ENDOMETRIUM KANSERI PDF

Tabar This type tends to be less differentiated and spread early via lymphatics or through Fallopian tubes into peritoneum, hence it is associated with poorer prognosis compared to type I lesions. Aside from this we also use screening methods such as ultrasound and tomography. Peripheral blood samples were taken and serum CA and HE-4 were tested. Hence, it is not possible for the patient to have children once she is diagnosed with endometrial cancer and goes through the surgical treatment. Currently, no clinically useful tumor marker is available for primary diagnosis in endometrial cancer.

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Usually, when cells grow old or get damaged, they die , and new cells take their place. Cancer starts when new cells form unneeded, and old or damaged cells do not die as they should. The buildup of extra cells often forms a mass of tissue called a growth or tumor.

These abnormal cancer cells have many genetic abnormalities that cause them to grow excessively. When a mutant version of p53 is overexpressed, the cancer tends to be particularly aggressive. Serous carcinomas are thought to develop from endometrial intraepithelial carcinoma.

Epigenetic silencing and point mutations of several genes are commonly found in Type I endometrial cancer. Pre-cancerous endometrial hyperplasias are also referred to as endometrial intraepithelial neoplasia.

This tissue is then examined histologically for characteristics of cancer. If cancer is found, medical imaging may be done to see whether the cancer has spread or invaded tissue. Examination[ edit ] Vaginal ultrasonography with an endometrial fluid accumulation darker area in a postmenopausal uterus, a finding that is highly suspicious for endometrial cancer Polypoidal endometrial carcinoma Routine screening of asymptomatic people is not indicated, since the disease is highly curable in its early, symptomatic stages.

Instead, women, particularly menopausal women, should be aware of the symptoms and risk factors of endometrial cancer. Changes in the size, shape or consistency of the uterus or its surrounding, supporting structures may exist when the disease is more advanced.

Some women with Lynch syndrome elect to have a prophylactic hysterectomy and salpingo-oophorectomy to greatly reduce the risk of endometrial and ovarian cancer. Ultrasound findings alone are not conclusive in cases of endometrial cancer, so another screening method for example endometrial biopsy must be used in conjunction. Other imaging studies are of limited use.

CT scans are used for preoperative imaging of tumors that appear advanced on physical exam or have a high-risk subtype at high risk of metastasis. Endometrial biopsy is the less invasive option, but it may not give conclusive results every time. Hysteroscopy only shows the gross anatomy of the endometrium, which is often not indicative of cancer, and is therefore not used, unless in conjunction with a biopsy.

These include a chest x-ray, liver function tests , kidney function tests , [21] and a test for levels of CA , a tumor marker that can be elevated in endometrial cancer.

Some tumors are difficult to classify and have features overlapping more than one category. High grade endometrioid tumors in particular tend to have both type I and type II features. There are many microscopic subtypes of endometrial carcinoma, but they are broadly organized into two categories, Type I and Type II, based on clinical features and pathogenesis.

The two subtypes are genetically distinct. In the United States they are more common in white women , particularly those with a history of endometrial hyperplasia. Type I endometrial cancers are often low-grade, minimally invasive into the underlying uterine wall myometrium , estrogen-dependent, and have a good outcome with treatment.

Type II endometrial cancers are often high-grade, with deep invasion into the underlying uterine wall myometrium , are of the serous or clear cell type, and carry a poorer prognosis.

They can appear to be epithelial ovarian cancer on evaluation of symptoms. Low-grade endometrioid adenocarcinomas have well differentiated cells, have not invaded the myometrium, and are seen alongside endometrial hyperplasia. Higher-grade endometrioid adenocarcinomas have less well-differentiated cells, have more solid sheets of tumor cells no longer organized into glands, and are associated with an atrophied endometrium. There are several subtypes of endometrioid adenocarcinoma with similar prognoses, including villoglandular, secretory, and ciliated cell variants.

There is also a subtype characterized by squamous differentiation. Some endometrioid adenocarcinomas have foci of mucinous carcinoma. The CTNNB1 beta-catenin gene is most commonly mutated in the squamous subtype of endometrioid adenocarcinoma.

Serous endometrial carcinoma is aggressive and often invades the myometrium and metastasizes within the peritoneum seen as omental caking or the lymphatic system. Histologically, it appears with many atypical nuclei, papillary structures , and, in contrast to endometrioid adenocarcinomas, rounded cells instead of columnar cells. Like serous cell carcinoma, it is usually aggressive and carries a poor prognosis. Mucinous endometrial carcinomas are most often stage I and grade I, giving them a good prognosis.

They typically have well-differentiated columnar cells organized into glands with the characteristic mucin in the cytoplasm. Mucinous carcinomas must be differentiated from cervical adenocarcinoma. They have a worse prognosis than grade III tumors. Histologically, these tumors show sheets of identical epithelial cells with no identifiable pattern.

Squamous cell carcinoma of the endometrium has a poor prognosis. For primary squamous cell carcinoma of the endometrium PSCCE to be diagnosed, there must be no other primary cancer in the endometrium or cervix and it must not be connected to the cervical epithelium. Because of the rarity of this cancer, there are no guidelines for how it should be treated, nor any typical treatment.

The common genetic causes remain uncharacterized. Its pathophysiology and treatments have not been characterized.

They are generally non-aggressive and, if they recur, can take decades. Metastases to the lungs and pelvic or peritoneal cavities are the most frequent. ESS makes up 0. The cancer usually first spreads into the myometrium and the serosa , then into other reproductive and pelvic structures. When the lymphatic system is involved, the pelvic and para-aortic nodes are usually first to become involved, but in no specific pattern, unlike cervical cancer.

More distant metastases are spread by the blood and often occur in the lungs, as well as the liver, brain, and bone. Grade II cancers are intermediate between grades I and III in terms of cell differentiation and aggressiveness of disease. The most common finding is a well-differentiated endometrioid adenocarcinoma, [44] which is composed of numerous, small, crowded glands with varying degrees of nuclear atypia, mitotic activity, and stratification.

This often appears on a background of endometrial hyperplasia. Frank adenocarcinoma may be distinguished from atypical hyperplasia by the finding of clear stromal invasion, or "back-to-back" glands which represent nondestructive replacement of the endometrial stroma by the cancer. With progression of the disease, the myometrium is infiltrated.

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