, and the prognostic value of SGO2 in LUAD was evaluated by survival analysis. In addition, the effects of SGO2 knockdown on lung cancer cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT) were studied in vitro. After that, the TIMER database and single-sample GSEA (ssGSEA) analysis were used to investigate the correlation between SGO2 and immune infiltration. Finally, the tumor mutational burden (TMB) of different SGO2 clusters and the efficacy of the two clusters in multiple treatments were evaluated. Results: High-risk genes associated with poor prognosis in LUAD are involved in cell cycle regulation and proliferation. Among these genes, SGO2 exhibited high expression in LUAD and corresponded with the TNM stage. Furthermore, the knockdown of SGO2 led to a decrease in the proliferation, migration, invasion, and EMT processes of lung cancer cells. Notably, high SGO2 expression may have poorer anti-tumor immunity and may therefore be more suitable for immunotherapy to re-establish immune function, while its high expression with a higher TMB could enable LUAD to benefit from multiple therapies. Conclusion: Our findings suggest that SGO2 may be a promising prognostic biomarker for LUAD, particularly in regulating the cell cycle and benefiting from multiple therapies.
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BACKGROUND: Inflammatory factors are well-established indicators for vascular disease, but the D-dimer to lymphocyte count ratio (DLR) is not measured in routine clinical care. Screening of DLR in individuals may identify individuals at in-hopital mortality of acute aortic dissection (AD). METHODS: A retrospective analysis of clinical data from 2013 to 2020 was conducted to identify which factors were related to in-hospital mortality risk of AD. Baseline clinical features, cardiovascular risk factors, and laboratory parameters were obtained from the hospital database. The end point was in-hospital mortality. Forward conditional logistic regression was performed to identify independent risk factors for AA in-hospital death. The cutoff value of the DLR should be ideally calculated by receiver operating characteristic (ROC) analysis. RESULTS: The in-hospital mortality rate was 15% (48 of 320 patients). Patients with in-hospital mortality had a higher admission mean DLR level than the alive group (1740 vs. 1010, P < .05). The cutoff point of DLR was 907. The in-hospital mortality rate in the high-level DLR group was significantly higher than that in the low-level DLR group (P < .05). Univariate analysis showed that 8 of 38 factors were associated with in-hospital mortality (P < .05), including admission WBC, neutrophils, lymphocytes, neutrophils/lymphocytes (NLR), prothrombin time (PT), heart rate (HR), D-dimer, and DLR. In multivariate analysis, DLR (odds ratio [OR] 2.127, 95% CI 1.034-4.373, P = 0.040), HR (odds ratio [OR] 1.016, 95% CI 1.002-1.030, P = 0.029) and PT (odds ratio [OR] 1.231, 95% CI 1.018-1.189, P = 0.032) were determined to be independent predictors of in-hospital mortality (P < .05). CONCLUSION: Compared with the common clinical parameters PT and HR, serum DLR level on admission is an uncommon but independent parameter that can be used to assess in-hospital mortality in patients with acute AD.
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Disección Aórtica , Mortalidad Hospitalaria , Humanos , Disección Aórtica/diagnóstico , Biomarcadores , Recuento de Linfocitos , Linfocitos , Neutrófilos , Pronóstico , Estudios Retrospectivos , Curva ROCRESUMEN
Extending the benefits of tumor molecular profiling for all cancer patients requires a comprehensive analysis of tumor genomes across distinct patient populations worldwide. In this study, we perform deep next-generation DNA sequencing (NGS) from tumor tissues and matched blood specimens from over 10,000 patients in China by using a 450-gene comprehensive assay, developed and implemented under international clinical regulations. We perform a comprehensive comparison of somatically altered genes, the distribution of tumor mutational burden (TMB), gene fusion patterns, and the spectrum of various somatic alterations between Chinese and American patient populations. Here, we show 64% of cancers from Chinese patients in this study have clinically actionable genomic alterations, which may affect clinical decisions related to targeted therapy or immunotherapy. These findings describe the similarities and differences between tumors from Chinese and American patients, providing valuable information for personalized medicine.
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Neoplasias , Pueblo Asiatico/genética , Biomarcadores de Tumor/genética , Secuenciación de Nucleótidos de Alto Rendimiento , Humanos , Mutación , Neoplasias/epidemiología , Neoplasias/genética , Neoplasias/terapia , Medicina de PrecisiónRESUMEN
BACKGROUND: Nil by mouth is considered the standard of care during the first days following esophagectomy. However, with the routine implementation of enhanced recovery after surgery, early oral intake is more likely to be the preferred mode of nutrition following esophagectomy. The present study aims to evaluate the safety and effectiveness of early oral intake following esophagectomy for esophageal cancer. METHODS: Comprehensive literature searches were conducted using PubMed, Web of Science, Embase, and Cochrane Library. Weighted mean differences (WMD) and odds ratios (OR) with 95% confidence intervals (CI) were calculated as the effect sizes for continuous and dichotomous variables, respectively. RESULTS: Fourteen studies with a total of 1947 patients were included. Length of hospital stay (WMD = - 3.94, CI: - 4.98 to - 2.90; P < 0.001), the time to first flatus (WMD = - 1.13, CI: - 1.25 to - 1.01; P < 0.001) and defecation (WMD = - 1.26, CI: - 1.82 to - 0.71; P < 0.001) favored the early oral intake group. There was no statistically significant difference in mortality (OR = 1.23, CI: 0.45 to 3.36; P = 0.69). Early oral intake also did not increase the risk of pneumonia and overall postoperative complications. CONCLUSIONS: Current evidence indicates early oral intake following esophagectomy seems to be safe and effective. It may be the preferred mode of nutrition following esophagectomy. However, more high-quality studies are still needed to further validate this conclusion.
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Neoplasias Esofágicas , Esofagectomía , Nutrición Enteral , Neoplasias Esofágicas/cirugía , Esofagectomía/efectos adversos , Humanos , Tiempo de Internación , Complicaciones Posoperatorias/epidemiologíaRESUMEN
OBJECTIVE: To determine the prognostic value of red cell distribution width (RDW) and circulating tumor cells with epithelial-mesenchymal transition phenotype (M-CTC) in lung adenocarcinoma (LUAD). PATIENTS AND METHODS: Clinical and laboratory data of 60 patients with LUAD were collected. CTCs were isolated from their peripheral blood using the CanPatrolTM CTC enrichment method. The indicators of RDW and neutrophil lymphocyte ratio (NLR) were calculated based on the laboratory standards. RESULTS: A total of 60 LUAD patients were enrolled, of which 19 (31.7%) had high RDW (>0.14) and 32 (53.3%) were positive for M-CTCs. There was no significant correlation between RDW and the clinical characteristics. M-CTC was not significantly associated with tumor size and differentiation, age, gender, tumor stage, and histological type but correlated significantly with lymphatic metastasis (P = 0.044), high NLR (>2.26, P = 0.023), and high RDW (>0.14, P = 0.036). Furthermore, the M-CTC+ LUAD patients had a significantly poor recurrence-free survival (RFS; Log rank P =0.001, HR = 2.749, 95% CI = 1.489-5.078) and overall survival (OS; Log rank P =0.022, HR = 2.283, 95% CI = 1.128-4.622) compared to the M-CTC- patients. Similarly, high RDW also correlated with worse RFS (Log rank P = 0.008, HR = 2.331, 95% CI = 1.248-4.353) and OS (Log rank P = 0.004, HR = 0.004, 95% CI = 1.398-5.525). CONCLUSION: M-CTC is significantly related to RDW and NLR, and an independent prognostic factor in LUAD.
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Circulating tumor cells (CTCs) are a heterogeneous population of tumor cells with distinct clinical and biological properties. The aim of the present study was to evaluate the relationship between CTCs with the epithelial-mesenchymal transition phenotype (CTC EMT) and the proliferative marker Ki67, and their prognostic value in non-small cell lung cancer (NSCLC). CTCs were isolated from the peripheral blood of 84 NSCLC patients using the CanPatrolTM CTC enrichment method, and the expression of Ki67 in tumor tissues were detected by immunohistochemistry. Almost two-thirds (61/84) of the patients were positive for CTC EMT, and 55 (65.4%) patients had high in-situ expression of Ki67 (≥ 14%) in the tumor tissues. CTC EMT was not significantly associated with tumor size and differentiation, age, gender and histological type, but correlated with lymphatic metastasis, tumor stage and Ki67 overexpression. Furthermore, the CTC EMT+ NSCLC patients had a significantly lower recurrence-free survival (RFS) and overall survival (OS) compared to the negative patients. Similarly, Ki67 levels ≥ 14% were associated with a significantly lower RFS and OS. In conclusion, CTC EMT is significantly related to Ki67 expression, and is a risk factor of NSCLC.
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@#Objective To explore the effect of 16F gastric tube on pain relief in postoperative lung cancer patients. Methods A total of 118 lung cancer patients were treated with radical resection of lung cancer in our hospital between January 2015 and May 2016. The patients were assigned into two groups: a 16F gastric tube group (16F group, 60 patients, 30 males and 30 females at age of 41-73 (52.13±7.83) years and a 28F drainage tube group (28F group, 58 patients, 25 males and 33 females at age of 45-75 (55.62±4.27) years. Clinical effects were compared between the two groups. Results There was no statistical difference in drainage time (4.47±1.03 d vs. 4.24±1.16 d, P=0.473), drainage amount (560.37±125.00 ml vs. 656.03±132.45 ml, P=0.478), incidences of pneumothorax (5/60 vs. 2/58, P=0.439), pleural effusion (6/60 vs. 3/58, P=0.522), and subcutaneous emphysema (3/60 vs. 1/58, P=0.635) between the two groups (P>0.05). The pain caused by the drainage tube in the16F group was less than that in the 28F drainage tube group with a statistical difference (F=4 242.996, P<0.001). The frequency of taking analgesics in the 16F group was significantly less than that in the 28F group (12/60 vs. 26/58, P<0.001). Conclusion The effects of draining pleural effusions and promoting lung recruitment are similar between the 16F group and the 28F group. However, the wound pain caused by 16F gastric tube is significantly less than that by 28F drainage tube.
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RATIONALE: Mesenchymal-to-epithelial transition (MET) exon 14 skipping mutation was a targetable alteration in nonsmall-cell lung cancer (NSCLC), and the MET inhibitor of crizotinib had the most efficacy among all the targeted drugs. Most of the cancer-related deaths are associated with metastasis. Circulating tumor cells (CTCs) have been a valuable biomarker in assessing metastasis. Recent experiences suggested that CTCs detection may help improve diagnosis and predict prognosis for patients with NSCLC. However, few literatures have reported the CTCs detection based on the (MET) exon 14 skipping, which are positive in NSCLC patients. PATIENT CONCERNS: The patient, a 69-year-old Chinese male, with a 50 years history of smoking. Because of the cough, the patient went to the hospital and found the upper right lung tumor and the right supraclavicular lymph node enlarged. He was worried that it was cancer. DIAGNOSES: The patient was performed biopsy of the right clavicle lymph node metastasis on October 12 and sent the tissue specimen for pathological evaluation. Finally, the patient was diagnosed to be with a pT3N3Mx stage IIIC lung adenocarcinoma. INTERVENTIONS: The patient began to take orally crizotinib 250âmg twice a day for the medical therapy after lymph node biopsy. At the same time, the CTCs were detected to observe the prognosis of the patients. OUTCOMES: Compared with the first CTCs result, the second test revealed a decrease in the amount of CTCs, while the mesenchymal CTCs have increased, indicating the possibility of distal metastasis. LESSONS: This is the first proof that CTCs can be quantitatively assayed by MET exon 14 skipping mutation, which demonstrates the clinical response to crizotinib. More cases should be reported and further evaluation for treatment options and prognosis evaluation is necessary.
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Adenocarcinoma/tratamiento farmacológico , Adenocarcinoma/patología , Neoplasias Pulmonares/tratamiento farmacológico , Neoplasias Pulmonares/patología , Células Neoplásicas Circulantes/efectos de los fármacos , Pirazoles/uso terapéutico , Piridinas/uso terapéutico , Adenocarcinoma del Pulmón , Anciano , Biomarcadores , Crizotinib , Transición Epitelial-Mesenquimal , Humanos , Masculino , Mutación , PronósticoRESUMEN
Recent studies report a correlation between excision repair cross-complementing group 2 (ERCC2) Lys751Gln polymorphism and an increased risk of lung cancer, but results are controversial and inconclusive. Thus, we conducted a comprehensive meta-analysis in order to assess the correlation between them. Our study uses an odds ratio (OR) with a 95% confidence interval (95% CI) to evaluate the strength of the association; we also performed Begg's funnel plot and the Egger's test to assess the publication bias of previous articles. Finally, our meta-analysis is comprised of 28 full studies, including 23,370 subjects (10,242 cases and 13,128 controls). Our overall research shows that ERCC2 Lys751Gln polymorphism carries an increased risk of developing lung cancer (C vs. A: OR = 1.160, 95% CI = 1.081-1.245, p = .000; CC vs. AA: OR = 1.252, 95% CI = 1.130-1.388, p = .000; CA vs. AA: OR = 1.152, 95% CI = 1.060-1.252, p = .001; CC+CA vs. AA: OR = 1.186, 95% CI = 1.089-1.292, p = .000; CC vs. CA+AA: OR = 1.196, 95% CI = 1.087-1.316, p = .000). In ethnic subgroup analyses, we find a significant risk among Caucasians (C vs. A: OR = 1.106, 95% CI = 1.048-1.166, p = .000; CC vs. AA: OR = 1.233, 95% CI = 1.103-1.378, p = .000; CC+CA vs. AA: OR = 1.113, 95% CI = 1.033-1.199, p = .005; CC vs. CA+AA: OR = 1.185, 95% CI = 1.069-1.313, p = .001) and among Asians under two genetic models (CA vs. AA: OR = 1.265, 95% CI = 1.034-1.549, p = .023; CC+CA vs. AA: OR = 1.252, 95% CI = 1.015-1.544, p = .036). These results were confirmed by similar findings, demonstrated by stratified analyses in study design and histological typing. This meta-analysis indicates that ERCC2 Lys751Gln polymorphism may lead to an increased susceptibility to lung cancer risk among Caucasians and Asians.
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Neoplasias Pulmonares/epidemiología , Neoplasias Pulmonares/genética , Proteína de la Xerodermia Pigmentosa del Grupo D/genética , Humanos , Neoplasias Pulmonares/enzimología , Oportunidad Relativa , Polimorfismo Genético , Factores de RiesgoRESUMEN
The association between excision repair cross complementing group 2 (ERCC2) Asp312Asn polymorphism and lung cancer has been reported by many articles recently, but the results were controversial and inconclusive. Therefore, a meta-analysis was conducted to assess the relationship between them. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association. A total of 22 full studies with 20,101 subjects (8719 cases and 11,382 controls) were included in our research. The meta-analysis result showed that no significant association was found between ERCC2 Asp312Asn polymorphism and lung cancer in overall analysis (AA vs. GG, OR=1.023, 95% CI=0.824-1.270, p=0.838; AG vs. GG, OR=1.003, 95% CI=0.936-1.074, p=0.942; AA+AG vs. GG, OR=1.013, 95% CI=0.949-1.082, p=0.697; AA vs. AG+GG, OR=1.033, 95% CI=0.841-1.270, p=0.755). In subset analyses of stratified ethnicity, significantly increased risk was found among Asians (AA vs. GG, OR=3.212, 95% CI=1.518-6.795, p=0.002; AA vs. AG+GG, OR=3.174, 95% CI=1.500-6.712, p=0.003), whereas the association was not found among Caucasians under any genetic models. When analyses were conducted based on the study design, it indicated that the risk of lung cancer might be significantly increased in a hospital-based study (AA vs. GG, OR=1.323, 95% CI=1.096-1.596, p=0.004; AA+AG vs. GG, OR=1.109, 95% CI=1.000-1.229, p=0.050; AA vs. AG+GG, OR=1.285, 95% CI=1.076-1.535, p=0.006). In addition, a significantly increased risk for nonsmokers was detected under the dominant model (AA+AG vs. GG, OR=1.460, 95% CI=1.095-1.948, p=0.010). In conclusion, this meta-analysis suggested ERCC2 Asp312Asn polymorphism may increase the risk of lung cancer among Asians, whereas not among Caucasians.