A method establishment and comparison of in vivo lung cancer model development platforms for evaluation of tumour metabolism and pharmaceutical efficacy

Phytomedicine ◽  
2021 ◽  
pp. 153831
Author(s):  
Tu-Liang Liang ◽  
Run-Ze Li ◽  
Chu-Tian Mai ◽  
Xiao-Xiang Guan ◽  
Jia-Xin Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Model Development ◽  
Cancer Model ◽  
Tumour Metabolism ◽  
Lung Cancer Model

Development of a Lung Cancer Model in Wistar Rat and In Silico Screening of its Biomarkers.

2020 ◽  
Vol 16 ◽  
Author(s):  
Nisat Alam ◽  
Hasina Najnin ◽  
Maidul Islam ◽  
Saleem Iqbal ◽  
Rana Zaidi
Keyword(s):  
Lung Cancer ◽  
In Silico ◽  
Wistar Rats ◽  
Molecular Targets ◽  
Total Binding Energy ◽  
Cancer Model ◽  
Lung Cancer Model ◽  
Male Wistar Rats ◽  
P38 Mapks

Background: Cancer is caused by three factors: Nutrition, inflammation and cigarette smoke. This study in rat experimental models would enable us to understand the mechanism of lung cancer caused by NNK to which humans are continuously exposed, help us understand possible molecular targets, design drugs for humans against lung cancer. Aim: A lung cancer model was developed by administering tobacco specific carcinogen: NNK [4-methylnitrosamino)-1-(3-pyridyl)-1-butanone] to male wistar rats in 24 weeks. Further, In silico approach was followed to screen the molecular targets. Methods: A method was established in which subcutaneous and intraperitoneal injections of NNK were administered to male wistar rats simultaneously. For authentication of lung cancer in vivo we performed molecular docking simulations with protein biomarkers:Cox-2, p53, p38 MAPKs and EGFR using Hex-Discovery Studio, Schrödinger-maestro software. Results: Lung morphology and histopathology indicated the initiation of bronchiolar epithelial hyperplasia, squamous dysplasia beginning in cancer 1 group after 16 weeks NNK exposure. 66.66% incidence of squamous cell carcinoma (SCC), 33.3% incidence of adenocarcinoma in cancer 2 group after being exposed to NNK. Results indicated that the SCC and adenocarcinoma gradually increased from 66.66% to 85.71% in cancer 2 group and 33.33% to 42.58% in cancer 3 groups respectively. Docking results indicate the total binding energy and glide energy of Cox-2, p53, p38 MAPKs, EGFR : 38.14, -211.58, -181.58, - 213.05 Kcal/mol and -39.25, -32.16,-36.49, -40.19 Kcal/mol, respectively. Conclusion: Pulmonary adenocarcinoma developed in 24 weeks, in silico experiments confirm EGFR to be the most potential target for NNK induced lung Cancer.

Improvement of lung cancer risk prediction adding SNPs to the HUNT Lung Cancer Model: A HUNT Study.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e20696-e20696 ◽  
Author(s):  
Oluf D. Røe ◽  
Olav Toai Duc Nguyen ◽  
Klio Lakiotaki ◽  
Ioannis Tsamardinos ◽  
Vincenzo Lagani ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Variable Selection ◽  
Risk Prediction ◽  
Cancer Susceptibility ◽  
Model Development ◽  
Genome Wide Association Studies ◽  
Cancer Model ◽  
Nested Models ◽  
Lung Cancer Model ◽  
Lung Cancer Susceptibility

e20696 Background: A novel validated model for risk prediction of lung cancer, the HUNT Lung Cancer Model predicts 6- and 16-year risk of lung cancer with a C-index = 0.879 and 6-year AUC = 0.87. The model is valid for smokers and ex-smokers of any intensity and quit time and includes seven variables; age, BMI, pack-years, smoking intensity (cigarettes per day), quit time, daily cough in periods of the year and hours of daily indoors smoke exposure. Genome-wide association studies (GWAS) have consistently identified specific lung cancer susceptibility regions. We aimed to improve performance of the HUNT model by integrating the most significant Single Nucleotide Polymorphisms (SNPs). Methods: Lung cancer cases (n = 484) and controls without other cancer (n = 50337) were genotyped for 22 SNPs located in GWAS-identified lung cancer susceptibility regions. Variable selection and model development used backwards feature selection with Akaike Information Criterion in multivariable Cox regression models. Internal validation used bootstrap to assess the change in area under the receiver operator characteristic curve (AUC) in order to compare nested models with and without genetic variables in the ever-smokers´ population (n = 456 cases, n = 28633 controls). We also used likelihood based methods for significance testing. Results: Variable selection and model development in the general population yielded six SNPs, rs1051730, rs11571833, rs13314271, rs2131877, rs2736100 and rs4488809. The added genetic information from these SNPs to the HUNT model, resulted in an improvement according to F test of the nested models (ANOVA p-value 0.000002425). The AUC of the augmented model was 0.881 (95% CI [0.869 0.892]) vs 0.869 without SNPs. Conclusions: In a highly predictive clinical risk prediction model, the integration of SNPs could further improve model performance according to likelihood based methods. Further refinement and validation of this integrated model is needed for clinical use.

Anti-lymphangiogenesis effects of a specific anti-interleukin 7 receptor antibody in lung cancer model in vivo

2013 ◽  
Vol 54 (2) ◽  
pp. 148-155 ◽  
Author(s):  
Ming Jian ◽  
Zhang Qingfu ◽  
Jiang Yanduo ◽  
Jiang Guocheng ◽  
Qiu Xueshan
Keyword(s):  
Lung Cancer ◽  
Cancer Model ◽  
Receptor Antibody ◽  
Interleukin 7 ◽  
Lung Cancer Model

scholarly journals Antitumor immune activity by chemokine CX3CL1 in an orthotopic implantation of lung cancer model in vivo

2012 ◽  
Vol 1 (1) ◽  
pp. 35-40 ◽  
Author(s):  
JI-YE KEE ◽  
YOSHIHISA ARITA ◽  
KANNA SHINOHARA ◽  
YASUKATA OHASHI ◽  
HIROAKI SAKURAI ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Model ◽  
Orthotopic Implantation ◽  
Immune Activity ◽  
Lung Cancer Model

In vivo cryochemotherapy of a human lung cancer model

Cryobiology ◽  
2005 ◽  
Vol 51 (1) ◽  
pp. 92-101 ◽  
Author(s):  
Valérie Forest ◽  
Michel Peoc’h ◽  
Claude Ardiet ◽  
Lydia Campos ◽  
Denis Guyotat ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Cancer Model ◽  
Lung Cancer Model

Bevacizumab combined with apatinib enhances antitumor and anti-angiogenesis effects in a lung cancer model in vitro and in vivo

2020 ◽  
Vol 28 (9) ◽  
pp. 961-969 ◽  
Author(s):  
Mingting Wang ◽  
Qin Zeng ◽  
Yuan Li ◽  
Saber Imani ◽  
Danna Xie ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Model ◽  
Lung Cancer Model

scholarly journals The lytic activity of VSV-GP treatment dominates the therapeutic effects in a syngeneic model of lung cancer

2019 ◽  
Vol 121 (8) ◽  
pp. 647-658
Author(s):  
Liesa-Marie Schreiber ◽  
Carles Urbiola ◽  
Krishna Das ◽  
Bart Spiesschaert ◽  
Janine Kimpel ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Adaptive Immune Response ◽  
Mouse Lung ◽  
Therapeutic Effects ◽  
Cancer Model ◽  
Adaptive Immune ◽  
Syngeneic Mouse ◽  
Tumour Spread ◽  
Lung Cancer Model

Abstract Background Oncolytic virotherapy is thought to result in direct virus-induced lytic tumour killing and simultaneous activation of innate and tumour-specific adaptive immune responses. Using a chimeric vesicular stomatitis virus variant VSV-GP, we addressed the direct oncolytic effects and the role of anti-tumour immune induction in the syngeneic mouse lung cancer model LLC1. Methods To study a tumour system with limited antiviral effects, we generated interferon receptor-deficient cells (LLC1-IFNAR1−/−). Therapeutic efficacy of VSV-GP was assessed in vivo in syngeneic C57BL/6 and athymic nude mice bearing subcutaneous tumours. VSV-GP treatment effects were analysed using bioluminescent imaging (BLI), immunohistochemistry, ELISpot, flow cytometry, multiplex ELISA and Nanostring® assays. Results Interferon insensitivity correlated with VSV-GP replication and therapeutic outcome. BLI revealed tumour-to-tumour spread of viral progeny in bilateral tumours. Histological and gene expression analysis confirmed widespread and rapid infection and cell killing within the tumour with activation of innate and adaptive immune-response markers. However, treatment outcome was increased in the absence of CD8+ T cells and surviving mice showed little protection from tumour re-challenge, indicating limited therapeutic contribution by the activated immune system. Conclusion These studies present a case for a predominantly lytic treatment effect of VSV-GP in a syngeneic mouse lung cancer model.

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