TY - CHAP
T1 - Analysis of Integrin Signaling in Genetically Engineered Mouse Models of Mammary Tumor Progression
AU - Pylayeva, Yuliya
AU - Guo, Wenjun
AU - Giancotti, Filippo G.
N1 - Funding Information:
We thank the Transgenic and Knock‐out Mouse Facility and the Molecular Cytology Facility of MSKCC for technical assistance. These studies were supported by the National Institutes of Health (grants R37 CA58976 to F.G.G., RO1 CA113996 to F.G.G., and P30 CA08748 to Memorial Sloan‐Kettering Cancer Center).
PY - 2007
Y1 - 2007
N2 - Cancer progression-the evolution of malignant tumors towards metastatic dissemination-is a complex, multistep process orchestrated by neoplastic cells but aided by elements of the tumor microenvironment such as macrophages, activated fibroblasts, and endothelial cells. During tumor progression, cancer cells acquire a number of traits, such as the ability to undergo unrestrained proliferation, to resist pro-apoptotic insults, and to invade through tissue boundaries. Genetic and epigenetic changes conspire to drive the emergence of these traits against the backdrop of host selection. It is becoming increasingly clear that certain integrins and integrin-signaling components amplify oncogenic signaling to promote tumor progression. Mouse models of cancer provide useful, if not necessary, experimental systems to study tumor initiation and progression in vivo and to test novel therapeutic approaches. We have utilized mouse models of mammary tumorigenesis to examine the role of integrin α6β4 signaling in tumor progression in vivo. In this chapter, we describe a collection of cell biological and genetic methods that may aid in characterizing the roles of integrin signals in mammary tumorigenesis.
AB - Cancer progression-the evolution of malignant tumors towards metastatic dissemination-is a complex, multistep process orchestrated by neoplastic cells but aided by elements of the tumor microenvironment such as macrophages, activated fibroblasts, and endothelial cells. During tumor progression, cancer cells acquire a number of traits, such as the ability to undergo unrestrained proliferation, to resist pro-apoptotic insults, and to invade through tissue boundaries. Genetic and epigenetic changes conspire to drive the emergence of these traits against the backdrop of host selection. It is becoming increasingly clear that certain integrins and integrin-signaling components amplify oncogenic signaling to promote tumor progression. Mouse models of cancer provide useful, if not necessary, experimental systems to study tumor initiation and progression in vivo and to test novel therapeutic approaches. We have utilized mouse models of mammary tumorigenesis to examine the role of integrin α6β4 signaling in tumor progression in vivo. In this chapter, we describe a collection of cell biological and genetic methods that may aid in characterizing the roles of integrin signals in mammary tumorigenesis.
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U2 - 10.1016/S0076-6879(07)26019-7
DO - 10.1016/S0076-6879(07)26019-7
M3 - Chapter
C2 - 17697895
AN - SCOPUS:35148889801
SN - 9780123739247
T3 - Methods in Enzymology
SP - 439
EP - 461
BT - Integrins
A2 - Cheresh, David
ER -