WordNet
- any malignant tumor derived from epithelial tissue; one of the four major types of cancer
- of or relating to the endometrium
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/12/22 15:08:08」(JST)
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| Endometrial cancer | |
|---|---|
| Synonyms | Uterine cancer |
| The location and development of endometrial cancer. | |
| Specialty | Oncology, gynecology |
| Symptoms | Vaginal bleeding, pain with urination or sexual intercourse, pelvic pain[1] |
| Usual onset | After menopause[2] |
| Risk factors | Obesity, excessive estrogen exposure, high blood pressure, diabetes, family history[1][3] |
| Diagnostic method | Endometrial biopsy[1] |
| Treatment | Abdominal hysterectomy, radiation therapy, chemotherapy, hormone therapy[4] |
| Prognosis | five-year survival rate ~80% (US)[5] |
| Frequency | 3.8 million (total affected in 2015)[6] |
| Deaths | 89,900 (2015)[7] |
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Endometrial cancer is a cancer that arises from the endometrium (the lining of the uterus or womb).[1] It is the result of the abnormal growth of cells that have the ability to invade or spread to other parts of the body.[8] The first sign is most often vaginal bleeding not associated with a menstrual period.[1] Other symptoms include pain with urination, pain during sexual intercourse, or pelvic pain.[1] Endometrial cancer occurs most commonly after menopause.[2]
Approximately 40% of cases are related to obesity.[3] Endometrial cancer is also associated with excessive estrogen exposure, high blood pressure and diabetes.[1] Whereas taking estrogen alone increases the risk of endometrial cancer, taking both estrogen and a progestogen in combination, as in most birth control pills, decreases the risk.[1][3] Between two and five percent of cases are related to genes inherited from the parents.[3] Endometrial cancer is sometimes loosely referred to as "uterine cancer", although it is distinct from other forms of uterine cancer such as cervical cancer, uterine sarcoma, and trophoblastic disease.[9] The most frequent type of endometrial cancer is endometrioid carcinoma, which accounts for more than 80% of cases.[3] Endometrial cancer is commonly diagnosed by endometrial biopsy or by taking samples during a procedure known as dilation and curettage.[1] A pap smear is not typically sufficient to show endometrial cancer.[4] Regular screening in those at normal risk is not called for.[10]
The leading treatment option for endometrial cancer is abdominal hysterectomy (the total removal by surgery of the uterus), together with removal of the fallopian tubes and ovaries on both sides, called a bilateral salpingo-oophorectomy.[4] In more advanced cases, radiation therapy, chemotherapy or hormone therapy may also be recommended.[4] If the disease is diagnosed at an early stage, the outcome is favorable,[4] and the overall five-year survival rate in the United States is greater than 80%.[5]
In 2012, endometrial cancers newly occurred in 320,000 women and caused 76,000 deaths.[3] This makes it the third most common cause of death in cancers which only affect women, behind ovarian and cervical cancer.[3] It is more common in the developed world[3] and is the most common cancer of the female reproductive tract in developed countries.[4] Rates of endometrial cancer have risen in a number of countries between the 1980s and 2010.[3] This is believed to be due to the increasing number of elderly people and increasing rates of obesity.[11]
Contents
- 1 Signs and symptoms
- 2 Risk factors
- 2.1 Hormones
- 2.2 Genetics
- 2.3 Other health problems
- 2.4 Protective factors
- 3 Pathophysiology
- 4 Diagnosis
- 4.1 Examination
- 4.2 Classification
- 4.2.1 Carcinoma
- 4.2.1.1 Endometrioid adenocarcinoma
- 4.2.1.2 Serous carcinoma
- 4.2.1.3 Clear cell carcinoma
- 4.2.1.4 Mucinous carcinoma
- 4.2.1.5 Mixed or undifferentiated carcinoma
- 4.2.1.6 Other carcinomas
- 4.2.2 Sarcoma
- 4.2.1 Carcinoma
- 4.3 Metastasis
- 4.4 Histopathology
- 4.5 Staging
- 5 Management
- 5.1 Surgery
- 5.2 Add-on therapy
- 5.2.1 Chemotherapy
- 5.2.2 Radiotherapy
- 5.2.3 Hormonal therapy
- 5.3 Monitoring
- 6 Prognosis
- 6.1 Survival rates
- 6.2 Recurrence rates
- 7 Epidemiology
- 8 Research
- 9 History and culture
- 10 References
- 11 External links
Signs and symptoms
Vaginal bleeding or spotting in women after menopause occurs in 90% of endometrial cancer.[2][12] Bleeding is especially common with adenocarcinoma, occurring in two-thirds of all cases.[2][10] Abnormal menstrual cycles or extremely long, heavy, or frequent episodes of bleeding in women before menopause may also be a sign of endometrial cancer.[10]
Symptoms other than bleeding are not common. Other symptoms include thin white or clear vaginal discharge in postmenopausal women. More advanced disease shows more obvious symptoms or signs that can be detected on a physical examination. The uterus may become enlarged or the cancer may spread, causing lower abdominal pain or pelvic cramping.[10] Painful sexual intercourse or painful or difficult urination are less common signs of endometrial cancer.[9] The uterus may also fill with pus (pyometrea).[13] Of women with these less common symptoms (vaginal discharge, pelvic pain, and pus), 10–15% have cancer.[14]
Risk factors
Risk factors for endometrial cancer include obesity, diabetes mellitus, breast cancer, use of tamoxifen, never having had a child, late menopause, high levels of estrogen, and increasing age.[13][14] Immigration studies (migration studies), which examine the change in cancer risk in populations moving between countries with different rates of cancer, show that there is some environmental component to endometrial cancer.[15] These environmental risk factors are not well characterized.[16]
Hormones
Most of the risk factors for endometrial cancer involve high levels of estrogens. An estimated 40% of cases are thought to be related to obesity.[3] In obesity, the excess of adipose tissue increases conversion of androstenedione into estrone, an estrogen. Higher levels of estrone in the blood causes less or no ovulation and exposes the endometrium to continuously high levels of estrogens.[11][17] Obesity also causes less estrogen to be removed from the blood.[17] Polycystic ovary syndrome (PCOS), which also causes irregular or no ovulation, is associated with higher rates of endometrial cancer for the same reasons as obesity.[15] Specifically, obesity, type II diabetes, and insulin resistance are risk factors for Type I endometrial cancer.[18] Obesity increases the risk for endometrial cancer by 300–400%.[19]
Estrogen replacement therapy during menopause when not balanced (or "opposed") with progestin is another risk factor. Higher doses or longer periods of estrogen therapy have higher risks of endometrial cancer.[17] Women of lower weight are at greater risk from unopposed estrogen.[3] A longer period of fertility—either from an early first menstrual period or late menopause—is also a risk factor.[20] Unopposed estrogen raises an individual's risk of endometrial cancer by 2–10 fold, depending on weight and length of therapy.[3] In trans men who take testosterone and have not had a hysterectomy, the conversion of testosterone into estrogen via androstenedione may lead to a higher risk of endometrial cancer.[21]
Genetics
The autosomal dominant inheritance pattern seen in Lynch syndrome
Genetic disorders can also cause endometrial cancer. Overall, hereditary causes contribute to 2–10% of endometrial cancer cases.[3][22] Lynch syndrome, an autosomal dominant genetic disorder that mainly causes colorectal cancer, also causes endometrial cancer, especially before menopause. Women with Lynch syndrome have a 40–60% risk of developing endometrial cancer, higher than their risk of developing colorectal (bowel) or ovarian cancer.[15] Ovarian and endometrial cancer develop simultaneously in 20% of people. Endometrial cancer nearly always develops before colon cancer, on average, 11 years before.[16] Carcinogenesis in Lynch syndrome comes from a mutation in MLH1 and/or MLH2: genes that participate in the process of mismatch repair, which allows a cell to correct mistakes in the DNA.[15] Other genes mutated in Lynch syndrome include MSH2, MSH6, and PMS2, which are also mismatch repair genes. Women with Lynch syndrome represent 2–3% of endometrial cancer cases; some sources place this as high as 5%.[16][19] Depending on the gene mutation, women with Lynch syndrome have different risks of endometrial cancer. With MLH1 mutations, the risk is 54%; with MSH2, 21%; and with MSH6, 16%.[23]
Women with a family history of endometrial cancer are at higher risk.[9] Two genes most commonly associated with some other women's cancers, BRCA1 and BRCA2, do not cause endometrial cancer. There is an apparent link with these genes but it is attributable to the use of tamoxifen, a drug that itself can cause endometrial cancer, in breast and ovarian cancers.[15] The inherited genetic condition Cowden syndrome can also cause endometrial cancer. Women with this disorder have a 5–10% lifetime risk of developing endometrial cancer,[3] compared to the 2–3% risk for unaffected women.[16]
Other health problems
Some therapies for other forms of cancer increase the lifetime risk of endometrial cancer, which is a baseline 2–3%.[16] Tamoxifen, a drug used to treat estrogen-positive breast cancers, has been associated with endometrial cancer in approximately 0.1% of users, particularly older women, but the benefits for survival from tamoxifen generally outweigh the risk of endometrial cancer.[24] A one to two-year course of tamoxifen approximately doubles the risk of endometrial cancer, and a five-year course of therapy quadruples that risk.[20] Raloxifene, a similar drug, did not raise the risk of endometrial cancer.[25] Previously having ovarian cancer is a risk factor for endometrial cancer,[26] as is having had previous radiotherapy to the pelvis. Specifically, ovarian granulosa cell tumors and thecomas are tumors associated with endometrial cancer.
Low immune function has also been implicated in endometrial cancer.[13] High blood pressure is also a risk factor,[19] but this may be because of its association with obesity.[23] Sitting regularly for prolonged periods is associated with higher mortality from endometrial cancer. The risk is not negated by regular exercise, though it is lowered.[27]
Protective factors
Smoking and the use of progestin are both protective against endometrial cancer. Smoking provides protection by altering the metabolism of estrogen and promoting weight loss and early menopause. This protective effect lasts long after smoking is stopped. Progestin is present in the combined oral contraceptive pill and the hormonal intrauterine device (IUD).[15][28] Combined oral contraceptives reduce risk more the longer they are taken: by 56% after four years, 67% after eight years, and 72% after twelve years. This risk reduction continues for at least fifteen years after contraceptive use has been stopped.[25] Obese women may need higher doses of progestin to be protected.[28] Having had more than five infants (grand multiparity) is also a protective factor,[13] and having at least one child reduces the risk by 35%. Breastfeeding for more than 18 months reduces risk by 23%. Increased physical activity reduces an individual's risk by 38–46%. There is preliminary evidence that consumption of soy is protective.[25]
Pathophysiology
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A diagram showing the female reproductive tract with the uterine wall enlarged and normal endometrium visible
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Endometrial cancer forms when there are errors in normal endometrial cell growth. 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.[9]
In 10–20% of endometrial cancers, mostly Grade 3 (the highest histologic grade), mutations are found in a tumor suppressor gene, commonly p53 or PTEN. In 20% of endometrial hyperplasias and 50% of endometrioid cancers, PTEN suffers a loss-of-function mutation or a null mutation, making it less effective or completely ineffective.[30] Loss of PTEN function leads to up-regulation of the PI3k/Akt/mTOR pathway, which causes cell growth.[19] The p53 pathway can either be suppressed or highly activated in endometrial cancer. When a mutant version of p53 is overexpressed, the cancer tends to be particularly aggressive.[30] P53 mutations and chromosome instability are associated with serous carcinomas, which tend to resemble ovarian and Fallopian carcinomas. Serous carcinomas are thought to develop from endometrial intraepithelial carcinoma.[19]
PTEN and p27 loss of function mutations are associated with a good prognosis, particularly in obese women. The Her2/neu oncogene, which indicates a poor prognosis, is expressed in 20% of endometrioid and serous carcinomas. CTNNB1 (beta-catenin; a transcription gene) mutations are found in 14–44% of endometrial cancers and may indicate a good prognosis, but the data is unclear.[30] Beta-catenin mutations are commonly found in endometrial cancers with squamous cells.[19] FGFR2 mutations are found in approximately 10% of endometrial cancers, and their prognostic significance is unclear.[30] SPOP is another tumor suppressor gene found to be mutated in some cases of endometrial cancer: 9% of clear cell endometrial carcinomas and 8% of serous endometrial carcinomas have mutations in this gene.[31]
Type I and Type II cancers (explained below) tend to have different mutations involved. ARID1A, which often carries a point mutation in Type I endometrial cancer, is also mutated in 26% of clear cell carcinomas of the endometrium, and 18% of serous carcinomas. Epigenetic silencing and point mutations of several genes are commonly found in Type I endometrial cancer.[3][29] Mutations in tumor suppressor genes are common in Type II endometrial cancer.[3] PIK3CA is commonly mutated in both Type I and Type II cancers.[29] In women with Lynch syndrome-associated endometrial cancer, microsatellite instability is common.[19]
Development of an endometrial hyperplasia (overgrowth of endometrial cells) is a significant risk factor because hyperplasias can and often do develop into adenocarcinoma, though cancer can develop without the presence of a hyperplasia.[17] Within ten years, 8–30% of atypical endometrial hyperplasias develop into cancer, whereas 1–3% of non-atypical hyperplasias do so.[32] An atypical hyperplasia is one with visible abnormalities in the nuclei. Pre-cancerous endometrial hyperplasias are also referred to as endometrial intraepithelial neoplasia.[33] Mutations in the KRAS gene can cause endometrial hyperplasia and therefore Type I endometrial cancer.[30] Endometrial hyperplasia typically occurs after the age of 40.[9] Endometrial glandular dysplasia occurs with an overexpression of p53, and develops into a serous carcinoma.[13]
Diagnosis
Diagnosis of endometrial cancer is made first by a physical examination and dilation and curettage (removal of endometrial tissue; D&C). 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
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. A cervical screening test, such as a Pap smear, is not a useful diagnostic tool for endometrial cancer because the smear will be normal 50% of the time.[10] A Pap smear can detect disease that has spread to the cervix.[9] Results from a pelvic examination are frequently normal, especially in the early stages of disease. Changes in the size, shape or consistency of the uterus and/or its surrounding, supporting structures may exist when the disease is more advanced.[10] Cervical stenosis, the narrowing of the cervical opening, is a sign of endometrial cancer when pus or blood is found collected in the uterus (pyometra or hematometra).[12]
Women with Lynch syndrome should begin to have annual biopsy screening at the age of 35. Some women with Lynch syndrome elect to have a prophylactic hysterectomy and salpingo-oophorectomy to greatly reduce the risk of endometrial and ovarian cancer.[10]
Transvaginal ultrasound to examine the endometrial thickness in women with postmenopausal bleeding is increasingly being used to aid in the diagnosis of endometrial cancer in the United States.[34] In the United Kingdom, both an endometrial biopsy and a transvaginal ultrasound used in conjunction are the standard of care for diagnosing endometrial cancer.[13] The homogeneity of the tissue visible on transvaginal ultrasound can help to indicate whether the thickness is cancerous. 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).[35] They can also be used to investigate extrapelvic disease.[13] An MRI can be of some use in determining if the cancer has spread to the cervix or if it is an endocervical adenocarcinoma.[35] MRI is also useful for examining the nearby lymph nodes.[13]
Dilation and curettage or an endometrial biopsy are used to obtain a tissue sample for histological examination. 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.[35] Hysteroscopy can be used to confirm a diagnosis of cancer. New evidence shows that D&C has a higher false negative rate than endometrial biopsy.[19]
Before treatment is begun, several other investigations are recommended. These include a chest x-ray, liver function tests, kidney function tests,[19] and a test for levels of CA-125, a tumor marker that can be elevated in endometrial cancer.[9]
Classification
Endometrial cancers may be tumours derived from epithelial cells (carcinomas), mixed epithelial and mesenchymal tumours (carcinosarcomas), or mesenchymal tumours.[36]
Traditional classification of endometrial carcinomas is based either on clinical and endocrine features (Type I and Type II), or histopathological characteristics (endometroid, serous, and clear-cell). Some tumours are difficult to classify and have features overlapping more than one category. High grade endometroid tumours in particular tend to have both type I and type II features.[36]
Carcinoma
The vast majority of endometrial cancers are carcinomas (usually adenocarcinomas), meaning that they originate from the single layer of epithelial cells that line the endometrium and form the endometrial glands. 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.[10]
Type I endometrial carcinomas occur most commonly before and around the time of menopause. In the United States they are more common in whites, 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.[10] Type I carcinomas represent 75–90% of endometrial cancer.[13][37]
Type II endometrial carcinomas usually occur in older, post-menopausal people, in the United States are more common in black women, and are not associated with increased exposure to estrogen or a history of endometrial hyperplasia. 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.[10][37] They tend to present later than Type I tumors and are more aggressive, with a greater risk of relapse and/or metastasis.[13]
Endometrioid adenocarcinoma
Gross pathology of an endometrial adenocarcinoma
A histologic view of an endometrial adenocarcinoma showing many abnormal nuclei
In endometrioid adenocarcinoma, the cancer cells grow in patterns reminiscent of normal endometrium, with many new glands formed from columnar epithelium with some abnormal nuclei. Low-grade endometrioid adenocarcinomas have well differentiated cells, have not invaded the myometrium, and are seen alongside endometrial hyperplasia. The tumor's glands form very close together, without the stromal tissue that normally separates them. 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.[38]
The genetic mutations most commonly associated with endometrioid adenocarcinoma are in the genes PTEN, a tumor suppressor; PIK3CA, a kinase; KRAS, a GTPase that functions in signal transduction; and CTNNB1, involved in adhesion and cell signaling. The CTNNB1 (beta-catenin) gene is most commonly mutated in the squamous subtype of endometrioid adenocarcinoma.[39]
Serous carcinoma
See also: Uterine papillary serous carcinoma
Serous carcinoma is a Type II endometrial tumor that makes up 5–10% of diagnosed endometrial cancer and is common in postmenopausal women with atrophied endometrium and black women. 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. Roughly 30% of endometrial serous carcinomas also have psammoma bodies.[17][37] Serous carcinomas spread differently than most other endometrial cancers; they can spread outside the uterus without invading the myometrium.[17]
The genetic mutations seen in serous carcinoma are chromosomal instability and mutations in TP53, an important tumor suppressor gene.[39]
Clear cell carcinoma
See also: Uterine clear-cell carcinoma
Clear cell carcinoma is a Type II endometrial tumor that makes up less than 5% of diagnosed endometrial cancer. Like serous cell carcinoma, it is usually aggressive and carries a poor prognosis. Histologically, it is characterized by the features common to all clear cells: the eponymous clear cytoplasm when H&E stained and visible, distinct cell membranes.[37] The p53 cell signaling system is not active in endometrial clear cell carcinoma.[13] This form of endometrial cancer is more common in postmenopausal women.[17]
Mucinous carcinoma
Mucinous carcinomas are a rare form of endometrial cancer, making up less than 1–2% of all diagnosed endometrial cancer. 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.[38]
Mixed or undifferentiated carcinoma
Mixed carcinomas are those that have both Type I and Type II cells, with one making up at least 10% of the tumor.[38] These include the malignant mixed Müllerian tumor, which derives from endometrial epithelium and has a poor prognosis.[40]
Undifferentiated endometrial carcinomas make up less than 1–2% of diagnosed endometrial cancers. They have a worse prognosis than grade III tumors. Histologically, these tumors show sheets of identical epithelial cells with no identifiable pattern.[38]
Other carcinomas
Non-metastatic squamous cell carcinoma and transitional cell carcinoma are very rare in the endometrium. Squamous cell carcinoma of the endometrium has a poor prognosis.[38] It has been reported fewer than 100 times in the medical literature since its characterization in 1892. 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.[41] Primary transitional cell carcinomas of the endometrium are even more rare; 16 cases had been reported as of 2008[update]. Its pathophysiology and treatments have not been characterized.[42] Histologically, TCCE resembles endometrioid carcinoma and is distinct from other transitional cell carcinomas.[43]
Sarcoma
Main article: Endometrial stromal sarcoma
Endometrioid endometrial adenocarcinoma—very high magnification—H&E stain
In contrast to endometrial carcinomas, the uncommon endometrial stromal sarcomas are cancers that originate in the non-glandular connective tissue of the endometrium. 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.[17] They typically have estrogen and/or progesterone receptors.[44] The prognosis for low-grade endometrial stromal sarcoma is good, with 60–90% five-year survival. High-grade undifferentiated endometrial sarcoma (HGUS) has a worse prognosis, with high rates of recurrence and 25% five-year survival.[45] HGUS prognosis is dictated by whether or not the cancer has invaded the arteries and veins. Without vascular invasion, the five-year survival is 83%; it drops to 17% when vascular invasion is observed. Stage I ESS has the best prognosis, with five-year survival of 98% and ten-year survival of 89%. ESS makes up 0.2% of uterine cancers.[46]
Metastasis
Endometrial cancer frequently metastasizes to the ovaries and Fallopian tubes[26] when the cancer is located in the upper part of the uterus, and the cervix when the cancer is in the lower part of the uterus. 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.[47] Endometrial cancer metastasizes to the lungs 20–25% of the time, more than any other gynecologic cancer.[48]
Histopathology
A stage I, grade I section of an endometrial cancer after hysterectomy
A stage III endometrioid adenocarcinoma that has invaded the myometrium
Metastatic endometrial cancer seen in a removed lung
There is a three-tiered system for histologically classifying endometrial cancers, ranging from cancers with well-differentiated cells (grade I), to very poorly-differentiated cells (grade III).[20] Grade I cancers are the least aggressive and have the best prognosis, while grade III tumors are the most aggressive and likely to recur. Grade II cancers are intermediate between grades I and III in terms of cell differentiation and aggressiveness of disease.[49]
The histopathology of endometrial cancers is highly diverse. The most common finding is a well-differentiated endometrioid adenocarcinoma,[40] 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.[50]
Staging
Endometrial carcinoma is surgically staged using the FIGO cancer staging system. The 2009 FIGO staging system is as follows:[51]
| Stage | Description |
|---|---|
| IA | Tumor is confined to the uterus with less than half myometrial invasion |
| IB | Tumor is confined to the uterus with more than half myometrial invasion |
| II | Tumor involves the uterus and the cervical stroma |
| IIIA | Tumor invades serosa or adnexa |
| IIIB | Vaginal and/or parametrial involvement |
| IIIC1 | Pelvic lymph node involvement |
| IIIC2 | Para-aortic lymph node involvement, with or without pelvic node involvement |
| IVA | Tumor invades bladder mucosa and/or bowel mucosa |
| IVB | Distant metastases including abdominal metastases and/or inguinal lymph nodes |
Myometrial invasion and involvement of the pelvic and para-aortic lymph nodes are the most commonly seen patterns of spread.[2] A Stage 0 is sometimes included, in this case it is referred to as "carcinoma in situ".[9] In 26% of presumably early-stage cancers, intraoperative staging revealed pelvic and distant metastases, making comprehensive surgical staging necessary.[23]
-
Stage IA and IB endometrial cancer
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Stage II endometrial cancer
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Stage III endometrial cancer
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Stage IV endometrial cancer
Management
Surgery
A keyhole hysterectomy, one possible surgery to treat endometrial cancer
The primary treatment for endometrial cancer is surgery; 90% of women with endometrial cancer are treated with some form of surgery.[20] Surgical treatment typically consists of hysterectomy including a bilateral salpingo-oophorectomy, which is the removal of the uterus, and both ovaries and Fallopian tubes. Lymphadenectomy, or removal of pelvic and para-aortic lymph nodes, is performed for tumors of histologic grade II or above.[14] Lymphadenectomy is routinely performed for all stages of endometrial cancer in the United States, but in the United Kingdom, the lymph nodes are typically only removed with disease of stage II or greater.[13] The topic of lymphadenectomy and what survival benefit it offers in stage I disease is still being debated.[19] In stage III and IV cancers, cytoreductive surgery is the norm,[14] and a biopsy of the omentum may also be included.[52] In stage IV disease, where there are distant metastases, surgery can be used as part of palliative therapy.[19] Laparotomy, an open-abdomen procedure, is the traditional surgical procedure; however, laparoscopy (keyhole surgery) is associated with lower operative morbidity. The two procedures have no difference in overall survival.[52] Removal of the uterus via the abdomen is recommended over removal of the uterus via the vagina because it gives the opportunity to examine and obtain washings of the abdominal cavity to detect any further evidence of cancer. Staging of the cancer is done during the surgery.[53]
The few contraindications to surgery include inoperable tumor, massive obesity, a particularly high-risk operation, or a desire to preserve fertility.[53] These contraindications happen in about 5–10% of cases.[19] Women who wish to preserve their fertility and have low-grade stage I cancer can be treated with progestins, with or without concurrent tamoxifen therapy. This therapy can be continued until the cancer does not respond to treatment or until childbearing is done.[54] Uterine perforation may occur during a D&C or an endometrial biopsy.[55] Side effects of surgery to remove endometrial cancer can specifically include sexual dysfunction, temporary incontinence, and lymphedema, along with more common side effects of any surgery, including constipation.[9]
Add-on therapy
There are a number of possible additional therapies. Surgery can be followed by radiation therapy and/or chemotherapy in cases of high-risk or high-grade cancers. This is called adjuvant therapy.[14]
Chemotherapy
Adjuvant chemotherapy is a recent innovation, consisting of some combination of paclitaxel (or other taxanes like docetaxel), doxorubicin (and other anthracyclines), and platins (particularly cisplatin and carboplatin). Adjuvant chemotherapy has been found to increase survival in stage III and IV cancer more than added radiotherapy.[14][19][20][56] Mutations in mismatch repair genes, like those found in Lynch syndrome, can lead to resistance against platins, meaning that chemotherapy with platins is ineffective in people with these mutations.[57] Side effects of chemotherapy are common. These include hair loss, low neutrophil levels in the blood, and gastrointestinal problems.[14]
In cases where surgery is not indicated, palliative chemotherapy is an option; higher-dose chemotherapy is associated with longer survival.[14][20][56] Palliative chemotherapy, particularly using capecitabine and gemcitabine, is also often used to treat recurrent endometrial cancer.[56]
Radiotherapy
Adjuvant radiotherapy is commonly used in early-stage (stage I or II) endometrial cancer. It can be delivered through vaginal brachytherapy (VBT), which is becoming the preferred route due to its reduced toxicity, or external beam radiotherapy (EBRT). Brachytherapy involves placing a radiation source in the organ affected; in the case of endometrial cancer a radiation source is placed directly in the vagina. External beam radiotherapy involves a beam of radiation aimed at the affected area from outside the body. VBT is used to treat any remaining cancer solely in the vagina, whereas EBRT can be used to treat remaining cancer elsewhere in the pelvis following surgery. However, the benefits of adjuvant radiotherapy are controversial. Though EBRT significantly reduces the rate of relapse in the pelvis, overall survival and metastasis rates are not improved.[2] VBT provides a better quality of life than EBRT.[19]
Radiotherapy can also be used before surgery in certain cases. When pre-operative imaging or clinical evaluation shows tumor invading the cervix, radiation can be given before a total hysterectomy is performed.[12] Brachytherapy and EBRT can also be used, singly or in combination, when there is a contraindication for hysterectomy.[19] Both delivery methods of radiotherapy are associated with side effects, particularly in the gastrointestinal tract.[2]
Hormonal therapy
Hormonal therapy is only beneficial in certain types of endometrial cancer. It was once thought to be beneficial in most cases.[2][14] If a tumor is well-differentiated and known to have progesterone and estrogen receptors, progestins may be used in treatment.[56] About 25% of metastatic endometrioid cancers show a response to progestins. Also, endometrial stromal sarcomas can be treated with hormonal agents, including tamoxifen, hydroxyprogesterone caproate, letrozole, megestrol acetate, and medroxyprogesterone.[17] This treatment is effective in endometrial stromal sarcomas because they typically have estrogen and/or progestin receptors. Progestin receptors function as tumor suppressors in endometrial cancer cells.[58] Preliminary research and clinical trials have shown these treatments to have a high rate of response even in metastatic disease.[44]
Monitoring
The tumor marker CA-125 is frequently elevated in endometrial cancer and can be used to monitor response to treatment, particularly in serous cell cancer or advanced disease.[26][35][59] Periodic MRIs or CT scans may be recommended in advanced disease and women with a history of endometrial cancer should receive more frequent pelvic examinations for the five years following treatment.[59] Examinations conducted every three to four months are recommended for the first two years following treatment, and every six months for the next three years.[19]
Women with endometrial cancer should not have routine surveillance imaging to monitor the cancer unless new symptoms appear or tumor markers begin rising. Imaging without these indications is discouraged because it is unlikely to detect a recurrence or improve survival, and because it has its own costs and side effects.[60] If a recurrence is suspected, PET/CT scanning is recommended.[19]
Prognosis
Survival rates
| Stage | 5-year survival rate |
|---|---|
| I-A | 88% |
| I-B | 75% |
| II | 69% |
| III-A | 58% |
| III-B | 50% |
| III-C | 47% |
| IV-A | 17% |
| IV-B | 15% |
The five-year survival rate for endometrial adenocarcinoma following appropriate treatment is 80%.[62] Most women, over 70%, have FIGO stage I cancer, which has the best prognosis. Stage III and especially Stage IV cancers has a worse prognosis, but these are relatively rare, occurring in only 13% of cases. The median survival time for stage III-IV endometrial cancer is nine to ten months.[63] Older age indicates a worse prognosis.[14] In the United States, white women have a higher survival rate than black women, who tend to develop more aggressive forms of the disease by the time of their diagnosis.[64] Tumors with high progesterone receptor expression have a good prognosis compared to tumors with low progesterone receptor expression; 93% of women with high progesterone receptor disease survived to three years, compared with 36% of women with low progesterone receptor disease.[4] Heart disease is the most common cause of death among those who survive endometrial cancer,[65] with other obesity-related health problems also being common.[66]
Recurrence rates
Recurrence of early stage endometrial cancer ranges from 3 to 17%, depending on primary and adjuvant treatment.[62] Most recurrences (75–80%) occur outside of the pelvis, and most occur two to three years after treatment, 64% after two years and 87% after three years.[48]
Higher-staged cancers are more likely to recur, as are those that have invaded the myometrium or cervix, or that have metastasized into the lymphatic system. Papillary serous carcinoma, clear cell carcinoma, and endometrioid carcinoma are the subtypes at the highest risk of recurrence.[20] High-grade histological subtypes are also at elevated risk for recurrence.[13]
The most common site of recurrence is in the vagina;[2] vaginal relapses of endometrial cancer have the best prognosis. If relapse occurs from a cancer that has not been treated with radiation, EBRT is the first-line treatment and is often successful. If a cancer treated with radiation recurs, pelvic exenteration is the only option for curative treatment. Palliative chemotherapy, cytoreductive surgery, and radiation are also performed.[67] Radiation therapy (VBT and EBRT) for a local vaginal recurrence has a 50% five-year survival rate. Pelvic recurrences are treated with surgery and radiation, and abdominal recurrences are treated with radiation and, if possible, chemotherapy.[19] Other common recurrence sites are the pelvic lymph nodes, para-aortic lymph nodes, peritoneum (28% of recurrences), and lungs, though recurrences can also occur in the brain (<1%), liver (7%), adrenal glands (1%), bones (4–7%; typically the axial skeleton), lymph nodes outside the abdomen (0.4–1%), spleen, and muscle/soft tissue (2–6%).[48]
Epidemiology
As of 2014[update], approximately 320,000 women are diagnosed with endometrial cancer worldwide each year and 76,000 die, making it the sixth most common cancer in women.[3] It is more common in developed countries, where the lifetime risk of endometrial cancer in people born with uteri is 1.6%, compared to 0.6% in developing countries.[14] It occurs in 12.9 out of 100,000 women annually in developed countries.[20]
In the United States, endometrial cancer is the most frequently diagnosed gynecologic cancer and, in women, the fourth most common cancer overall,[11][17] representing 6% of all cancer cases in women.[68] In that country, as of 2014[update] it was estimated that 52,630 women were diagnosed yearly and 8,590 would die from the disease.[23] Northern Europe, Eastern Europe, and North America have the highest rates of endometrial cancer, whereas Africa and West Asia have the lowest rates. Asia saw 41% of the world's endometrial cancer diagnoses in 2012, whereas Northern Europe, Eastern Europe, and North America together comprised 48% of diagnoses.[3] Unlike most cancers, the number of new cases has risen in recent years, including an increase of over 40% in the United Kingdom between 1993 and 2013.[14] Some of this rise may be due to the increase in obesity rates in developed countries,[20] increasing life expectancies, and lower birth rates.[11] The average lifetime risk for endometrial cancer is approximately 2–3% in people with uteruses.[16] In the UK, approximately 7,400 cases are diagnosed annually, and in the EU, approximately 88,000.[19]
Endometrial cancer appears most frequently during perimenopause (the period just before, just after, and during menopause), between the ages of 50 and 65;[17] overall, 75% of endometrial cancer occurs after menopause.[2] Women younger than 40 make up 5% of endometrial cancer cases and 10–15% of cases occur in women under 50 years of age. This age group is at risk for developing ovarian cancer at the same time.[17] The worldwide median age of diagnosis is 63 years of age;[19] in the United States, the average age of diagnosis is 60 years of age. White American women are at higher risk for endometrial cancer than black American women, with a 2.88% and 1.69% lifetime risk respectively.[23] Japanese-American women and American Latina women have a lower rates and Native Hawaiian women have higher rates.[25]
Research
There are several experimental therapies for endometrial cancer under research, including immunologic, hormonal, and chemotherapeutic treatments. Trastuzumab (Herceptin), an antibody against the Her2 protein, has been used in cancers known to be positive for the Her2/neu oncogene, but research is still underway. Immunologic therapies are also under investigation, particularly in uterine papillary serous carcinoma.[30]
Cancers can be analyzed using genetic techniques (including DNA sequencing and immunohistochemistry) to determine if certain therapies specific to mutated genes can be used to treat it. PARP inhibitors are used to treat endometrial cancer with PTEN mutations,[3] specifically, mutations that lower the expression of PTEN. The PARP inhibitor shown to be active against endometrial cancer is olaparib. Research is ongoing in this area as of the 2010s.[22][69][70]
Research is ongoing on the use of metformin, a diabetes medication, in obese women with endometrial cancer before surgery. Early research has shown it to be effective in slowing the rate of cancer cell proliferation.[18][29] Preliminary research has shown that preoperative metformin administration can reduce expression of tumor markers. Long-term use of metformin has not been shown to have a preventative effect against developing cancer, but may improve overall survival.[18]
Temsirolimus, an mTOR inhibitor, is under investigation as a potential treatment.[19] Research shows that mTOR inhibitors may be particularly effective for cancers with mutations in PTEN.[3] Ridaforolimus (deforolimus) is also being researched as a treatment for people who have previously had chemotherapy. Preliminary research has been promising, and a stage II trial for ridaforolimus was completed by 2013.[19] There has also been research on combined ridaforolimus/progestin treatments for recurrent endometrial cancer.[71] Bevacizumab and tyrosine kinase inhibitors, which inhibit angiogenesis, are being researched as potential treatments for endometrial cancers with high levels of vascular endothelial growth factor.[3] Ixabepilone is being researched as a possible chemotherapy for advanced or recurrent endometrial cancer.[71] Treatments for rare high-grade undifferentiated endometrial sarcoma are being researched, as there is no established standard of care yet for this disease. Chemotherapies being researched include doxorubicin and ifosfamide.[45]
There is also research in progress on more genes and biomarkers that may be linked to endometrial cancer. The protective effect of combined oral contraceptives and the IUD is being investigated. Preliminary research has shown that the levonorgestrel IUD placed for a year, combined with 6 monthly injections of gonadotropin-releasing hormone, can stop or reverse the progress of endometrial cancer in young women.[72] An experimental drug that combines a hormone with doxorubicin is also under investigation for greater efficacy in cancers with hormone receptors. Hormone therapy that is effective in treating breast cancer, including use of aromatase inhibitors, is also being investigated for use in endometrial cancer. One such drug is anastrozole, which is currently being researched in hormone-positive recurrences after chemotherapy.[71] Research into hormonal treatments for endometrial stromal sarcomas is ongoing as well. It includes trials of drugs like mifepristone, a progestin antagonist, and aminoglutethimide and letrozole, two aromatase inhibitors.[44]
Research continues into the best imaging method for detecting and staging endometrial cancer. In surgery, research has shown that complete pelvic lymphadenectomy along with hysterectomy in stage 1 endometrial cancer does not improve survival and increases the risk of negative side effects, including lymphedema. Other research is exploring the potential of identifying the sentinel lymph nodes for biopsy by injecting the tumor with dye that shines under infrared light. Intensity modulated radiation therapy is currently under investigation, and already used in some centers, for application in endometrial cancer, to reduce side effects from traditional radiotherapy. Its risk of recurrence has not yet been quantified. Research on hyperbaric oxygen therapy to reduce side effects is also ongoing. The results of the PORTEC 3 trial assessing combining adjuvant radiotherapy with chemotherapy were awaited in late 2014.[71]
History and culture
Endometrial cancer is not widely known by the general populace, despite its frequency. There is low awareness of the symptoms, which can lead to later diagnosis and worse survival.[73]
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External links
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| Wikimedia Commons has media related to Endometrial cancer. |
- American Cancer Society's Detailed Guide: Endometrial Cancer
- U.S. National Cancer Institute: Endometrial cancer
- Anatomical pathology images
Tumors: female urogenital neoplasia (C51–C58/D25–D28, 179–184/218–221)
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UpToDate Contents
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- 1. 子宮体癌：臨床的特徴および診断 endometrial carcinoma clinical features and diagnosis
- 2. 子宮体癌の概要 overview of endometrial carcinoma
- 3. 子宮体癌の補助化学療法の考え方 approach to adjuvant treatment of endometrial cancer
- 4. 子宮体癌：治療前評価、病期分類、および外科治療 endometrial carcinoma pretreatment evaluation staging and surgical treatment
- 5. 中等度リスクの子宮体癌に対する補助化学療法 adjuvant treatment of intermediate risk endometrial cancer
English Journal
- Endometrial carcinoma recurrence according to race and ethnicity: An NRG Oncology/Gynecologic Oncology Group 210 Study.
- Felix AS1, Brasky TM2, Cohn DE3, Mutch DG4, Creasman WT5, Thaker PH4, Walker JL6, Moore RG7, Lele SB8, Guntupalli SR9, Downs LS10, Nagel C11, Boggess JF12, Pearl ML13, Ioffe OB14, Deng W8, Miller DS15, Brinton LA16.
- International journal of cancer.Int J Cancer.2018 Mar 15;142(6):1102-1115. doi: 10.1002/ijc.31127. Epub 2017 Nov 6.
- PMID 29063589
- Can the apparent diffusion coefficient differentiate the grade of endometrioid adenocarcinoma and the histological subtype of endometrial cancer?
- Yan B1, Zhao T2, Liang X1, Niu C2, Ding C3.
- Acta radiologica (Stockholm, Sweden : 1987).Acta Radiol.2018 Mar;59(3):363-370. doi: 10.1177/0284185117716198. Epub 2017 Jul 11.
- PMID 28696169
- Pathologic Staging of Endometrial Carcinomas: Selected Areas of Difficulty.
- McCluggage WG1.
- Advances in anatomic pathology.Adv Anat Pathol.2018 Mar;25(2):71-84. doi: 10.1097/PAP.0000000000000182.
- PMID 29356713
Japanese Journal
- Dose Volume Analysis of Radiotherapy for Inoperable Patients with Stage I-II Endometrial Carcinoma
- OHKUBO Yu,KATO Shingo,KIYOHARA Hiroki,TSURUOKA Ichiro,TAMAKI Tomoaki,NODA Shin-ei,OHNO Tatsuya,NAKANO Takashi
- Journal of radiation research 52(5), 666-673, 2011-09-16
- NAID 10029456132
- 内膜細胞診が診断の契機となった子宮内膜上皮内癌の1例
- 森村 豊,有我 こずえ,佐藤 陽子,原田 仁稔,渡辺 尚文,西山 浩,添田 周,藤森 敬也
- 日本臨床細胞学会雑誌 50(3), 176-180, 2011-05-22
- NAID 10028110053
Related Links
- Endometrial cancer (also referred to as corpus uterine cancer or corpus cancer) is the most common female genital cancer in the developing world, with adenocarcinoma of the endometrium the most common type. [] In ...
- American College of Obstetricians and Gynecologists. ACOG practice bulletin, clinical management guidelines for obstetrician-gynecologists, number 65, August 2005: management of endometrial cancer. Obstet Gynecol 2005; 106 ...
Related Pictures
★リンクテーブル★
| リンク元 | 「子宮体癌」「endometrial neoplasm」「cancer of the endometrium」「corpus uteri cancer」「uterine body cancer」 |
| 関連記事 | 「endometrial」「endometria」 |
「子宮体癌」
- 英
- uterine corpus cancer, carcinoma of uterine corpus, cancer of the uterine body
- ラ
- carcinoma corporis uteri
- 同
- 子宮内膜癌 endometrial carcinoma endometrial cancer
- 関
- 子宮、腫瘍、産婦人科学、子宮内膜増殖症(前癌病変)
- G9M.157(進行期分類)
定義
- 子宮体部内膜に発生する上皮性悪性腫瘍。
疫学
- 発生頻度は欧米に多く、日本では少ない(女性人口10万当たり4)→高齢化、生活習慣との関連
- 発症年齢は50歳代が最も多く、閉経後が7割を占める。40歳以下の婦人は5%程度。
- 妊娠中および分娩後5年以内に体癌が発見されることはほとんどない。
- 日本では近年増加傾向。子宮癌全体の30%を占める(みえる9.150)
リスクファクター
- プロゲステロンに拮抗されずに、エストロゲンに長期暴露されることによる
- 典型像：60歳くらいの太った未産の女性
- 未婚、不妊、閉経後、高い初婚・初妊年齢、少ない妊娠・出産回数、卵胞ホルモン服用歴、肥満
- 卵巣機能異常(無排卵周期症、PCOSなどの既往) → 正常量のエストロゲンが存在するものの、これに拮抗するプロゲステロンが欠乏する
- 出典不明
症状
子宮体癌の組織的分類
- ()内の頻度はG9M.155
- 子宮内膜癌
- 腺癌：ほとんどが腺癌
- 扁平上皮癌
- 混合癌
- 未分化癌
G9M.155
- 腺癌(95%以上)
- 類内膜癌(80-90%) → 類内膜腺癌(60-70%)、扁平上皮への分化を伴う類内膜腺癌(20-30%)
- 細胞異型が強い場合にはGradeを上げる。
- Grade1(高分化型)充実増殖の占める割合が腺癌成分の5%以下。プロゲステロン受容体陽性率高。予後良好
- Grade2(中分化型)充実増殖の占める割合が腺癌成分の6-50%。プロゲステロン受容体陽性率中。予後中等度
- Grade3(低分化型)充実増殖の占める割合が腺癌成分の50%超。プロゲステロン受容体陽性率低。予後不良
- その他(扁平上皮癌など(5%以下))
発生機序による分類
- type I：エストロゲン依存性。発症は遺伝子変異とエストロゲンの長期持続刺激による子宮内膜細胞の異常増殖
- 若年者の子宮体癌は多嚢胞性卵巣に由来するものがある
- type II：エストロゲン非依存性。子宮内膜異型増殖症を介さないで癌化する
| I型子宮体癌 | II型子宮体癌 | |
| 発生機序 | エストロゲンへの長期暴露 | de novo癌 |
| 好発年齢 | 閉経前-閉経早期 | |
| 頻度 | 80-90% | 10-20% |
| 病巣周辺の 子宮内膜異型増殖症 |
あり | なし |
| 組織型 | 類内膜腺癌 | 漿液性腺癌 明細胞腺癌 |
| 分化度 | 高分化型 | 低分化型 |
| 筋層浸潤 | 軽度 | 高度 |
| 予後 | 比較的良好 | 不良 |
| 遺伝子変異 | K-ras, PTEN | p53 |
検査
超音波エコー(経膣超音波)
- 子宮内膜の肥厚が認められる。
腫瘍マーカー
MRI
- T2画像が有用。
- junctional zoneの菲薄化・欠損
- 子宮内膜＞腫瘍＞筋層＞junctional zone
診断
- スクリーニング：細胞診
- 子宮腔内の吸引あるいは擦過細胞診による検出率：90%以上
- 子宮頚・腟部からの細胞採取による検出率：50%以下
- 確定診断：子宮内膜の試験掻爬組織診
手術進行期分類 (日産婦 1995,FIGO1998)
- 原則として手術進行期分類を用い、手術を行っていない例では臨床進行期分類を用いる
体 → 頚 → 骨盤内 → 骨盤外
- 0期： 子宮内膜異型増殖症
- I期： 子宮体部に限局
- Ia期： 子宮内膜に限局
- Ib期： 浸潤が子宮筋層1/2以内
- Ic期： 浸潤が子宮筋層1/2を越える
- II期： 子宮頸部に及ぶ
- IIa期： 頸管腺のみ
- IIb期： 頸部間質浸潤
- III期： 子宮外に広がるが小骨盤腔を越えない、または所属リンパ節転移
- IV期： 小骨盤腔を越える、または明らかな膀胱または腸粘膜を侵す
- IVa期： 膀胱、腸粘膜へ浸潤
- IVb期： 遠隔転移（腹腔内リンパ節、鼠径リンパ節転移を含む）
転移
- 直接浸潤
- リンパ行性転移
症状
- 不正性器出血、腹痛
治療
- 手術療法、放射線療法、薬物療法(抗ガン剤、ホルモン療法)
- 治療法の基本は手術療法(単純子宮全摘術、準広汎子宮全摘術、広汎子宮全摘術)。
- 補助的に摘出術を追加することがある：両側付属器切除術、リンパ節郭清、部分大網切除術
- 薬物療法・放射線療法：手術不能例、再発例、術後の補助療法
薬物療法
抗悪性腫瘍薬
- シスプラチン、アドリアマイシン、タキサン系の多剤併用療法
化学療法のレジメン
- 参考：http://medical.nikkeibp.co.jp/leaf/all/nmk/cr/report/200702/502818.htm
- 世界ではアドリアマイシン単剤療法(A)に対してアドリアマイシンとシスプラチンの併用療法(AP)の治療効果、あるいはアドリアマイシンとシスプラチンの併用療法(AP)に対してアドリアマイシン、シスプラチン、およびパクリタキセルの三剤併用療法(TAP)の治療効果を比較した臨床研究がなされている。それぞれの後者の方が奏効率が高い。しかし、TAP療法は毒性が高く、子宮体癌に対する標準治療としては2006年の段階で認められていない。
- 現在は卵巣癌の標準化学療法として知られているパクリタキセルとカルボプラチンの併用療法は、子宮体癌に対しても奏効率が非常に高く、標準化学療法としての期待が高まっている。
- GOG(the gynecologic oncology group)ではTC療法とTAP療法を直接比較する試験を進行させている。結果が出るまでには数年かかる。
ガイドライン的には「アンスラサイクリン系とプラチナ製剤を含む薬剤の選択が薦められている(グレードB)。タキサン系製剤も併用さているが、その十分な根拠は得られていない(グレードC)。(子宮体癌の治療ガイドライン2006年)
一般的な抗腫瘍薬による副作用
ホルモン療法
- ホルモン療法単体：挙児希望のGrade1のIa期：高用量MPA
- 術後補助療法：再発リスクの低い場合、高用量黄体ホルモン療法は非推奨(グレードD)(参考2)
手術療法
- 1. 子宮摘出術
- 単純子宮全摘術
- 子宮体部に限局しているとき
- 準広汎子宮全摘術
- 子宮体部に限局しているとき
- 広汎子宮全摘術
- MRIや肉眼で明らかな頸部間質浸潤が認められるとき。
- 2. 両側付属器切除術
- 3. リンパ節郭清
- 骨盤リンパ節郭清：基本的に施行。省略するのは、類内膜癌Grade1で、画像診断で病変が子宮内膜に限局すると推定される場合のみ。
- 傍大動脈リンパ節郭清
- 鼠径リンパ節郭清
- 4. 部分大網切除術
傍大動脈リンパ節郭清術と部分大網切除術の適応
- 転移リスクが高いため
放射線療法
- 子宮頚癌(扁平上皮癌)より放射線は有効ではない。 → 放射線療法は腺癌に奏効しづらい！！！
子宮温存を希望する若年性子宮体癌
- 根治治療ではなく、いずれは子宮全摘が必要。
- 再発例では子宮全摘
適応
- 画像診断上Ia期(内膜限局)
- G1の類内膜腺癌
治療
- 子宮内膜全面掻爬
- 高用量黄体ホルモン療法
予後
予後規定因子
- 筋層浸潤の深さ、頚部浸潤、子宮外進展、リンパ節転移、病理組織型、組織学的分化度、血管・リンパ管侵襲
5年生存率
| 臨床進行期 | 5年生存率(%) | |
| 出典不明(相対) | NGY.229 | |
| I | 86 | 79 |
| II | 68 | 66.8 |
| III | 42 | 37.5 |
| IV | 16 | 8.5 |
国試
症例
- 55歳の女性。不正性器出血を主訴に来院した。未経妊、閉経51歳。不妊治療をした経験がある。子宮は鶏卵大で卵巣は両側とも触知しない。経膣超音波で子宮内膜の肥厚が見られる。
子宮体癌治療ガイドライン(2006年)
- FIGOは子宮体癌の手術進行期分類を採用。
- 1)進行期決定のために手術術式の選択が必要である。
- 2)子宮体癌は放射線感受性が低く、抗ガン剤の標準治療の確立が遅れている。
- このことから子宮体癌では手術療法が第一選択。高齢や内科的合併症などの理由で、放射線療法が選択される場合もある。
参考
- 1.
- 2. 子宮体がん治療ガイドライン2009年版：（金原出版）
- 3. ガイドライン
「endometrial neoplasm」
「cancer of the endometrium」
子宮内膜癌、子宮内膜がん
「corpus uteri cancer」
子宮体癌、子宮体がん
「uterine body cancer」
子宮体癌、子宮体がん
「endometrial」
- adj.
- 子宮内膜の