Inflammation and Lung Cancer (Record no. 13868)
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000 -LEADER | |
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fixed length control field | 02923nam a22001697a 4500 |
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION | |
fixed length control field | 210521b |||||||| |||| 00| 0 eng d |
020 ## - INTERNATIONAL STANDARD BOOK NUMBER | |
International Standard Book Number | 9781493927234 |
International Standard Book Number | 9781493927241 |
100 ## - MAIN ENTRY--PERSONAL NAME | |
Personal name | Steven M. Dubinett |
9 (RLIN) | 10806 |
245 ## - TITLE STATEMENT | |
Title | Inflammation and Lung Cancer |
260 ## - PUBLICATION, DISTRIBUTION, ETC. | |
Place of publication, distribution, etc. | New York |
Name of publisher, distributor, etc. | Springer Science+Business Media |
Date of publication, distribution, etc. | 2015 |
300 ## - PHYSICAL DESCRIPTION | |
Extent | 215 Pages |
500 ## - GENERAL NOTE | |
General note | Includes References and Index |
520 ## - SUMMARY, ETC. | |
Summary, etc. | The inflammatory tumor microenvironment (TME) has a multifaceted role in tumor<br/>initiation, progression, and metastasis. Whereas genetic changes are critical for the<br/>malignant transformation of epithelial cells, we now understand that components<br/>of the developing lung TME are active participants in the events precipitating lung<br/>cancer initiation and progression. Inflammation can influence the TME to orchestrate creation of a hypoxic environment, increased angiogenesis and invasion, as<br/>well as expand stem cell phenotypes.<br/>Although the origin of the inflammatory TME is an active area of investigation,<br/>two pathways have been postulated. In the intrinsic pathway, the inflammatory microenvironment is generated by genetic alterations within premalignant or neoplastic cells that lead to increased production of inflammatory mediators. Conversely, in<br/>the extrinsic pathway, the inflammatory environment is accommodating to cancer<br/>development and progression. Thus, inflammation could be present due to an unresolved infection or chronic exposure to carcinogens.<br/>A body of evidence exists at the preclinical, clinical, epidemiological, molecular,<br/>and pathological levels suggesting that inflammation is strongly associated with<br/>the development of lung cancer. Here, inflammation and lung cancer is addressed<br/>in the context of the molecular pathology of the disease as well as the relationship<br/>to chronic obstructive pulmonary disease. In addition, the important relationships<br/>between inflammation, epithelial mesenchymal transition (EMT), and lung cancer<br/>initiation and metastases are reviewed. Our understanding regarding inflammationdependent regulation of angiogenesis and eicosanoid metabolism has opened new<br/>opportunities to translate findings to clinical interventions in prevention and therapy.<br/>Finally, research in understanding the nature of inflammation and immunity in<br/>the lung cancer TME has led to ground-breaking studies applying immunotherapeutic approaches for lung cancer. The phenotype of the adaptive immune infiltrate<br/>and the diversity of cellular elements that either promote eradication of malignancy<br/>or facilitate an immunosuppressive TME favoring tumor progression are being assessed in the context of the mutational landscape of evolving and established lung<br/>cancer. These studies, reviewed here, hold promise for additional progress in controlling inflammation and leading to further improvements in immunotherapy for<br/>lung cancer. |
654 ## - SUBJECT ADDED ENTRY--FACETED TOPICAL TERMS | |
General subdivision | Oncology |
942 ## - ADDED ENTRY ELEMENTS (KOHA) | |
Source of classification or shelving scheme | ddc |
Koha item type | BOOKS |
Withdrawn status | Lost status | Source of classification or shelving scheme | Damaged status | Not for loan | Collection | Home library | Current library | Shelving location | Date acquired | Total checkouts | Barcode | Date last seen | Price effective from | Koha item type |
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MWALIMU NYERERE LEARNING RESOURCES CENTRE-CUHAS BUGANDO | MWALIMU NYERERE LEARNING RESOURCES CENTRE-CUHAS BUGANDO | 05/21/2021 | EBS3470 | 05/21/2021 | 05/21/2021 | BOOKS |