Biomaterial Database

Estrogen dependency in uterine endometrial cancers. 1998

J Fujimoto, and R Hirose, and H Sakaguchi, and T Tamaya

Department of Obstetrics and Gynecology, Gifu University School of Medicine, Tsukasa-machi, Gifu City, Japan.

Estrogen dependency in uterine endometrial cancers involves complicated tumor biology. A transformed phenotype of uterine endometrial cancers is supported by estrogen-dependent oncogene (c-Ha-ras, c-fos and c-jun) expressions. The relative overexpression of estrogen receptor exon 5 splicing variant and the damaged expression of progesterone receptor A, which belong to a lack of estrogen dependency, are related to metastatic potential. The estrogen-related metastatic processes, detachment, invasion and angiogenesis in some uterine endometrial cancers can be inhibited by progestins.

UI	MeSH Term	Description	Entries
D009361	Neoplasm Invasiveness	Ability of neoplasms to infiltrate and actively destroy surrounding tissue.	Invasiveness, Neoplasm,Neoplasm Invasion,Invasion, Neoplasm
D009376	Neoplasms, Hormone-Dependent	Certain tumors that 1, arise in organs that are normally dependent on specific hormones and 2, are stimulated or caused to regress by manipulation of the endocrine environment.	Hormone-Dependent Neoplasms,Hormone Dependent Neoplasms,Hormone-Dependent Neoplasm,Neoplasm, Hormone-Dependent,Neoplasms, Hormone Dependent
D011960	Receptors, Estrogen	Cytoplasmic proteins that bind estrogens and migrate to the nucleus where they regulate DNA transcription. Evaluation of the state of estrogen receptors in breast cancer patients has become clinically important.	Estrogen Receptor,Estrogen Receptors,Estrogen Nuclear Receptor,Estrogen Receptor Type I,Estrogen Receptor Type II,Estrogen Receptors Type I,Estrogen Receptors Type II,Receptor, Estrogen Nuclear,Receptors, Estrogen, Type I,Receptors, Estrogen, Type II,Nuclear Receptor, Estrogen,Receptor, Estrogen
D011980	Receptors, Progesterone	Specific proteins found in or on cells of progesterone target tissues that specifically combine with progesterone. The cytosol progesterone-receptor complex then associates with the nucleic acids to initiate protein synthesis. There are two kinds of progesterone receptors, A and B. Both are induced by estrogen and have short half-lives.	Progesterone Receptors,Progestin Receptor,Progestin Receptors,Receptor, Progesterone,Receptors, Progestin,Progesterone Receptor,Receptor, Progestin
D004967	Estrogens	Compounds that interact with ESTROGEN RECEPTORS in target tissues to bring about the effects similar to those of ESTRADIOL. Estrogens stimulate the female reproductive organs, and the development of secondary female SEX CHARACTERISTICS. Estrogenic chemicals include natural, synthetic, steroidal, or non-steroidal compounds.	Estrogen,Estrogen Effect,Estrogen Effects,Estrogen Receptor Agonists,Estrogenic Agents,Estrogenic Compounds,Estrogenic Effect,Estrogenic Effects,Agents, Estrogenic,Agonists, Estrogen Receptor,Compounds, Estrogenic,Effects, Estrogen,Effects, Estrogenic,Receptor Agonists, Estrogen
D005260	Female		Females
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D013997	Time Factors	Elements of limited time intervals, contributing to particular results or situations.	Time Series,Factor, Time,Time Factor
D015854	Up-Regulation	A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.	Receptor Up-Regulation,Upregulation,Up-Regulation (Physiology),Up Regulation
D015972	Gene Expression Regulation, Neoplastic	Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.	Neoplastic Gene Expression Regulation,Regulation of Gene Expression, Neoplastic,Regulation, Gene Expression, Neoplastic