Cordycepin suppresses vascular inflammation, apoptosis and oxidative stress of arterial smooth muscle cell in thoracic aortic aneurysm with VEGF inhibition.

BACKGROUND: Thoracic aortic aneurysm (TAA) is a type of common and serious vascular disease, in which inflammation, apoptosis and oxidative stress are strongly involved in the progression. Cordycepin, a bioactive compound from Cordyceps militaris, exhibits anti-inflammatory and anti-oxidative activities. This study aimed to address the role and mechanism of cordycepin in TAA. METHODS: The thoracic aortas were perivascularly administrated with calcium chloride (CaCl2), and human aortic smooth muscle cells (HASMCs) were incubated with angiotensin II (Ang II) to simulate the TAA model in vivo and in vitro, respectively. The effect and mechanism of cordycepin in TAA were explored by hematoxylin and eosin (HE) staining, immunohistochemistry (IHC), immunofluorescence (IF), western blot, biochemical test, cell counting kit-8 (CCK-8), and terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL) assays. RESULTS: Cordycepin improved the CaCl2-induced the aneurysmal alteration and disappearance of normal wavy elastic structures of the aorta tissues, TAA incidence and thoracic aortic diameter in rats, and Ang II-induced the cell viability of HASMCs. Cordycepin reversed the CaCl2-induced the relative protein expression of cleaved caspase 9, cleaved caspase 3, interleukin (IL)-6, tumor necrosis factor (TNF)-α and IL-1ß, and the relative levels of glutathione (GSH), malonaldehyde (MDA) and reactive oxygen species (ROS) in vivo, or Ang II-induced these changes in vitro. Mechanically, cordycepin reduced the relative protein expressions of vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2), cluster of differentiation 31 (CD31) and endothelial nitric oxide synthase (eNOS) in the Ang II-induced HASMCs. Correspondingly, overexpression of VEGF increased the levels of the indicators involved in apoptosis, inflammation and oxidative stress, which were antagonized with the cordycepin incubation in the Ang II-induced HASMCs. CONCLUSION: Cordycepin inhibited apoptosis, inflammation and oxidative stress of TAA through the inhibition of VEGF.

Management of Penetrating Injury to the Esophagus Into the Aorta by a Fishbone.

A 66-year-old man was reported to have persistent chest pain for 4 hours after accidentally swallowing a fishbone. An isolated esophageal foreign body (EFB) was suspected in the community hospital. In our center, an emergency chest CT scan revealed an EFB in the upper part of the esophagus of the patient which penetrated the left esophageal wall as well as the distal aortic arch. However, the experience of the treatment strategy for this lesion is still not enough available. Considering the surgical trauma and the risk associated with advanced age of the patient, the option for open surgery was waived. In addition, there was also a risk of sudden death due to aortic rupture that could occur after direct removal of the fishbone. Therefore, emergency thoracic endovascular aortic repair was performed and the fishbone was removed under an endoscope. The patient successfully pulled through without any discomfort, with no complications.

General features, management strategies, and outcomes of symptomatic spontaneous isolated celiac artery dissection.

Objectives: Spontaneous isolated celiac artery dissection (SICAD) is a rare condition that has not been fully investigated and reported, and very little is known regarding its prognosis and management. Here, we aimed to provide more evidence on the management strategy and outcome for symptomatic SICAD based on the experience of a single center. Methods: From January 2018 to December 2021, a total of consecutive 51 patients with symptomatic SICAD were retrospectively included in this study. These patients had been selectively treated with conservative treatment (n = 31) or endovascular treatment (n = 20). Baseline data, imaging findings, treatment strategy, outcomes, and follow-up data have been described and analyzed. Results: The mean age of the patients was 53.2 ± 9.6 years, 44 (86.3%) were male, and 36 (70.6%) had hypertension. The median length of stay was 10.0 days. The complete remission rate was 92.2% on discharge. The median follow-up time was 21.0 months. A secondary intervention was required for two patients during follow-up in the conservative group, wherein one underwent a stent placement three months after discharge because of progression of symptoms and extension of dissection, and the other required intervention one month after discharge because of symptomatic progression. No secondary intervention was required in the endovascular group. Occasional and mild relapse of symptoms occurred in two patients in both the conservative and endovascular groups, with no secondary intervention. The length of dissection (25.5 ± 11.8 mm vs. 19.1 ± 7.4 mm, P = 0.022) and complete remodeling rate (85.7% vs. 15.4%, P < 0.001) in the endovascular group were greater than that in the conservative group. Conclusion: Patients with symptomatic SICAD who were selectively treated with conservative treatment or endovascular treatment had satisfactory early and medium-term outcomes. Endovascular treatment showed significant advantages in the complete remodeling of the celiac artery and presented with a lower rate of secondary intervention. Moreover, it was found to be a safe and effective remedy for failed conservative treatment.

Activation of AMP-activated protein kinase ablated the formation of aortic dissection by suppressing vascular inflammation and phenotypic switching of vascular smooth muscle cells.

BACKGROUND: Aortic dissection (AD) is a fatal vascular disease in absence of effective pharmaceutical therapy. Adenosine monophosphate-activated protein kinase α (AMPKα) plays a critical role in various cardiovascular diseases. Whether AMPKα is involved in the pathogenesis of aortic dissection remains unknown. We aimed to determine whether activation of AMPKα prevents the formation of AD. METHODS AND RESULTS: Reduced expression of phosphorylated AMPKα (Thr172) and exacerbated phenotypic switching were observed in human aortic tissues from aortic dissection patients compared with those in tissues from controls. In vivo, the formation of aortic dissection in ApoE-/- mice was successfully induced by continuous infusion of angiotensin II (AngII) for two weeks, characterized by the activation of vascular inflammation, infiltration of macrophages and phenotypic switching of vascular smooth muscle cells (VSMCs). rAAV2-mediated overexpression of constitutively active AMPKα (CA-AMPKα) enhanced the expression of phosphorylated AMPKα (Thr172) and attenuated AngII-induced occurrence of aortic dissection by suppressing the infiltration of macrophages, activation of vascular inflammation and phenotypic switching of VSMCs. The pathogenesis above was conversely exacerbated by rAAV2-mediated overexpression of dominant negative AMPKα2 (DN-AMPKα). In vitro, we demonstrated that the administration of an AMPK agonist (AICAR) or transfection of CA-AMPKα induced the activation of AMPKα and then ameliorated AngII-induced phenotypic switching in the VSMCs and inflammation in the bone marrow-derived macrophages (BMDMs). This could be reversed by the addition of AMPK inhibitor compound C or transfection of DN-AMPKα. CONCLUSION: Impaired activation of AMPKα may increase the susceptibility to aortic dissection. Our findings verified the protective effects of AMPKα on the formation of aortic dissection and may provide evidence for clinical prevention or treatment.

Application of patient decision aids in treatment selection of cardiac surgery patients: a scoping review.

BACKGROUND: The choice of treatment is an unavoidable challenge faced in the day to day medical decision making pertaining to patients with organic heart disease. As a professional discipline, cardiac surgery focuses on creating and using the most advanced evidence-based patient decision aids (PtDAs) to achieve high-quality decision-making. OBJECTIVES: To describe the basic situation, influencing factors, and the outcome of indicators of PtDAs among cardiac surgery patients. METHODS: Seven electronic databases were systematically searched for relevant reviews on the application of PtDAs among cardiac surgery patients. The methodological framework proposed by Arskey and O'Malley was used to guide the scoping review. The extracted data was analyzed qualitatively and quantitatively. RESULTS: After dual, blinded screening of titles and abstracts, 12 articles were included in the review. 10 were quantitative studies, 1 was a mixed study, 1 was a qualitative study. CONCLUSIONS: Compared with the burden of heart disease and the huge evidence base, the application of PtDAs in cardiac surgery is obviously insufficient. The published literature mainly provide information about the factors to be solved from the perspective of researchers, and also summarize obstacle factors. This is the basis for the application and construction of PtDAs in cardiac surgery patients.

Nuclear Paraspeckle Assembly Transcript 1 Enhances Hydrogen Peroxide-Induced Human Vascular Smooth Muscle Cell Injury by Regulating miR-30d-5p/A Disintegrin and Metalloprotease 10.

BACKGROUND: Nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported to be involved in the progression of many cancers; however, the role and mechanisms underlying NEAT1 in abdominal aortic aneurysm (AAA) remain unclear.Methods and Results: The expression of NEAT1, miR-30d-5p and A disintegrin and metalloprotease 10 (ADAM10) was measured by qRT-PCR and western blot. Functional experiments were conducted by using a CCK-8 assay, EDU assay, flow cytometry, western blot, ELISA, and commercial kits. The target relation was confirmed by dual-luciferase reporter assay and the RIP assay. It was then found that NEAT1 was upregulated in peripheral blood of AAA patients ~3.46-fold, smooth muscle cells (SMCs) isolated from AAA tissues ~2.6-fold and in a hydrogen peroxide (H2O2)-induced injury model of human vascular SMC (HVSMCs) ~2.0- and 3.9-fold at 50 µmol/L and 200 µmol/L H2O2treatment, respectively. NEAT1 deletion attenuated H2O2-induced cell proliferation promotion (40.0% vs. 74.3%), apoptosis inhibition (25.0% vs. 13.5%), and reduction of inflammatory response and oxidative stress in HVSMCs. Mechanistically, NEAT1 targeted miR-30d-5p to prevent the degradation of its target, ADAM10, in HVSMCs. Further rescue experiments suggested miR-30d-5p inhibition mitigated the effects of NEAT1 deletion on H2O2-induced HVSMCs. Moreover, ADAM10 overexpression counteracted the inhibitory functions of miR-30d-5p on H2O2-evoked HVSMC injury. CONCLUSIONS: NEAT1 promoted H2O2-induced HVSMC injury by inducing cell apoptosis, inflammation and oxidative stress through miR-30d-5p/ADAM10 axis, indicating the possible involvement of NEAT1 in the pathogenesis of AAA.

LncRNA LBX2-AS1 facilitates abdominal aortic aneurysm through miR-4685-5p/LBX2 feedback loop.

Long noncoding RNAs (LncRNAs) are involved in multiple processes of human malignancy, and emerge as crucial molecules in RNA biology. However, the function of lncRNAs has not been well illustrated in abdominal aortic aneurysm (AAA). In this research, the effects of dysregulated ladybird homeobox 2 antisense RNA 1 (LBX2-AS1) or ladybird homeobox 2 (LBX2) on vascular smooth muscle cell (VSMC) biological processes were surveyed via cell counting kit-8 (CCK-8), methyl thiazolyl tetrazolium (MTT), terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) and caspase-3 activity assays. LBX2-AS1 and LBX2 both possessed pro-apoptosis and anti-proliferation functions in AAA. Mechanically, the regulation role of LBX2-AS1 on miR-4685-5p or that of miR-4685-5p on LBX2 was investigated by quantitative real-time polymerase chain reaction (qRT-PCR). Additionally, the competing endogenous RNA (ceRNA) network was confirmed by luciferase reporter, RNA pull-down, and RNA immunoprecipitation (RIP) assays. LBX2-AS1 sequestered miR-4685-5p to release LBX2 expression via ceRNA mechanism. Further, LBX2 could act as a transcriptional activator of LBX2-AS1. A positive feedback loop was formed by LBX2-AS1, miR-4685-5p and LBX2, deteriorating AAA formation and progression. To sum up, our data suggested that LBX2-AS1, miR-4685-5p and LBX2 constituted a positive feedback loop in promoting AAA development, implying a potential usage of LBX2-AS1/miR-4685-5p/LBX2 axis in AAA management.

Network analysis of differentially expressed smoking-associated mRNAs, lncRNAs and miRNAs reveals key regulators in smoking-associated lung cancer.

Lung cancer is the leading cause of cancer-associated mortality worldwide. Smoking is one of the most significant etiological contributors to lung cancer development. However, the molecular mechanisms underlying smoking-induced induction and progression of lung cancer have remained to be fully elucidated. Furthermore, long non-coding RNAs (lncRNAs) are increasingly recognized to have important roles in diverse biological processes. The present study focused on identifying differentially expressed mRNAs, lncRNAs and micro (mi)RNAs in smoking-associated lung cancer. Smoking-associated co-expression networks and protein-protein interaction (PPI) networks were constructed to identify hub lncRNAs and genes in smoking-associated lung cancer. Furthermore, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses of differentially expressed lncRNAs were performed. A total of 314 mRNAs, 24 lncRNAs and 4 miRNAs were identified to be deregulated in smoking-associated lung cancer. PPI network analysis identified 20 hub genes in smoking-associated lung cancer, including dynein axonemal heavy chain 7, dynein cytoplasmic 2 heavy chain 1, WD repeat domain 78, collagen type III α 1 chain (COL3A1), COL1A1 and COL1A2. Furthermore, co-expression network analysis indicated that relaxin family peptide receptor 1, receptor activity modifying protein 2-antisense RNA 1, long intergenic non-protein coding RNA 312 (LINC00312) and LINC00472 were key lncRNAs in smoking-associated lung cancer. A bioinformatics analysis indicated these smoking-associated lncRNAs have a role in various processes and pathways, including cell proliferation and the cyclic guanosine monophosphate cGMP)/protein kinase cGMP-dependent 1 signaling pathway. Of note, these hub genes and lncRNAs were identified to be associated with the prognosis of lung cancer patients. In conclusion, the present study provides useful information for further exploring the diagnostic and prognostic value of the potential candidate biomarkers, as well as their utility as drug targets for smoking-associated lung cancer.

Left atrial myxoma with versus without cerebral embolism: length of symptoms, morphologic characteristics, and outcomes.

The aim of this study was to evaluate the embolic sequelae of left atrial myxomas and their influence on diagnosis, treatment, and prognosis. Seventy-eight patients were retrospectively investigated. According to their symptoms and neurologic-imaging findings, these patients were classified into 2 groups: embolism (15 patients, 19%) and nonembolism (63 patients, 81%). The time from the first onset of symptoms to diagnosis (that is, the duration of symptoms) was significantly longer in the embolism group than in the nonembolism group (105 ± 190 vs 23 ± 18 d; P <0.01). The myxomas were divided into 2 types on the basis of clinicopathologic findings: type 1, with an irregular or villous surface and a soft consistency, and type 2, with a smooth surface and a compact consistency. There were 42 patients with type 1 myxoma and 36 with type 2. Type 1 myxoma was more frequently found in the embolism group (12 patients, 29%) than was type 2 myxoma (3 patients, 8%). The difference was significant (P=0.04). There were 2 perioperative deaths in the nonembolism group. No recurrence of cardiac myxoma or death was recorded in either group during follow-up. In the embolism group, neurologic symptoms were relieved by surgery, and no subsequent neurologic event was reported. Because surgical resection is highly effective in left atrial myxoma, we should strive for early diagnosis in order to shorten the duration of symptoms and to avoid worse neurologic damage in patients in whom an embolic event is the initial manifestation.

Focal organizing pneumonia mimicking lung cancer: a surgeon's view.

Focal organizing pneumonia is a unique form of organizing pneumonia. Little is known regarding its clinical and radiological feature, diagnosis, management, and outcome. Twenty patients with focal organizing pneumonia were investigated and compared with 40 patients with bronchogenic carcinoma. There were 38 men (63.3%) and 22 women (36.7%). The mean age was 55 ± 9.9 years. No specific feature in clinical and radiological manifestation was found to distinguish between focal organizing pneumonia and bronchogenic carcinoma. In patients with focal organizing pneumonia, wedge resection was performed in 12 cases and lobectomy in eight cases. Follow-up was complete with a median period of 26 months (range, 6 to 104 months). All patients were free from recurrence of organizing pneumonia. Clinical and radiologic findings of focal organizing pneumonia are nonspecific, and this unique form of organizing pneumonia is difficult to differentiate from lung cancer. Surgical resection allows both diagnosis and cure. However, considering the benign nature of this disease, major pulmonary resections should be avoided.

Multimodality FDG PET/CT appearance of pulmonary tuberculoma mimicking lung cancer and pathologic correlation in a tuberculosis-endemic country.

OBJECTIVES: Differentiation between pulmonary tuberculoma and malignancy by preoperative diagnostic imaging sometimes proves difficult. The purpose of this study is to investigate variable manifestations of pulmonary tuberculoma mimicking lung cancer on fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) image and pathologic correlation. PATIENTS AND METHODS: Twenty-five patients with a high suspicion of malignancy and histopathologically diagnosed as pulmonary tuberculoma were included. Their FDG PET/CT images, clinical data, and pathologic findings were investigated. RESULTS: There were 18 men and seven women. The mean age was 52 ± 8.8 years. The maximal diameter of pulmonary tuberculoma ranged from 1.7 to 4.2 cm. CT scan revealed that abnormal signs associated with malignancy such as spicular radiation, notching, and pleural indentation also frequently manifested in tuberculoma. During early imaging, positive FDG uptake was identified in 21 patients (84%), intermediate uptake in 3 patients (12%) and negative uptake in 1 patient (4%). During delayed imaging, 16 patients (64%) showed persistent elevated FDG accumulation and 8 patients (32%) experienced a slight drop of FDG accumulation. Pathologically active tuberculoma showed significantly higher FDG radioactivity during both early and delayed imaging than inactive lesion (P < 0.05). Lymphadenopathy with positive FDG uptake was identified in nine patients (36%). CONCLUSION: Pulmonary tuberculomas mimicking lung cancer, most of which were pathologically active lesions, commonly displayed abnormal appearances in CT scan and an increase in FDG uptake, similar to changes seen on malignancy. Coexistent lymphadenopathy made differential diagnosis even more complicated. These results suggested that positive FDG PET/CT findings should be interpreted with caution in tuberculosis-endemic regions.

[Relationship between Glut-1, Glut-3 expression and fluorodeoxyglucose uptake in NSCLC and benign pulmonary lesion.].

BACKGROUND: It has been known that facilitative glucose transporter (GLUT) is the main carrier which intervenes the glucose uptake of cell. The expression of Glut-1, Glut-3 has close relationship with the uptake of (18)Fluoro-2-deoxyglucose (FDG). The aim of this study is to discuss the relationship between expression of glucose transporter-1, 3 (Glut-1, Glut-3) and FDG uptake in NSCLC and benign pulmonary lesion. METHODS: Eighty-four NSCLC patients and twenty-four benign pulmonary lesion patients received PET/CT scan before operation. The expression of Glut-1, Glut-3 was detected by immunohistochemistry. The relationship among these factors was investigated. RESULTS: The range of average SUV (SUVave) of the eighty-four patients was 3.6-13.2, and the average value was 7.8+/-3.0. The range of average SUV (SUVave) of the twenty-four patients was 1.2-9.2, and the average value was 3.2+/-1.9. In NSCLC tissues, the average immunohistochemical staining intensity of Glut-1, Glut-3 was 4.4+/-1.3 and 2.6+/-1.9, respectively. In benign pulmonary lesion, the average immunohistochemical staining intensity of Glut-1, Glut-3 was 0.9+/-0.9 and 1.2+/-1.4, respectively. Both of the Glut-1 and the Glut-3 expression levels were significantly higher in NSCLC than those in benign pulmonary lesion (P <0.01). Glut-1 expression was positively correlated to SUVave (r =0.78, P <0.01) in NSCLC patients. Glut-3 expression was positively correlated to SUVave (r =0.45, P =0.03) in benign pulmonary lesion patients. CONCLUSIONS: The results show Glut-1 and Glut-3 express not only in NSCLC but also in benign pulmonary lesion. Glut-1 play an important role in FDG uptake in NSCLC. Glut-3 play an important role in FDG uptake in benign pulmonary lesion.

Correlation of photodynamic activity and fluorescence signaling for free and pegylated mTHPC in mesothelioma xenografts.

BACKGROUND/OBJECTIVES: Correlation of photodynamic activity (PDT) and fluorescence signaling for free and pegylated meta-tetrahydroxyphenylchlorin (mTHPC) in nude mice with mesothelioma xenografts. STUDY DESIGN/MATERIALS AND METHODS: Twelve animals received light delivery (20 J/cm(2), 150 mW/cm(2), spot size 1.2 cm) on the tumor and the hind leg 3 days after sensitization with 0.15 mg/kg free mTHPC (n = 6) or equimolar-dosed pegylated mTHPC (n = 6). Groups of three animals each were sensitized with 0.15 and 0.5 mg/kg free mTHPC or equimolar dosed pegylated mTHPC followed after 3 days by fluorescence microscopy measurements. RESULTS: Pegylated mTHPC resulted in a similar extent of PDT-related tumor necrosis but in lower skin phototoxicity than free mTHPC. Both mTHPC formulations were heterogeneously distributed in the tumor and were mainly localized in perivascular areas. Pegylated mTHPC revealed a higher tumor to skin fluorescence intensity ratio than free mTHPC (P<0.001). CONCLUSIONS: Fluorescence signaling measurement has the potential to predict the photodynamic activity for both mTHPC formulations in mesothelioma xenografts.

Antegrade versus retrograde isolated lung perfusion: doxorubicin uptake and distribution in a sarcoma model.

BACKGROUND: Antegrade and retrograde doxorubicin-based isolated lung perfusions were compared in rodents bearing a sarcomatous tumor in the perfused lung. Inasmuch as these tumors derive their vascularization from the bronchial artery system, we hypothesized that retrograde isolated lung perfusion through the pulmonary vein might result in an improved tumor drug uptake. METHODS: Single-pass antegrade (n = 9) and retrograde (n = 9) isolated left lung perfusions were performed with 100 microg of doxorubicin in Fischer rats 10 days after subpleural tumor cell injection. The perfusion, washout, and recirculation times were 20, 10, and 60 minutes, respectively, followed by harvesting of the lung. The doxorubicin concentration and compartmental distribution in the tumor and in normal parenchyma of each perfused lung were measured by high-pressure liquid chromatography (6 animals of each group) and fluorescence microscopy (3 animals of each group). RESULTS: Doxorubicin concentration and pattern of doxorubicin-based fluorescence signaling were comparable for both perfusion techniques in normal lung tissue. Antegrade and retrograde isolated lung perfusion resulted in similar tumor drug uptake, which was lower than in normal lung parenchyma, and in weak and sporadic fluorescence signaling emerging from the tumor periphery and from blood vessels situated within the tumor tissue. CONCLUSIONS: Retrograde isolated lung perfusion did not confer a better doxorubicin uptake in the tumor as compared with antegrade lung perfusion despite the fact that the tumor vascularization in this model is based on the bronchial artery circulation.

Preclinical comparison of mTHPC and verteporfin for intracavitary photodynamic therapy of malignant pleural mesothelioma.

Efficacy and tumour selectivity of photodynamic therapy with two clinically approved sensitizers (mTHPC, verteporfin) were assessed for focal intracavitary photodynamic therapy (PDT) in rodents with malignant pleural mesothelioma (MPM) at recommended drug-light conditions and at escalating sensitizer dosages. MPM tumours were generated in 15 Fischer rats by subpleural mediastinal tumour cell injection followed after 5 days by intracavitary PDT with light delivery monitored by in situ dosimetry. Animals were intravenously sensitized either with mTHPC (0.1 mg/kg, n = 3; 0.2 mg/kg, n = 3) followed after 4 days by illumination with 20 J/cm(2) at 652 nm, or with verteporfin (0.6 mg/kg, n = 3; 1.2 mg/kg, n = 3) followed after 20 min by illumination with 100 J/cm(2) at 689 nm. Three untreated tumour-bearing animals served as controls. Histological evaluation of the treated tumour and of adjacent normal organs was performed 10 days after tumour implantation. The extent of PDT-induced tumour necrosis was compared to the non-necrosed area and expressed in percentage. A locally invasive growing MPM tumour (3.1 +/- 1 mm diameter) without spontaneous necrosis diameter was found in all animals. For both sensitizers, focal intracavitary PDT was well tolerated at drug-light conditions recommended for clinical applications. Mediastinal organs were spared for both sensitizers but verteporfin resulted in a higher extent of tumour necrosis (80%) than mTHPC (50%). Drug dose escalation revealed a higher extent of PDT-related tumour necrosis for both sensitizers (mTHPC 55%, verteporfin 88%), however, verteporfin-PDT was associated with a higher toxicity than mTHPC-PDT.

[Relationship between tumor size and lymph node metastasis in squamous cell carcinoma and adenocarcinoma of the lung].

BACKGROUND: Lymphatic dissemination is the main approach of metastasis in lung cancer, and it is also an important prognostic factor. The aim of this study is to explore the relationship between tumor size and lymph node metastasis in squamous cell carcinoma and adenocarcinoma of the lung. METHODS: A total of 240 patients diagnosed as squamous cell carcinoma and adenocarcinoma were studied. The relationship between tumor size and lymph node metastasis was analyzed. RESULTS: Lymph node metastasis rate in maximum diameter (d)≤2cm, 2cm < d≤3cm, 3cm < d≤6cm, 6cm < d≤10cm, and d > 10cm groups was 50.0%, 35.1%, 52.8%, 52.1% and 71.4%, respectively. There was no correlation between tumor size and lymph node metastasis (r=0.10, P > 0.05). Lymph node metastasis occurred more frequently in adenocarcinoma (58.8%) than that in squamous cell carcinoma (42.9%) (P < 0.05). Mediastinal lymph node metastasis was found in 7 patients (16.3%) with d≤3cm, who were all diagnosed as moderate or poor differentiation. CONCLUSIONS: Lymph node metastasis is not related to tumor size. Lymph node metastasis occurs more frequently in adenocarcinoma than it does in squamous cell carcinoma. Mediastinal lymph node metastasis can be found in tumor with d≤3cm, and differentiation grade may play an important role in lymph node metastasis.