scholarly journals Lobectomy for Indeterminate Lung Tumors with a Strong Suspicion of Lung Cancer

2012 ◽  
Vol 18 (3) ◽  
pp. 243-246 ◽  
Author(s):  
Noritoshi Nishiyama ◽  
Koshi Nagano ◽  
Nobuhiro Izumi ◽  
Keiko Tei ◽  
Shoji Hanada ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Tumors ◽  
Strong Suspicion

scholarly journals NNK-Induced Lung Tumors: A Review of Animal Model

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Hua-Chuan Zheng ◽  
Yasuo Takano
Keyword(s):  
Lung Cancer ◽  
Animal Model ◽  
Animal Models ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Genetic Mutation ◽  
Lung Tumors ◽  
Chemotherapeutic Agents ◽  
Signal Pathways ◽  
Lung Carcinogenesis

The incidence of lung adenocarcinoma has been remarkably increasing in recent years due to the introduction of filter cigarettes and secondary-hand smoking because the people are more exposed to higher amounts of nitrogen oxides, especially 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone(NNK), which is widely applied in animal model of lung tumors. In NNK-induced lung tumors, genetic mutation, chromosome instability, gene methylation, and activation of oncogenes have been found so as to disrupt the expression profiles of some proteins or enzymes in various cellular signal pathways. Transgenic animal with specific alteration of lung cancer-related molecules have also been introduced to clarify the molecular mechanisms of NNK in the pathogenesis and development of lung tumors. Based on these animal models, many antioxidant ingredients and antitumor chemotherapeutic agents have been proved to suppress the NNK-induced lung carcinogenesis. In the future, it is necessary to delineate the most potent biomarkers of NNK-induced lung tumorigenesis, and to develop efficient methods to fight against NNK-associated lung cancer using animal models.

scholarly journals Modulation of the PD-1/PD-L1 immune checkpoint axis during inflammation-associated lung tumorigenesis

2020 ◽  
Vol 41 (11) ◽  
pp. 1518-1528
Author(s):  
Sreekanth Chanickal Narayanapillai ◽  
Yong Hwan Han ◽  
Jung Min Song ◽  
Manaye Ebabu Kebede ◽  
Pramod Upadhyaya ◽  
...  
Keyword(s):  
Lung Cancer ◽  
T Lymphocytes ◽  
Immune Checkpoint ◽  
Significant Risk ◽  
Lung Tumors ◽  
Tumor Formation ◽  
Normal Lung ◽  
Dependent Manner ◽  
Cd8 T Lymphocytes ◽  
Immunosuppressive Microenvironment

Abstract Chronic obstructive pulmonary disease (COPD) is a significant risk factor for lung cancer. One potential mechanism through which COPD contributes to lung cancer development could be through generation of an immunosuppressive microenvironment that allows tumor formation and progression. In this study, we compared the status of immune cells and immune checkpoint proteins in lung tumors induced by the tobacco smoke carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) or NNK + lipopolysaccharide (LPS), a model for COPD-associated lung tumors. Compared with NNK-induced lung tumors, NNK+LPS-induced lung tumors exhibited an immunosuppressive microenvironment characterized by higher relative abundances of PD-1+ tumor-associated macrophages, PD-L1+ tumor cells, PD-1+ CD4 and CD8 T lymphocytes and FOXP3+ CD4 and CD8 T lymphocytes. Also, these markers were more abundant in the tumor tissue than in the surrounding ‘normal’ lung tissue of NNK+LPS-induced lung tumors. PD-L1 expression in lung tumors was associated with IFNγ/STAT1/STAT3 signaling axis. In cell line models, PD-L1 expression was found to be significantly enhanced in phorbol-12-myristate 13-acetate activated THP-1 human monocytes (macrophages) treated with LPS or incubated in conditioned media (CM) generated by non-small cell lung cancer (NSCLC) cells. Similarly, when NSCLC cells were incubated in CM generated by activated THP-1 cells, PD-L1 expression was upregulated in EGFR- and ERK-dependent manner. Overall, our observations indicate that COPD-like chronic inflammation creates a favorable immunosuppressive microenvironment for tumor development and COPD-associated lung tumors might show a better response to immune checkpoint therapies.

A Review of the Histopathology of Cigarette Smoke–Induced Lung Cancer in Rats and Mice

2007 ◽  
Vol 26 (4) ◽  
pp. 307-313 ◽  
Author(s):  
Fletcher F. Hahn ◽  
Andrew P. Gigliotti ◽  
Julie A. Hutt ◽  
Thomas H. March ◽  
Joe L. Mauderly
Keyword(s):  
Lung Cancer ◽  
Cigarette Smoke ◽  
Malignant Tumors ◽  
Lung Tumors ◽  
The Past ◽  
Lifetime Exposure ◽  
Low Incidence ◽  
Epithelial Lesions ◽  
Induced Changes ◽  
Rats And Mice

In the past several years an increased number of lung tumors has been reported in laboratory studies of rats and mice after lifetime exposure to mainstream cigarette smoke. Proliferative epithelial lesions are present in the lungs of both species and are apparent antecedent lesions to benign and malignant tumors. Both species have alveolar epithelia hyperplasia, alveolar adenomas, and alveolar carcinomas. The incidence of all three are more in the rats. In addition, mice also have bronchiolar epithelial hyperplasia and bronchial papillomas not found in rats. Rats have a low incidence of squamous cyst that is not found in mice. Lung tumors in rats and mice are found at the end of the life span and rarely metastasize. The characteristics of the lung tumors, and the proliferative changes associated with the tumors, are important in helping understand the mechanisms of lung cancer induction. These studies in rats and mice allow new approaches to the study of cigarette smoke–induced changes in the lung.

Pulmonary Adenocarcinoma: The Expanding Spectrum of Histologic Variants

2006 ◽  
Vol 130 (7) ◽  
pp. 958-962 ◽  
Author(s):  
Cesar A. Moran
Keyword(s):  
Lung Cancer ◽  
Lung Tumors ◽  
Pulmonary Adenocarcinoma ◽  
Current Review ◽  
Poorly Differentiated ◽  
Histopathologic Features

Abstract Pulmonary adenocarcinoma is one of the most common types of lung cancer. Traditionally, adenocarcinomas have been divided based on their degree of resemblance to their parent tissues into 3 histopathologic types: well, moderately, and poorly differentiated. In the majority of cases, this schema is sufficient to categorize these lung tumors. However, there is a considerable group of tumors in which the histology is not that of the classic gland-forming neoplasm. Thus, although the terminology of adenocarcinoma is applied in such cases, the histopathologic features are different from those of the more conventional variants. The current review addresses these unusual variants and the importance of recognizing and properly categorizing them to avoid unnecessary additional workup or possible misdiagnosis.

scholarly journals ZEB1 suppression sensitizes KRAS mutant cancers to MEK inhibition by an IL17RD-dependent mechanism

2019 ◽  
Vol 11 (483) ◽  
pp. eaaq1238 ◽  
Author(s):  
David H. Peng ◽  
Samrat T. Kundu ◽  
Jared J. Fradette ◽  
Lixia Diao ◽  
Pan Tong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Mapk Signaling ◽  
Lung Tumors ◽  
Mitogen Activated Protein Kinase ◽  
Mek Inhibition ◽  
Mitogen Activated Protein

Mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitors have failed to show clinical benefit in Kirsten rat sarcoma (KRAS) mutant lung cancer due to various resistance mechanisms. To identify differential therapeutic sensitivities between epithelial and mesenchymal lung tumors, we performed in vivo small hairpin RNA screens, proteomic profiling, and analysis of patient tumor datasets, which revealed an inverse correlation between mitogen-activated protein kinase (MAPK) signaling dependency and a zinc finger E-box binding homeobox 1 (ZEB1)–regulated epithelial-to-mesenchymal transition. Mechanistic studies determined that MAPK signaling dependency in epithelial lung cancer cells is due to the scaffold protein interleukin-17 receptor D (IL17RD), which is directly repressed by ZEB1. Lung tumors in multiple Kras mutant murine models with increased ZEB1 displayed low IL17RD expression, accompanied by MAPK-independent tumor growth and therapeutic resistance to MEK inhibition. Suppression of ZEB1 function with miR-200 expression or the histone deacetylase inhibitor mocetinostat sensitized resistant cancer cells to MEK inhibition and markedly reduced in vivo tumor growth, showing a promising combinatorial treatment strategy for KRAS mutant cancers. In human lung tumor samples, high ZEB1 and low IL17RD expression correlated with low MAPK signaling, presenting potential markers that predict patient response to MEK inhibitors.

TA 4-SCC versus CEA Sensitivity for Lung Cancer

1988 ◽  
Vol 74 (4) ◽  
pp. 393-395 ◽  
Author(s):  
Fernando Pecchio ◽  
Marco Rapellino ◽  
Elia Ricci ◽  
Caterina Casadio ◽  
Donatella Moscato ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Marker ◽  
Lung Tumors ◽  
Stage I ◽  
Histologic Types

The sensitivity of a new tumor marker, TA 4-SCC, for lung tumors is examined and compared with the performance of the already established CEA. TA 4-SCC sensitivity is only moderate (30 %), and it presents no significant differences among the various histologic types of lung cancer. In addition, unlike CEA, TA 4-SCC is present in large amounts in the serum of many stage I and II patients. In fact, its sensitivity in still curatively operable tumors reaches 30 % compared to 10 % with CEA.

New microRNA-based diagnostic test for lung cancer classification.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 10528-10528
Author(s):  
Ranit Aharonov ◽  
Gila Lithwick Yanai ◽  
Hila Benjamin ◽  
Mats Olot Sanden ◽  
Marluce Bibbo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Carcinoma ◽  
Expression Profiles ◽  
Lung Tumors ◽  
Small Cell ◽  
Diagnostic Methods ◽  
Expression Levels ◽  
Qrt Pcr ◽  
Cancer Types

10528 Background: Lung cancer is the leading cause of cancer deaths in the US. Treatment options are determined by tumor subtyping, for which there is lack of standardized, objective, and highly accurate techniques. In 20%-30% of cases significant limitations of tumor quantity and quality prevent full classification of the tumor using traditional diagnostic methods. Using microRNA microarray data generated from over a hundred formalin-fixed, paraffin-embedded (FFPE) primary lung cancer samples, we have identified microRNA expression profiles that differ significantly for the main lung cancer types. Based on these findings, we have developed and validated a microRNA-based qRT-PCR assay that differentiates primary lung cancers into four types: squamous cell carcinoma, non-squamous non-small cell lung cancer, carcinoid and small cell carcinoma. Methods: Over 700 primary tumor samples from different histological types of lung cancer were collected. Samples included FFPE blocks from resection or biopsies and cell blocks from cytology specimens including fine needle aspiration, bronchial brushing and bronchial washing. High-quality RNA was extracted from the samples using proprietary protocols. Expression levels of potential microRNA biomarkers were profiled using microarrays followed by a sensitive and specific qRT-PCR platform. An assay for lung tumors classification using 8 microRNAs on qRT-PCR was developed based on data from 261 samples. This assay was validated on an independent blinded set of 451 cytological and pathological samples. Results: Using the expression levels of 8 microRNAs measured in qRT-PCR, accurate classification of the primary lung tumors into the four main cancer types is obtained. The microRNA-based assay reached an accuracy of 94%. Moreover, cytological samples composed over 50% of the validation set and reached an accuracy of 95%. Conclusions: We present here a new microRNA-based assay for the classification of the four main types of lung cancer based only on the expression of 8 microRNAs. This assay displays very high levels of accuracy for both pathological and cytological samples. The assay comprises a standardized, well-tested and objective tool which can assist physicians in the diagnosis of lung cancer.

Report of four cases of pulmonary malignant tumors treated with SBRT using BODYFIX plus 4D-CBCT image guidance technique.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e20050-e20050
Author(s):  
Lei Wu ◽  
Tao Li ◽  
Qifeng Wang
Keyword(s):  
Lung Cancer ◽  
Range Of Motion ◽  
Treatment Planning ◽  
Radiation Treatment ◽  
Lung Tumors ◽  
Planning System ◽  
Target Area ◽  
Radiation Treatment Planning ◽  
Short Term ◽  
Cbct Image

e20050 Background: To monitor the range of motion in SBRT treatment of lung tumors by using BODYFIX combined with four-dimensional cone beam CT (4D-CBCT), and provide evidence for delineating the reasonable internal target area (ITV) of lung cancer, and observe the short-term outcom of treatment and treatment of complications. Methods: 4D-CT was used to locate CT scan, delineate the GTV of the tumor, make a simple radiation treatment planning, determine the treatment center point, and then use line accelerator 4D-CBCT to perform pre-SBRT treatment on 4 patients with lung malignant tumor. The system automatically reconstructs the image and matches the CT image of the treatment plan to obtain the placement error of the patient in the head and foot (SI), left and right (LR), and front and rear (AP) directions. The double registration technique is used to correct the correction first. Positioning error, the 4D-CBCT dynamic image is again registered with the target area, the range of motion within the tumor is observed, and the time-weighted 4D-CBCT image is transmitted back to the Monaco planning system to delineate the target area to accurately determine the range of the ITV. According to this target area, a radiation treatment planning was developed, GTV 20Gy/f, 1 to 3 fractions, and then 4D-CBCT scan was performed in each SBRT treatment to observe the range of tumor motion in real time. Results: 3 of the 4 patients the lung tumors were CR at 3 months after treatment, and 1 patient was SD. No serious complications occurred during the treatment or within 3 months after radiotherapy. Conclusions: The BODYFIX plus 4D-CBCT image can more accurately outline the ITV range of lung cancer. The patient is well tolerated and the short-term outcom is good.

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