Improving cancer therapies by targeting the physical and chemical hallmarks of the tumor microenvironment. Ivey, J. W., Bonakdar, M., Kanitkar, A., Davalos, R. V., & Verbridge, S. S. Cancer Lett, 380(1):330-9, 2016. 1872-7980 Ivey, Jill W Bonakdar, Mohammad Kanitkar, Akanksha Davalos, Rafael V Verbridge, Scott S R21 CA173092/CA/NCI NIH HHS/United States R21 CA192042/CA/NCI NIH HHS/United States R21 EB019123/EB/NIBIB NIH HHS/United States Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review Ireland 2016/01/03 Cancer Lett. 2016 Sep 28;380(1):330-9. doi: 10.1016/j.canlet.2015.12.019. Epub 2015 Dec 24.doi abstract bibtex Tumors are highly heterogeneous at the patient, tissue, cellular, and molecular levels. This multi-scale heterogeneity poses significant challenges for effective therapies, which ideally must not only distinguish between tumorous and healthy tissue, but also fully address the wide variety of tumorous sub-clones. Commonly used therapies either leverage a biological phenotype of cancer cells (e.g. high rate of proliferation) or indiscriminately kill all the cells present in a targeted volume. Tumor microenvironment (TME) targeting represents a promising therapeutic direction, because a number of TME hallmarks are conserved across different tumor types, despite the underlying genetic heterogeneity. Historically, TME targeting has largely focused on the cells that support tumor growth (e.g. vascular endothelial cells). However, by viewing the intrinsic physical and chemical alterations in the TME as additional therapeutic opportunities rather than barriers, a new class of TME-inspired treatments has great promise to complement or replace existing therapeutic strategies. In this review we summarize the physical and chemical hallmarks of the TME, and discuss how these tumor characteristics either currently are, or may ultimately be targeted to improve cancer therapies.
@article{RN180,
author = {Ivey, J. W. and Bonakdar, M. and Kanitkar, A. and Davalos, R. V. and Verbridge, S. S.},
title = {Improving cancer therapies by targeting the physical and chemical hallmarks of the tumor microenvironment},
journal = {Cancer Lett},
volume = {380},
number = {1},
pages = {330-9},
note = {1872-7980
Ivey, Jill W
Bonakdar, Mohammad
Kanitkar, Akanksha
Davalos, Rafael V
Verbridge, Scott S
R21 CA173092/CA/NCI NIH HHS/United States
R21 CA192042/CA/NCI NIH HHS/United States
R21 EB019123/EB/NIBIB NIH HHS/United States
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Ireland
2016/01/03
Cancer Lett. 2016 Sep 28;380(1):330-9. doi: 10.1016/j.canlet.2015.12.019. Epub 2015 Dec 24.},
abstract = {Tumors are highly heterogeneous at the patient, tissue, cellular, and molecular levels. This multi-scale heterogeneity poses significant challenges for effective therapies, which ideally must not only distinguish between tumorous and healthy tissue, but also fully address the wide variety of tumorous sub-clones. Commonly used therapies either leverage a biological phenotype of cancer cells (e.g. high rate of proliferation) or indiscriminately kill all the cells present in a targeted volume. Tumor microenvironment (TME) targeting represents a promising therapeutic direction, because a number of TME hallmarks are conserved across different tumor types, despite the underlying genetic heterogeneity. Historically, TME targeting has largely focused on the cells that support tumor growth (e.g. vascular endothelial cells). However, by viewing the intrinsic physical and chemical alterations in the TME as additional therapeutic opportunities rather than barriers, a new class of TME-inspired treatments has great promise to complement or replace existing therapeutic strategies. In this review we summarize the physical and chemical hallmarks of the TME, and discuss how these tumor characteristics either currently are, or may ultimately be targeted to improve cancer therapies.},
keywords = {*Ablation Techniques/methods
Animals
Antineoplastic Agents/*administration & dosage
Drug Carriers
*Drug Delivery Systems/methods
Drug Resistance, Neoplasm
Humans
Hydrogen-Ion Concentration
Neoplasms/metabolism/pathology/*therapy
Tumor Hypoxia
*Tumor Microenvironment
Chemcical tumor microenvironment
Electroporation therapy
Physical tumor microenvironment
Tumor microenvironment targeting},
ISSN = {0304-3835 (Print)
0304-3835},
DOI = {10.1016/j.canlet.2015.12.019},
year = {2016},
type = {Journal Article}
}
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