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Endometrium

Endometrium

Updated June 2016

FIGO Staging​

Distribution of patients and approximate Five Year Survival by Surgical Stage/Sub-stage [REVISED FIGO STAGE 2009]

(corrected to exclude death from intercurrent disease)

FIGO stage

Substage

Definition

Proportion of all patients

5-year overall survival

I

Tumour confined to corpus uteri

 

 

 

IA

Tumour limited to endometrium or invades less than one half of the myometrium

56%

90%

IB

Tumour invades one half or more of the myometrium

20%

81%

II

 

Tumour invades stromal connective tissue of the cervix but does not extend beyond uterus

7%

67%

III

Local and/or regional spread

 

 

 

IIIA

Tumour involves serosa and/or adnexae (direct extension or metastases)

8%

60%

IIIB

Vaginal involvement (direct extension or metastasis) or parametrial involvement

2%

41%

IIIC

Metastases to pelvic and/or para-aortic lymph nodes

4%

32%

IIIC1

Regional lymph node metastases to pelvic lymph nodes

 

 

IIIC2

Regional lymph node metastasis to para-aortic lymph nodes, with or without positive pelvic lymph nodes

 

 

IV

Tumour invades bladder mucosa and/or bowel mucosa, and/or distant metastases

 

 

 

IVA

Tumour invades bladder mucosa and/or bowel mucosa (bullous edema is not sufficient to classify a tumour as T4)

1%

20%

IVB

Distant metastases (includes metastases to inguinal lymph nodes, intraperitoneal disease, or lung, liver, or bone metastases)

3%

5%

Changes from previous staging system:

  1. FIGO no longer includes Stage 0 (carcinoma in situ)
  2. Stage IA/IB combined into Stage IA; Stage IB now includes deep myometrial invasion (previous Stage IC)
  3. Endocervical glandular involvement only should be classified as Stage I – it is no longer stage II
  4. Peritoneal cytology no longer included in staging system
  5. Stage IIIC subdivided into pelvic nodes alone (Stage IIIC1) or involved para-aortics (Stage IIIC2)

NB: Omentum or peritoneal disease = Stage IVB

It should be noted that these figures are approximations of five-year survival data collected from large numbers of patients within a given stage (FIGO data). Caution should be used in attempting to use these data to assign prognosis in an individual case as outcomes within these substages will worsen depending on grade and histotype (e.g., papillary serous and MMMT).

1. Predisposing Factors/Prevention

Updated December 2015

Risk Factors:

This cancer is the fourth most common malignancy affecting women in BC, and the most common gynecologic malignancy.  According to Canadian Cancer Statistics, the incidence of this cancer has been increasing over the last 30 years.
 
There are two types of endometrial cancer: Type 1 is characterized by an excess of estrogen, which can be attributed to obesity (conversion of androstenedione to estrone in adipose tissue), anovulatory conditions (polycystic ovarian syndrome, which results in a deficiency of progesterone), and exogenous estrogen (estrogen hormone replacement therapy, or tamoxifen, a selective estrogen receptor modulator, which acts as an estrogen agonist in the uterus).  Although associated with obesity, type 2 diabetes is also an independent risk factor for Type 1 cancers, related to hyperinsulinemia.  Type 1 cancers account for approximately 80-85% of all uterine cancers.  They are endometrioid histology, most commonly grade 1 (well differentiated), and early stage.  Approximately 15-20% of all women with Type 1 cancers are premenopausal. In general, Type 1 cancers are associated with a good prognosis, particularly if they present as Stage I, grade 1.  

Type 2 endometrial cancer is characterized by non-endometrioid histotypes, and are high-grade tumours. These include uterine papillary serous carcinoma (high-grade serous carcinoma), malignant mixed mullerian tumour (carcinosarcoma), and clear cell carcinoma.  These cancers are more likely to present at an advanced stage compared to endometrioid carcinomas.  Even among those who present with Stage I disease, there is a higher likelihood of recurrence compared to endometrioid carcinomas, and therefore these patients with Type 2 cancers are often offered adjuvant chemotherapy and radiotherapy, even if they have Stage I disease.  These patients do not have the same risk factors as those with Type 1 cancers.  These patients with Type 2 cancers tend to be older, they are more likely to have a normal body mass index (BMI) and they do not appear to be related to an excess of estrogen.  These cancers have a molecular profile that is different (p53 mutations) from those with endometrioid cancers (PTEN mutations).

Endometrial cancer is also seen as part of Lynch syndrome (Hereditary non-polyposis colorectal cancer, HNPCC).  This hereditary cancer syndrome is characterized by a very high lifetime risk of endometrial and colorectal cancers (both approximately 60%), as well as ovarian (lifetime risk of 10%), gastric, small bowel, ureter, and renal pelvis.  This syndrome is caused by an inherited mutation in one of the DNA mismatch repair genes (mutations in MLH1, MSH2, MSH6, PMS2 account for 99% of all Lynch Syndrome).  The endometrial cancer histotypes and outcomes in Lynch Syndrome are similar to those in the general population.

Prevention:

With respect to prevention, weight loss in obese women and improving glycemic control in diabetic women may have the most potential for reducing risk in these specific populations. The use of combination oral contraceptives has been shown to decrease risk by 50% if used for 5 or more years. The addition of a progestin to estrogen replacement therapy counteracts the adverse effects of unopposed estrogen on the endometrium.  Women who are identified as having Lynch Syndrome are advised to consider risk-reducing surgery (hysterectomy and bilateral salpingo-oophorectomy) to reduce their risk of endometrial and ovarian cancers.  Screening for endometrial and ovarian cancer using endometrial biopsy, transvaginal ultrasound, and CA125 has not been proven to decrease the incidence or mortality from cancer in these high-risk women.

References:

  1. ​Kelsey J, Whittemore AS. Epidemiology and primary prevention of cancers of the breast, endometrium and ovary: a brief review. Ann Epidemiology 1994;4:89-95. 
  2. Miller AB. Planning cancer control strategies. Chronic Dis Can 1992;13:S1-S40. 
  3. Schmeler KM et al, Prophylactic surgery to reduce the risk of gynecologic cancers in the Lynch Syndrome. N Engl J Med 2006;354(3):261-9. 


2. Screening/Early Detection

​Updated December 2015

Screening for endometrial cancer (endometrial biopsy, transvaginal ultrasound, CA125) has never proven to be effective in asymptomatic women.  There is a role for endometrial biopsy to gauge response to therapy for women who are using progestins as fertility-sparing or conservative management for endometrial hyperplasia/cancer. Women on tamoxifen have an increased risk of endometrial cancer.  However, screening asymptomatic women on tamoxifen is not recommended. Only those who develop abnormal uterine bleeding need endometrial sampling.

Patients with endometrioid ovarian cancers and adult granulosa cell tumors of ovary have an increased risk for endometrial cancer, and hysterectomy is recommended routinely as part of their management. If fertility preservation is important, this should be discussed with the gynecologic oncologists at BC Cancer Agency.

It must be emphasized that Pap smear is not a satisfactory screening procedure for endometrial cancer (it is only a screening test for cervical cancer).  All cases of post-menopausal and intermenstrual bleeding or spotting require investigation, which includes a pelvic examination and endometrial tissue sampling. Post-menopausal women who develop a sudden onset of an unusual vaginal discharge in the absence of an identifiable vaginal cause may be suffering from endometrial cancer and require similar investigation. A variety of techniques are available to evaluate patients including endometrial biopsies, hysteroscopy and D&C.  Pelvic ultrasound may be helpful to determine if there is a thickened endometrium, which may suggest endometrial pathology (polyp, cancer).  However, a biopsy is still required to obtain a tissue diagnosis.

NB: A normal endometrial thickness on ultrasound does not rule out endometrial cancer.

3. Diagnosis

​Udpated 23 November 2012

3.1 WHO/ISGP Classification of Endometrial Carcinoma

  • Endometrioid
    • Typical
    • Variants
      • Villoglandular (papillary)
      • With squamous differentiation
      • Secretory
      • Ciliated
  • High grade serous (HGS) adenocarcinoma (also known as serous carcinoma or uterine papillary serous carcinoma)
  • Clear cell adenocarcinoma
  • Mucinous adenocarcinoma
  • Squamous cell carcinoma
  • Undifferentiated carcinoma
  • Mixed carcinoma
    • (two of above histological types in which minor component accounts for 10% or more of the tumour)

Mixed Epithelial-Mesenchymal Tumors

  1. Adenofibroma
  2. Adenomyoma including atypical polypoid adenomyoma
  3. Adenosarcoma, homologous and heterologous
  4. Carcinofibroma
  5. Carcinosarcoma (also known as malignant mullerian mixed tumor - MMMT), homologous and heterologous. This is now recognized as representing high grade, metaplastic adenocarcinoma and treated as such.

3.2 Diagnosis/Surgical Management

An endocervical curettage is no longer recommended as part of clinical staging as it is not accurate for assessing cervical stromal invasion, and the presence of endocervical glandular involvement only is no longer part of the FIGO staging system. All patients with potential clinical involvement of the cervix should be referred for assessment regarding possible surgical staging.  Patients who are deemed to have inoperable disease by the gynecologic oncology team will be referred for preoperative chemotherapy plus or minus radiotherapy. These patients are at a higher risk of both locoregional and distant recurrence and require multidiscipli​nary care, which may include chemotherapy, radiotherapy and surgery.

In 1988 FIGO adopted a surgical staging system for cancer of the uterine corpus (Endometrium), which was revised in 2009. Careful intraoperative exploration, including nodal assessment, is the responsibility of the operating surgeon. Only those skilled and experienced in lymph node dissection should carry out such procedures (see Surgery Table 1).

Lymph node dissection is not routinely performed for grade 1 endometrioid tumors because the risk of nodal involvement is outweighed by the potential perioperative risks associated with this procedure, and therefore these cases may have surgery performed by a general gynecologist. Although full lymphadenectomy is not routinely performed for grade 2 and 3 endometrioid tumors, these cases have a higher risk of lymph node involvement and may require nodal sampling. Therefore, it is recommended that these patients have their surgery performed by a gynecologic oncologist. Lymph node dissection is routinely performed on all cases with non-endometrioid histology (Type 2 cancers such as high grade serous or clear cell carcinoma), as they may have lymph node involvement in the absence of high-risk uterine factors such as deep myometrial invasion.

At the time of the staging procedure careful evaluation of pelvic and para-aortic nodal areas should be carried out and any large lymph nodes should be biopsied/removed. In the setting of enlarged nodes, debulking of these nodes rather than complete node dissection is preferred, as these patients will receive postoperative XRT, and single modality treatment diminishes the rate of morbidity, particularly if there are enlarged para-aortic nodes and extended field radiotherapy is required. The patient should be referred as soon as a diagnosis is made for planning of chemotherapy and radiotherapy

Proper handling of a hysterectomy specimen by the pathologist is essential for evaluating tumour factors that may affect postoperative adjuvant treatment in patients with endometrial adenocarcinoma. If the specimen is not going to be fixed promptly (e.g., surgery on Friday afternoon, or before a holiday), the gynecologist should open the uterus at the 3 and 9 o'clock positions on the cervix, extend these incisions from the external os laterally along the sides of the uterus up to the fundus, and promptly place the specimen in formalin for overnight fixation. Lack of prompt fixation may result in severely autolyzed hysterectomy specimens that will preclude accurate histologic grading and assessment of depth of invasion, which are essential for prognosis and treatment planning.


4. Staging

Updated December 2015

4.1 Clinico-Pathologic Considerations

Gross Description

Gross description of the hysterectomy specimen should include:

  1. Whether the tumour is in a polyp or not
  2. Location of the tumour within the uterus (fundus, or lower uterine segment)
  3. The depth of myometrial invasion (luminal or serosal half)
  4. The presence or absence of cervical stromal involvement

Microscopic Description

  1. The histologic type
  2. The histologic grade (1-3) 
  3. Myometrial invasion if present 
    • Luminal half (less than 50% invasion)
    • Serosal half (more than 50% invasion)
  4. The presence or absence of lymphatic or vascular invasion and extent
  5. Perilymphatic inflammation (slight, moderate, marked)
  6. Cervical involvement (endocervical or stromal involvement)
  7. Lymph node involvement
  8. Adnexal involvement
  9. Cytology of peritoneal fluid, if obtained

4.2 Staging Di​​agram

Corpus uteri.pdf

4.3 Preoperative Investigations for Staging

  • chest x-ray 
  • imaging with CT or U/S as appropriate (if suspicion of extrauterine disease, or if unable to assess the size of the uterus)
  • tumor markers: CA 125 is most helpful, as an elevated CA125 is associated with extrauterine disease, CA 19-9, CA 15-3, CEA

5. Management

Updated February 2016

5.1 Surgery

A. Primary Surgery (If the cancer appears to be confined to the uterus, i.e., clinical Stage I):

Preoperative Grade 1: Hysterectomy and bilateral salpingo-oophorectomy (HBSO*) by gynecologist

Preoperative Grade 2 or 3:  HBSO, possible lymph node sampling or nodal debulking by gynecologic oncologist

Preoperative Type 2 cancer (high grade serous, clear cell carcinoma, carcinosarcoma): HBSO, lymphadenectomy, omentectomy, peritoneal washings**, tumour debulking by gynecologic oncologist

*HBSO can be accomplished by laparotomy or minimally invasive approach (vaginal, laparoscopic assisted, total laparoscopic, robotic assisted).

** Status of washings is no longer considered part of FIGO staging, nor does it influence adjuvant treatment decisions for Type 1 (endometrioid) cancers.  However, it may still be useful in those with Type 2 cancers, which have atypical patterns of metastases (peritoneal washings may be positive in the absence of metastatic disease).

B. Delayed primary surgery (if surgery upfront is not possible):

Clinical Stage II (bulky cervical involvement)

Clinical Stage IIIC (with bulky/unresectable nodes)

Clinical Stage IV (metastatic disease on preoperative imaging, or bladder/bowel involvement)

These patients will receive chemotherapy +/- radiotherapy first, followed by repeat imaging and assessment by a gynecologic oncologist after the 2nd cycle of chemotherapy to determine response to treatment and suitability for delayed primary surgery.  If there has been a good response to treatment, surgery will usually be considered after the 3rd cycle of chemotherapy.  This will be followed by an additional 3 cycles of chemotherapy, with or without radiotherapy, to be determined by the multidisciplinary team.

Indications for referral to a Gynecologic Oncologist: 

  1. preoperative grade 2 or 3
  2. preoperative high-risk histology (Type 2 cancers) including papillary serous, clear cell or carcinosarcoma
  3. clinically advanced stage endometrial cancer – clinical stage II and beyond

5.2 Adjuvant Therapy

5.2.1 Endometrioid Carcinomas

Risk Group

Number of Risk Factors

​​​​Stage/grade

Risk of recurrence without adjuvant therapy

Low Risk

0

Stage IA, grade 1 or 2

3-5%

Intermediate Risk

1

Stage IA, grade 3 or Stage 1B, grade 1

10%

High Risk

2

Stage IB, grade 3

25%

Adjuvant pelvic radiation is offered to those whose disease appears to be confined to the pelvis (uterus, cervix, adnexae, pelvic nodes), but remain at risk for pelvic recurrence after surgery. Adjuvant vault radiation is offered to those whose disease appears to be confined to the uterus, but have at least one high-risk uterine factor (deep myometrial invasion, or Grade 3 tumour) that increases their risk for vault recurrence. 

Patients with LVSI (+) and low-risk and intermediate-risk disease are considered at high risk of recurrence and pelvic radiation is recommended.  Most of these recurrences in the absence of adjuvant therapy occur in the pelvis.  There is insufficient evidence that patients with low-risk or intermediate-risk disease with LVSI+ should receive chemotherapy. 

Patients with Stage I high-risk disease (deep myometrial invasion and grade 3 tumour) as well as Stage II disease are at high risk of locoregional as well as distant recurrence, regardless of their lymph node status (negative or unknown).  They should be referred for consideration of chemotherapy and radiotherapy.  For those with Stage I high-risk disease, the standard is 3 cycles of chemotherapy, followed by radiotherapy, and for those with Stage II or III disease, the recommendation is 6 cycles of chemotherapy and radiotherapy in either a “sandwich” or “sequential” protocol.  The “sandwich” protocol consists of 3 cycles of chemotherapy, radiotherapy, then 3 more cycles of chemotherapy, and the “sequential” protocol includes 6 cycles of chemotherapy followed by radiotherapy.  For those with Stage IIIC disease (node-positive), radiotherapy to the para-aortic nodes will be considered.  The multidisciplinary team (medical and radiation oncology) should collectively determine the optimal protocol for each eligible patient.

Stage IVB. With upper abdominal disease present, the likelihood of distant recurrence is very high, in which case chemotherapy alone for 6 cycles is generally recommended. 

Table 1. Adjuvant therapy guidelines for endometrioid carcinomas:

 

 IA

 IB

 II**

 IIIA /B

IIIC^ IV

 Grade 1

 O

 V

 C, P, V C+P C+P C

 Grade 2 

 O

 V

 C, P, V

 C+P

 C+P C

 Grade 3

 V

C+P

 C, P, V

 C+P

 
 C+P C


O=observation
V=vault brachytherapy
P=pelvic radiation
C=chemotherapy

* For Stage IA or IB recommend pelvic radiotherapy if there is LVSI (any extent)

**For Stage II, recommend chemotherapy if there is at least one additional high-risk uterine factor (deep myometrial invasion, or grade 3 tumour).  

^Pelvic radiotherapy will include extended field to cover para-aortic nodes if positive pelvic or para-aortic nodes


5.2.2 Non-Endometrioid Carcinomas

These cancers have an atypical pattern of metastatic spread.  Unlike endometrioid carcinomas, there can be extrauterine involvement even in the absence of myometrial invasion.  Non-endometrioid carcinomas are all considered high-risk, even when confined to the endometrium.  The only exception is if patients have undergone a complete surgical staging procedure and are proven to have no myometrial invasion.  These patients do not require any adjuvant therapy as their recurrence risk is less than 10%.  For those who have undergone a full surgical staging procedure and have Stage I disease limited to less than 50% myometrial invasion, vault brachytherapy will suffice for local control, in additional to chemotherapy for distant control.  However, if there is deep myometrial invasion despite negative nodes (Stage IB), these patients are at high risk of pelvic recurrence and should receive pelvic radiotherapy, in addition to chemotherapy.  Although these patients have Stage I disease, they are considered high-risk and should receive 6 cycles of chemotherapy (with radiotherapy as per sandwich or sequential protocol). 

Table 2.  Adjuvant therapy guidelines for non-endometrioid carcinomas:

IA M- IS M+ IB, II, III** IV***
Fully staged*ObservationC+VC+PC
Incompletely stagedRestaging, or C+PC+PC+PC

M–: no myometrial invasion; M+: myometrial invasion

*Fully staged includes complete lymphadenectomy, omentectomy, washings 

**Pelvic radiotherapy will include extended field to cover para-aortic nodes if positive pelvic or para-aortic nodes

Consider using hormones instead of chemotherapy as first-line therapy for stage IVB grade 1.  Grade 1 tumors have a response rate up to 30% whereas it is around 10% for Grade 3. Treatment options include: Tamoxifen 20 mg po od, Letrozole 2.5 mg po od, Megace 160 mg po od, or Provera 200 mg po od. If hormone therapy fails, the next choice would be standard chemotherapy.

5.3 Chemotherapy

Carboplatin/paclitaxel (GOENDCAT) is the recommended protocol based upon the superiority of taxane-platin containing regimens over platinum-anthracycline regimens and lower toxicity of carboplatin-paclitaxel compared to cisplatin/adriamycin/paclitaxel.

Special Histologies/Situations

1.  Small Cell Carcinomas
     Rare tumour in endometrium. See cervix protocol (SMCC2)
2.  Isolated pelvic relapse: refer to BCCA for immediate assessment as cure may be possible.

References

  1. Kwon JS et al. Are uterine risk factors more important than nodal status in predicting survival in endometrial cancer? Obstet Gynecol 2009;114(4):736-43. 
  2. Fleming GF et al. Phase III trial of doxorubicin plus cisplatin with or without paclitaxel plus filgrastim in advanced endometrial carcinoma:  a Gynecologic Oncology Group study. J Clin Oncol 2004;22(11):2159-66. 
  3. Hoskins PJ et al. Paclitaxel and carboplatin, alone or with irradiation, in advanced or recurrent endometrial cancer: a Phase II study.  J Clin Oncol 2001;19(20):4048-53. 
  4. Carey MS et al. Systematic review of systemic therapy for advanced or recurrent endometrial cancer. Gyn Oncol 2006;101(1):158-67. 

5.4 Mismatch Repair 

In the Vancouver Coastal Health Authority Region, all endometrial cancers are currently tested using immunohistochemistry (IHC) for 4 mismatch repair (MMR) proteins as a reflex screening test for Lynch Syndrome.  Approximately 20-25% of all endometrial cancers have abnormal MMR (deficiency of staining for one of the MMR proteins).  Women with abnormal MMR should be referred for genetic counselling and testing through the Hereditary Cancer Program at the BCCA, regardless of age and family history.  Abnormal MMR does not necessarily mean that the patient has a germline mutation in the corresponding gene.  However those with abnormal MSH2 or MSH6 on IHC have at least a 50% risk of having a mutation, and therefore having Lynch Syndrome.  Those with abnormal MLH1 have about a 10% risk of having a mutation.  The remaining 90% of those with abnormal MLH1 have a somatic phenomenon called hypermethylation of the MLH1 promoter, which is not associated with Lynch Syndrome.  

Referral to the Hereditary Cancer Program at BCCA is important for these women even though they have already had endometrial cancer because: (1) they may still be at risk for colorectal cancer, and therefore they can undergo more frequent screening to prevent this cancer; (2) they may have unaffected first degree relatives who could benefit from this information, and undergo risk-reducing interventions to prevent endometrial and colorectal cancers. 

Screening for MMR may become routine for all endometrial cancers in British Columbia in the near future.  At the present time, any woman diagnosed with endometrial cancer under the age of 50 in British Columbia is eligible for MMR IHC, but a direct request for testing must be submitted to BCCA.

References

  1. Kwon JS et al. Testing women with endometrial cancer to detect Lynch Syndrome.  J Clin Oncol 2011;29(16):2247-52.  
  2. Buchanan DD et al. Tumor mismatch repair immunohistochemistry and DNA MLH1 methylation testing of patients with endometrial cancer diagnosed at age younger than 60 years optimizes triage for population-level germline mismatch repair gene mutation testing.  J Clin Oncol 2014;32(2):90-100.  

5.5 Estrogen Replacement Therapy

Endometrial tumours that develop on estrogen replacement therapy tend to be well differentiated and minimally invasive, and therefore these women generally have a good prognosis.  However, the known association between estrogen and endometrial cancer causes concern when women with a history of endometrial carcinoma request hormone replacement. 

Many of these patients are asymptomatic. There is a small proportion of patients (usually premenopausal) who suffer from extreme vasomotor symptoms. Unfortunately, there are limited non-hormonal alternatives to estrogen, such as clonidine or venlafaxine.

For premenopausal women, thorough discussion of the risks and benefits of estrogen replacement is essential. . The absence of hormone replacement therapy in young women who have surgery including bilateral salpingo-oophorectomy before age 50 is known to be associated with an increased risk of death sec​ondary to coronary heart disease, osteoporosis, thromboembolic events, and cancers such as lung and colorectal cancer1.  There is no evidence that estrogen replacement therapy use alters the prognosis in women who have had treatment for endometrial cancer2.

References

  1. Parker WH et al. Long-term mortality associated with oophorectomy compared with ovarian conservation in the Nurses’ Health Study. Obstet Gynecol 2013;121(4):709-16.  
  2. Barakat RR et al. Randomized double-blind trial of estrogen replacement therapy versus placebo in Stage I or II endometrial cancer:  A Gynecologic Oncology Group study J Clin Oncol 2006;1;24(4):587-92.  




6. Follow-up

Upd​ated December 2015

Follow-up for Endometrial Cancer

  1. Early recognition and prompt management of treatment-related complications
  2. Early detection of persistent or recurrent disease
  3. Collection of meaningful data regarding the efficacy of existing treatment policies and their complications so that any appropriate modifications can be instituted
  4. Risk factors for endometrial cancer are similar to those for other cancers such as breast and colorectal.  Women who have endometrial cancer are at increased risk for these cancers and should be advised to undergo regular screening

In all situations outlined below, history and physical exam, including pelvirectal examination, are recommended. Patients do not need routine bloodwork, pap smear, or imaging, unless indicated by symptoms or signs on examination.

I. Patients in whom no adjuvant treatment is recommended

These patients are at low risk of recurrence (<5%), which is most likely to occur within the first 2 years after primary treatment. The most likely site of recurrence is the vaginal vault, therefore these patients need to be counselled about vaginal bleeding. Their follow-up care can be provided by their referring physician.

Years 1 through 5: every 6 months

Year 5+: annually

II. Patients treated with adjuvant vaginal vault radiation alone

These patients are still at low risk of recurrence (5-10%), which is most likely to occur within the first 2-3 years after primary treatment. They can recur in the pelvis/vault, but some will recur distantly. These patients need to be counselled about vaginal bleeding, pelvic pain, bloating, increased abdominal girth. Their follow-up care can be provided by their referring physician. 

Years 1 2: every 3-6 months

Years 3-5: every 6 months

Year 5+: annually

III. Patients treated with adjuvant pelvic radiation +/- chemotherapy

These patients are at high risk of recurrence, which may be distant or locoregional. Their recurrences are also most likely to occur within the first 2-3 years after primary treatment. These patients will typically be seen at least once following completion of radiotherapy by the radiation oncologist at the BCCA to review/manage side-effects of treatment. Further follow-up care can then be provided by the referring physician. 

Years 1-2: every 3-6 months

Years 3-5: every 6 months

Year 5: annually

IV. Patients who have been recommended adjuvant treatment but have declined

These patients should be followed more frequently as they have the potential for salvage treatment. Their follow-up care can be provided by their referring physician. 

Years 1 and 2: every 3 - 4 months

Years 3 - 5: every 6 months

Year 5+: annually

References

  1. Colombo N et al.  Endometrial cancer:  EMSO clinical practice guidelines for diagnosis, treatment, and follow-up.  Ann Oncol 2013;24(suppl6):vi33-vi38
  2. Canadian Cancer Society 2015 http://www.cancer.ca/en/cancer-information/cancer-type/uterine/treatment/follow-up
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