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COPD AND lung cancer AND microenvironment

Dhruv R Seshadri, Anand Ramamurthi
The use of nanomaterials to modulate the tumor microenvironment has great potential to advance outcomes in patients with lung cancer. Nanomaterials can be used to prolong the delivery time of therapeutics enabling their specific targeting to tumors while minimizing and potentially eliminating cytotoxic effects. Using nanomaterials to deliver small-molecule inhibitors for oncogene targeted therapy and cancer immunotherapy while concurrently enabling regeneration of the extracellular matrix could enhance our therapeutic reach and improve outcomes for patients with non-small cell lung cancer (NSCLC) and chronic obstructive pulmonary disease (COPD)...
2018: Frontiers in Pharmacology
Jérôme Biton, Hanane Ouakrim, Agnès Dechartres, Marco Alifano, Audrey Mansuet-Lupo, Han Si, Rebecca Halpin, Todd Creasy, Claudie Bantsimba-Malanda, Jennifer Arrondeau, François Goldwasser, Pascaline Boudou-Rouquette, Ludovic Fournel, Nicolas Roche, Pierre-Régis Burgel, Jeremy Goc, Priyanka Devi-Marulkar, Claire Germain, Marie-Caroline Dieu-Nosjean, Isabelle Cremer, Ronald Herbst, Diane Damotte
RATIONALE: Patients with chronic obstructive pulmonary disease (COPD) have a higher prevalence of lung cancer. The chronic inflammation associated with COPD probably promotes the earliest stages of carcinogenesis. However, once tumors have progressed to malignancy, the impact of COPD on the tumor immune microenvironment remains poorly defined, and its effects on immune-checkpoint blockers' efficacy are still unknown. OBJECTIVES: To study the impact of COPD on the immune contexture of non-small cell lung cancer (NSCLC)...
March 8, 2018: American Journal of Respiratory and Critical Care Medicine
Nicholas M Mark, Julia Kargl, Stephanie E Busch, Grace H Y Yang, Heather E Metz, Huajia Zhang, Jesse J Hubbard, Sudhakar N J Pipavath, David K Madtes, A McGarry Houghton
RATIONALE: Chronic obstructive pulmonary disease (COPD) and non-small cell lung cancer (NSCLC) are interrelated diseases with substantial mortality, and the pathogenesis of both involves aberrant immune functioning. OBJECTIVES: To profile immune cell composition and function in patients with NSCLC and describe the effects of COPD on lung and tumor microenvironments. METHODS: We profiled resected lung and tumor tissue using flow cytometry and T-cell receptor sequencing in patients with and without COPD from a prospective cohort of patients undergoing resection of NSCLC...
February 1, 2018: American Journal of Respiratory and Critical Care Medicine
C Jungnickel, L H Schmidt, L Bittigkoffer, L Wolf, A Wolf, F Ritzmann, A Kamyschnikow, C Herr, M D Menger, T Spieker, R Wiewrodt, R Bals, C Beisswenger
Chronic obstructive pulmonary disease (COPD) is associated with an increased risk for lung cancer and an aberrant microbiota of the lung. Microbial colonization contributes to chronic neutrophilic inflammation in COPD. Nontypeable Haemophilus influenzae (NTHi) is frequently found in lungs of stable COPD patients and is the major pathogen triggering exacerbations. The epithelial cytokine interleukin-17C (IL-17C) promotes the recruitment of neutrophils into inflamed tissues. The purpose of this study was to investigate the function of IL-17C in the pulmonary tumor microenvironment...
July 20, 2017: Oncogene
Mingxing Wang, Guoyin Li, Zhiwei Yang, Lei Wang, Lei Zhang, Ting Wang, Yimeng Zhang, Shengli Zhang, Yong Han, Lintao Jia
Hypoxic microenvironment is critically involved in the response of non-small cell lung cancer (NSCLC) to chemotherapy, the mechanisms of which remain largely unknown. Here, we found that NSCLC patients exhibited increased chemotherapeutic resistance when complicated by chronic obstructive pulmonary disease (COPD), a critical cause of chronic hypoxemia. The downregulation of uncoupling protein 2 (UCP2), which is attributed to hypoxia-inducible factor 1 (HIF-1)-mediated suppression of the transcriptional factor peroxisome proliferator-activated receptor γ (PPARγ), was involved in NSCLC chemoresistance, and predicted a poor survival rate of patients receiving routine chemotherapy...
January 31, 2017: Oncotarget
Lei Gong, Mauricio da Silva Caetano, Amber M Cumpian, Soudabeh Daliri, Alejandra Garza Flores, Seon Hee Chang, Cesar E Ochoa, Christopher M Evans, Zhentao Yu, Seyed Javad Moghaddam
Tumor necrosis factor (TNF) is known as an important regulator of tumor microenvironment and inflammation. TNF levels are markedly elevated in the bronchoalveolar lavage fluid (BALF) of patients with chronic obstructive pulmonary disease (COPD), which is an independent risk factor for lung cancer. We have previously shown that COPD-like airway inflammation promotes lung cancer in a K-ras mutant mouse model (CC-LR mouse). This was associated with a significant increase of neutrophils in BALF, accompanied by a marked increase in TNF level, suggesting a link between COPD, TNF, and lung cancer promotion...
2016: Oncoimmunology
Diane C Wang, Lin Shi, Zhenhua Zhu, Danyan Gao, Yong Zhang
Genetic variations in COPD and lung cancer may be one of the molecular mechanisms responsible for COPD-lung cancer transformation. The present review highlights main genetic variations co-existed in COPD and lung cancer and integrates the varied genes into four molecular mechanisms, e.g. activated cell proliferation pathway, tumor suppressor and DNA repair gene dysfunction, chronic inflammatory microenvironment, and impaired immune response, by which COPD epithelial cells may be transformed into tumorigenic status...
February 2017: Seminars in Cancer Biology
Teresa W-M Fan, Marc O Warmoes, Qiushi Sun, Huan Song, Jadwiga Turchan-Cholewo, Jeremiah T Martin, Angela Mahan, Richard M Higashi, Andrew N Lane
Cancer and stromal cell metabolism is important for understanding tumor development, which highly depends on the tumor microenvironment (TME). Cell or animal models cannot recapitulate the human TME. We have developed an ex vivo paired cancerous (CA) and noncancerous (NC) human lung tissue approach to explore cancer and stromal cell metabolism in the native human TME. This approach enabled full control of experimental parameters and acquisition of individual patient's target tissue response to therapeutic agents while eliminating interferences from genetic and physiological variations...
July 2016: Cold Spring Harbor Molecular Case Studies
Mauricio S Caetano, Huiyuan Zhang, Amber M Cumpian, Lei Gong, Nese Unver, Edwin J Ostrin, Soudabeh Daliri, Seon Hee Chang, Cesar E Ochoa, Samir Hanash, Carmen Behrens, Ignacio I Wistuba, Cinthya Sternberg, Humam Kadara, Carlos Gil Ferreira, Stephanie S Watowich, Seyed Javad Moghaddam
Activating mutations of K-ras are the most common oncogenic alterations found in lung cancer. Unfortunately, attempts to target K-ras-mutant lung tumors have thus far failed, clearly indicating the need for new approaches in patients with this molecular profile. We have previously shown NF-κB activation, release of IL6, and activation of its responsive transcription factor STAT3 in K-ras-mutant lung tumors, which was further amplified by the tumor-enhancing effect of chronic obstructive pulmonary disease (COPD)-type airway inflammation...
June 1, 2016: Cancer Research
Rinat Zaynagetdinov, Taylor P Sherrill, Linda A Gleaves, Pierre Hunt, Wei Han, Allyson G McLoed, Jamie A Saxon, Harikrishna Tanjore, Peter M Gulleman, Lisa R Young, Timothy S Blackwell
Nuclear Factor (NF)-κB is positioned to provide the interface between COPD and carcinogenesis through regulation of chronic inflammation in the lungs. Using a tetracycline-inducible transgenic mouse model that conditionally expresses activated IκB kinase β (IKKβ) in airway epithelium (IKTA), we found that sustained NF-κB signaling results in chronic inflammation and emphysema by 4 months. By 11 months of transgene activation, IKTA mice develop lung adenomas. Investigation of lung inflammation in IKTA mice revealed a substantial increase in M2-polarized macrophages and CD4+/CD25+/FoxP3+ regulatory T lymphocytes (Tregs)...
February 2, 2016: Oncotarget
Vivek Mittal, Tina El Rayes, Navneet Narula, Timothy E McGraw, Nasser K Altorki, Mary Helen Barcellos-Hoff
The tumor microenvironment (TME) represents a milieu that enables tumor cells to acquire the hallmarks of cancer. The TME is heterogeneous in composition and consists of cellular components, growth factors, proteases, and extracellular matrix. Concerted interactions between genetically altered tumor cells and genetically stable intratumoral stromal cells result in an "activated/reprogramed" stroma that promotes carcinogenesis by contributing to inflammation, immune suppression, therapeutic resistance, and generating premetastatic niches that support the initiation and establishment of distant metastasis...
2016: Advances in Experimental Medicine and Biology
Severin Schmid, Markus Kübler, C Korcan Ayata, Zsofia Lazar, Benedikt Haager, Madelon Hoßfeld, Anja Meyer, Sanja Cicko, Mirjam Elze, Sebastian Wiesemann, Gernot Zissel, Bernward Passlick, Marco Idzko
OBJECTIVES: Purines are well-known as intracellular sources for energy but they also act as extracellular signaling molecules. In the recent years, there has been a growing interest in the therapeutic potential of purinergic signaling for cancer treatment. This is the first study to analyze lung purine levels and purinergic receptors in non-small-cell lung cancer (NSCLC) patients. MATERIALS AND METHODS: In this prospective clinical trial we enrolled 26 patients with NSCLC and 21 patients with chronic obstructive pulmonary disease (COPD) without signs of malignancy...
December 2015: Lung Cancer: Journal of the International Association for the Study of Lung Cancer
Yu Fujita, Nobuyoshi Kosaka, Jun Araya, Kazuyoshi Kuwano, Takahiro Ochiya
Increasing attention is being paid to the role of extracellular vesicles (EVs) in various lung diseases. EVs are released by a variety of cells, including respiratory cells and immune cells, and they encapsulate various molecules, such as proteins and microRNAs, as modulators of intercellular communication. Cancer cell-derived EVs play crucial roles in promoting tumor progression and modifying their microenvironment. By contrast, noncancerous cell-derived EVs demonstrate protective functions against injury, such as tissue recovery and repair, to maintain physiological homeostasis...
September 2015: Trends in Molecular Medicine
Halina Batura-Gabryel, Beata Brajer-Luftmann, Agata Nowicka, Mariusz Kaczmarek, Jan Sikora
SESSION TITLE: COPD BiomarkersSESSION TYPE: Original Investigation SlidePRESENTED ON: Monday, October 27, 2014 at 07:30 AM - 08:30 AMPURPOSE: COPD is an independent risk factor for lung cancer. The pathogenesis of both diseases plays a crucial role specific microenvironment created by chronic inflammation. COPD is characterized by increased accumulation of granulocytes, macrophages, lymphocytes and dendritic cells. Little is known about the impact of COPD on the microenvironment of different subpopulations of T lymphocytes other than Th1 i Th2 (Th9, Th17, Th22)...
October 1, 2014: Chest
Yasuo Sekine, Atsushi Hata, Eitetsu Koh, Kenzo Hiroshima
Chronic obstructive pulmonary disease (COPD) and lung cancer are closely related. The annual incidence of lung cancer arising from COPD has been reported to be 0.8-1.7 %. Treatment of lung cancer from COPD is very difficult due to low cardiopulmonary function, rapid tumor growth, and resistance to molecularly targeted therapies. Chronic inflammation caused by toxic gases can induce COPD and lung cancer. Carcinogenesis in the inflammatory microenvironment occurs during cycles of tissue injury and repair. Cellular damage can induce induction of necrotic cell death and loss of tissue integrity...
July 2014: General Thoracic and Cardiovascular Surgery
György Marko-Varga, Akos Végvári, Melinda Rezeli, Kaiu Prikk, Peeter Ross, Magnus Dahlbäck, Goutham Edula, Ruth Sepper, Thomas E Fehniger
UNLABELLED: BACKGROUND: For many common global diseases, such as cancer, diabetes, neurodegenerative and cardiovascular diseases there is an unmet need for diagnosing early indications of disease that could enable medical intervention and early treatment. The treatment of these diseases will require detailed knowledge of targeted pathways involved in disease pathogenesis but also the mode of drug actions at the biological location on these targets. Translational medicine is a new area of research where expert from different disciplines involved in basic science and clinical disciplines meet and join forces...
2012: Clinical and Translational Medicine
Vijaya Karoor, Mysan Le, Daniel Merrick, Karen A Fagan, Edward C Dempsey, York E Miller
Patients with chronic obstructive pulmonary disease (COPD) are at an increased risk for the development of lung cancer, the mechanisms for which are incompletely understood. We hypothesized that the hypoxic pulmonary microenvironment present in COPD would augment lung carcinogenesis. Mice were subjected to chemical carcinogenesis protocols and placed in either hypoxia or normoxia. Mice exposed to chronic hypoxia developed tumors with increased volume compared with normoxic controls. Both lungs and tumors from hypoxic mice showed a preferential stabilization of HIF-2α and increased expression of VEGF-A, FGF2, and their receptors as well as other survival, proliferation, and angiogenic signaling pathways regulated by HIF-2α...
August 2012: Cancer Prevention Research
Jiun-Lih Lin, Mark H Bonnichsen, Emily U Nogeh, Mark J Raftery, Paul S Thomas
Asthma, chronic obstructive pulmonary disease (COPD) and lung cancer cause extensive mortality and morbidity worldwide. However, the current state-of-the-art diagnosis and management schemes of these diseases are suboptimal as the incidence of asthma has risen by 250% over the last two decades and the 5-year mortality rate of lung cancer remains at 88%. Proteomic analysis is at the frontier of medical research and demonstrates tremendous potential in the early detection, diagnosis and staging, as well as providing novel therapeutic targets for improved management of smoking-related lung diseases...
June 2010: Expert Review of Proteomics
Tonya Walser, Xiaoyan Cui, Jane Yanagawa, Jay M Lee, Eileen Heinrich, Gina Lee, Sherven Sharma, Steven M Dubinett
Worldwide over 1 million people die due to lung cancer each year. It is estimated that cigarette smoking explains almost 90% of lung cancer risk in men and 70 to 80% in women. Clinically evident lung cancers have multiple genetic and epigenetic abnormalities. These abnormalities may result in activation of oncogenes and inactivation of tumor-suppressor genes. Chronic inflammation, which is known to promote cancer, may result both from smoking and from genetic abnormalities. These mediators in turn may be responsible for increased macrophage recruitment, delayed neutrophil clearance, and increase in reactive oxygen species (ROS)...
December 1, 2008: Proceedings of the American Thoracic Society
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