الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Endometrial carcinoma is the most frequent gynecologic malignancy in industrialized countries. Factors contributing to the increased incidence of endometrial cancer include increasing life expectancy, increasing population obesity, fewer hysterectomies performed for benign disease and tamoxifen use. Most cases are diagnosed in women over 50, although 20-25% of women are pre-menopausal at diagnosis. Early recognition contributes to generally high cure rates but approximately25% of women will have poorer outcomes due to more aggressive histological types, later presentation and problems associated with co-morbid conditions such as cardiovascular disease. The great majority of primary endometrial cancers (>80%) are endometrioid adenocarcinomas. These usually arise on a background of atypical hyperplasia, a precursor lesion. Up to 50% of cases of severe atypical hyperplasia are upgraded to invasive endometrial cancer on the hysterectomy specimen. Endometrioid tumors are assigned a grade (1-3) depending on the degree of differentiation and nuclear features. Serous, clear cell, squamous and undifferentiated carcinomas are less common and have a poorer prognosis due to a tendency to early extra-uterine spread. Relatively little is known of the molecular events that precede a diagnosis of non-endometrioid carcinoma although a pre-cursor lesion for serous endometrial carcinoma Endometrial Intra-epithelial Carcinoma (EIC) has been identified. Other types of endometrial cancer are less common still. Endometrial cancers are rarely metastatic from other tumors. Breast carcinoma is the most likely to metastasize to the endometrium though metastases from ovary, lung, stomach, colorectal and melanoma are all reported.
Endometrial carcinomas spread by direct extension to the cervix, vagina and myometrium. Vaginal metastases can also occur as a result of haematogenous spread. Deeper myometrial invasion eventually leads to breach of the uterine serosa and parametrial involvement. Lymph node involvement in endometrial cancer is directly related to depth of myometrial invasion as well as grade.
Lymphatic spread occurs to the external iliac, internal iliac and obturator nodes in the pelvis and to para aortic nodes. Para-aortic node involvement is less common when the pelvic nodes are uninvolved although para-aortic spread can arise directly via lymphatic channels draining the upper uterus. Trans-tubal spread occurs via the fallopian tubes to the ov aries and peritoneal cavity. The lungs are the most common site for distant haematogenous metastasis. Non-endometrioid tumors have a tendency to early dissemination. Even minimal myometrial invasion in these tumors may be associated with extra-uterine disease. Expert histopathological assessment with accurate grading of disease, classification of histological sub-type and assessment of the final surgical specimen, is important in planning appropriate investigations and guiding treatment.
Surgical management of early-stage endometrial cancer includes peritoneal cytology, total hysterectomy with bilateral salpingo-oophorectomy and lymph node sampling. Histological grade, the depth of myometrial involvement and lymph node status are the main prognostic factors in endometrial cancer. Alternative modes for assessing the status of pelvic lymph nodes, including imaging techniques, have not yet equaled the ‘gold standard’ method, namely histological examination of nodes from the pelvic dissection specimen.
Lymphatic mapping with sentinel lymph node biopsy has emerged as an alternative to systematic lymphadenectomy, and also reduces the morbidity of this procedure. The sentinel no