Estrogen upregulates DNA2 expression through the PI3K-AKT pathway in endometrial carcinoma / 浙江大学学报(英文版)(B辑:生物医学和生物技术)
Journal of Zhejiang University. Science. B
;
(12): 262-268, 2023.
Article
in English
| WPRIM
| ID: wpr-971485
ABSTRACT
Endometrial cancer is the most common gynecological malignancy, affecting up to 3% of women at some point during their lifetime (Morice et al., 2016; Li and Wang, 2021). Based on the pathogenesis and biological behavioral characteristics, endometrial cancer can be divided into estrogen-dependent (I) and non-estrogen-dependent (II) types (Ulrich, 2011). Type I accounts for approximately 80% of cases, of which the majority are endometrioid carcinomas, and the remaining are mucinous adenocarcinomas (Setiawan et al., 2013). It is generally recognized that long-term stimulation by high estrogen levels with the lack of progesterone antagonism is the most important risk factor; meanwhile, there is no definite conclusion on the specific pathogenesis. The incidence of endometrial cancer has been on the rise during the past two decades (Constantine et al., 2019; Gao et al., 2022; Luo et al., 2022). Moreover, the development of assisted reproductive technology and antiprogestin therapy following breast cancer surgery has elevated the risk of developing type I endometrial cancer to a certain extent (Vassard et al., 2019). Therefore, investigating the influence of estrogen in type I endometrial cancer may provide novel concepts for risk assessment and adjuvant therapy, and at the same time, provide a basis for research on new drugs to treat endometrial cancer.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Breast Neoplasms
/
Endometrial Neoplasms
/
DNA Helicases
/
Phosphatidylinositol 3-Kinases
/
Estrogens
/
Proto-Oncogene Proteins c-akt
Limits:
Female
/
Humans
Language:
English
Journal:
Journal of Zhejiang University. Science. B
Year:
2023
Type:
Article
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