Origin of carcinoma associated fibroblasts

被引：95

作者：

Haviv, Izhak ^{[1
,2
]}

Polyak, Kornelia ^{[4
,5
]}

Qiu, Wen ^{[2
,6
]}

Hu, Min ^{[4
,5
]}

Campbell, Ian ^{[3
,6
]}

机构：

[1] Baker IDI Inst, Prahran, Vic, Australia

[2] Univ Melbourne, Sch Med, Dept Biochem, Melbourne, Vic, Australia

[3] Univ Melbourne, Sch Med, Dept Pathol, Melbourne, Vic, Australia

[4] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA

[5] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA

[6] Peter MacCallum Canc Ctr, VBCRC Canc Genet Lab, Melbourne, Vic 8006, Australia

来源：

CELL CYCLE | 2009年 / 8卷 / 04期

关键词：

oncology; cancer associated fibroblasts; micro-environment; cancer etiology; STROMAL-EPITHELIAL INTERACTIONS; OVARIAN SURFACE EPITHELIUM; GROWTH-FACTOR-BETA; MESENCHYMAL STEM-CELLS; HUMAN BREAST-CANCER; TUMOR-STROMA; IN-VIVO; GENETIC ALTERATIONS; SOMATIC MUTATIONS; PROSTATE-CANCER;

D O I：

10.4161/cc.8.4.7669

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Recent evidence on the genomic integrity of non-malignant cells surrounding carcinoma cells has reinvigorated the discussion about the origin of the altered phenotype exhibited by carcinoma associated fibroblasts. Many hypotheses have been proposed for the origin of these altered cells, including standard connective tissue acute phase and stress response, fibroblast senescence, reciprocal interactions with the cancer cells, fibroblast specific somatic mutations, differentiation precursors and infiltrating mesenchymal stem cells. Here we review the definition of CAF phenotype and the evidence for each of those hypotheses, in the context of our current understanding of cancer etiology.

引用

页码：589 / 595

页数：7

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