@article {336,
	title = {Forcing form and function: biomechanical regulation of tumor evolution.},
	journal = {Trends Cell Biol},
	volume = {21},
	year = {2011},
	month = {2011 Jan},
	pages = {47-56},
	abstract = {<p>Cancer cells exist in a constantly evolving tissue microenvironment of diverse cell types within a proteinaceous extracellular matrix. As tumors evolve, the physical forces within this complex microenvironment change, with pleiotropic effects on both cell- and tissue-level behaviors. Recent work suggests that these biomechanical factors direct tissue development and modulate tissue homeostasis, and, when altered, crucially influence tumor evolution. In this review, we discuss the biomechanical regulation of cell and tissue homeostasis from the molecular, cellular and tissue levels, including how modifications of this physical dialogue could contribute to cancer etiology. Because of the broad impact of biomechanical factors on cell and tissue functions, an understanding of tumor evolution from the biomechanical perspective should improve risk assessment, clinical diagnosis and the efficacy of cancer treatment.</p>
},
	keywords = {Animals, Biomechanical Phenomena, Cell Transformation, Neoplastic, Extracellular Matrix, Humans, Neoplasms, Signal Transduction},
	issn = {1879-3088},
	doi = {10.1016/j.tcb.2010.08.015},
	author = {Yu, Hongmei and Mouw, Janna Kay and Weaver, Valerie M}
}
@article {366,
	title = {Matrix crosslinking forces tumor progression by enhancing integrin signaling.},
	journal = {Cell},
	volume = {139},
	year = {2009},
	month = {2009 Nov 25},
	pages = {891-906},
	abstract = {<p>Tumors are characterized by extracellular matrix (ECM) remodeling and stiffening. The importance of ECM remodeling to cancer is appreciated; the relevance of stiffening is less clear. We found that breast tumorigenesis is accompanied by collagen crosslinking, ECM stiffening, and increased focal adhesions. Induction of collagen crosslinking stiffened the ECM, promoted focal adhesions, enhanced PI3 kinase (PI3K) activity, and induced the invasion of an oncogene-initiated epithelium. Inhibition of integrin signaling repressed the invasion of a premalignant epithelium into a stiffened, crosslinked ECM and forced integrin clustering promoted focal adhesions, enhanced PI3K signaling, and induced the invasion of a premalignant epithelium. Consistently, reduction of lysyl oxidase-mediated collagen crosslinking prevented MMTV-Neu-induced fibrosis, decreased focal adhesions and PI3K activity, impeded malignancy, and lowered tumor incidence. These data show how collagen crosslinking can modulate tissue fibrosis and stiffness to force focal adhesions, growth factor signaling and breast malignancy.</p>
},
	keywords = {Aging, Animals, Breast Neoplasms, Collagen, Epidermal Growth Factor, Extracellular Matrix, Female, Fibrosis, Genes, ras, Humans, Integrins, Mammary Glands, Human, Mice, Mice, Inbred BALB C, Protein-Lysine 6-Oxidase, Signal Transduction},
	issn = {1097-4172},
	doi = {10.1016/j.cell.2009.10.027},
	author = {Levental, Kandice R and Yu, Hongmei and Kass, Laura and Lakins, Johnathon N and Egeblad, Mikala and Erler, Janine T and Fong, Sheri F T and Csiszar, Katalin and Giaccia, Amato and Weninger, Wolfgang and Yamauchi, Mitsuo and Gasser, David L and Weaver, Valerie M}
}
