Influence of blood glucose fluctuations on chemotherapy efficacy and safety in type 2 diabetes mellitus patients complicated with lung carcinoma

BACKGROUND Patients with type 2 diabetes mellitus(T2DM)have large fluctuations in blood glucose(BG),abnormal metabolic function and low immunity to varying degrees,which increases the risk of malignant tumor diseases and affects the efficacy of tumor chemotherapy.Controlling hyperglycemia may have important therapeutic implications for cancer patients.AIM To clarify the influence of BG fluctuations on chemotherapy efficacy and safety in T2DM patients complicated with lung carcinoma(LC).METHODS The clinical data of 60 T2DM+LC patients who presented to the First Affiliated Hospital of Ningbo University between January 2019 and January 2021 were retrospectively analyzed.All patients underwent chemotherapy and were grouped as a control group(CG;normal BG fluctuation with a mean fluctuation<3.9 mmol/L)and an observation group(OG;high BG fluctuation with a mean fluctuation≥3.9 mmol/L)based on their BG fluctuations,with 30 cases each.BGrelated indices,tumor markers,serum inflammatory cytokines and adverse reactions were comparatively analyzed.Pearson correlation analysis was performed to analyze the correlation between BG fluctuations and tumor markers.RESULTS The fasting blood glucose and 2-hour postprandial blood glucose levels in the OG were notably elevated compared with those in the CG,together with markedly higher mean amplitude of glycemic excursions(MAGE),mean of daily differences,largest amplitude of glycemic excursions and standard deviation of blood glucose(P<0.05).In addition,the OG exhibited evidently higher levels of carbohydrate antigen 19-9,carbohydrate antigen 125,carcinoembryonic antigen,neuron-specific enolase,cytokeratin 19,tumor necrosis factor-α,interleukin-6,and highsensitivity C-reactive protein than the CG(P<0.05).Pearson analysis revealed a positive association of MAGE with serum tumor markers.The incidence of adverse reactions was significantly higher in the OG than in the CG(P<0.05).CONCLUSION The greater the BG fluctuation in LC patients after chemotherapy,the more unfavorable the therapeutic effect of chemotherapy;the higher the level of tumor markers and inflammatory cytokines,the more adverse reactions the patient experiences.

Smart Lung Tumor Prediction Using Dual Graph Convolutional Neural Network

A significant advantage of medical image processing is that it allows non-invasive exploration of internal anatomy in great detail.It is possible to create and study 3D models of anatomical structures to improve treatment outcomes,develop more effective medical devices,or arrive at a more accurate diagnosis.This paper aims to present a fused evolutionary algorithm that takes advantage of both whale optimization and bacterial foraging optimization to optimize feature extraction.The classification process was conducted with the aid of a convolu-tional neural network(CNN)with dual graphs.Evaluation of the performance of the fused model is carried out with various methods.In the initial input Com-puter Tomography(CT)image,150 images are pre-processed and segmented to identify cancerous and non-cancerous nodules.The geometrical,statistical,struc-tural,and texture features are extracted from the preprocessed segmented image using various methods such as Gray-level co-occurrence matrix(GLCM),Histo-gram-oriented gradient features(HOG),and Gray-level dependence matrix(GLDM).To select the optimal features,a novel fusion approach known as Whale-Bacterial Foraging Optimization is proposed.For the classification of lung cancer,dual graph convolutional neural networks have been employed.A com-parison of classification algorithms and optimization algorithms has been con-ducted.According to the evaluated results,the proposed fused algorithm is successful with an accuracy of 98.72%in predicting lung tumors,and it outper-forms other conventional approaches.

Early Diagnosis of Lung Tumors for Extending Patients’ Life Using Deep Neural Networks

The medical community has more concern on lung cancer analysis.Medical experts’physical segmentation of lung cancers is time-consuming and needs to be automated.The research study’s objective is to diagnose lung tumors at an early stage to extend the life of humans using deep learning techniques.Computer-Aided Diagnostic(CAD)system aids in the diagnosis and shortens the time necessary to detect the tumor detected.The application of Deep Neural Networks(DNN)has also been exhibited as an excellent and effective method in classification and segmentation tasks.This research aims to separate lung cancers from images of Magnetic Resonance Imaging(MRI)with threshold segmentation.The Honey hook process categorizes lung cancer based on characteristics retrieved using several classifiers.Considering this principle,the work presents a solution for image compression utilizing a Deep Wave Auto-Encoder(DWAE).The combination of the two approaches significantly reduces the overall size of the feature set required for any future classification process performed using DNN.The proposed DWAE-DNN image classifier is applied to a lung imaging dataset with Radial Basis Function(RBF)classifier.The study reported promising results with an accuracy of 97.34%,whereas using the Decision Tree(DT)classifier has an accuracy of 94.24%.The proposed approach(DWAE-DNN)is found to classify the images with an accuracy of 98.67%,either as malignant or normal patients.In contrast to the accuracy requirements,the work also uses the benchmark standards like specificity,sensitivity,and precision to evaluate the efficiency of the network.It is found from an investigation that the DT classifier provides the maximum performance in the DWAE-DNN depending on the network’s performance on image testing,as shown by the data acquired by the categorizers themselves.

Endostatin enhances antitumor effect of tumor antigen-pulsed dendritic cell therapy in mouse xenograft model of lung carcinoma

Objective： To investigate the antitumor effect of endostatin combined with tumor antigen-pulsed dendritic cell （DC）-T cell therapy on lung cancer. Methods： Transplanted Lewis lung cancer （LLC） models of C57BL/6 mice were established by subcutaneous injection of LLC cells in left extremity axillary. Tumor antigen-pulsed DC-T cells from spleen cells and bone of mice were cultured in vitro. Tumor-bearing mice were randomly divided into three groups, including DC- T＋endostatin group, DC-T group, and phosphate-buffered saline （PBS） control group. Microvessel density （MVD） of tumor tissue in tumor-bearing mice was determined by immunohistochemistry （IHC）. The expressions of vascular endothelial growth factor （VEGF） and hypoxia-inducible factor-1α （HIF-1α） were determined by Western blotting and IHC staining. The proportions of CD8＋ T cells, mature dendritic cells （mDC）, tumor-associated macrophages [TAM （M1/M2）], and myeloid-derived suppressor cells （MDSC） in suspended cells of tumor tissue were determined by flow cytometry. The expressions of inter｜eukin （IL）-6, IL-10, IL-17, transforming growth factor-β（TGF-β） and interferon-γ （IFN-γ） in suspended cells of tumor tissue were detected by enzyme-linked immune sorbent assay （ELISA）. Results： DC-T cells combined with endostatin remarkably suppressed tumor growth. MVD of mice in DC- T＋endostatin group was significantly lower than that of the control group and DC-T monotherapy group. The expressions of VEGF, IL-6 and IL-17 in tumors were markedly decreased, but IFN-γ, and HIF-1α increased after treating with DC-T cells combined with endostatin, compared to control group and DC-T group. In the DC- T＋endostatin group, the proportions of MDSC and TAM （M2 type） were significantly decreased, mDC and TAM （Nil type） were up-regulated, and CD8＋ T cells were recruited to infiltrate tumors, in contrast to PBS control and DC-T monotherapy. DC-T cells combined with endostatin potently reduced the expressions of IL-6, IL-10, TGF-β and IL-17 in tumor tissue, and enhanced the expression of IFN-γ. Conclusions： The study indicated the synergic antitumor effects between endostatin and tumor antigen-pulsed DC-T cells, which may be a prospective therapy strategy to achieve potent antitumor effects on lung cancer.

Inhibitory Effect of MiR-449b on Cancer Cell Growth and Invasion through LGR4 in Non-Small-Cell Lung Carcinoma

Non-small-cell lung carcinoma （NSCLC） is one of the most frequently diagnosed malignancies worldwide. Previous studies have shown that microRNA-449b （miR-449b） functions as a tumor suppressor in many cancers. However, the role of miR- 449b in NSCLC is still unknown. In the present study, miR-449b was significantly down- regulated in NSCLC samples and cell lines. Bioinformatics analysis revealed that 3＇-UTR region of leucine rich repeat containing G protein-coupled receptor 4 （LGR4） mRNA had putative complementary sequences to miR-449b, which was further confirmed by the luciferase assay. Western blotting showed that restoration of miR-449b in NSCLC cells decreased the expression of LGR4. Interestingly, over-expression of miR-449b inhibited growth and invasion of NSCLC cells in vitro. Furthermore, ectopic expression of LGR4 reversed miR-449b-suppressed proliferation and invasion of NSCLC cells. Therefore, the data of the present study demonstrate that miR-449b inhibits tumor cell growth and invasion by targeting LGR4 in NSCLC.

Inhibition of lymphangiogenesis,nodal and lung metastasis by dihydroartemisinin in mice bearing Lewis lung carcinoma

Objective:To investigate the activity of anti-malarial dihydroartemisinin (DHA) on tumor growth, lymphangiogenesis, nodal and lung metastasis and survival in mice bearing Lewis lung carcimoma (LLC). Methods: The models of C57BL/6 mice transplantation tumors were established via subcutaneous injection of LLC cells and divided into 4 groups: control group, DHA group, DHA+ferrous sulfate (FS) group and FS group, with 25 mice in each group. Tumor volumes and weights, nodal and lung metastasis, and survival were monitored. Tumor lymphatic microvessel density (LMVD) was determined by lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) immnohistochemistry. After LLC cells were treated with DHA or DHA+FS, protein and mRNA levels of vascular endothelial growth factor (VEGF) -C were evaluated by Western blotting and real time quantitative RT-PCR, respectively. Results: Oral administration of DHA or DHA+FS inhibited lymph node and lung metastasis, and prolonged survival. However, no significant tumor growth retardation effect was observed when mice were treated with DHA alone. The inhibited tumor metastasis was related to the decreased LMVD in the peritumoral regions, but not in the intratumoral regions. DHA significantly down-regulated the expression of VEGF-C protein and mRNA in LLC cells. Conclusion: DHA effectively inhibits LLC transplantation tumor lymphangiogenesis, nodal and lung metastasis, and may be a promising chemotherapeutic agent for controlling lung cancer metastasis by decreasing VEGF-C expression.

EFFECT OF PROCYANIDIN ON CELL CYCLE IN MURINE LEWIS LUNG CARCINOMA

Objective: To investigate the anti-tumor effect of procyanidin (WeiMaiNing, WMN) on a murine Lewis lung carcinoma cell line (3LL) and the influence on the cell cycle. Methods: The inhibitory rate of 3LL growth was detected in the model of murine Lewis lung carcinoma. The effect of the drug on 3LL cell cycle and the influence of the drug on the expression of cyclin D1 protein were investigated by flow cytometry, immunohistochemical staining. Results: The inhibitory rates of WMN in 3LL were 19.14%, 33.59% and 51.56% respectively at dosages 100 mg穔g-1穌-1, 150 mg穔g-1穌-1 and 250 mg穔g-1穌-1. The inhibitory effect was in a dose-dependent manner. We found WMN significantly increased (P<0.01) the number of 3LL cells in G0-G1 phase (35.97% vs. 27.2% at 150 mg穔g-1穌-1 WMN; 40.10% vs. 27.2% at 250 mg穔g-1穌-1 WMN) and decreased the expression of cyclin D1, PCNA protein. Conclusion: WeiMaiNing inhibits the growth of 3LL cells in vivo by decreasing the expression of PCNA and cyclin D1, blocking the cells in G0-G1 phase and preventing the cells transition from G1 to S phase while DNA is replicated.

Short-Term Test for the Induction of Lung Tumor in Mouse by Chloroprene

In a previous study by the authors,positive results from both a case-control study and a cohort study were reported.In the present study a short-term test for the induction of mouse lung tumor by chloroprene was conducted to confirm whether chloroprene monomer itself can induce tumors.Kunming albino mice weaned at 2 weeks were subjected to inhaling 0,2.9±0.3, 19.2±1.9,and 189.0±13.3 mg/m^3 chloroprene(GC purity,99.8%)4 h daily(except Sunday) for 7 months.All survivors were killed at the end of the 8th month or when moribund.No lung tumors were found before the 6th month.Thus,survivors at the 6th month were counted as effective animals.Most lung tumors observed were papilloadenomas(50/57),and a few were adenomas(7/57).The tumor incidence in the 2.9 mg/m^3 group was 8.1% in comparison to 1.3% in the control group,with the significance level at P<0.05.The higher the concentration,the higher the incidence.Examination of the multiplicity of tumor induction also demonstrated a dose-response relationship,and the number of tumors per mouse in the 189 mg/m^3 group was significant at P<0.01.1989 Academic Press,Inc.

Accuracy of endoscopic ultrasound-guided needle aspiration specimens for molecular diagnosis of non-small-cell lung carcinoma

BACKGROUND Endoscopic ultrasonography-guided fine-needle aspiration(EUS-FNA)and endobronchial ultrasound-guided transbronchial needle aspiration(EBUS-TBNA)are highly sensitive for diagnosing and staging lung cancer.In recent years,targeted therapy has shown great significance in the treatment of non-small cell lung carcinoma(NSCLC).Using these minimally invasive techniques to obtain specimens for molecular testing will provide patients with a more convenient diagnostic approach.AIM To evaluate the feasibility and accuracy of tissue samples obtained using EUSFNA and EBUS-TBNA for molecular diagnosis of NSCLC.METHODS A total of 83 patients with NSCLC underwent molecular testing using tissues obtained from EUS-FNA or EBUS-TBNA at the Tianjin Medical University Cancer Hospital from January 2017 to June 2019.All enrolled patients underwent chest computed tomography or positron emission tomography/computed tomography prior to puncture.We detected abnormal expression of EGFR,KRAS,MET,HER2,ROS1 and anaplastic lymphoma kinase protein.Two patients failed to complete molecular testing due to insufficient tumor tissue.The clinical features,puncture records,molecular testing results and targeted treatment in the remaining 81 patients were summarized.RESULTS In a total of 99 tissue samples obtained from 83 patients,molecular testing was successfully completed in 93 samples with a sample adequacy ratio of 93.9%(93/99).Biopsy samples from two patients failed to provide test results due to insufficient tumor tissue.In the remaining 81 patients,62 cases(76.5%)were found to have adenocarcinoma,11 cases(13.6%)had squamous cell carcinoma,3 cases(3.7%)had adenosquamous carcinoma and 5 cases(6.2%)had NSCLC-not otherwise specified.The results of molecular testing showed EGFR mutations in 21 cases(25.9%),KRAS mutations in 9 cases(11.1%),ROS-1 rearrangement in 1 case(1.2%)and anaplastic lymphoma kinase-positive in 5 cases(6.2%).Twentyfour patients with positive results received targeted therapy.The total effectiveness rate of targeted therapy was 66.7%(16/24),and the disease control rate was 83.3%(20/24).CONCLUSION Tissue samples obtained by EUS-FNA or EBUS-TBNA are feasible for the molecular diagnosis of NSCLC and can provide reliable evidence for clinical diagnosis and treatment.

Detection of Lung Tumor Using ASPP-Unet with Whale Optimization Algorithm

The unstructured growth of abnormal cells in the lung tissue creates tumor.The early detection of lung tumor helps the patients avoiding the death rate and gives better treatment.Various medical image modalities can help the physicians in the diagnosis of disease.Many research works have been proposed for the early detection of lung tumor.High computation time and misidentification of tumor are the prevailing issues.In order to overcome these issues,this paper has proposed a hybrid classifier of Atrous Spatial Pyramid Pooling(ASPP)-Unet architecture withWhale Optimization Algorithm(ASPP-Unet-WOA).To get a fine tuning detection of tumor in the Computed Tomography(CT)of lung image,this model needs pre-processing using Gabor filter.Secondly,feature segmentation is done using Guaranteed Convergence Particle Swarm Optimization.Thirdly,feature selection is done using Binary Grasshopper Optimization Algorithm.This proposed(ASPPUnet-WOA)is implemented in the dataset of National Cancer Institute(NCI)Lung Cancer Database Consortium.Various performance metric measures are evaluated and compared to the existing classifiers.The accuracy of Deep Convolutional Neural Network(DCNN)is 93.45%,Convolutional Neural Network(CNN)is 91.67%,UNet obtains 95.75%and ASPP-UNet-WOA obtains 98.68%.compared to the other techniques.

Glabridin and Anti-Non-Muscle Myosin IIA Therapy Disrupts Non-Small Cell Lung Carcinoma Motility

Lung cancer is the leading cause of cancer related death in the United States killing over 130,000 people each year. While a combination of chemo and radiation therapy may be effective, surgery is still required for many patients. Without surgery, the disease may progress and lead to metastases. We sought to determine if treatment with anti-non-muscle myosin IIA antibody would inhibit movement of the cells in the presence and absence of glabridin (an isoflavonoid compound shown to inhibit cell migration by inhibiting myosin). We compared inhibition by glabridin to that of an anti-non-muscle myosin IIA antibody and a combination therapy of both at 12 and 24 hours post wound creation. Cells that took up the anti-non-muscle myosin IIA antibody were greatly inhibited in motility and exhibited no significant change in wound healing. Glabridin treatment resulted in a dramatic increase in wound size within 12 hours and regeneration within 24 hours. The greatest decrease in motility was observed in cells treated with the combination of both glabridin and anti-non-muscle myosin IIA antibody. By 24 hrs, cell migration had halted due to death of the cells resulting from this combination. Further testing needs to be done to determine a safe mode of delivery of the combination therapy to ensure only local distribution. Controlled release drug delivery depot systems have been used as a means to provide local release of drugs intra-tumorally or adjacent to the cancerous tissue after surgical resection and have great potential.

Effect of Bcl-2 Antisense Oligodeoxynucleotides on Human Lung Carcinoma Transplanted Subcutaneously in Nude Mice

Objective： To investigate the inhibitory effects of the Bcl-2 antisense oligodeoxynucleotides （ASODN） on tumor formation and growth of human lung carcinoma transplanted subcutaneously in nude mice. Methods： Human NCI-H460 cells treated with Bcl-2 ASODN or nonesense oligodeoxynucleotide （NSODN） and untreated NCI-H460 cells were respectively implanted subcutaneously into nude mice. When the diameters of tumor were above 0.5 cm after untreated NCI-H460 cells injection, the mice bearing tumor were randomly divided into three groups： saline control group, Bcl-2 ASODN group, NSODN group. ODN was directly injected into the tumor body for 3 weeks. The weight and volume of subcutaneous tumors were measured, and the morphology of tumor cells was observed. Results： The tumorigenic ability of the treated NCI-H460 cells by Bcl-2 ASODN was reduced. The mean time at which tumor can be detected was prolonged up to 12.6 days （P〈0.01）. The maximum tumor growth inhibitory rate was 87.5%. In therapeutic efficacy, growth of tumor was significantly inhibited in Bcl-2 ASODN group as compared with that in NSODN group, saline-treated group （P〈0.01）. The NSODN control was ineffective. In comparison with NSODN-treated, saline-treated mice, those treated with Bcl-2 ASODN showed a significant decrease in median weight of subcutaneous tumors （P〈0.01）. The growth inhibitory rate was 71.0% in ASODN group. Conclusion： Bcl-2 ASODN could inhibit tumor formation and tumor growth in nude mice.

Expressions of FEZ1 and Survivin, and their significance in small cell lung cancer and squamous cell lung carcinoma

Objective： To detect the expressions of FEZ1 and Survivin in small cell lung cancer （SOLO） and poorly differentiated squamous cell carcinoma （PDSCC）, and to approach a theoretical basis for clinical diagnosis and treatment. Methods： Immunohistochemical and flow cytometry method were used to detect the expressions of FEZ1 and Survivin. Apoptosis ratio and cell proliferation index in normal lung tissue, SCLC and PDSCC were analyzed. Results： The expressions of FEZ1 and Survivin were significantly different between SCLC and PDSCC （P 〈 0.05）. The apoptosis ratio and proliferation index of normal lung tissue were lower than those of PDSCC and SOLO, with a significant difference （P 〈 0.05）. Conclusion： The expressions of FEZ1 and Survivin are significantly different between SCLC and PDSCC, indicating that detecting the expressions of the two indexes may be helpful for clinical diagnosis.

Development for the lung tumor model of newborn mice induced by diethylstilbestrol

Objective： To explore a economical and effective method for building lung tumor model induced by diethylstibestrol （DES）. Methods： The carcinogenic effect of neonatal mice treated by DES was studied. The newborn mice were divided into DES, Urethan （U） and U ＋ DES groups. U group was given in 500 mg/kg dose by ip at postnatal 14 day, DES group was administered by ip at the 1 d, 8 d, 15 d in the dose of 1/7, 2/7 and 4/7 LD50 of the day when they were injected respectively for DES （I）, DES （M）, DES （H） groups. Until 26 weeks, they were anatomized and checked the formation of tumors. The organ index, tumor incidence ratio and mean number of tumors were calculated. Results： Lung tumors were apparently induced in tested neonatal mice. The incidence of lung tumor of DES （L, M, H） groups were 16.7%, 22.4% and 43.1% respectively, the U ＋ DES （L, M, H） groups were 70.4%, 90.9% and 70.8% respectively, and the U group was 53.1%. The mean numbers of lung tumors of U ＋ DES （L, M） groups were higher than those of the DES （L, M） groups respectively （P 〈 0.05）. Conclusion： The higher ratio of lung tumor incidence had been induced by DES and U joined action to neonatal mice, which may be a useful and economical method to establish a lung tumor model induced by DES.

Hypercalcemia-Leukocytosis syndrome and adenosquamous lung carcinoma:An overlooked conjugation

Hypercalcaemia and leukocytosis are two paraneoplastic conditions associated with poor prognosis.Adenosquamous carcinoma is a rare and aggressive histological subtype of lung cancer consisting of adenocarcinoma and squamous cell components.We report the case of a 57-year-old male smoker who was admitted to the Emergency Room with skull and neck tumefactions,confusion and deteriorated general condition.The complementary study in the ER revealed severe hypercalcaemia(19.8 mg/dL),leukocytosis(18.7×10^(9)/L)and extensive osteolytic lesions of the skull on cranioencephalic computer tomography(CT).The patient was stabilized and admitted.Thoracoabdominopelvic CT showed lung parenchyma consolidation with necrotic areas,supra and infradiaphragmatic adenopathies and scattered osteolytic lesions.Percutaneous lymph node biopsy was consistent with metastasis of adenosquamous lung carcinoma.The patients’clinical situation evolved unfavourably after hospital-acquired infection.This case is characterized by a rare presentation of advanced stage adenosquamous lung carcinoma with scattered osteolytic lesions and severe hypercalcaemia-leukocytosis syndrome,an underrecognized marker of poor prognosis.

EXPRESSION OF p^(53) c-erbB-2, PCNA AND DAN CONTENT IN LUNG CARCINOMA

Theexpressionofp53Protein,c-erbB-2oncoprotein,Proliferatingcennuclearantigen(usA)werestudiedbythestreptavidinperotidaseconjugated(S-P)immunohistochemicalmethodandDNAcontentinsituwastested,inordertoexplorethesignificanceofP53,c-erbB-2,PCNAinPrimallUng...

Solitary pancreatic metastasis from squamous cell lung carcinoma: A case report and review of literature

BACKGROUND Pancreatic metastases from squamous cell lung carcinoma(SCLC)are unusual.These lesions are often asymptomatic and detected incidentally or during followup investigations,occasionally several years after removal of the primary tumor.CASE SUMMARY A 56-year-old male with SCLC developed jaundice 1 mo after the cancer diagnosis.An abdominal computed tomography(CT)scan showed a mass in the pancreatic head with distention of both intra-and extrahepatic biliary ducts.Endoscopic retrograde cholangiopancreatography and sphincterotomy were performed first,culminating with plastic biliary stent placement.Cytological examination of the pancreatic mass sample collected by fine-needle aspiration(FNA)under endoscopic ultrasound(EUS)guidance revealed the presence of malignant cells compatible with well-differentiated squamous cell carcinoma.After liver function normalized,chemotherapy was initiated with carboplatin and paclitaxel;however,4 d later,the patient presented dysphagia.Cervico-thoracoabdominal CT showed tracheoesophageal fistula and stent migration.After replacement with a 10 cm/10 mm uncovered metallic biliary stent and treatment of the tracheoesophageal fistula with a fully covered esophageal stent,the patient was able to start oral feeding progressively.He died 9 mo after the initial diagnosis.CONCLUSION The diagnosis of pancreatic metastasis from SCLC is challenging for clinicians.EUS-FNA is the primary exam for confirmatory diagnosis.

Relevance of EGFR gene mutation with pathological features and prognosis in patients with non-small-cell lung carcinoma

Objective:To study the relevance of EGFR gene mutation with pathological features and prognosis in patients with non-small-cell lung carcinoma.Methods:A total of 297 patients from July 2009 to May 2013 were chosen as objects.EGFR gene mutation were detected with fluorescence quantitative PCR.Relevance of EGFR gene mutation with clinical and pathological features was analyzed,and the prognosis of EGFR- mutant-patients and that of EGFR- wide type-patients was compared.Results:In 297 patients.136(45.79%) showed EGFR gene mutation.EGFR gene mutation had no significant relevance with age.gender,smoking history,family history of cancer and clinical stage(P>0.05);there was significant relevance between EGFR gene mutation and blood type,pathologic types,differentiation and diameter of cancer(P<0.05).The difference between prognosis of EGFR- mutant-patients and that of EGFR- wide type-patients was statistical significance(P<0.05).Conclusions:EGFR gene mutation has significant relevance with pathological features,the prognosis of EGFRmutant-paticnts is better than that of EGFR- wide type-patients.

Mechanism of miR-21 via Wnt/β-catenin signaling pathway in human A549 lung cancer cells and Lewis lung carcinoma in mice

Objective:To study the mechanism of effect of miR-21 via Wnt/ β-catenin signaling pathway in human A549 lung cancer cells and Lewis lung carcinoma in mice.Methods:The effect of miR-21 on A549 cells were detected by MTT method.MiR-21 expression levels were overexpressed or inhibited in A549 cells by transfecting with miR-21 mimics or inhibitors.Correlation among key molecules(Wnt1,β-catenin.CyclinD1 and miR-21) of mRNA and protein levels in Wnt/β-catenin signaling pathway were studied by Real-time PCR and Western blot hybridization assay.Invasive ability of A549 cells was determined via Transwell chamber cell invasion assay;the role of miR-21 in A549 cells was explored via the Wnt/β-catenin signaling pathway.A Lewis lung carcinoma animal model was established to detect miR-21 expressions in tumor animals and controlled animal tissues,and verify expression changes of the above moleculesin the Wnt / β-catenin signaling pathway was determined in the animal level.Results:MTT assay results showed that miR-21 overexpression could markedly enhance cell absorbance value;that is,miR-21 could increase the ability proliferation of A549 cells.β-catenin and CyclinD1 expression levels were significantly higher in miR-21 mimic transfected cells(P<0.05),and Wnt 1 gene had no significant change.Wnt 1,β-catenin and CyclinD1 gene expression showed no significant change when miR-21 expression was suppressed,compared with controls.After cells were transfected with miR-21 mimics,cell invasion assay revealed that the perforated cells was significantly higher than the perforated cells in the control group(P<0.01).Lewis lung assay revealed that miR-21 expression levels in the Lewis lung carcinoma were significantly higher;and at the same time.Wnt1,β-catenin and CyclinD1 gene expression levels were significantly increased,compared to controls.Conclusions:In A549 human lung cancer cells and Lewis lung carcinoma in mice,key molecules β-catenin and CyclinD1 of miR-21 expressions and the Wnt/ β-catenin signaling pathway are positively correlated.

Up-Regulation of the Gap Junction Intercellular Communication by Tea Polyphenol in the Human Metastatie Lung Carcinoma Cell Line

Our previous study has proven that tea polyphenol has a role in lung neoplasms. The present communication was to investage the anti-proliferation effect of tea polyphenol on the PG cells, which was a high metastatic human lung carcinoma cell line, by 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-diphenytetrazoliumromide (MTT) cell viability assay, and to study the change of intracellular calcium concentration, connexin43 (Cx43) expression, gap junctional intercellular communication (GJIC) and cell cycle distribution after the tea polyphenol treatment by laser scanning confocal microscopy and flow cytometry. The results showed that 1) tea polyphenol could kill the PG cells in a dose-depent manner via inhibiting the PG cell proliferation and blocking the PG cell cycle progression staying in G0/G1 phase and not transfering in S and G2/M phases to reduce the PG cell proliferation index;2) the increases of intracellular calcium concentration, GJIC and Cx43 expression were related with the tea polyphenol doses. The data suggested that tea polyphenol could inhibit the growth of PG cells, which mechanism was associated with the up-regulation of GJIC.