The paramesonephric duct is responsible for the development of the female reproductive system. The fallopian tubes are formed by bilateral paramesonephric ducts, which combine to produce the uterus and the upper section of the vaginal canal. The uterus is held together in the pelvis by numerous ligaments, which are responsible for its anteverted and anteflexed position.
In the uterus, the embryo implants and develops into a foetus. The placenta, which is connected to the endometrium, acts as a conduit for nutrition and oxygen transport between maternal and foetal blood. The endometrium sheds every month in the absence of pregnancy, resulting in cyclic menstrual bleeding.
The uterus is made of these three layers:
Endometrium (Innermost layer)
Myometrium (Middle layer)
Serosa (Outermost layer)
Uterine cancer either develops in the myometrium or the endometrium. Sarcomas also develop in the middle muscular layer of the uterus, but they are rare. Uterine Sarcomas are aggressive, so they require rapid treatment. In developed countries, endometrial carcinoma is the most common gynecological cancer.
It’s also the 2nd most common gynaecological cancer in developing countries, following cervical cancer. According to the age-incidence curve endometrial cancer is mostly diagnosed in the 7th decade of life. According to the American Cancer Society, 63,230 new instances of uterine cancer were detected in 2018.
Uterine cancer kills 4.6 out of every 100,000 women in the United States, according to estimates. These figures indicate that uterine cancer is a significant burden on the health-care system, and that early detection, diagnosis, and treatment can improve patient outcomes while also reducing the strain on the system.
Epidemiology
In developed countries, endometrial carcinoma is the 4th most common cancer affecting women. 65,000 women develop uterine cancers each year, and endometrial carcinoma is responsible for 90% of these cases. The mean age of incidence is 61 years, and black women are twice more likely to be affected.
Black women also present a poorer prognosis in comparison to white women. Unfortunately, fatality rates for endometrial carcinoma have doubled over the past two decades. Although fatality rates for other cancers are declining in women, deaths due to uterine cancer are still on the rise.
Most women who develop uterine cancer are postmenopausal, with only 15-25% patients that are diagnosed pre-menopause.25% of women are diagnosed between 64-75, and incidentally the fatality rates between these age is the most at 32%.
Reasons for worse outcome in this age are:
Aggressive tumors
Advanced disease at diagnosis
Reluctance to surgical treatment of disease
Worse treatment outcomes
Anatomy
Pathophysiology
Endometrioid cancer occurs as a result of unopposed oestrogen exposure, resulting in hyperplasia and eventually dysplasia of the endometrial glands, and is thus referred to as adenocarcinoma. Numerous studies have established a relationship between endometrial cancer and intrinsic variables that increase blood oestrogen levels, such as obesity and type II diabetes mellitus.
Extrinsic variables, such as estrogen-only hormone replacement treatment and tamoxifen, also contribute to an increased risk of endometrial adenocarcinoma development. Serous endometrial cancer develops as a result of endometrial atrophy and is frequently associated with genetic abnormalities. There are two forms of uterine cancer based on molecular characteristics and oestrogen sensitivity.
Type I cancer is caused by unopposed oestrogen, but type II cancer that occurs in postmenopausal women, is not caused by oestrogen, and has a worse prognosis. PTEN, k-ras, and microsatellite instability inception mutations are frequently observed in type I, whereas p53 and HER2/neu mutations are frequently observed in type II. This classification also provides critical information about therapies and prognosis. The most often occurring mutations are in p53 and HER/neu, which have a dismal prognosis.
Etiology
The most frequent subtype of endometrial cancer is endometrial adenocarcinoma or endometrioid carcinoma. Endometrial adenocarcinoma occurs as a result of oestrogen exposure that is unopposed. Estrogen stimulates endometrial proliferation, resulting in endometrial hyperplasia.
Proliferation that is not monitored results in dysplasia and, eventually, cancer. Because adipose tissue in the body converts androgens to oestrogen, diseases such as obesity, metabolic syndrome, and type II diabetes mellitus result in elevated oestrogen levels, which can raise the risk of endometrial cancer.
Over 50% of endometrial malignancies are caused solely by obesity. As obesity rates have risen over the years, so has the incidence of endometrial cancer. Conditions which lead to unopposed oestrogen exposure substantially increase the risk of endometrial cancer. The increased oestrogen exposure is due to an unusually high amount of ovulatory cancers, caused by early menarche, polycystic ovarian syndrome, nulliparity, and late menopause.
Tamoxifen, a breast cancer medication, also raises the risk of endometrial cancer. Tamoxifen inhibits oestrogen receptors in breast tissue but stimulates oestrogen receptors in the endometrium. In postmenopausal women, estrogen-only hormone replacement therapy can also stimulate the endometrium, resulting in the development of endometrial cancer.
Genetics
Prognostic Factors
According to the SEER database, the 5-year survival rates are extremely positive for localised endometrial cancers, and extremely unfavourable for patients for which the cancer has spread to other parts of the boy such as liver, lungs, and bones.
Regional endometrial cancers have a 71% survival rate, whereas patients with localised cancers have a 96% 5-year survival rate. Only 1 out of 5 patients diagnosed with the distant stage of endometrial carcinoma survive 5 years after diagnosis.
The paramesonephric duct is responsible for the development of the female reproductive system. The fallopian tubes are formed by bilateral paramesonephric ducts, which combine to produce the uterus and the upper section of the vaginal canal. The uterus is held together in the pelvis by numerous ligaments, which are responsible for its anteverted and anteflexed position.
In the uterus, the embryo implants and develops into a foetus. The placenta, which is connected to the endometrium, acts as a conduit for nutrition and oxygen transport between maternal and foetal blood. The endometrium sheds every month in the absence of pregnancy, resulting in cyclic menstrual bleeding.
The uterus is made of these three layers:
Endometrium (Innermost layer)
Myometrium (Middle layer)
Serosa (Outermost layer)
Uterine cancer either develops in the myometrium or the endometrium. Sarcomas also develop in the middle muscular layer of the uterus, but they are rare. Uterine Sarcomas are aggressive, so they require rapid treatment. In developed countries, endometrial carcinoma is the most common gynecological cancer.
It’s also the 2nd most common gynaecological cancer in developing countries, following cervical cancer. According to the age-incidence curve endometrial cancer is mostly diagnosed in the 7th decade of life. According to the American Cancer Society, 63,230 new instances of uterine cancer were detected in 2018.
Uterine cancer kills 4.6 out of every 100,000 women in the United States, according to estimates. These figures indicate that uterine cancer is a significant burden on the health-care system, and that early detection, diagnosis, and treatment can improve patient outcomes while also reducing the strain on the system.
In developed countries, endometrial carcinoma is the 4th most common cancer affecting women. 65,000 women develop uterine cancers each year, and endometrial carcinoma is responsible for 90% of these cases. The mean age of incidence is 61 years, and black women are twice more likely to be affected.
Black women also present a poorer prognosis in comparison to white women. Unfortunately, fatality rates for endometrial carcinoma have doubled over the past two decades. Although fatality rates for other cancers are declining in women, deaths due to uterine cancer are still on the rise.
Most women who develop uterine cancer are postmenopausal, with only 15-25% patients that are diagnosed pre-menopause.25% of women are diagnosed between 64-75, and incidentally the fatality rates between these age is the most at 32%.
Reasons for worse outcome in this age are:
Aggressive tumors
Advanced disease at diagnosis
Reluctance to surgical treatment of disease
Worse treatment outcomes
Endometrioid cancer occurs as a result of unopposed oestrogen exposure, resulting in hyperplasia and eventually dysplasia of the endometrial glands, and is thus referred to as adenocarcinoma. Numerous studies have established a relationship between endometrial cancer and intrinsic variables that increase blood oestrogen levels, such as obesity and type II diabetes mellitus.
Extrinsic variables, such as estrogen-only hormone replacement treatment and tamoxifen, also contribute to an increased risk of endometrial adenocarcinoma development. Serous endometrial cancer develops as a result of endometrial atrophy and is frequently associated with genetic abnormalities. There are two forms of uterine cancer based on molecular characteristics and oestrogen sensitivity.
Type I cancer is caused by unopposed oestrogen, but type II cancer that occurs in postmenopausal women, is not caused by oestrogen, and has a worse prognosis. PTEN, k-ras, and microsatellite instability inception mutations are frequently observed in type I, whereas p53 and HER2/neu mutations are frequently observed in type II. This classification also provides critical information about therapies and prognosis. The most often occurring mutations are in p53 and HER/neu, which have a dismal prognosis.
The most frequent subtype of endometrial cancer is endometrial adenocarcinoma or endometrioid carcinoma. Endometrial adenocarcinoma occurs as a result of oestrogen exposure that is unopposed. Estrogen stimulates endometrial proliferation, resulting in endometrial hyperplasia.
Proliferation that is not monitored results in dysplasia and, eventually, cancer. Because adipose tissue in the body converts androgens to oestrogen, diseases such as obesity, metabolic syndrome, and type II diabetes mellitus result in elevated oestrogen levels, which can raise the risk of endometrial cancer.
Over 50% of endometrial malignancies are caused solely by obesity. As obesity rates have risen over the years, so has the incidence of endometrial cancer. Conditions which lead to unopposed oestrogen exposure substantially increase the risk of endometrial cancer. The increased oestrogen exposure is due to an unusually high amount of ovulatory cancers, caused by early menarche, polycystic ovarian syndrome, nulliparity, and late menopause.
Tamoxifen, a breast cancer medication, also raises the risk of endometrial cancer. Tamoxifen inhibits oestrogen receptors in breast tissue but stimulates oestrogen receptors in the endometrium. In postmenopausal women, estrogen-only hormone replacement therapy can also stimulate the endometrium, resulting in the development of endometrial cancer.
According to the SEER database, the 5-year survival rates are extremely positive for localised endometrial cancers, and extremely unfavourable for patients for which the cancer has spread to other parts of the boy such as liver, lungs, and bones.
Regional endometrial cancers have a 71% survival rate, whereas patients with localised cancers have a 96% 5-year survival rate. Only 1 out of 5 patients diagnosed with the distant stage of endometrial carcinoma survive 5 years after diagnosis.
The paramesonephric duct is responsible for the development of the female reproductive system. The fallopian tubes are formed by bilateral paramesonephric ducts, which combine to produce the uterus and the upper section of the vaginal canal. The uterus is held together in the pelvis by numerous ligaments, which are responsible for its anteverted and anteflexed position.
In the uterus, the embryo implants and develops into a foetus. The placenta, which is connected to the endometrium, acts as a conduit for nutrition and oxygen transport between maternal and foetal blood. The endometrium sheds every month in the absence of pregnancy, resulting in cyclic menstrual bleeding.
The uterus is made of these three layers:
Endometrium (Innermost layer)
Myometrium (Middle layer)
Serosa (Outermost layer)
Uterine cancer either develops in the myometrium or the endometrium. Sarcomas also develop in the middle muscular layer of the uterus, but they are rare. Uterine Sarcomas are aggressive, so they require rapid treatment. In developed countries, endometrial carcinoma is the most common gynecological cancer.
It’s also the 2nd most common gynaecological cancer in developing countries, following cervical cancer. According to the age-incidence curve endometrial cancer is mostly diagnosed in the 7th decade of life. According to the American Cancer Society, 63,230 new instances of uterine cancer were detected in 2018.
Uterine cancer kills 4.6 out of every 100,000 women in the United States, according to estimates. These figures indicate that uterine cancer is a significant burden on the health-care system, and that early detection, diagnosis, and treatment can improve patient outcomes while also reducing the strain on the system.
In developed countries, endometrial carcinoma is the 4th most common cancer affecting women. 65,000 women develop uterine cancers each year, and endometrial carcinoma is responsible for 90% of these cases. The mean age of incidence is 61 years, and black women are twice more likely to be affected.
Black women also present a poorer prognosis in comparison to white women. Unfortunately, fatality rates for endometrial carcinoma have doubled over the past two decades. Although fatality rates for other cancers are declining in women, deaths due to uterine cancer are still on the rise.
Most women who develop uterine cancer are postmenopausal, with only 15-25% patients that are diagnosed pre-menopause.25% of women are diagnosed between 64-75, and incidentally the fatality rates between these age is the most at 32%.
Reasons for worse outcome in this age are:
Aggressive tumors
Advanced disease at diagnosis
Reluctance to surgical treatment of disease
Worse treatment outcomes
Endometrioid cancer occurs as a result of unopposed oestrogen exposure, resulting in hyperplasia and eventually dysplasia of the endometrial glands, and is thus referred to as adenocarcinoma. Numerous studies have established a relationship between endometrial cancer and intrinsic variables that increase blood oestrogen levels, such as obesity and type II diabetes mellitus.
Extrinsic variables, such as estrogen-only hormone replacement treatment and tamoxifen, also contribute to an increased risk of endometrial adenocarcinoma development. Serous endometrial cancer develops as a result of endometrial atrophy and is frequently associated with genetic abnormalities. There are two forms of uterine cancer based on molecular characteristics and oestrogen sensitivity.
Type I cancer is caused by unopposed oestrogen, but type II cancer that occurs in postmenopausal women, is not caused by oestrogen, and has a worse prognosis. PTEN, k-ras, and microsatellite instability inception mutations are frequently observed in type I, whereas p53 and HER2/neu mutations are frequently observed in type II. This classification also provides critical information about therapies and prognosis. The most often occurring mutations are in p53 and HER/neu, which have a dismal prognosis.
The most frequent subtype of endometrial cancer is endometrial adenocarcinoma or endometrioid carcinoma. Endometrial adenocarcinoma occurs as a result of oestrogen exposure that is unopposed. Estrogen stimulates endometrial proliferation, resulting in endometrial hyperplasia.
Proliferation that is not monitored results in dysplasia and, eventually, cancer. Because adipose tissue in the body converts androgens to oestrogen, diseases such as obesity, metabolic syndrome, and type II diabetes mellitus result in elevated oestrogen levels, which can raise the risk of endometrial cancer.
Over 50% of endometrial malignancies are caused solely by obesity. As obesity rates have risen over the years, so has the incidence of endometrial cancer. Conditions which lead to unopposed oestrogen exposure substantially increase the risk of endometrial cancer. The increased oestrogen exposure is due to an unusually high amount of ovulatory cancers, caused by early menarche, polycystic ovarian syndrome, nulliparity, and late menopause.
Tamoxifen, a breast cancer medication, also raises the risk of endometrial cancer. Tamoxifen inhibits oestrogen receptors in breast tissue but stimulates oestrogen receptors in the endometrium. In postmenopausal women, estrogen-only hormone replacement therapy can also stimulate the endometrium, resulting in the development of endometrial cancer.
According to the SEER database, the 5-year survival rates are extremely positive for localised endometrial cancers, and extremely unfavourable for patients for which the cancer has spread to other parts of the boy such as liver, lungs, and bones.
Regional endometrial cancers have a 71% survival rate, whereas patients with localised cancers have a 96% 5-year survival rate. Only 1 out of 5 patients diagnosed with the distant stage of endometrial carcinoma survive 5 years after diagnosis.
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