Endometrial intraepithelial neoplasia: Difference between revisions
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EIN arises due to genetic and hormonal factors that lead to the abnormal growth of endometrial cells. One of the key genetic alterations associated with EIN is the inactivation of the [[PTEN]] tumor suppressor gene. This inactivation results in unregulated cell proliferation and increased risk of progression to cancer. | EIN arises due to genetic and hormonal factors that lead to the abnormal growth of endometrial cells. One of the key genetic alterations associated with EIN is the inactivation of the [[PTEN]] tumor suppressor gene. This inactivation results in unregulated cell proliferation and increased risk of progression to cancer. | ||
The condition is often associated with prolonged exposure to [[estrogen]] without the counterbalancing effect of [[progesterone]], which can occur in conditions such as [[polycystic ovary syndrome]] (PCOS), obesity, and [[estrogen replacement therapy]] without progesterone. | The condition is often associated with prolonged exposure to [[estrogen]] without the counterbalancing effect of [[progesterone]], which can occur in conditions such as [[polycystic ovary syndrome]] (PCOS), obesity, and [[estrogen replacement therapy]] without progesterone. | ||
Latest revision as of 18:37, 21 February 2025
Endometrial Intraepithelial Neoplasia[edit]
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Endometrial intraepithelial neoplasia (EIN) is a precancerous condition of the endometrium, the lining of the uterus. It is characterized by an abnormal proliferation of the endometrial glands, which can lead to the development of endometrial cancer. EIN is considered a precursor lesion to endometrioid endometrial carcinoma, the most common type of endometrial cancer.
Pathophysiology[edit]
EIN arises due to genetic and hormonal factors that lead to the abnormal growth of endometrial cells. One of the key genetic alterations associated with EIN is the inactivation of the PTEN tumor suppressor gene. This inactivation results in unregulated cell proliferation and increased risk of progression to cancer.
The condition is often associated with prolonged exposure to estrogen without the counterbalancing effect of progesterone, which can occur in conditions such as polycystic ovary syndrome (PCOS), obesity, and estrogen replacement therapy without progesterone.
Diagnosis[edit]
The diagnosis of EIN is typically made through endometrial biopsy or dilation and curettage (D&C). Histopathological examination reveals glandular crowding, architectural complexity, and cytological atypia. Immunohistochemical staining for PTEN can aid in the diagnosis by demonstrating loss of PTEN expression in the affected tissue.
Treatment[edit]
Management of EIN involves addressing the underlying hormonal imbalance and may include the use of progestin therapy to counteract the effects of estrogen. In cases where there is a high risk of progression to cancer, surgical intervention such as hysterectomy may be recommended.
Prognosis[edit]
The prognosis for patients with EIN depends on the timely diagnosis and appropriate management of the condition. With effective treatment, the risk of progression to endometrial cancer can be significantly reduced.
