Am J Clin Exp Obstet Gynecol 2013;1(1):1-16
Review Article
From endometrial glandular dysplasia to endometrial serous carcinoma:
insights into underlying biological aspects
Lucy M Han, Linxuan Wei, Donna C Ferguson, Setsuko K Chambers, Oluwole Fadare, Yiying Wang, Wenxin Zheng
College of Medicine, University of Arizona, Tucson, AZ, USA; Department of Obstetrics and Gynecology, Qilu Hospital,
Shandong University, Jinan, Shandong, China; Department of Obstetrics and Gynecology, University of Arizona,
Tucson, AZ, USA; Arizona Cancer Center, University of Arizona, Tucson, AZ, USA; Department of Pathology,
Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Obstetrics and
Gynecology, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Obstetrics and Gynecology,
Henan Province People’s Hospital, Zhengzhou, Henan, China; Department of Pathology, University of Arizona College
of Medicine, Tucson, AZ, USA
Received November 3, 2013; Accepted November 18, 2013; Epub December 7, 2013; Published December 15, 2013
Abstract: Endometrial serous carcinoma (ESC), a clinically aggressive gynecologic cancer, is the prototypical type II
endometrial carcinoma. In 2004, we first proposed a model of endometrial serous carcinogenesis that has, with
additional evidence, developed into a robust, step-wise model of ESC development based on the progressive
accumulation of molecular alterations. In this model, the cancer progresses from a resting endometrium into
endometrial glandular dysplasia (EmGD), then serous endometrial intraepithelial carcinoma (SEIC), and eventually
advances into ESC. Though various studies have discussed the key molecular alterations involved in ESC
development, the pathways and relationships between different players are unclear. In this review, we have
summarized the current state of knowledge on key pathways and on relationships between the molecular factors
involved in endometrial serous carcinogenesis and discussed potential prevention and therapeutic strategies.
(AJCEOG1311001).
Keywords: Endometrial serous carcinoma, endometrial glandular dysplasia, endometrial intraepithelial carcinoma,
p53 mutation, PI3K-AKT-mTOR pathway, targeted therapies
Address correspondence to: Dr. Wenxin Zheng, Department Pathology and Gynecology, College of Medicine,
University of Arizona, Tucson, AZ 85724, USA. Tel: 520-626-6032; Fax: 520-626-1027; E-mail: zhengw@email.arizona.
edu
Review Article
From endometrial glandular dysplasia to endometrial serous carcinoma:
insights into underlying biological aspects
Lucy M Han, Linxuan Wei, Donna C Ferguson, Setsuko K Chambers, Oluwole Fadare, Yiying Wang, Wenxin Zheng
College of Medicine, University of Arizona, Tucson, AZ, USA; Department of Obstetrics and Gynecology, Qilu Hospital,
Shandong University, Jinan, Shandong, China; Department of Obstetrics and Gynecology, University of Arizona,
Tucson, AZ, USA; Arizona Cancer Center, University of Arizona, Tucson, AZ, USA; Department of Pathology,
Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Obstetrics and
Gynecology, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Obstetrics and Gynecology,
Henan Province People’s Hospital, Zhengzhou, Henan, China; Department of Pathology, University of Arizona College
of Medicine, Tucson, AZ, USA
Received November 3, 2013; Accepted November 18, 2013; Epub December 7, 2013; Published December 15, 2013
Abstract: Endometrial serous carcinoma (ESC), a clinically aggressive gynecologic cancer, is the prototypical type II
endometrial carcinoma. In 2004, we first proposed a model of endometrial serous carcinogenesis that has, with
additional evidence, developed into a robust, step-wise model of ESC development based on the progressive
accumulation of molecular alterations. In this model, the cancer progresses from a resting endometrium into
endometrial glandular dysplasia (EmGD), then serous endometrial intraepithelial carcinoma (SEIC), and eventually
advances into ESC. Though various studies have discussed the key molecular alterations involved in ESC
development, the pathways and relationships between different players are unclear. In this review, we have
summarized the current state of knowledge on key pathways and on relationships between the molecular factors
involved in endometrial serous carcinogenesis and discussed potential prevention and therapeutic strategies.
(AJCEOG1311001).
Keywords: Endometrial serous carcinoma, endometrial glandular dysplasia, endometrial intraepithelial carcinoma,
p53 mutation, PI3K-AKT-mTOR pathway, targeted therapies
Address correspondence to: Dr. Wenxin Zheng, Department Pathology and Gynecology, College of Medicine,
University of Arizona, Tucson, AZ 85724, USA. Tel: 520-626-6032; Fax: 520-626-1027; E-mail: zhengw@email.arizona.
edu
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