Regulation of tumor progression and metastasis by bone marrow-derived microenvironments

Research output: Chapter in Book/Report/Conference proceedingChapter

Tina El Rayes, Dingcheng Gao, Nasser K. Altorki, Thomas R. Cox, Janine T. Erler, Vivek Mittal

Activating mutations in driver oncogenes and loss-of-function mutations in tumor suppressor genes contribute to tumor progression and metastasis. Accordingly, therapies targeting key tumor cell-intrinsic signaling pathways are being used in clinical trials, and some have met FDA approval. However, these treatments benefit only a small proportion of patients harboring key driver mutations, and acquired resistance to these therapies presents a major impediment to effective treatment. More recently, the contribution of the tumor microenvironment (TME) has been an area of active investigation and has begun to provide critical insights into carcinogenesis. The host stromal cells in the TME coevolve with tumors and contribute to carcinogenesis in several ways. Among the host cells, bone marrow (BM)-derived cells constitute a significant fraction and directly contribute to proliferation, invasion, intravasation, extravasation, and outgrowth at the metastatic site. While the tumor-reprogrammed BM cells constitute attractive targets for anticancer therapy, recent studies have also begun to unravel their role as prognostic and predictive molecular markers of the disease.

Original languageEnglish (US)
Title of host publicationBiomarkers of the Tumor Microenvironment
Subtitle of host publicationBasic Studies and Practical Applications
PublisherSpringer International Publishing
Pages303-328
Number of pages26
ISBN (Electronic)9783319391472
ISBN (Print)9783319391458
DOIs
StatePublished - Aug 2 2017

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Regulation of tumor progression and metastasis by bone marrow-derived microenvironments. / El Rayes, Tina; Gao, Dingcheng; Altorki, Nasser K.; Cox, Thomas R.; Erler, Janine T.; Mittal, Vivek.

Biomarkers of the Tumor Microenvironment: Basic Studies and Practical Applications. Springer International Publishing, 2017. p. 303-328.

Research output: Chapter in Book/Report/Conference proceedingChapter

Harvard

El Rayes, T, Gao, D, Altorki, NK, Cox, TR, Erler, JT & Mittal, V 2017, Regulation of tumor progression and metastasis by bone marrow-derived microenvironments. in Biomarkers of the Tumor Microenvironment: Basic Studies and Practical Applications. Springer International Publishing, pp. 303-328. https://doi.org/10.1007/978-3-319-39147-2_13

APA

El Rayes, T., Gao, D., Altorki, N. K., Cox, T. R., Erler, J. T., & Mittal, V. (2017). Regulation of tumor progression and metastasis by bone marrow-derived microenvironments. In Biomarkers of the Tumor Microenvironment: Basic Studies and Practical Applications (pp. 303-328). Springer International Publishing. https://doi.org/10.1007/978-3-319-39147-2_13

Vancouver

El Rayes T, Gao D, Altorki NK, Cox TR, Erler JT, Mittal V. Regulation of tumor progression and metastasis by bone marrow-derived microenvironments. In Biomarkers of the Tumor Microenvironment: Basic Studies and Practical Applications. Springer International Publishing. 2017. p. 303-328 https://doi.org/10.1007/978-3-319-39147-2_13

Author

El Rayes, Tina ; Gao, Dingcheng ; Altorki, Nasser K. ; Cox, Thomas R. ; Erler, Janine T. ; Mittal, Vivek. / Regulation of tumor progression and metastasis by bone marrow-derived microenvironments. Biomarkers of the Tumor Microenvironment: Basic Studies and Practical Applications. Springer International Publishing, 2017. pp. 303-328

BibTeX

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title = "Regulation of tumor progression and metastasis by bone marrow-derived microenvironments",
abstract = "Activating mutations in driver oncogenes and loss-of-function mutations in tumor suppressor genes contribute to tumor progression and metastasis. Accordingly, therapies targeting key tumor cell-intrinsic signaling pathways are being used in clinical trials, and some have met FDA approval. However, these treatments benefit only a small proportion of patients harboring key driver mutations, and acquired resistance to these therapies presents a major impediment to effective treatment. More recently, the contribution of the tumor microenvironment (TME) has been an area of active investigation and has begun to provide critical insights into carcinogenesis. The host stromal cells in the TME coevolve with tumors and contribute to carcinogenesis in several ways. Among the host cells, bone marrow (BM)-derived cells constitute a significant fraction and directly contribute to proliferation, invasion, intravasation, extravasation, and outgrowth at the metastatic site. While the tumor-reprogrammed BM cells constitute attractive targets for anticancer therapy, recent studies have also begun to unravel their role as prognostic and predictive molecular markers of the disease.",
keywords = "Anti-cancer therapy, Bone marrow, Bone marrow-derived cells, Metastasis, Pre-metastatic niche, Tumor microenvironment, Tumor progression",
author = "{El Rayes}, Tina and Dingcheng Gao and Altorki, {Nasser K.} and Cox, {Thomas R.} and Erler, {Janine T.} and Vivek Mittal",
year = "2017",
month = "8",
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pages = "303--328",
booktitle = "Biomarkers of the Tumor Microenvironment",
publisher = "Springer International Publishing",

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RIS

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T1 - Regulation of tumor progression and metastasis by bone marrow-derived microenvironments

AU - El Rayes, Tina

AU - Gao, Dingcheng

AU - Altorki, Nasser K.

AU - Cox, Thomas R.

AU - Erler, Janine T.

AU - Mittal, Vivek

PY - 2017/8/2

Y1 - 2017/8/2

N2 - Activating mutations in driver oncogenes and loss-of-function mutations in tumor suppressor genes contribute to tumor progression and metastasis. Accordingly, therapies targeting key tumor cell-intrinsic signaling pathways are being used in clinical trials, and some have met FDA approval. However, these treatments benefit only a small proportion of patients harboring key driver mutations, and acquired resistance to these therapies presents a major impediment to effective treatment. More recently, the contribution of the tumor microenvironment (TME) has been an area of active investigation and has begun to provide critical insights into carcinogenesis. The host stromal cells in the TME coevolve with tumors and contribute to carcinogenesis in several ways. Among the host cells, bone marrow (BM)-derived cells constitute a significant fraction and directly contribute to proliferation, invasion, intravasation, extravasation, and outgrowth at the metastatic site. While the tumor-reprogrammed BM cells constitute attractive targets for anticancer therapy, recent studies have also begun to unravel their role as prognostic and predictive molecular markers of the disease.

AB - Activating mutations in driver oncogenes and loss-of-function mutations in tumor suppressor genes contribute to tumor progression and metastasis. Accordingly, therapies targeting key tumor cell-intrinsic signaling pathways are being used in clinical trials, and some have met FDA approval. However, these treatments benefit only a small proportion of patients harboring key driver mutations, and acquired resistance to these therapies presents a major impediment to effective treatment. More recently, the contribution of the tumor microenvironment (TME) has been an area of active investigation and has begun to provide critical insights into carcinogenesis. The host stromal cells in the TME coevolve with tumors and contribute to carcinogenesis in several ways. Among the host cells, bone marrow (BM)-derived cells constitute a significant fraction and directly contribute to proliferation, invasion, intravasation, extravasation, and outgrowth at the metastatic site. While the tumor-reprogrammed BM cells constitute attractive targets for anticancer therapy, recent studies have also begun to unravel their role as prognostic and predictive molecular markers of the disease.

KW - Anti-cancer therapy

KW - Bone marrow

KW - Bone marrow-derived cells

KW - Metastasis

KW - Pre-metastatic niche

KW - Tumor microenvironment

KW - Tumor progression

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UR - http://www.scopus.com/inward/citedby.url?scp=85034855129&partnerID=8YFLogxK

U2 - 10.1007/978-3-319-39147-2_13

DO - 10.1007/978-3-319-39147-2_13

M3 - Chapter

SN - 9783319391458

SP - 303

EP - 328

BT - Biomarkers of the Tumor Microenvironment

PB - Springer International Publishing

ER -

ID: 38736426