TY - JOUR
T1 - Epithelial ovarian cancer
T2 - Focus on genetics and animal models
AU - Shan, Weiwei
AU - Liu, Jinsong
N1 - Funding Information:
We sincerely apologize for being not able to cite all the references relevant to this topic. This work was supported by Research Scholar Grant RSG-04-028-1-CCE from the American Cancer Society, grant RO1 CA131183-02 from the National Institutes of Health/ National Cancer Institute, and an institutional research grant from The University of Texas M.D. Anderson Cancer Center (all to J.L.).
PY - 2009/3/1
Y1 - 2009/3/1
N2 - Despite rapid advances in understanding ovarian cancer etiology, epithelial ovarian cancer remains the most lethal form of gynecologic cancers in the United States. The four morphologically-defined epithelial ovarian cancer subtypes-serous, endometrioid, mucinous, and clear cell carcinomas - are generally believed to originate from ovarian epithelial cells. Although it remains unclear how this single cell layer gives rise to morphologically distinct cancers, it has been suggested that early genetic events may direct the differentiation of ovarian epithelial cells. A number of genetic alterations are frequently encountered during ovarian tumorigenesis, including oncogenic activities of KRAS, BRAF and AKT, and silencing mutations of TP53, RB and PTEN. However, knowledge about how these genetic elements are coordinated during ovarian cancer initiation and progression is very limited. The establishment of cell-culture systems and rodentbased models has made big strides towards a better understanding of the genetic bases of human epithelial ovarian tumorigenesis. More importantly, the rise of genetically-engineered rodent and human models, particularly in the past five years, has provided key insight in the role of specific genes during ovarian tumorigenesis. In this review, we offer a comprehensive coverage of currently-available in vitro and in vivo models of human epithelial ovarian cancer, focusing on latest updates of genetically-modified rodent and human models and the valuable information conveyed by them.
AB - Despite rapid advances in understanding ovarian cancer etiology, epithelial ovarian cancer remains the most lethal form of gynecologic cancers in the United States. The four morphologically-defined epithelial ovarian cancer subtypes-serous, endometrioid, mucinous, and clear cell carcinomas - are generally believed to originate from ovarian epithelial cells. Although it remains unclear how this single cell layer gives rise to morphologically distinct cancers, it has been suggested that early genetic events may direct the differentiation of ovarian epithelial cells. A number of genetic alterations are frequently encountered during ovarian tumorigenesis, including oncogenic activities of KRAS, BRAF and AKT, and silencing mutations of TP53, RB and PTEN. However, knowledge about how these genetic elements are coordinated during ovarian cancer initiation and progression is very limited. The establishment of cell-culture systems and rodentbased models has made big strides towards a better understanding of the genetic bases of human epithelial ovarian tumorigenesis. More importantly, the rise of genetically-engineered rodent and human models, particularly in the past five years, has provided key insight in the role of specific genes during ovarian tumorigenesis. In this review, we offer a comprehensive coverage of currently-available in vitro and in vivo models of human epithelial ovarian cancer, focusing on latest updates of genetically-modified rodent and human models and the valuable information conveyed by them.
KW - Epithelial ovarian cancer
KW - Genetically-modified animal models
KW - Ovarian epithelial cells
KW - Review
KW - Tumorigenesis
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U2 - 10.4161/cc.8.5.7848
DO - 10.4161/cc.8.5.7848
M3 - Review article
C2 - 19221485
AN - SCOPUS:62449340297
SN - 1538-4101
VL - 8
SP - 731
EP - 735
JO - Cell Cycle
JF - Cell Cycle
IS - 5
ER -