GYNECOLOGY
Topic: Uterine Cancer
Lecturer: Dr. Villanueva (FAV)
ENDOMETRIAL CANCER
 Among the cancers of the genital tract, there are 2 cancers which are
relatively kind. One is endometrial cancer and the other one is vulvar
cancer because these two manifest very early so therefore can be
diagnosed very early  curable
 Endometrial cancer  present as heavy menstrual bleeding and it has
a characteristic appearance, usually seen in woman who are
overweight (obese), has history of DM and hypertension
 The most common gyne malignancy in the U.S.
 6% of all cancers in women
o Approximately 3 women in 100 in the U.S. will develop this
disease during their life
 Generally high rate of survival due to early diagnosis
 Curve rises sharply after age 45 and peaks between 55 and 60; then
there is gradual decrease
Epidemiology
 Primarily in Perimenopausal and postmenopausal years
 Frequently diagnosed between ages 50 and 65
 Can also develop in young women in their reproductive years
o 5% diagnosed in women < 40 years
o 10-15% in women < 50 years
 < 50 – also at risk for synchronous ovarian cancer
Risk Factors
 Endometrial cancer has premalignant lesions  catching a woman at
this premalignant phase = you can prevent the cancer from developing
 Epidemiologic differences:
o Risk related to hormonal stimulation or unrelated to estrogen
at all.
 Estrogen-related endometrial cancer (Type I) tends
to be lower grade histologically.
 Better prognosis compared to Type II
 Endometrial cancers unrelated to hormones (Type II)
tend to be a higher grade and stage
 E.g. Papillary serous or clear cell tumors
How Endometrial Hyperplasia is associated with Endometrial Cancer
 Endometrial hyperplasia is a continuum …
o Simple hyperplasia  complex hyperplasia without atypia 
complex hyperplasia with atypia  endometrial cancer (well
differentiated adenocarcinoma)
 Simple hyperplasia – 1% progress to endometrial cancer
o 99% of simple hyperplasia will regress
 Complex hyperplasia – 3%
 Complex hyperplasia with atypia – 28%
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Strength in knowledge
 In simple hyperplasia and complex hyperplasia, what we normally do is
give progesterone for a long-term and then assess after 6 months to
make sure that it has not progressed
 In complex hyperplasia with atypia, normally we do hysterectomy
because the chance of it developing into endometrial cancer is very high
o Complex atypical hyperplasia – results from increased
estrogenic stimulation of the endometrium
o It is a precursor to endometrioid endometrial cancer
o Some endometrioid cancers develop without previous
hyperplasia
o These non-estrogen-related carcinomas including serous
histology tend to be poorly differentiated and clinically more
aggressive
 30 - 40% of endometrial cancers are found in a background of atypical
hyperplasia. Overall, these tend to be lower grade tumors
o Even if atypical hyperplasia is not cancer automatically, we do
hysterectomy
 Microscopically:
o Simple hyperplasia  proliferation of glands but there is still
stroma in between
 Other term for simple hyperplasia = Swiss cheese
o Complex hyperplasia  proliferation also of well-defined
glands but stroma in between is very little
Image on Left: Complex hyperplasia with atypia
 Increased N:C ratio
 Nuclear abnormalities
 Atypical cells
 Mitotic figures
CASE:
 45 year old nulligravid consulted because of profuse vaginal bleeding
of 6 months duration.
 She is hypertensive, diabetic, with BMI of 35
QUESTIONS:
 What are the differential diagnosis?
 What is the most probable complete diagnosis?
 What is the plan of management?
FIGO-AUB
P – Polyp C – Coagulopathy
A – Adenomyosis O – Ovulatory dysfunction
L – Leiomyoma E – Endometrium
M – Malignancy and Hyperplasia I – Iatrogenic
N – Not classified
Lecture Discussion:
To answer the 1st question we have now the mnemonics PALM COEIN. These
are our differentials in a patient who has heavy menstrual bleeding
 Ovulatory dysfunction  an anovulatory bleeding
 Endometrium  problems with prostaglandins being produced.
More of the vasodilators than vasoconstrictors
 Iatrogenic  giving of medicine which is causing the bleeding
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 GYNECOLOGY
Topic: Uterine Cancer
Lecturer: Dr. Villanueva (FAV)
Obesity
 A BMI of 30 and above – there is 2-5 times the risk for endometrial
cancer
 Risk is linear  the higher the BMI, the higher that chance that a woman
can get endometrial cancer
 What is the explanation for that?
o This is due to the peripheral conversion of androgens to
estrogens inside the adipose tissues
o Patients who are fat (obese) have a lot of adipose tissues so
whatever androgens are circulating in the body are converted
to estrogen  elevated estrogen will go to the uterus and
cause unopposed estrogen stimulation
For Type I Diseases, What would be some common exogenous estrogen
source?
 Unopposed in HRT (Hormone Replacement Therapy)
 Tamoxifen
Estrogen in HRT
 Benefits: helps relieve hot flashes, vaginal dryness, and prevents
osteoporosis
o Estrogen is given as a hormone replacement therapy in
menopause because we want to relieve the hot flashes, vaginal
dryness and osteoporosis
 Unopposed estrogen increases the risk of endometrial hyperplasia
and endometrial cancer.
o Unfortunately, if we only give estrogen (which is unopposed
because there is no progesterone)  the risk of endometrial
hyperplasia and cancer increases
 In unopposed estrogen 20-50% of women will have developed
endometrial hyperplasia after 1 year risk of endometrial cancer is
related BOTH to dose and duration of treatment. Thus, in women taking
estrogen alone for 10 years, the incidence of endometrial cancer goes
from 1/1000 to 42/1000. May be a less aggressive cancer…
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Strength in knowledge
 The practice now in HRT is that we don’t just give estrogen alone. We
also add progesterone  this will protect the uterus against
endometrial cancer
Tamoxifen
 Tamoxifen – a competitive inhibitor of estrogen binding to estrogen
receptors that also has partial agonist activity (Tamoxifen is a weak
estrogen); Selective estrogen receptor modulator (SERM)
o Used in patients with early stage breast cancer
 Especially to those with ER/PR (+) breast cancer
o As treatment of recurrent disease
o Risk reduction in high risk women
 Unfortunately while it suppresses breast tissue growth, it stimulates
endometrial lining.
o Tamoxifen will bind to the estrogen receptors in the
endometrium stimulate the endometrium and cause it to
thicken
 Probably a 2 to 3 fold risk of endometrial cancer with Tamoxifen.
 Especially in women older than 50
From Comprehensive Gyne:
 Majority of endometrial cancers that developed in Tamoxifen users
were endometrioid histology and low grade and stage.
 However, high-grade endometrial CA and sarcomas have also been
reported in women taking Tamoxifen.
 Screening include Transvaginal ultrasound and office endometrial
sampling
 High false-positive rate in Transvaginal ultrasound because Tamoxifen
causes subendometrial cyst formation (endometrial stripe appear
abnormally thick)
 Counsel women that Tamoxifen increases risk of endometrial cancer
and all women n Tamoxifen who have irregular vaginal bleeding
(premenopausal) or any vaginal bleeding (postmenopausal) should
undergo endometrial sampling or Dilation & Curettage.
What’s ACOG have to say about Tamoxifen?
 Even though Tamoxifen is associated with endometrial cancer, the
benefits in treating women with breast CA outweigh the risks … but …
o Women need a yearly gyne exam
o Women should monitor themselves for abnormal and vaginal
symptoms., eg Bleeding, discharge, etc
o Screening such as pelvic ultrasound is NOT recommended (too
many false positives)
o However ultrasound can be helpful
o US – not end-all, will not tell you exactly if there’s a
problem; “suggestive” that there might be a problem
o 1st imaging of choice
o Limit Tamoxifen use to 5 years (not longer)
o If there is a typical endometrial hyperplasia, treat and reassess
Tamoxifen (i.e. Consider hysterectomy)
Unopposed Estrogen stimulation
 Strongly associated with endometrial cancer
 4-8x ↑ risk for woman using estrogen alone for menopausal
replacement therapy
 ↑ risk with higher doses of estrogen (> 0.625 mg conjugated
estrogens) and more prolonged use
 Reduced with the use of Progestin
 GYNECOLOGY
Topic: Uterine Cancer
Lecturer: Dr. Villanueva (FAV)

What would be endogenous sources of estrogen as a risk factor for  Lynch syndrome – ~2% of all endometrial cancers, < 10% in synchronous
endometrial cancer? endometrial and ovarian cancers
 Nulliparity  Women with endometrial cancer and Family History of Colon,
o Prolonged estrogen exposure endometrial, or ovarian cancer should be referred for genetic evaluation
 Anovulatory cycles and colonoscopy.
o PCOS (↑ estrogen level, unopposed estrogen)  Personal History of both endometrial and colon cancer have significant
 Estrogen secreting tumors risk for Lynch syndrome and should be referred.
o Granulosa cell tumors  secrete estrogen  Hyperplasia
 Late menopause Parity
 Nulliparity in and of itself is not a risk factor as much as the Anovulatory
Other Risk Factors for Endometrial Cancer cycles that are associated with infertility
Diabetes and Hypertension
 A risk factor because these conditions are often associated with obesity, Diet
and also because of the effects of hyperinsulinemia and insulin-like  Especially High fat
growth factors.
 Diabetes – independent risk factor for endometrial CA and since Menarche/Menopause
Diabetics are also hypertensive. HTN is also associated with endometrial  Early menarche and late menopause essentially prolonged estrogen
CA. exposure without the protection of progesterone.
 Hypertension – often related to Obesity and Diabetes but not
considered an independent risk factor Recall:
EXOgenous Estrogen Sources ENDOgenous Estrogen Sources
Recall: Genital tract cancers and their Risk factors Unopposed estrogen in HRT Nulliparity
Tamoxifen Anovulatory cycles
Cervical CA risk factors?
 Sexual promiscuity  increased chance of getting exposed to HPV Estrogen secreting tumors
Late menopause
Endometrial CA risk factors?
 Fat PROTECTIVE FACTORS
 Female
 Oral contraceptives: decrease both the risk of ovarian and endometrial
 HTN
cancer (RR = 0.6 if used for one year … effect lasts for 15 years!)
 Diabetic
 In the 40s to 50s  However, oral contraceptives which are used for more than 5 years
increases the chance of cervical cancer
Ovarian CA risk factors?
 Protective effect probably due to progesterone
 Ovulation
o Combination (Progestin-containing) oral contraceptives
decrease the risk
Chronic Anovulation
 Usually seen in women with PCOS
HISTOPATHOLOGY
 Many women with chronic Anovulation have plenty of estrogen since
 Most common types of endometrial cancer:
androgens can be converted peripherally to estrogen, but Anovulatory
o Endometrioid adenocarcinoma (70-80%)
cycles lack progesterone (luteal phase). Thus even though these women
 Most common type of endometrial cancer is
have hyperandrogenism, they also have chronic estrogen stimulation
Adenocarcinoma (Type I)
and can develop endometrial hyperplasia even at a young age
o Clear cell and serous tumors are more aggressive and probably
present at an advance age (together 5-10%)
Familial Predisposition
o Mucinous and squamous about 2%
 E.g. Lynch syndrome II: hereditary nonpolyposis colorectal cancer
(HNPCC), endometrial carcinoma, collection of cancers
CLINICAL PRESENTATION
 (Up to 43% of women of affected families will develop ovarian cancer)
 The “classic symptom” is abnormal uterine bleeding
 Unclear if there’s a risk with BRCA 1 and 2
o Usually heavy, profuse, or prolonged bleeding
 20-30% of women with post-menopausal bleeding will have uterine
From Comprehensive Gyne:
cancer
Lynch Syndrome/HNPCC
 (the risk is higher the farther they are away from menopause)
 Autosomal dominant hereditary cancer susceptibility syndrome caused
 Abnormal pap smear
by a germline defect in a DNA mismatch repair gene
o Not a reliable means of picking up endometrial CA
 Lifetime risk for developing
 The presence of endometrial cells on a pap smear in women > 40 is an
o Endometrial cancer – 40 – 60%
indication for biopsy. Even more likely if cells are atypical … if cancer
o Colon cancer – 40 – 60%
present, is often of higher grade, with deeper invasion more advanced
o Ovarian cancer – 12 %
stage
 Endometrial CA can be of any histology or grade
o Hyperplasia in 36%
o Most endometrial CA with Lynch syndrome were in the early
o AdenoCA in 11%
stage
o Approximately ¼ high grade, high stage, or poor histology
 Screening recommendation: Annual endometrial biopsy and TVS to
evaluate the ovaries
 After childbearing is complete, prophylactic hysterectomy and salpingo-
oophorectomy to decrease endometrial and ovarian cancer.

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Strength in knowledge
 GYNECOLOGY
Topic: Uterine Cancer
Lecturer: Dr. Villanueva (FAV)

DIAGNOSIS
 Abnormal vaginal bleeding is the most frequent symptom of
There is something there in the
endometrial hyperplasia.
endometrium and it is very thick
 Premenopausal women with irregular vaginal bleeding and (>2 cm thickness)  think of
postmenopausal women with any vaginal bleeding should be evaluated cancer especially if it has color
with an office endometrial sampling or a D & C like this
 Easy to do with office EMB
 Hysterescopy with D&C (Gold standard)
o Detection rates of endometrial CA, by pipelle was between 91
and 99%
o Detection of hyperplasia was 81%
 Recommendation: EMB as initial test; Hysteroscopy/ D&C if EMB
inconclusive or high suspicion (hyperplasia with atypia, pyometria,
presence of necrosis, or persistent bleeding) ENDOMETRIAL CANCER STAGING
 Staging is always done surgically
Symptoms, Signs, and Diagnosis:  Requires a total hysterectomy, BSO (Bilateral salpingo-oophorectomy)
 Primary symptoms of endometrial carcinoma: Postmenopausal  Uterine specimen opened in the room to evaluate extent of disease
bleeding, abnormal premenopausal bleeding, and perimenopausal  Can omit LN sampling, if risk of lymph node spread is low.
bleeding
 Diagnosis of endometrial carcinoma established by Histologic
examination of the endometrium
 Initial diagnosis can frequently be made on an outpatient basis, with an
Office endometrial biopsy.
o (+) endometrial carcinoma  Endocervical curettage (rule out
Endocervix invasion)
 Routine cytologic examination (Pap smear) from Exocervix
o Screens for cervical neoplasia
o Detects endometrial carcinoma approximately 50% of cases
 Endocervix first sampled to rule out cervical involvement by
endometrial cancer
o Hysteroscopy  visualize endometrial cavity and then complete
uterine curettage is performed

 Transvaginal ultrasound
o In postmenopausal women, an endometrial thickness of 4-5
mm or less is pretty reassuring (only 1% will have endometrial
CA)
o Adjunct for the diagnosis of endometrial hyperplasia and
cancer
o A thicker endometrium requires EMB, hysteroscopy / D&C.
o Especially useful for women on estrogen who have bleeding,
but overall TVS is not recommended as a screening tool.
o It is still recommended to do an EMB rather than rely on TVS **Will not be asked on the exam According to Dr. Villanueva**
results in evaluating abnormal bleeding.
 So even if TVS says that the endometrium is thin, you Importance of Staging  can predict prognosis
still need to do endometrial biopsy to evaluate further
the abnormal bleeding Prognostic Factors:
 Divided into Clinical and Pathological Factors
Clinical Factors Pathologic Factors
 Diagnosis  Tumor grade
 Race  Histologic Type
This is the uterus, if you get a  Clinical tumor stage  Tumor size
very thin endometrium like this  Depth of myometrial invasion
(0.18 cm)  you are practically  Involvement of vascular spaces in the
sure that this is normal. It is not uterus by tumor
cancer  Spread of tumor outside the uterus to the
retroperitoneal lymph nodes, peritoneal
cavity, or uterine adnexa

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 GYNECOLOGY
Topic: Uterine Cancer
Lecturer: Dr. Villanueva (FAV)

Patterns of Metastatic Spread

 Pelvic and paraaortic lymph nodes, lung, inguinal and Supraclavicular
nodes, liver, peritoneal cavity, bone, brain, and vagina

Pre-op Imaging
 CXR  check for lung metastasis
 CT (not necessary unless you think there’s extra pelvic disease – it
doesn’t alter treatment and doesn’t really let you know of depth of
invasion etc. – MRI would be better in assessing invasion)

Laboratory Tests
 CA-125
o Usually used in cases of ovarian cancer.
Tumor stage – well-recognized prognostic factor for endometrial carcinoma. o Elevated CA-125 Pre-Op  often indicate extrauterine disease
Fortunately, most cases are diagnosed in Stage 1 o Particularly useful marker for those with serous carcinoma of
Histologic Grade – major determinant of prognosis the endometrium
 Determined by the percentage of solid components found in the tumor  LFT’s
 Grade 1 – well-differentiated; < 5% solid components  CBC
 Grade 2 – intermediate differentiation, < 6-50% solid components  Renal
 Grade 3 – poorly differentiated, > 50% solid components
Going back to the CASE:
Recurrence:
 1st management you do for the case is endometrial biopsy
 Recurrence rate is low for Grade I
 If it is benign (hyperplasia)  give progesterone (long-term) and
 The higher the Grade, the higher the chance of recurrence
investigate every 6 months
 If it is malignant (or even just complex hyperplasia with atypia)  do
hysterectomy or TAHBSO
 If severe bleeding  give blood transfusion first before doing the
procedure

**From Previous Trans**

HNPCC AND SCREENING
 Since 40-60% of patients with this develop endometrial CA, do an EMB
at age 35
o Women with HNPCC-associated mutations
o Women with a family member with this mutation
o Women from families with autosomal dominant predisposition
to colon CA
 Doing an ultrasound is not enough!

Progestins
 Progestational agents valuable against endometrial cancer, particularly
in patients with recurrent disease
 Side effects: weight gain, edema, thrombophlebitis, headache, and
occasional hypertension
 This shows the node that may be involved in endometrial cancer:
 Current recommendations for Progestin Therapy:
o Paraaortic
o Oral medroxyprogesterone acetate (Provera)
o Common iliac o Intramuscular medroxyprogesterone acetate (Depo-
o Internal iliac Provera)
o External iliac o Megestrol acetate (Megace)
o Inguinal  Increase likelihood of response to hormonal therapy:
 If lymph nodes are already involved  Stage III o Low grade tumor
o Presence of steroid hormone receptor (ER+ & PR+)
Plentl and Friedman noted four major channels of lymphatic drainage from o Longer disease-free interval
the uterus that serve as sites for extrauterine spread of tumor: Tamoxifen
1. A small lymphatic branch along the round ligament that runs to the  1st generation SERMs
inguinal femoral nodes  Mixed estrogenic agonist and antagonist
2. Branches from the tubal and  Grade 1 and 2 tumors were more likely to respond to Tamoxifen than
3. Ovarian pedicles (infundibulopelvic ligaments; large lymphatics that Grade 3 tumors
drain into the paraaortic nodes)  Short-term administration of Tamoxifen can cause an increase in the
4. The broad ligament lymphatics (drain directly to the pelvic nodes) progesterone levels in postmenopausal women with endometrial
cancer
The pelvic and paraaortic node drainage sites (2, 3, and 4) are the most
Anastrazole
important clinically
 Oral Nonsteroidal aromatase inhibitor
 For postmenopausal women with progressive breast cancer
following Tamoxifen therapy

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Strength in knowledge
 GYNECOLOGY
Topic: Uterine Cancer
Lecturer: Dr. Villanueva (FAV)

ENDOMETRIAL
FINDINGS MANAGEMENT
HYPERPLASIA
 Endometrium with dilated glands
 May contain some outpouching and abundant
endometrial stroma
Simple Hyperplasia  Cystic hyperplasia – dilation of endometrial glands which
often occur in a Hyperplastic endometrium in a
post/menopausal woman (cystic atrophy)
 1 % risk of developing endometrial cancer
 Diagnostic D & C can also be therapeutic
 Glands are crowded with very little endometrial stroma
 Progestins or combination oral contraceptive agents
 Complex gland pattern
 Out-pouching formations
Complex Hyperplasia  Variant of adenomatous hyperplasia with moderate to
(without Atypia) severe degrees of architectural atypia but with no
cytologic atypia
 Low malignant potential
 3 % risk of developing endometrial cancer
Women who desire preservation of child-bearing function:
 Megestrol acetate (high-dose progestin), 40 mg 3-4x/day
 Long term follow up
 Periodic sampling (1st at 3 mos., at least every 6 mos.
thereafter)
 Periodic progestin tx or oral contraception until patient
 Hyperplasias that contain glands with cytologic atypia
chooses to get pregnant (dt risk factors which are likely to
Complex Atypical  Premalignant; Greatest malignant potential (29 %)
remain)
Hyperplasia  Increase in the nuclear/cytoplasmic ratio with irregularity
in the size and shape of the nuclei
Older patients, moderate or severe atypical hyperplasia:
Hysterectomy generally recommended
 If Hysterectomy not advisable: Long term high-dose
progestin – Megestrol acetate 160mg/d or its equivalent
depending on endometrial response.
 Periodic sampling of endometrium

MANAGEMENT:
 Surgery – primary treatment modality for patients with endometrial carcinoma
 Complete surgical staging (Hysterectomy with/without Bilateral salpingo-oophorectomy, pelvic and paraaortic
lymphadenectomy)
o EXCEPTION: Women with significant medical comorbidities, Young, Premenopausal women who desire
future fertility with Grade 1 endometrial adenocarcinoma associated with endometrial hyperplasia
Stage I  Minimally invasive surgery in the treatment of early stage endometrial cancer has become standard of care
 Patients with significant medical comorbidities, Radiation therapy alone can be used
 For those who cannot tolerate surgery or external beam therapy, treatment by intracavitary radiation alone offers
some benefit
 Occasionally, morbidly obese patients are encountered for whom an abdominal operation is risky.
Three therapeutic options have been employed for the treatment of Stage II carcinoma of the endometrium that also
involves the Endocervix:
1) Primary operation (Radical hysterectomy and pelvic and paraaortic lymph node dissection)
Stage II
2) Primary radiation (intrauterine and vaginal implant and external irradiation – 45 Gy) followed by an operation
(extrafascial hysterectomy)
3) Simple Hysterectomy followed by an external beam radiation
 Adjuvant treatment (Combination of tumor-directed radiation and systemic chemotherapy)
 Optimal surgical debulking
Stage III or IV
 Combination therapy; Doxorubicin (1st drug w/ good activity against endometrial CA) and Cisplatin, Paclitaxel and
Recurrent Endometrial
Carboplatin (1st line standard of care for advanced and recurrent endometrial cancers)
cancer
 Clinical trials and target therapy should be considered in women who fail 1st line chemotherapy
 Radiotherapy can be useful for patients with an isolated recurrence in the pelvis

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 GYNECOLOGY
Topic: Uterine Cancer
Lecturer: Dr. Villanueva (FAV)
KEY POINTS
 Endometrial carcinoma is the most common malignancy of the female
genital tract. In the United States, the lifetime risk of endometrial
cancer is 3%.
 Most women who develop endometrial cancer are between 50 and 65
years of age.
 Women with Lynch syndrome (hereditary nonpolyposis colorectal
cancer syndrome) have a 40% to 60% lifetime risk of endometrial
cancer, which is similar to their lifetime risk of colon cancer.
 Chronic unopposed estrogen stimulation of the endometrium leads to
endometrial hyperplasia and in some cases adenocarcinoma. Other
important predisposing factors include obesity, nulliparity, late
menopause, and diabetes.
 The risk of a woman developing endometrial carcinoma increases three
times if her body mass index is greater than 30 kg/m2.
 Tamoxifen use increases the risk of endometrial neoplasia two to
threefold.
 The primary symptom of endometrial carcinoma is postmenopausal
bleeding. Women with abnormal bleeding should undergo an
endometrial sampling to rule out endometrial pathology.
 Cytologic atypia in endometrial hyperplasia is the most important
factor in determining malignant potential.
 Simple hyperplasia will develop into endometrial cancer in 1% of
patients, whereas complex hyperplasia will develop into cancer in 29%
of patients.
 Studies have found that there is a 40% concurrent rate of endometrial
cancer in patients with a preoperative diagnosis of complex atypical
hyperplasia.
 Prognosis in endometrial carcinoma is related to tumor grade, tumor
stage, histologic type, and degree of myometrial invasion.
 Older patients with atypical hyperplasia are at increased risk of
malignant progression compared with younger patients.
 A key determinant of the risk of nodal spread of endometrial carcinoma
is depth of myometrial invasion, which is often related to tumor grade.
 Well-differentiated (grade 1) endometrial carcinomas usually express
steroid hormone receptors, whereas poorly differentiated (grade 3)
tumors usually do not express receptors.
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 Uterine serous carcinoma is an aggressive histologic subtype
associated with metastatic disease even in the absence of myometrial
invasion.
 Ninety percent of recurrences of adenocarcinoma of the endometrium
occur within 5 years.
 Overall survival rates for patients with adenocarcinoma of the
endometrium by stage are as follows: stage I, 86%; stage II, 66%; stage
III, 44%; stage IV, 16% (overall there is a 72.7% 5-year survival rate
combining clinical and operative staging systems).
 Histologic variants of endometrial carcinoma with a poor prognosis
include uterine serous carcinoma and clear-cell carcinoma.
 Patients with uterine serous or clear-cell carcinoma of the
endometrium should have a full staging laparotomy similar to that for
ovarian carcinoma.
 The most frequent sites of distant metastasis of adenocarcinoma of the
endometrium are the lung, retroperitoneal nodes, and abdomen.
 Primary treatment of endometrial cancer includes hysterectomy,
bilateral salpingo-oophorectomy, pelvic cytology, bilateral pelvic and
paraaortic lymphadenectomy, and resection of all disease. The
exceptions include young premenopausal women with stage I and
grade 1 endometrial carcinoma associated with endometrial
hyperplasia, and women with increased risk of mortality secondary to
medical comorbidities.
 Postoperative adjuvant radiation has not been shown to improve
overall survival.
 Patients with high-stage or recurrent disease should be treated in a
multimodality approach including chemotherapy, radiation, or
hormone therapy.
 Uterine sarcomas make up less than 5% of uterine malignancies.
 Uterine sarcomas are treated primarily by operation including removal
of the uterus, tubes, and ovaries.
 Endometrial stromal sarcomas are low-grade sarcomas with an
indolent course.
 Multiagent chemotherapeutic regimens are usually prescribed for
metastatic sarcomas; complete responses are rare and usually
temporary.