The microenvironment of lung cancer and therapeutic implications

Research output: Chapter in Book/Report/Conference proceedingChapter

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 infl ammation, immune suppression, therapeutic resistance, and generating premetastatic niches that support the initiation and establishment of distant metastasis. The lungs present a unique milieu in which tumors progress in collusion with the TME, as evidenced by regions of aberrant angiogenesis, acidosis and hypoxia. Infl ammation plays an important role in the pathogenesis of lung cancer, and pulmonary disorders in lung cancer patients such as chronic obstructive pulmonary disease (COPD) and emphysema, constitute comorbid conditions and are independent risk factors for lung cancer. The TME also contributes to immune suppression, induces epithelial-to-mesenchymal transition (EMT) and diminishes effi cacy of chemotherapies. Thus, the TME has begun to emerge as the “Achilles heel” of the disease, and constitutes an attractive target for anti-cancer therapy. Drugs targeting the components of the TME are making their way into clinical trials. Here, we will focus on recent advances and emerging concepts regarding the intriguing role of the TME in lung cancer progression, and discuss future directions in the context of novel diagnostic and therapeutic opportunities.

Original languageEnglish (US)
Title of host publicationAdvances in Experimental Medicine and Biology
PublisherSpringer New York
Pages75-110
Number of pages36
Volume890
DOIs
StatePublished - Oct 1 2016

Publication series

NameAdvances in Experimental Medicine and Biology
Volume890
ISSN (Print)00652598
ISSN (Electronic)22148019

PMID: 26703800

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The microenvironment of lung cancer and therapeutic implications. / Mittal, Vivek; El Rayes, Tina; Narula, Navneet; McGraw, Timothy E.; Altorki, Nasser K.; Barcellos-Hoff, Mary Helen.

Advances in Experimental Medicine and Biology. Vol. 890 Springer New York, 2016. p. 75-110 (Advances in Experimental Medicine and Biology; Vol. 890).

Research output: Chapter in Book/Report/Conference proceedingChapter

Harvard

Mittal, V, El Rayes, T, Narula, N, McGraw, TE, Altorki, NK & Barcellos-Hoff, MH 2016, The microenvironment of lung cancer and therapeutic implications. in Advances in Experimental Medicine and Biology. vol. 890, Advances in Experimental Medicine and Biology, vol. 890, Springer New York, pp. 75-110. https://doi.org/10.1007/978-3-319-24932-2_5

APA

Mittal, V., El Rayes, T., Narula, N., McGraw, T. E., Altorki, N. K., & Barcellos-Hoff, M. H. (2016). The microenvironment of lung cancer and therapeutic implications. In Advances in Experimental Medicine and Biology (Vol. 890, pp. 75-110). (Advances in Experimental Medicine and Biology; Vol. 890). Springer New York. https://doi.org/10.1007/978-3-319-24932-2_5

Vancouver

Mittal V, El Rayes T, Narula N, McGraw TE, Altorki NK, Barcellos-Hoff MH. The microenvironment of lung cancer and therapeutic implications. In Advances in Experimental Medicine and Biology. Vol. 890. Springer New York. 2016. p. 75-110. (Advances in Experimental Medicine and Biology). https://doi.org/10.1007/978-3-319-24932-2_5

Author

Mittal, Vivek ; El Rayes, Tina ; Narula, Navneet ; McGraw, Timothy E. ; Altorki, Nasser K. ; Barcellos-Hoff, Mary Helen. / The microenvironment of lung cancer and therapeutic implications. Advances in Experimental Medicine and Biology. Vol. 890 Springer New York, 2016. pp. 75-110 (Advances in Experimental Medicine and Biology).

BibTeX

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title = "The microenvironment of lung cancer and therapeutic implications",
abstract = "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 infl ammation, immune suppression, therapeutic resistance, and generating premetastatic niches that support the initiation and establishment of distant metastasis. The lungs present a unique milieu in which tumors progress in collusion with the TME, as evidenced by regions of aberrant angiogenesis, acidosis and hypoxia. Infl ammation plays an important role in the pathogenesis of lung cancer, and pulmonary disorders in lung cancer patients such as chronic obstructive pulmonary disease (COPD) and emphysema, constitute comorbid conditions and are independent risk factors for lung cancer. The TME also contributes to immune suppression, induces epithelial-to-mesenchymal transition (EMT) and diminishes effi cacy of chemotherapies. Thus, the TME has begun to emerge as the “Achilles heel” of the disease, and constitutes an attractive target for anti-cancer therapy. Drugs targeting the components of the TME are making their way into clinical trials. Here, we will focus on recent advances and emerging concepts regarding the intriguing role of the TME in lung cancer progression, and discuss future directions in the context of novel diagnostic and therapeutic opportunities.",
keywords = "Angiogenesis, Bone marrow, Endothelial cells, Hypoxia, Immune cells, Immunotherapy, Infl ammation, Lung cancer, Microenvironment, Radiation, Resistance, Therapy",
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RIS

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T1 - The microenvironment of lung cancer and therapeutic implications

AU - Mittal, Vivek

AU - El Rayes, Tina

AU - Narula, Navneet

AU - McGraw, Timothy E.

AU - Altorki, Nasser K.

AU - Barcellos-Hoff, Mary Helen

PY - 2016/10/1

Y1 - 2016/10/1

N2 - 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 infl ammation, immune suppression, therapeutic resistance, and generating premetastatic niches that support the initiation and establishment of distant metastasis. The lungs present a unique milieu in which tumors progress in collusion with the TME, as evidenced by regions of aberrant angiogenesis, acidosis and hypoxia. Infl ammation plays an important role in the pathogenesis of lung cancer, and pulmonary disorders in lung cancer patients such as chronic obstructive pulmonary disease (COPD) and emphysema, constitute comorbid conditions and are independent risk factors for lung cancer. The TME also contributes to immune suppression, induces epithelial-to-mesenchymal transition (EMT) and diminishes effi cacy of chemotherapies. Thus, the TME has begun to emerge as the “Achilles heel” of the disease, and constitutes an attractive target for anti-cancer therapy. Drugs targeting the components of the TME are making their way into clinical trials. Here, we will focus on recent advances and emerging concepts regarding the intriguing role of the TME in lung cancer progression, and discuss future directions in the context of novel diagnostic and therapeutic opportunities.

AB - 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 infl ammation, immune suppression, therapeutic resistance, and generating premetastatic niches that support the initiation and establishment of distant metastasis. The lungs present a unique milieu in which tumors progress in collusion with the TME, as evidenced by regions of aberrant angiogenesis, acidosis and hypoxia. Infl ammation plays an important role in the pathogenesis of lung cancer, and pulmonary disorders in lung cancer patients such as chronic obstructive pulmonary disease (COPD) and emphysema, constitute comorbid conditions and are independent risk factors for lung cancer. The TME also contributes to immune suppression, induces epithelial-to-mesenchymal transition (EMT) and diminishes effi cacy of chemotherapies. Thus, the TME has begun to emerge as the “Achilles heel” of the disease, and constitutes an attractive target for anti-cancer therapy. Drugs targeting the components of the TME are making their way into clinical trials. Here, we will focus on recent advances and emerging concepts regarding the intriguing role of the TME in lung cancer progression, and discuss future directions in the context of novel diagnostic and therapeutic opportunities.

KW - Angiogenesis

KW - Bone marrow

KW - Endothelial cells

KW - Hypoxia

KW - Immune cells

KW - Immunotherapy

KW - Infl ammation

KW - Lung cancer

KW - Microenvironment

KW - Radiation

KW - Resistance

KW - Therapy

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U2 - 10.1007/978-3-319-24932-2_5

DO - 10.1007/978-3-319-24932-2_5

M3 - Chapter

VL - 890

T3 - Advances in Experimental Medicine and Biology

SP - 75

EP - 110

BT - Advances in Experimental Medicine and Biology

PB - Springer New York

ER -

ID: 18792828