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Objectives

The following module was designed to supplement medical students’ learning in the clinic. Please take the time to read through each module by clicking the headings below. For quick reference, all objectives are answered in point form in the very last page of this module. Summary tables are also placed at the end of every section.

By the end of the tutorial, the following objectives should be addressed:

  1. Review the anatomy of the female pelvis
  2. Describe the blood supply and lymphatic drainage of the cervix, uterus and associated structures
  3. State the incidence of endometrial cancer in Canada
  4. List the risk factors for development of endometrial cancer
  5. State the standard screening protocol for endometrial cancer
  6. Describe possible signs and symptoms of endometrial neoplasia
  7. List a differential diagnosis for abnormal vaginal bleeding
  8. Describe how you would investigate a woman with abnormal vaginal bleeding
  9. Discuss the malignant transformation of the endometrium and its relationship to hormonal influence in endometrial hyperplasia and cancer
  10. Describe the pathology for endometrial hyperplasia and adenocarcinoma of the uterus
  11. Outline the staging system for endometrial cancer
  12. Describe the principles of surgical, radiation and hormonal therapies for endometrial cancer

Anatomy Review

The female pelvis holds important structures such as the bowels, bladder, uterus and ovaries/fallopian tubes in a structural framework created by bone and muscle. We concentrate our discussion on the relevant reproductive anatomy.

Uterus and Ovaries

The uterus is comprised of the uterine corpus and the uterine cervix. The corpus, or body, is the shape of an inverted triangle, or pear, while the uterine cervix is a tubular structure that is the conduit between the vagina and endometrial cavity. Take a moment to inspect the figure above and notice the differences in epithelium located in each region.

The most superior portion of the uterine corpus, or body, is called the fundus, the most inferior portion the isthmus. The uterus itself is made up of three layers of distinct tissue: the endometrium, myometrium, and serosa. The endometrium is the lining of the uterine cavity, with a superficial layer of glandular epithelium and stroma. It is this endometrial thickness that changes with the menstrual cycle or other hormonal influences. The myometrium is the thickest layer of the uterus and composed of smooth muscle fibers. The serosa is the thin outer lining of the uterus, which consists of visceral peritoneum – this invests the body of the uterus.

Uterine support structures of note include:

  • The Round Ligament – is an extension of the uterine musculature that attaches at the uterine fundus and travels retroperitoneally to enter the inguinal canal, finally terminating in the labia majora.
  • The Broad Ligament – consists of a double layer of visceral and parietal peritoneum that invests the lateral body of the uterus and upper cervix. Subsections have been named, such as the mesosalpinx near the fallopian tubes and the mesovarium near the ovary. These structures are indicated in the diagram below.
  • The Utero-ovarian Ligament – attaches the ovaries to the uterus, suspending the ovaries
  • Suspensory Ligament of the Ovary/ Infundibulopelvic Ligament – attaches ovary to the pelvic sidewall and carries the ovarian vessels.
  • Note the relationship between the uterus, bladder and bowels.

Pelvic Vasculature

The aorta supplies blood to the pelvic structures and descends as the abdominal aorta. From this abdominal aorta comes the first artery of note: the ovarian or gonadal arteriesh that branch off just below the renal arteries. The ovarian arteries descend in the suspensory ligament of the ovary. The abdominal aorta continues, then bifurcates at vertebrae L5 into the Right and Left Common Iliac Arteries. Then, the common iliacs divide into internal and external iliac arteries. The external iliac gives off several branches including inferior epigastric arteries, recurrent obturator artery and super vesical artery.

The internal iliac artery branches into anterior and posterior divisions. The posterior branches into lateral sacral, iliolumbar and superior gluteal arteries. The anterior division has several branches including obliterated umbilical artery, uterine artery, superior vesical artery, obturator artery, vaginal artery and interior gluteal/pudendal arteries. It is these arteries that become very important in supplying the reproductive organs. The internal iliac is also commonly called the hypogastric artery and is useful to ligate during pelvic hemorrhage.

Summary

Epidemiology

Incidence

Endometrial cancer is the most common gynecological cancer in Canada, being the 4th most common cancer in women after breast, lung and colorectal cancers. The incidence is 21 per 100,000 people. The lifetime probability of developing endometrial cancer is 1 in 40. An estimated 5600 new cases of endometrial cancer are expected to be diagnosed in 2013, with 4500 cases having been diagnosed in 2012. (1) However, the 5 year overall survival ratio is 84% – so it’s worth learning how to diagnose and treat!

The median age of diagnosis is 61 yrs of age, and as such is considered a disease of postmenopausal women – however 25% of cases occur in premenopausal women. (2)

Risk Factors for Developing Endometrial Cancer

There are two types of endometrial cancer that are recognized, with each class having different risk factors. Type 1 and Type 2 Risk factors are presented.

Type 1 Risk Factors

FIGURE 1: TYPE 1 ENDOMETRIAL CARCINOMA RISK FACTORS
Age
  • Endometrial carcinomas tend to occur in post menopausal women.
Endogenous Estrogen Sources
  • Obesity – adipose tissue converts adrenal precurors to estradiol. Comorbidities include diabetes mellitus and hypertension
  • Chronic Anovulation – in a state of anovulation, sex steroids are produced non-cyclically, resulting in an irregular uterine bleed. The continued proliferation of the endometrium can lead to hyperplasia or carcinoma. Common associated syndromes are Polycystic Ovary Syndrome, and thyroid dysfunction.
  • Estrogen-secreting tumours
  • Late menopause (after age 55) – results in prolonged estrogen stimulation
  • Early menarche – results in prolonged estrogen stimulation
  • Nulliparity and Infertility – these are not independent risk factors but rather are associated with high frequency of anovulatory cycles in infertile women
Exogenous Estrogen Sources
  • Tamoxifen therapy – (breast cancer treatment)
  • Postmenopausal estrogen therapy
  • Unopposed estrogen therapy – estrogen therapy that is unopposed by a progestin results in increased risk of endometrial hyperplasia or carcinoma
Genetic Factors
  • Lynch Syndrome – Lynch Syndrome is also known as hereditary nonpolyposis colorectal cancer, and is an autosomal dominant disorder
  • BRCA gene mutation – some data suggests that BRCA1 mutations are associated with endometrial carcinoma
SUMMARY: RISK FACTORS FOR TYPE 1 ENDOMETRIAL CANCER
  1. Increasing Age
  2. Estrogen Exposure – early or late menarche, nulliparity, anovulation, obesity, PCOS, thyroid dysfunction
  3. Genetics – Lynch Syndrome, BCRA1 Mutation
  • It is notable that protective factors for endometrial carcinoma include estrogen-progestin oral contraceptives, physical activity, tea and coffee.

Type 2 Risk Factors

  • Non estrogen related factors
  • P53 mutations are the predominate molecular finding.

Summary

Screening

With the exception of women with genetic syndromes – discussed below – routine screening for endometrial cancer is not advised. Data does not support efficacy of screening and there is currently no screening test that is sensitive, specific and acceptable to patients and physicians. Cytology from Pap smear and transvaginal ultrasound to assess endometrial thickness have low sensitivity and specificity. Biopsy is invasive but does meet sensitivity and specificity requirements.

As such the American Cancer Society suggests that women at an average or increased risk (such as those of advanced age, with anovulatory conditions or nulliparity) should be well-informed of symptoms such as abnormal uterine bleed and encouraged to report them should they occur.(1)

Two genetic syndromes are of note in this discussion. The first is a rare autosomal dominant condition called Cowden Syndrome that is a result of mutation in the PTEN tumour suppressor gene. The lifetime risk of endometrial cancer in women with Cowden syndrome is 13-28 percent. There are no established guidelines for screening but management is similar to that of Lynch Syndrome, the second genetic syndrome of note.

Lynch Syndrome, or Hereditary Nonpolyposis Colorectal Cancer (HNPCC) is an autosomal dominant inherited cancer susceptibility syndrome caused by mutation in certain DNA mismatch repair genes. The syndrome predisposes an individual to a variety of cancers, namely colorectal and endometrial cancer. Women with Lynch syndrome have a 27-71% risk of endometrial cancer, and as such management includes surveillance, chemoprevention and risk reducing surgery.(2)

Screen with annual endometrial sampling, starting 5-10 years before earliest age of Lynch-related cancer diagnosed in the family. Transvaginal ultrasound to assess endometrial thickness is useful in postmenopausal women, if endometrial sampling is not acceptable. Risk reducing hysterectomy and bilateral salpingo-oophrectomy is effective prevention.

Summary

Classification

Endometrial carcinomas may be Type 1 or Type 2, depending on light microscopic appearance, clinical behavior and epidemiology.

TABLE: COMPARISON OF TYPE 1 AND TYPE 2 ENDOMETRIAL CANCER

*Non-endometroid tissue includes serous, clear cell, mucinous, squamous, transitional cell and undifferentiated

Signs and Symptoms

A classic presentation of endometrial cancer is postmenopausal bleeding. Premenopausal women may present with heavy/or irregular periods and this may be associated with vaginal discharge. Signs on pelvic examination include bulky uterus, with bleeding or vaginal discharge from the os apparent. However, it is often that no physical signs can be detected.

Occasionally abnormal endometrial cells will be detected incidentally on a pap smear.

Considering the possible mechanisms of spread is important when considering presenting symptoms:

Local Invasion – to myometrium, cervix, fallopian tubes, ovaries, bladder, rectumLymphatic Spread – to pelvic or lumbar lymph nodesHematogenous – to lungs or boneWith these mechanisms of spread and organs in mind, other symptoms such as change in bowel or bladder habits, bony pain or cough maybe present. For this reason, it is very important complete a full history, with an emphasis on any associated symptoms.

Summary of Signs and Symptoms

Abnormal Uterine BleedAbnormal Cytology (pap) findings noted incidentally on papIncidental finding from other procedure : eg hysterectomy

Diagnosis

Differential Diagnosis for Abnormal Vaginal Bleeding

Though abnormal bleeding from the female genital area is often attributed to a uterine source, it may arise from any site in the lower genital tract, upper genital tract or from a non-gynecological source such as the urethra, bowels, or local trauma. It may also be helpful to separate possible causes depending on if the patient is pre or post menopausal.(1)

Premenopausal – fibroids, polyps, anoulavtory cycles (PCOS), cervical cancer (post coital)Postmenopausal – atrophy (50%), polyps, cervical cancer, endometrial hyperplasia, endometrial cancer** Note that this differential does not take into account Tamoxifen therapy (which can also cause gynecological bleed), coagulation abnormalities, herbal supplements or trauma.

Approach

Abnormal uterine or vaginal bleeding has a wide array of etiologies and needs thorough investigation beginning with a history and physical examination. A differential diagnosis will change based on age, reproductive status, underlying conditions and family history.(2) Note that terminology around changes in bleed frequency, time, and duration have become so elaborate that “abnormal uterine bleeding” is now more often used in place of terms such as menorrhagia, amenorrha, oligomenorrhea etc.(3)The following page will take you through the steps required to investigate a woman with abnormal uterine bleed.

History – Key aspects (initial approach)

  • Gain more information about the symptom: frequency, duration, volume, relationship to sexual activity.  Note bleeding between periods is usually related to a structural lesion such as fibroid whereas irregular but heavy periods are typically ovulatory in nature.
  • Review medications including contraception use, intrauterine device use
  • Assess family/personal history : coagulopathy, Lynch Syndrome or BRCA
  • Pregnancy: pregnancy related bleeding should be considered in women of reproductive age
  • Review gynecological history
  • Ask for any associated symptoms:
  • Pain in lower abdomen or back, fever and or vaginal discharge could signal infection
  • Extreme pain (consider ectopic pregnancy)
  • Bladder or bowel function – changes  here may suggest a mass from local neoplasm
  • Headaches,  breast discharge, hot flashes and acne or symptoms of hypo- or hyperthyroidism may suggest endocrinologic dysfunction (2,3)

Physical

  • Determine if there is bleeding on an external surface – vulva, urethra, anus
  • Note any masses, lacerations, ulcerations, vaginal discharge
  • Uterus Assessment: determine size, contour, position, tenderness. Assess for presence of fibroids, infection or pregnancy
  • Examine adnexa for ovarian masses
  • General Exam looking for systemic illness: endocrine abnormalities, enlarged lymph nodes, fever.(3)

Investigations

  • Pregnancy test – to rule out an intrauterine or ectopic pregnancy, a serum or urine test should be performed. Gestational trophoblastic disease can present with uterine bleeding and a positive pregnancy test, anywhere from weeks to years after a pregnancy.
  • Cervical cytology – to exclude cervical cancer
  • Transvaginal ultrasound in postmenopausal women – transvaginal ultrasound as a measurement of endometrial thickness is an alternative to biopsy in postmenopausal women only, not in premenopausal women whose endometrial thickness varies with time of month

Confirmative diagnosis of endometrial carcinoma is made based on pathology of tissue obtained via biopsy, curettage or hysterectomy.(4) If biopsy confirms endometrial cancer, additional measures will need to be taken, namely:

  • Imaging: Chest X-ray, CT of abdomen and pelvis
  • In some cases: IVP, Cystoscopy , Proctosigmoidoscopy

Summary

All patients with suspected endometrial cancer should have a complete:

  • History
  • Physical
  • Pelvic Ultrasound
  • Endometrial sampling: D&C (Dilation and Curettage) or endometrial biopsy
  • Additional staging investigations may include: CXR, CT scan, ultrasound and/or proctoscopy if there is local invasion5

Pathology

Endometrial hyperplasia is characterized by a proliferation of endometrial glands that results in a greater gland to stroma ratio than would be seen in normal endometrial tissue.  It is characterized by proliferation of endometrial glands that almost always results from chronic estrogen stimulation unopposed by progesterone. The hyperplasia may be non-neoplastic or neoplastic, however neoplastic hyperplasia is a precursor to the most common form of endometrial carcinoma – so the presence of either type of hyperplasia is notable.(1)

The World Health Organization’s classification system for endometrial hyperplasia is based on the architecture of the glands and stroma, and level of nuclear atypia. Nuclear atypia is defined as the presence of nuclear enlargement where the chromatin may be arranged in a clump pattern or be evenly dispersed. These two dimensions yield four categories, seen below with more information.  For comparison, normal endometrium exhibits no crowding of glands in the stroma – thus is said to have less than 50% gland:stroma ratio. (1)

  • Simple hyperplasia – Glands mildly crowded ( <50% gland:stroma ratio)
  • Complex hyperplasia – Glands crowded ( 50% gland:stroma ratio)
  • Simple atypical hyperplasia – Normal glands but nuclear atypia present
  • Complex atypical hyperplasia – Crowded glands + nuclear atypia

For simple and complex hyperplasia, the risk of developing endometrial cancer is approximately 1-3%. Complex atypical hyperplasia however is considered synonymous with carcinoma-in-situ and 30% of these cases will develop into endometrial carcinomas.(2)

The World Health Organization and International Society of Gynecological Pathologists have developed the following classification system for endometrial carcinomas.(3)

  • Endometrioid Carcinoma: the most common type of endometrial carcinoma, associated with unopposed estrogen exposure.
  • Serous and Clear Cell Carcinoma: highly aggressive cancers that usually present at a more advanced stage, and thus confer a poorer prognosis than endometrioid carcinomas
  • Mixed Pattern Cancers: these carcinomas presents with growth patterns characteristic of both serous and endometrioid tissues. It is the ratio of serous to endometrioid tissue that helps determine classification
  • Rare Subtypes: mucinous, transitional cell, small cell and squamous cell carcinomas together comprise less than 2% of endometrial carcinomas. (3)

Staging

Staging of endometrial cancer is based on the joint 2010 International Federation of Gynecology and Obstetrics (FIGO)/TNM classification system, an abbreviated version of which is below:

Treatment

The standard treatment of endometrial carcinoma is Total Abdominal Hysterectomy and Bilateral Salpingo-Oophorectomy (TAH-BSO). Surgery alone is reserved for patients with low recurrence risk, such as those with Grade 1 or 2 lesions as adjuvant therapy has not been shown to improve overall survival. Adjuvant therapy is recommended for those with risk factors. Surgery may be undesirable  for some due to its implications for fertility.(1)

Adjuvant therapies that may be offered include:

pelvic radiation, or vaginal brachytherapy chemotherapyhormone/high-dose progestin treatments. (4)

The decision to pursue adjuvant therapy is based on the risk of persistent or recurrent disease and is guided by stratifying patients into low, intermediate or high risk groups as outlined below.

Risk Stratification

Low Risk – women with grade 1 or 2 endometrioid cancers that are limited to the endometrium.

  • Initial treatment is TAH-BSO without adjuvant therapy as it does not improve overall survival
  • As there is very low risk of distant metastases, chemotherapy is not used in this group (1)

Intermediate risk – if the cancer invades the myometrium, or cervical stroma or is of grade 2 or 3.

  • A combination of factors including stage and grade are considered to determine if radiation would be beneficial.  Radiation may be delivered to the pelvis  and vaginal vault or the vaginal vault alone.
  • Grade 3 tumours and Stage 2 or greater may also be candidates for chemotherapy

High Risk – stage 3 disease, uterine sarcoma or clear cell carcinoma of any stage. 

  • A combination of surgery, adjuvant therapies and chemotherapies are offered
  • Other factors affecting risk include lower uterine segment involvement, positive peritoneal cytology, age and ethnicity. (4)

Prognosis

Prognostic Factors

  • Age (1)
  • Tumor grade 
    – grade 1 or 2 tumours typically have favorable outomes. grade 3+ tumours have poor prognoses. (1)
  • Stage or degree of spread 
    – the rate of five-year survival for stage 1 disease is approximately 80-90%, for stage II is 70-80%, and for stages III,IV is 20-60%. (2)
  • Cell type 
    – among cell types, papillary serous, squamous, undifferentiated and clear cells are associated with poor outcomes. (3)

Follow-Up

A large percentage of endometrial carcinoma recurrences occur within three years post-treatment, with the most common sites of recurrence being the vaginal vault, pelvis, abdomen, and lungs. Around 70% of recurrences are associated with symptoms; symptoms suggestive of recurrence include vaginal bleeding, abdominal or pelvic pain, persistent cough, or unexplained weight loss.(1)

The BC Cancer Society has carrying recommendations for follow up, dependent on the treatments given to patients. A history and physical is always recommended, followed by any investigations that are indicated by symptoms or signs on exam. A summary table can be found below. (2)

Summary

1. Describe the blood supply and lymphatic drainage of the cervix, uterus and gonads.

2. State the incidence of endometrial cancer in Canada.

Endometrial cancer is the most common gynecological cancer in Canada, being the 4th most common cancer in women after breast, lung and colorectal cancers. The incidence is 21 per 100,000 people. The lifetime probability of developing endometrial cancer is 1 in 40.

3. List the risk factors for development of endometrial cancer

Type 1 Risk Factors Endometrial Cancer are:

  • Increasing Age
  • Estrogen Exposure – early or late menarche, nulliparity, anovulation, obesity, PCOS, thyroid dysfunction
  • Genetics – Lynch Syndrome, BRCA1 Mutation

It is notable that protective factors for endometrial  carcinoma include estrogen-progestin oral contraceptives, physical activity tea and coffee.

Type 2 Risk Factors

  • Non estrogen related factors
  • p53 mutations are the predominate molecular finding

4. Describe how the cancer develops and how it spreads

  • Develops mostly due to unopposed estrogen exposure
  • Local Invasion – to myometrium, cervix, fallopian tubes, ovaries, bladder, rectum
  • Lymphatic Spread – to pelvic or lumbar lymph nodes
  • Hematogenous – to lungs or bone

5. State the screening protocol for endometrial cancer.

Screening is not recommended unless a genetic syndrome is identified.

6. Describe the possible signs and symptoms of endometrial cancer.

  • Abnormal Uterine Bleed
  • Abnormal Cytology (pap) findings noted incidentally on pap
  • Incidental finding from other procedure (eg. hysterectomy)

7. List a differential diagnosis for abnormal vaginal bleeding in pre and post menopausal women

Premenopausal – fibroids, polyps, anoulavtory cycles (PCOS), cervical cancer (post coital)Postmenopausal – atrophy (50%), polyps, cervical cancer, endometrial hyperplasia, endometrial cancer

** note that this differential does not take into account Tamoxifen therapy (which can also cause gynecological bleed), coagulation abnormalities, herbal supplements or trauma.

8. Describe how you would investigate a woman with abnormal vaginal bleeding

  • History (gyne hx, family hx, pregnancy, symptom characterization)
  • Physical (pelvic exam, asses for general unwell)
  • Biopsy/D&C/hysteroscopy – need endometrial tissue to diagnose endometrial cancer

9. Discuss the malignant transformation of the endometrium and its relationship to hormonal influence in endometrial hyperplasia and cancer.

Endometrial hyperplasia is characterized by a proliferation of endometrial glands that results in a greater gland to stroma ratio than would be seen in normal endometrial tissue.  It is characterized by proliferation of endometrial glands that almost always results from chronic estrogen stimulation unopposed by progesterone. The hyperplasia may be non-neoplastic or neoplastic.

10. Describe the pathology for endometrial hyperplasia and adenocarcinoma of the uterus

Pathologically, endometrial carcinoma can be classified based on cell type with a correlated prognosis.

11. Outline the staging system for endometrial cancer

12. Describe the principles of surgical, radiation and hormonal therapies for endometrial cancer

Virtual Patient Case

This case study was designed to supplement your knowledge on the workup of endometrial cancer and test what you have learned after going through module. Use your mouse to click through the slides and answer each question in the text box provided.

Note: This case can be completed on an iPad. To do this download the (free) Articulate Mobile Player for the iPad by clicking here.

References

Anatomy Review

  1. Barber MD, Park AJ. Surgical Pelvic Female Anatomy. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  2. Netter Anatomy [internet]. Elsevier. Available from: http://www.netteranatomy.com/anatomylab/subregions.cfm?subregionID=R55

Epidemiology

  1. Canadian Cancer Society’s Advisory Committee on Cancer Statistics. Canadian Cancer Statistics II 2013. Toronto, ON: Canadian Cancer Society; 2013.
  2. Halperin EC, Perez CA, Brady LW.Principles and Practice of Radiation Oncology. 5th ed.Phladelphia: Lippincott Williams & Wilkins;2008.
  3. Lee-May,C, Berek JS. Endometrial Carcinoma: epidemiology and risk factors. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  4. Lomo LC, Hecht JL. Endometrial Carcinoma: histopathology and pathogenesis. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.

Screening

  1. Lee-May,C, Berek JS. Endometrial carcinoma: epidemiology and risk factors. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  2. Lu KH, Schmeler KM. Endometrial and ovarian cancer screening and prevention in women with Lynch Syndrome (hereditary nonpolyposis colorectal cancer). In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.

Classification

  1. Lomo LC, Hecht JL. Endometrial Carcinoma: histopathology and pathogenesis. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.

Signs and Symptoms

  1. Neal; AJ, Hoskin, PJ. Clinical Oncology: Basic Principles and Practice. 3rd ed. New York: Oxford University Press; 2003.
  2. Lee-May,C, Berek JS. Endometrial Carcinoma: epidemiology and risk factors. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.

Diagnosis

  1. Goodman,A. Overview of causes of genital tract bleeding in women. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  2. Goodman A. Initial approach to the premenopusal woman with abnormal uterine bleeding. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  3. Goodman A. Terminology and evaluation of abnormal uterine bleeding in premenopausal women. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  4. Lee-May,C, Berek JS. Endometrial Carcinoma: epidemiology and risk factors. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  5. Murphy GP, Lawrence WM, Lenhard RE. American Cancer Society Textbook of Clinical Oncology. 2nd ed. American Cancer Society: Atlanta; 1995

Pathology

  1. Giuntoli RL, Zacur HA. Classification and diagnosis of endometrial hyperplasia. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  2. Murphy GP, Lawrence WM, Lenhard RE. American Cancer Society Textbook of Clinical Oncology. 2nd ed. American Cancer Society: Atlanta; 1995
  3. Lomo LC, Hecht JL. Endometrial Carcinoma: histopathology and pathogenesis. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.

Staging

  1. 1) Plaxe SC. Endometrial carcinoma: pretreatment evaluation, staging and surgical treatment. In: UpToDate,Rose, BD (Ed), UpToDate, Waltham, Ma, 2013

Management

  1. Plaxe SC, Mundt AJ. Treatment of low-risk endometrial cancer. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  2. Murphy GP, Lawrence WM, Lenhard RE. American Cancer Society Textbook of Clinical Oncology. 2nd ed. American Cancer Society: Atlanta; 1995
  3. Plaxe SC, Mundt AJ. Overview of Endometrial Carcinoma. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  4. Giuntoli RL, Zacur HA. Classification and diagnosis of endometrial hyperplasia. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  5. Plaxe and Mundt. Approach to adjuvant treatment of endometrial cancer. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.

Prognosis

  1. Lomo LC, Hecht JL. Endometrial Carcinoma: histopathology and pathogenesis. In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  2. Plaxe SC. Endometrial carcinoma: pretreatment evaluation, staging and surgical treatment. In: UpToDate,Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  3. Murphy GP, Lawrence WM, Lenhard RE. American Cancer Society Textbook of Clinical Oncology. 2nd ed. American Cancer Society: Atlanta; 1995

Follow-up

  1. Plaxe SC, Mundt AJ. Overview of Endometrial Carcinoma In: UpToDate, Rose, BD (Ed), UpToDate, Waltham, Ma, 2013.
  2. Endometrium Cancer Follow-up Guidelines. BC Cancer Agency. 2013. Available at: http://www.bccancer.bc.ca/HPI/CancerManagementGuidelines/Gynecology/Endometrium/FU.htm. Accessed July 30, 2013.

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