Co-evolution of tumor cells and their microenvironment

被引:480
作者
Polyak, Kornelia [1 ,2 ]
Haviv, Izhak [3 ,4 ]
Campbell, Ian G. [5 ,6 ]
机构
[1] Dana Farber Canc Inst, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Boston, MA 02115 USA
[3] Baker IDI Inst, Blood & DNA Profiling Facil, Melbourne, Vic 3000, Australia
[4] Univ Melbourne, Sch Med, Dept Biochem, Melbourne, Vic 3010, Australia
[5] Peter MacCallum Canc Ctr, VBCRC Canc Genet Lab, Melbourne, Vic 3002, Australia
[6] Univ Melbourne, Sch Med, Dept Pathol, Melbourne, Vic 3010, Australia
关键词
STROMAL-EPITHELIAL INTERACTIONS; CANCER-ASSOCIATED FIBROBLASTS; HUMAN BREAST TISSUES; GENETIC ALTERATIONS; HUMAN COLON; MICRODISSECTED STROMA; TP53; MUTATIONS; MAMMARY-GLAND; IN-SITU; PROGRESSION;
D O I
10.1016/j.tig.2008.10.012
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Increasing evidence indicates that tumor-stromal cell interactions have a crucial role in tumor initiation and progression. These interactions modify cellular compartments, leading to the co-evolution of tumor cells and their microenvironment. Although the importance of microenvironmental alterations in tumor development is recognized, the molecular mechanisms underlying these changes are only now beginning to be understood. Epigenetic and gene expression changes have consistently been reported in cancer-associated stromal cells and the influence of the host genotype on tumorigenesis is also well documented. However, the presence of clonally selected somatic genetic alterations within the tumor microenvironment has been controversial. A thorough understanding of the co-evolution of these two cellular compartments will require carefully executed molecular studies combined with mathematical modeling.
引用
收藏
页码:30 / 38
页数:9
相关论文
共 75 条
[31]  
Kerbel Robert S, 2008, Proc Natl Acad Sci U S A, V105, pE55, DOI 10.1073/pnas.0804876105
[32]  
Kerner M, 2001, MICROBIAL ECOL, V41, P69
[33]   Smad4 signalling in T cells is required for suppression of gastrointestinal cancer [J].
Kim, Byung-Gyu ;
li, Cuing Li ;
Qiao, Wenhui ;
Mamura, Mizuko ;
Kasperczak, Barbara ;
Anver, Miriam ;
Wolfraim, Lawrence ;
Hong, Suntaek ;
Mushinski, Elizabeth ;
Potter, Michael ;
Kim, Seong-Jin ;
Fu, Xin-Yuan ;
Deng, Chuxia ;
Letterio, John J. .
NATURE, 2006, 441 (7096) :1015-1019
[34]   A novel 3D in vitro culture model to study stromal-epithelial interactions in the mammary gland [J].
Krause, Silva ;
Maffini, Maricel V. ;
Soto, Ana M. ;
Sonnenschein, Carlos .
TISSUE ENGINEERING PART C-METHODS, 2008, 14 (03) :261-271
[35]   Cancer and aging: a model for the cancer promoting effects of the aging stroma [J].
Krtolica, A ;
Campisi, J .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2002, 34 (11) :1401-1414
[36]   Reconstruction of functionally normal and malignant human breast tissues in mice [J].
Kuperwasser, C ;
Chavarria, T ;
Wu, M ;
Magrane, G ;
Gray, JW ;
Carey, L ;
Richardson, A ;
Weinberg, RA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (14) :4966-4971
[37]   Genetic model of multi-step breast carcinogenesis involving the epithelium and stroma: clues to tumour-microenvironment interactions [J].
Kurose, K ;
Hoshaw-Woodard, S ;
Adeyinka, A ;
Lemeshow, S ;
Watson, PH ;
Eng, C .
HUMAN MOLECULAR GENETICS, 2001, 10 (18) :1907-1913
[38]   Frequent somatic mutations in PTEN and TP53 are mutually exclusive in the stroma of breast carcinomas [J].
Kurose, K ;
Gilley, K ;
Matsumoto, S ;
Watson, PH ;
Zhou, XP ;
Eng, C .
NATURE GENETICS, 2002, 32 (03) :355-357
[39]   BRCA1 regulates human mammary stem/progenitor cell fate [J].
Liu, Suling ;
Ginestier, Christophe ;
Charafe-Jauffret, Emmanuelle ;
Foco, Hailey ;
Kleer, Celina G. ;
Merajver, Sofia D. ;
Dontu, Gabriela ;
Wicha, Max S. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2008, 105 (05) :1680-1685
[40]   The stroma as a crucial target in rat mammary gland carcinogenesis [J].
Maffini, MV ;
Soto, AM ;
Calabro, JM ;
Ucci, AA ;
Sonnenschein, C .
JOURNAL OF CELL SCIENCE, 2004, 117 (08) :1495-1502