Archive for the Uterine cancer category.
Sarcomas of the uterus are rare; they comprise only 3-5% of all uterine tumors. These tumors primarily arise from two tissues: endometrial sarcomas from endometrial glands and stroma and leiomyosarcomas from the uterine muscle itself. Other sarcomas arise in supporting tissues and are very rare. Sarcomas have been classified as pure (composed of one cell type only) and mixed (composed of more than one cell type). The site of origin has also been used in the classification of sarcomas, with homologous tumors defined as those that contain tissue elements entirely indigenous to the uterus and heterologous tumors defined as those that contain tissue elements foreign to the uterus. Although several classifications have been suggested and used over the years, a simplified classification is endorsed by the Gynecologic Oncology Group and has been used successfully:
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• Leiomyosarcomas
• Endometrial stromal sarcomas
• Mixed homologous müllerian sarcomas (carcinosarcomas)
• Mixed heterologous müllerian sarcomas (mixed mesodermal sarcoma)
• Other uterine sarcomas
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Particularly with leiomyosarcomas, the diagnosis of this entity is determined almost solely on the basis of mitotic index (the number of mitoses per 10 high-power fields). Cellular atypia has also been used by some investigators.
Sarcomas are usually found in postmenopausal women; leiomyosarcomas are identified about 10 years earlier than mixed mesodermal sarcomas and endometrial stromal sarcoma. Menorrhagia and postmenopausal bleeding are common symptoms. Abdominal pain or mass is a frequent complaint. Particularly in the postmenopausal patient, a rapidly enlarging uterus should suggest sarcoma as a possible etiology. A large friable polypoid mass extending through a dilated cervix into the vagina also should raise suspicion of sarcoma, particularly in the postmenopausal patient. A mixed mesodermal tumor and endometrial stromal sarcoma can usually be diagnosed with a directed or endometrial biopsy, whereas a leiomyosarcoma may or may not be identified preoperatively.
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Total abdominal hysterectomy and bilateral salpingo-oophorectomy are considered the hallmarks of therapy for uterine sarcomas. In many instances, patients with sarcomas tend to have extrauterine disease, which may be present intraperitoneally or in the lymph nodes. This is particularly true for homologous and heterologous mixed müllerian tumors. Although radiation therapy has been used for a long time in patients with uterine sarcoma, it has not been associated with any improvement in survival compared with surgery alone. There does appear to be less local recurrence after radiation therapy, but because most patients that have recurrence have it at distant sites, the overall survival has not been affected. Adjunctive therapy with chemotherapeutic agents has been evaluated; however, none have been shown to improve survival even in patients with limited disease. Unfortunately, many patients with stage I uterine sarcomas will develop a recurrence. The use of adjuvant chemotherapy has to date minimally affected the survival of these patients. Preliminary data regarding the use of ifosfamide, mesna, and cisplatin suggest encouraging response rates, but their impact on survival awaits further evaluation.
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Estrogen Replacement Therapy after Endometrial Cancer
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Estrogen replacement therapy can be used safely in patients who have had endometrial cancer. This suggestion is based on the fact that patients with a disease with a good prognosis, although estrogen-progesterone receptor positive, nevertheless have no remaining cancer cells after their treatment. Those patients with a lesion with a poor prognosis are usually receptor poor; therefore, replacement therapy theoretically would have no impact on development of recurrences. There are now five studies in the literature (none of them prospective and randomized), and all suggest that hormone replacement therapy is not detrimental to these patients. Some investigators will start the patient taking estrogen replacement therapy immediately after primary therapy for her cancer, although others think that waiting a number of months or even years is necessary to be safe. A Committee Opinion of the American College of Obstetricians and Gynecologists stated that in women with a history of endometrial carcinoma, estrogens can be used for the same indications as they are used for any other woman, except that the selection of appropriate candidates should be based on prognostic indicators and the risk that the patient is willing to assume. A prospective, randomized study of estrogen replacement therapy in endometrial cancer patients is anticipated to begin shortly under the auspices of the Gynecology Oncology Group. The experience over the last 10-15 years would suggest that if estrogen replacement therapy is detrimental to patients with endometrial cancer, the risk is extremely small. Because most patients with endometrial cancer are long-term survivors, the risks of cardiovascular disease and osteoporosis appear to be significant and higher than the risk of recurrence of the endometrial cancer. Benefits of estrogen replacement therapy, therefore, appear to greatly outweigh the theoretical risk in patients who have had endometrial cancer.
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Endometrial Hyperplasia
Both the diagnosis and management of endometrial hyperplasia have generated tremendous confusion. The natural history would suggest that some of these lesions revert to normal spontaneously or with medical therapy, some persist, and a few will progress to endometrial adenocarcinoma. Most endometrial hyperplasias are thought to result from persistent or prolonged estrogenic stimulation of the endometrium, either endogenously (anovulatory cycle or hormone-producing tumor) or with unopposed exogenous estrogen. In the mid-1980s, a new classification was developed by the International Society of Gynecologic Pathologists, which eliminated a plethora of terms that carried different connotations.
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The diagnosis of endometrial hyperplasia is made pathologically, usually on an endometrial biopsy that is obtained because of irregular or postmenopausal bleeding. Four categories of hyperplasia are now recognized: simple, simple atypical, complex, and complex atypical. It would appear that only those patients with atypical hyperplasia are at risk of developing endometrial cancer if the hyperplasia is allowed to go untreated for varying periods (up to and more than 10 years). The diagnosis of atypical hyperplasia is based on cytologic atypia. Architectural changes that previously were thought to indicate high risk for developing endometrial cancer no longer carry that implication unless atypia is present. Even when complex atypical hyperplasia is present, data suggest that only one fourth to one third of these patients might develop endometrial adenocarcinoma some years in the future.
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In the patient who has atypical hyperplasia on an endometrial biopsy, a thorough curettage is usually recommended because as many as one third of these patients will have a coexistent adenocarcinoma. In the patient with hyperplasia without atypia, curettage is usually not warranted. Hyperplasias, both with and without atypia, can be treated successfully in most instances with progestins. Various progesterone regimens (ie, use of medroxyprogesterone acetate or its equivalent for a few months) have been effective. The younger patient usually needs a higher dose. The goal is to make the endometrium atrophic, and a rebiopsy is recommended 2-3 months after commencement of the pro-gestin therapy. If hyperplasia persists on biopsy, progestin may be continued for another period. In many patients with atypical hyperplasia, particularly if they are postmenopausal, a simple hysterectomy and bilateral salpingo-oophorectomy have been advocated. These surgical patients may use estrogen replacement therapy postoperatively.
Simple hysterectomy and bilateral salpingo-oophorectomy remain the hallmarks of therapy for corpus cancer. After complete surgical staging, if disease is limited to the uterus, most patients need no further therapy. The one exception is patients with a poorly differentiated, deeply invasive cancer. Nonrandomized studies controlled for prognostic factors suggest that pelvic radiation in this group may prevent both local and distant recurrence. In all other instances, radiation therapy did not appear to be of benefit. In the only prospective, randomized study comparing radiation with no radiation, it appeared that radiation decreased local recurrence but overall survival was the same.
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The role of brachytherapy postoperatively does not appear to be efficacious in most surgical stage I cancers because vaginal vault recurrence appears to be no more than 1-2%, irrespective of whether the patient receives radiation. Fortunately, most adenocarcinomas of the endometrium are surgical stage I, and most of those are adequately treated with surgery only.
When disease is present outside of the uterus, there is no general agreement as to optimal therapy. Unfortunately, prospective, randomized studies have not been done, and the clinician’s experience, both published and unpublished, affects the therapeutic recommendation. The question that has been raised is whether surgical staging is only diagnostic and therefore has no impact on survival. Data are now appearing in the literature suggesting that lymphadenectomy can be therapeutic to a greater degree than simple hysterectomy and bilateral salpingo-oophorectomy patients with true stage II disease has not been investigated in any depth. Again, most oncologists would probably treat these patients with postoperative radiation, although some have suggested that surgery may be definitive, particularly for those with stage IIA cancers. The role of radical hysterectomy in patients with clinical stage II disease has essentially been discarded from our armamentarium. In patients with surgical stage III and IV disease, treatment is usually individualized and combination therapy with surgery and radiation is common. The use of chemotherapy and hormones both in adjuvant and therapeutic modes in patients with advanced disease has not proved to be efficacious. Multiple regimens have been attempted, but response rates remain suboptimal.
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Recurrent disease historically has been treated in many different ways. If a local recurrence appears in the vaginal vault, surgery alone or in combination with radiation therapy has saved many of these patients. If recurrence is in the lower vagina, success has been limited. For metastatic disease, progestins have been primarily used; reports have noted an objective response in about one third of patients. More recent data suggest that the response rate is 15-20%. Original grade of tumor, length of time from primary treatment to recurrence, and hormone receptor status of the original tumor all appear to be indicative of the patient’s response to progestin. Several cytotoxic agents have been used with objective responses noted. The most experience has been with adriamycin and cyclophosphamide, cisplatin with or without adriamycin, and more recently paclitaxel. Unfortunately, when there is a response, it is relatively short lived. The ideal single or combination regimen for recurrent endometrial cancer has not yet been identified.
Stage IA G 1, 2, 3 Tumor limited to endometrium
Stage IB G 1, 2, 3 Invasion to less than one half of the myometrium
Stage IC G 1, 2, 3 Invasion to more than one half of the myometrium
Stage IIA G 1, 2, 3 Endocervical glandular involvement only
Stage IIB G 1, 2, 3 Cervical stromal invasion
Stage IIIA G 1, 2, 3 Tumor invades serosa and/or adnexa, and/or positive peritoneal cytology
Stage IIIB G 1, 2, 3 Vaginal metastases
Stage IIIC G 1, 2, 3 Metastases to pelvic and/or paraaortic lymph nodes
Stage IVAG 1, 2, 3 Tumor invasion of bladder and/or bowel mucosa
Stage IVB Distant metastases including intraabdominal and/or inguinal lymph nodes
Histopathology–Degree of Differentiation
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Cases of carcinoma of the corpus should be classified (or graded) according to the degree of
histologic differentiation as follows:
G1 = 5% or less of a nonsquamous or nonmorular solid growth pattern
G2 = 6-50% of a nonsquamous or nonmorular solid growth pattern
G3 = more than 50% of a nonsquamous or nonmorular solid growth pattern
Notes on Pathological Grading
1. Notable nuclear atypia, inappropriate for the architectural grade, raises the grade of a grade 1 or grade 2 tumor by 1.
2. In serous adenocarcinomas, clear-cell adenocarcinomas, and squamous cell carcinomas, nuclear grading takes precedence.
3. Adenocarcinomas with benign squamous differentiation are graded according to the nuclear grade of the glandular component.
Rules Related to Staging
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1. Because corpus cancer is now staged surgically, procedures previously used for determination of stages are no longer applicable, such as the findings from fractional dilation and curettage to differentiate between stage I and stage II.
2. It is appreciated that there may be a small number of patients with corpus cancer who will be treated primarily with radiation therapy. If that is the case, the clinical staging adopted by FIGO in 1971 would still apply, but designation of that staging system would be noted.
3. Ideally, width of the myometrium should be measured along with the width of tumor invasion.
Many of the prognostic factors noted above require surgical staging for adequate delineation. Until 1988, staging for endometrial cancer was clinical. It became readily apparent that clinical staging failed to identify the true extent of disease in a large number of patients. Up to one fourth of patients who were thought to have clinical stage disease I had extrauterine disease when surgical staging was done. The margin of error for stage II was even greater, with studies suggesting that 50-60% of patients who were thought to have stage II disease in fact did not. In many instances, the patients had only stage I disease. This misclassification resulted in radiation therapy that probably was unnecessary. Because of lack of sensitivity of clinical staging, FIGO in 1988 determined that corpus cancer should be surgically staged (see the box). Initially, concern was voiced that a considerable number of patients with this disease were elderly and could not withstand the surgical procedure or were quite obese, making surgery technically difficult to perform. Experience has shown that this number appears to be very small. With surgical staging, more specific postoperative therapy, if indicated, could be optimally identified and directed. The role of preoperative radiation in this disease entity has become minimal.
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Endometrial cancer is a surgically staged disease, and many of the traditional diagnostic procedures advocated before 1988 are no longer necessary. These include a fractional dilation and curettage and endocervical curettage. A chest X-ray is important pretreatment and could affect final staging. Other scanning techniques, unless clinically indicated, are not advocated on a routine basis.
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Surgical staging consists of primary total abdominal hysterectomy and bilateral salpingo-oophorectomy as well as full surgical staging. This includes peritoneal cytology on opening the abdomen, surgical exploration of the abdominal contents, appropriate biopsies, and bilateral pelvic and paraaortic lymphadenectomy. The universal role of the lymphadenectomy continues to be debated, particularly in patients with well-differentiated adenocarcinomas that are superficially invasive. Data suggest that the chance of lymph node metastasis in this group of patients approaches zero, although some authors have found occasional metastasis in this group of patients. The incidence of nodal metastasis, both pelvic and paraaortic, in patients with poorly differentiated or deeply invasive lesions is high enough to warrant the added surgical procedure. Although this lymphadenectomy was originally termed “selective” or “limited,” it is felt that a fairly thorough lymphadenectomy should be performed. Some investigators have suggested that lymph nodes on top of the vessels from the inguinal ligament to the retroperitoneal duodenum should be removed as well as those from the obturator space above the nerve. Numerous nodes should be obtained with such a procedure. The practice of identifying clinically enlarged nodes as those to be removed should not be advocated because the vast majority of metastases to lymph nodes from carcinoma of the uterus are usually microscopic. Such a practice can create a false sense of security.
Multiple prognostic factors have been identified in endometrial adenocarcinoma. Patient age, histology, degree of differentiation, depth of invasion, and surgical staging are all important prognostic factors. Younger patients have a better prognosis than older individuals. This may be because younger patients tend to have a better-differentiated, superficially invasive cancer. Adenocarcinoma with its variants are by far the most common histologic type. Current data suggest that grade of adenocarcinoma is a more important prognostic indicator than presence of a squamous component.
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Uterine papillary serous carcinoma is recognized as a distinct, highly aggressive carcinoma of the uterus. Patients tend to be older, parous, not obese, and with a high tumor grade. Extrauterine disease is identified frequently with uterine papillary serous carcinoma. Even when disease appears to be limited to the uterus, prognosis is considerably poorer than with adenocarcinoma of similar extent. Fortunately, these tumors are unusual; however, they appear to be diagnosed with increasing frequency. Clear-cell carcinomas occur infrequently, and most studies suggest that clear-cell carcinomas have a poorer prognosis than pure adenocarcinomas.
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The differentiation of the adenocarcinoma has long been recognized as an important prognostic factor. Surgical stage I disease survival is directly related to the grade of the tumor. The grade of the tumor correlates generally with the depth of uterine muscle invasion. As the tumor becomes less differentiated, the chances of deep myometrial involvement increase. These two factors correlate well with extrauterine disease. As a general rule, cancers that are poorly differentiated are associated with greater adnexal and lymph node metastasis and other extrauterine spread. This is also true as the depth of myometrial invasion increases. The role of full surgical staging in determining true extent of the disease becomes apparent. Most studies suggest that the presence of malignant cells in peritoneal cytology is a poor prognostic factor. Tumor cells found in capillary-like spaces within the myometrium have been shown to be predictive of extrauterine metastasis, particularly to the lymph nodes. Other prognostic factors that have been suggested include hormone receptor status, tumor ploidy analysis, and S-phase fraction. Although predictive of prognosis, they have not generally been used in the routine evaluation of endometrial cancer.