<unk>  lesions was first described in the 1990s. Endometrial hyperplasia may be classified according to new World Health Organization (WHO2014) into two groups; hyperplasia without atypia (non-neoplastic) and atypical hyperplasia (endometrial<unk>  neoplasm).<unk>  arises from premalignant endometrial glands , which are risk of transmutatain to endometrial edometrioid carcinoma. Inactivation (mutation or deletion) of the PTEN tumor suppressor gene, inactivation of PAX2 gene, KRAS mutations, Microsatellite instability, Mutation in p53 gene are involved in the pathogenesis of<unk>  <unk> .<unk>  may be caused by estrogenic stimulation of the endometrium that is unopposed by progestin. On microscopic histopathological analysis, individual glands are lined by a single layer of pseudostratified epithelium which is a characteristic finding of<unk> . In 2002, the incidence of<unk>  <unk>  was estimated to be 144 cases per 100,000 individuals worldwide. The hallmark symptom of<unk>  is postmenopausal abnormal uterine bleeding. There are no specific laboratory findings associated with<unk> . Transvaginal ultrasonography is the imaging modality of choice for<unk> . Progestin therapy is recommended among patients with<unk> . Hysterectomy is the mainstay of treatment for<unk>  to prevent endometrial carcinoma.
Endometrial intraepithelial neoplasia
Cervical intraepithelial neoplasia
Cervical polyp
Cervical dysplasia
Adenomyosis
Endometrial cancer
Cervical cancer pathophysiology
Endometrial hyperplasia