13.     With regard to endometrial carcinoma.  

Introduction.

There are a lot of headings and sub-headings.

If you don't like hopping about using the links, just keep scrolling down and you will cover everything.

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List of contents.

1. introduction

2. abbreviations

3. key facts for the DRCOG

4. expanded information for the MRCOG

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Abbreviations.

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Key facts for the DRCOG.

1. risk factors, real and otherwise

2.     oestrogen

3.     HRT

4.     the Pill

5.     menstrual history

6.     pregnancy

7.     endometrial hyperplasia   

8.     obesity

9.     diabetes

10.     HNPCC. Lynch type II syndrome

11.     PCOS

12.     oestrogen-sectreting tumours

13.     tamoxifen

14.      talcum powder

15. signs and symptoms

16. investigation

17. factors affecting prognosis

18. prognosis

19. treatment

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Risk factors.

These are commonly asked about in MCQs etc.

Risk factors: oestrogen.

Oestrogen stimulates the endometrium.

Given on its own, “unopposed oestrogen”, it increases the risk.

Adding a progesterone-type drug counteracts this effect.

If a woman never produced oestrogen, e.g. in Turner’s syndrome, she would be at reduced risk (see MCQ4, question 24 and MCQ5, question 14).

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Risk factors: HRT.

Oestrogen-based HRT increases the risk,

    unless a progestogen is given all the time: continuous, combined HRT,

    in which case the risk of cancer actually declines.

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Risk factors: the Pill.

The Pill is not a risk factor.

The incidence is reduced by it.

It also reduces the risk of ovarian cancer.   

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Risk factors: menstrual history.

A late menarche or early menopause reduce the years of oestrogen exposure and the risk.

Nulliparity is a risk factor.

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Pregnancy.

Pregnancy reduces the risk.

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Risk factors: endometrial hyperplasia.

“Simple”, “Complex” and “Atypical” hyperplasia feature in the exam, so you need to know their significance.

The main risk lies with atypical hyperplasia.

There is thickening of the endometrium and distortion of its architecture.

More importantly, there are cytological features of pre-malignancy: 

    increased size and pigmentation of the nuclei,

    and an increased cell division rate, reflected in the number of mitoses.

Malignancy develops in 25-50%.

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Risk factors: obesity.

Obesity roughly doubles the risk.

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Risk factors: diabetes.

Diabetes is a weak risk factor but quoted.

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Risk factors: Lynch type II (HNPCC) families.

Hereditary non-polyposis colorectal cancer, HNPCC, (Lynch type II syndrome) is an autosomal dominant condition.

Women with the HNPCC gene are at increased risk of endometrial cancer.

Some studies put the risk as high as 60%, which is some risk!

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Risk factors: PCOS.

Polycystic ovary syndrome (PCOS) is a risk factor.

Ovulation does not occur as often as normal.

So more time is spent with just oestrogen.

And it is oestrogen which stimulates the endometrium.

See also MCQ4, question 9 "PCOS" and MCQ4, question 12 "Treatment for PCOS".

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Risk factors: oestrogen-secreting tumours.

Oestrogen-secreting granulosa and theca cell tumours produce continuous oestrogen and are obvious risk factors.

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Risk factors: Tamoxifen.

Tamoxifen (see MCQ10, question 22) is now commonly used to reduce the risk of recurrence of breast cancer.

It acts effectively against oestrogen in the breast and reduces the risk of recurrence of breast cancer.

But it acts like oestrogen in the endometrium and increases the risk of benign and malignant disease.

So you have to pay particular heed to patients on Tamoxifen with abnormal bleeding.

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Risk factors: Talcum powder.

There have been research papers suggesting talcum powder as a risk factor.

Sounds a bit far fetched, but it is true!

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Signs and symptoms.

Endometrial cancer usually presents with postmenopausal bleeding.

Less often the presentation will be with postmenopausal discharge.

Occasionally atypical glandular cells are seen on a cervical smear and give rise to the diagnosis.

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Investigation.

“One-stop” clinics are becoming the norm for seeing these patients.

The key investigations are:

    taking a history - the frequency & duration of the bleeding, risk factors etc.,

    examination - looking for signs of signs of primary & secondary disease or possible explanations like polyps, atrophic vaginitis,

    TVS (an endometrial thickness < 4 mm is reassuring) 

    and hysteroscopy and biopsy.

MRI and CT scanning are done to estimate the degree and site of any spread.

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Factors influencing prognosis.

The prognosis in endometrial cancer worsens if:

    the tumour is poorly differentiated,

    or it has extended to the outer third of the myometrium,

    or has extended down to the cervix, whence it may spread fairly readily via the cervical lymphatics,

    or has spread outside the uterus.

Spread may be along the round ligaments to the groin nodes.

Though this is rare, it is one of those stupid questions favoured by those who set examinations.

The other big risk factor is the histology.

Well-differentiated tumours are less aggressive and respond best to treatment.

Poorly-differentiated and anaplastic tumours are very bad news.

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Prognosis.

It is almost as if there were two diseases.

Early, well-differentiated tumours are usually cured with treatment.

Five-year survival is > 80%

Poorly-differentiated tumours that have spread outside the uterus are usually lethal.

Five-year survival rates of 10% being quoted.

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Treatment.

Treatment is usually by hysterectomy and removal of ovaries.

In the more advanced case, the addition of removal of pelvic and para-aortic nodes is appropriate.

Some patients will benefit from post-operative radiotherapy.

In the past some believed that progestagens improved the outlook, but this is no longer believed.

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Expanded information for the MRCOG.

1. useful reading materials

2. prevalence

3. staging

4. risk factors

5.     oestrogen

6.     HRT

7.     the Pill

8.     tamoxifen

9.     alcohol, diabetes, diet, exercise, obesity

10.     PCOS

11.     endometrial hyperplasia

12.     HNPCC: Lynch type II syndrome

13.     oestrogen-secreting tumours

14.    talcum powder

15. signs and symptoms

16. investigation

17. prognosis

18. treatment

    1. surgical: hysterectomy and lymphadenectomy

    2. sentinel nodes

    3. radiotherapy

    4. chemotherapy

    5. HRT use after treatment

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Suggested reading.

FIGO staging in vulval and endometrial cancer: Katharine Edey & John Murdoch. TOG: 2010. October. Vol 12, issue 4, pages 245 - 249.

Endometrial cancer. Catherine Holland. OGRM. April 2010 (Vol. 20, Issue 4, Pages 116-120)

The changing role of the gynaecologist ..... in gynaecological cancer. RCOG SAC Opinion Paper 10.

Cancerhelp.org.uk: womb-cancer-risks-and-causes

Creasman: Emedicine.

Chiang: Emedicine.

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Prevalence.

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Staging.

Staging of tumours is one of the topics for the night before the exam.

An immediate and obvious problem is that staging needs PL and PAL.

Yet the role of lymphadenectomy is still debateable.

The standard view, after ASTEC, is that it does not improve prognosis in women with early disease.

And there is no argument, as there is for adjuvant radiotherapy, that it prevents nasty secondaries.

It would be OK to do it just for staging, if there were no risks.

But it carries risks of vessel damage during surgery and post-operative lymphoedema and cannot be justified in early disease.

There is evidence that it improves prognosis in advanced disease, so is done for these women.

You might also wonder why Stage I includes superficial involvement of the cervical canal.

For many decades we have recognied that prognosis  of disease confined to the uterus was seriously affected by a number of things:

poor differentiation on histology,

invasion of the outer 1/3 of the myometrium,

extension to the cervix.

The point we would make about the cervix is that the body of the uterus has little by way of lymphatics.

But the cervix has very good lymphatic drainage.

EC that got into the substance of the cervix could invade these lymphatics and metastasise easily.

But not while it was only in the superficial layers.

As superficial extension to the endocervical canal has little effect on prognosis, there is sense in it being included in StageI.

Make out a card.

Go through it the night before the exam so that it is with you the next day.

It probably won't last much longer unless you are a trainee oncologist!

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Risk factors

Oestrogen.

Oestrogen stimulates the endometrium.

Given on its own, “unopposed oestrogen”, it increases the risk.

Adding a progesterone-type drug counteracts this effect.

Oestrogen-only HRT (ooHRT) roughly doubles the risk.

Some studies say that there is still a slightly increased risk with added progestogen taken sequentially.

Others that the risk is reduced.

Luesley and Baker say it is decreased with a RR of 0.8, so I'd go with that for the exam.

Continous combined HRT (ccHRT) significantly reduces the risk

The Million Women Study reported on this matter.

ccHRT had a RR of 0.71.

Sequential combined HRT (scHRT)was neutral with a RR of 1.05.

ooHRT had a RR of 1.45.

Tibolone had a RR of 1.79.

Jaakkola et al looked at all Finnish women > 50 years who had had oestrogen-progestogen therapy prescribed from 1994 - 2006.

Obstet Gynecol. 2009 Dec;114(6):1197-204.

They then matched this data with information about endometrial cancer from the Finnish Cancer Registry.

There were 1,364 type I and 38 type II endometrial cancers.

They reached the following conclusions:

    ccHRT taken for 3 or more years was associated with a 76% reduction in the risk of type 1 endometrial cancer,

    scHRT taken for > 5 years was associated with:

        a 68% increase in incidence with the progestogen taken monthly,

        and a 276% increase in incidence if the progestogen was taken 3 monthly.

Oral and transdermal preparation showed similar increases in risk.

There was no difference in risk depending on the three main progestogens:

    dydrogesterone,

    medroxyprogesterone acetate

    and norethisterone.

The WHI study recorded a reduced risk for endometrial cancer for women on ccHRT

With a hazard ratio of 0.81 (95% CI, 0.48-1.36).

 

Unopposed oestrogen secretion also occurs with:

    oestrogen-secreting tumours,

    anovulatory cycles

       e.g. polycystic ovary syndrome. 

 

Wells reported on over 500 women who took ccHRT in the form of oestradiol 2 mg. and norethisterone 1 mg. daily.

BMJ 2002;325:239 ( 3 August ).

Endometrial samples were obtained:

    before admission to the study

    after 9 months on ccHRT,

    after 24 - 36 months on ccHRT,

    and after 5 years of ccHRT.

On entry to the study, complex hyperplasio was noted in:

    21 women who had been on scHRT,

    and 1 woman who had been on ooHRT.

398 women completed the 5 year course of treatment.

Data were obtained on:

    526 women at 9 months,

    465 women at 24 - 36 months

    and 398 women at five years.

There were no cases of endometrial hyperplasia or malignancy on any of the biopsies.

69% of the women who completed the five years' treatment had atrophic or "unassessable" endometrium.

Presumably the "unassessable" was due to paltry specimens and an indication of atrophy.

They concluded:

    "These findings provide reassurance about the long term safety of this continuous combined regimen in terms of the endometrium".

If a woman never produced oestrogen, e.g. in Turner’s syndrome, she would be at reduced risk (see MCQ4, question 24 and MCQ5, question 14).

Similarly, a late menarche and early menopause reduce the years of oestrogen exposure and the risk.

Nulliparity is a risk factor.

Diabetes is a weak risk factor but quoted.

Obesity increases the risk – androgens from the adrenals are converted into oestrogen in fatty tissue even after the menopause.

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Risk factors: HRT.

Oestrogen-only HRT is reckoned to roughly double the risk.

There is a slight decrease in  incidence with the usual combined sequential HRT.

But a significant reduction for combined HRT taken continuously.

This is dealt with in detail in the section on oestrogen as a risk factor.

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Risk factors: the Pill.

The Pill is not a risk factor.

It reduces the risk of endometrial cancer.

It also reduces the risk of ovarian cancer.   

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Risk factors: endometrial hyperplasia.

“Simple”, “Complex” and “Atypical” hyperplasia feature in the exam, so you need to know their significance.

Simple hyperplasia and complex hyperplasia carry small additional risks compared to the usual atrophic postmenopausal endometrium.

They imply thickening and abnormality of the structure of the endometrium, but the individual cells show no sign of malignancy.

If you give any woman unopposed oestrogen the endometrium will become abnormally thickened – simple hyperplasia.

The main risk lies with atypical hyperplasia.

There is thickening of the endometrium and distortion of its architecture.

More importantly, there are cytological features of pre-malignancy: 

    increased size and pigmentation of the nuclei,

    and an increased cell division rate, reflected in the number of mitoses.

Malignancy develops in 25-50%.

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Risk factors: Tamoxifen.

Tamoxifen (see MCQ10, question 22) is now commonly used to reduce the risk of recurrence of breast cancer.

It is a selective oestrogen-receptor modulator “SERM”. See MCQ9, question 20.

As such, it acts like oestrogen in some sites and against oestrogen in others.

Tamoxifen isn’t perfect.

It acts effectively against oestrogen in the breast and reduces the risk of recurrence of breast cancer.

But it acts like oestrogen in the endometrium and increases the risk of benign and malignant disease.

The risk of the latter is reckoned to double or triple.

So you have to pay particular heed to patients on Tamoxifen with abnormal bleeding.

In addition, it causes endometrial thickening which may not be malignant, making the results of TVS more difficult to interpret.

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Risk factors: alcohol, diabetes diet, exercise, obesity.

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Risk factors: PCOS.

Polycystic ovary syndrome (PCOS) is a risk factor.

See also MCQ4, question 9 "PCOS" and MCQ4, question 12 "Treatment for PCOS".

Progesterone production is mainly in the two weeks after ovulation

In PCOS ovulation is often infrequent.

This makes for long intervals of oestrogen production without progesterone.

And unopposed oestrogen is a major source of risk.

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Endometrial hyperplasia.

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Risk factors: HNPCC.

What about HNPCC, Lynch type II families and endometrial cancer? 

Hereditary non-polyposis colorectal cancer (HNPCC) is a familial condition inherited as an autosomal dominant.

It increases the risk of colorectal cancer.

It is reckoned to account for ~ 5% of colon cancer.

It is due to inheritance of mutations in key DNA repair genes, particularly MLH1, MSH2, MSH6, and PMS2, which make up more than 80% of the total.

Ashkenazi Jews are at particular risk of having these mutations.

When DNA is being replicated at cell division, errors can occur in the bases that are encoded and there is a system for identifying and repairing them: mismatch repair or MMR.

The risk of the different cancers varies with the mutation.

HNPCC is the most quoted example of a problem arising from flawed human MMR.

There are other examples of flawed MMR in humans, some of which also predispose to endometrial cancer.

I doubt that anyone will expect you to know anything about it, even for the MRCOG.

The story starts in the late 1800s.

Pauline Gross, a seamstress, told Dr. Aldred Warthin that she anticipated an early death because of her family history.

Her prognosis proved correct as she died of uterine cancer before she was 30.

Warthin went on to write up a series of family histories of apparent hereditary cancer.

This included family G, the Gross family.

Lynch developed and refined the theme and the Lynch syndromes emerged. (Arch. Intern. Med. 117: 206-212, 1966.)

HNPCC is sub-divided into Lynch Type I and Lynch Type II, of which I am sure you have heard mention.

Lynch Type I predisposes to "site-specific" disease. I.e. these families are at risk of colon cancer, but not cancer elsewhere. 

Lynch Type II families are at risk of other cancers too, particularly endometrial cancer, with the risk as high as 60%.

An increased, but much smaller risk of biliary tract, small bowel, stomach, ovarian and ureteric cancers has been described.

The risk of endometrial cancer may be as high as 60%.

A NCBI “Gene Review” put the risks as follows:

The risk for other Lynch syndrome-related cancers is lower, though substantially increased over general population rates.

It is reckoned that HNPCC women account for 1-3% of endometrial cancer.

Some advocate that women from these families should have screening.

Lindor et al proposed is annual endometrial sampling from a young age (e.g. 30 - 35) as the cancers start at an earlier age than normal – the average age is mid-40s.

They also advise prophylactic hysterectomy as soon as their families are complete.

Catherine Holland, in the OGRM article detailed in the "suggested reading" section., stated:

"Prophylactic hysterectomy + BSO are recommended for those who have completed their family.

Endometrial surveillance with annual endometrial imaging is offered to women ... who wish to retain their uterus

although this is not proven to be effective in prevention".

I think that younger women would baulk at the BSO bit and I doubt that it will make much difference if the uterus has been removed.

You could argue that with retrograde menstruation there would still be a risk of cancer arising from ectopic endometrium.

But EC almost always arises in the uterus, so you would have thought that its removal would be effective for prophylaxis.

Anyway, it is obviously the policy in her hospital, but there is no national screening programme as far as I am aware.

CancerHelp UK just says that these women are at increased risk and may benefit from screening.

The age of 30 has been suggested as research, e.g. that by Parc et al, Journal of Medical Genetics 2003;40:208-213). 

They found 30 to be the youngest age at which endometrial cancer occurred.

There are obvious parallels with BRCA1 and BRCA2. (See MCQ3, question 27). I suspect that gynaecological screening will become part of the routine for these families, who already have bowel screening with colonoscopy.

A trial was started in 2007 to look at whether hormone therapy can reduce the risk of endometrial cancer in these families.

I am sure that you will want to know that it is called: “Modulation Of Putative Surrogate Endpoint Biomarkers In Endometrial Biopsies From Women With HNPCC”.

A similar trial called “POET”, “Prevention  Of Endometrial Tumours“, was set up in 2007. 

It was designed to look at the use of the Mirena in HNPCC women.

This is of no relevance to the DRCOG, but might affect clinical practice in the years ahead.

(January 2012. I was informed by Louise Wan during a recent MRCOG tutorial that the trial has foundered due to failure to recruit enough women.

This does not surprise me given my own experience of never having had a woman from an HNPCC family referred for advice.)

Endometrial cancer is rare under the age of 40. Patients who develop it young should be considered likely to belong to a HNPCC family, with all that implies.

This is just another example of the exponential effect of genetics on routine clinical practice.

And a reminder that it is a subject in which you will need to stay well versed.

I don’t think that HNPCC and endometrial cancer will feature significantly in the DRCOG.

At most, HNPCC could be a single entry in a list of risk factors for endometrial cancer in a multiple choice question.

But it is likely to become a feature of your practice as you may well have such a family on your books.

MRCOG candidates need to know about it as it would be likely to get a point or two in an essay on postmenopausal bleeding, endometrial cancer or familial gynaecological cancer.

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Risk factors: oestrogen-secreting tumours.

Oestrogen-secreting granulosa and theca cell tumours produce continuous oestrogen and are obvious risk factors.

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Risk factors: talcum powder.

Talcum powder is often applied to the nether regions.

This practice has been implicated in the  causation of cancer including ovarian and endometrial cancer.

For example, in the paper by  Karageorgi et al who found that the risk might go up by 24%.

Cancer Epidemiol Biomarkers Prev. 2010 May;19(5):1269-75.

It might just be in the MCQ database.

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Signs and symptoms.

Endometrial cancer usually presents with postmenopausal bleeding.

Less often the presentation will be with postmenopausal discharge.

Occasionaly atypical glandular cells are seen on a cervical smear and give rise to the diagnosis.

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Investigation.

“One-stop” clinics are becoming the norm for seeing these patients.

They have facilities for transvaginal ultrasound scanning (TVS) and outpatient hysteroscopy.

Lotfallah et al reported that 70% of patients were reassured and discharged at the initial visit. (J Reprod Med. 2005 Feb;50(2):101-7.)

The key investigations are:

    taking a history - the frequency & duration of the bleeding, risk factors etc.,

    examination - looking for signs of signs of primary & secondary disease or possible explanations like polyps, atrophic vaginitis,

    TVS (an endometrial thickness < 4 mm is reassuring) 

    and hysteroscopy and biopsy.

There is increasing evidence that narrow-band hysteroscopy gives better detection rates than using white light.

Narrow-band uses only a band of blue light at 415nm plus a green band at 540nm.

This highlights blood vessels just beneath the epithelium.

I suspect that wider adoption of narrow-band technology is only likely to come if narrow-band + biopsy is found to give better detection rates that the current white light + biopsy, as biopsy tends to be done in all cases of possible malignancy.

If the patient is seen in an ordinary gynae clinic, Pipelle endometrial sampling may be done.

A negative result does not exclude malignancy -  the Pipelle only samples about 4% of the endometrium.

Fractional curettage might still be in the College database but is now of historical interest only.

With the fantastic developments in ultrasound, MR scanning etc. it is now of historical interest only.

It involved taking the biopsies at D&C from different levels.

You started low in the uterus and worked upwards in a progressive fashion, sending samples from each level. 

In this way some idea could be obtained of the location and local spread of the tumour.

E.g. has it got down to the cervix, which is important for prognosis.

In the endometrial cavity, the tumour is walled-off by the myometrium.

The myometrium has few lymphatics, so it restricts secondary spread until the tumour reaches its outer margins.

But the cervix has oodles of lymphatics.

So an endometrial tumour that reaches the cervix is likely to metastasise. 

 

TVS will give a good idea of the depth of myometrial invasion and involvement of the cervix.

These are major factors in determining staging, optimum management and prognosis.

MR scanning is more accurate than TVS, but more expensive and often not so easily available.

CT scanning is as good as MR in assessing lymphatic spread, but not so good at assessing myometrial invasion and extension to the cervix.

So MR scanning is the current gold standard.

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Prognosis.

There is a tendency to regard endometrial cancer as relatively benign with high cure rates from simple hysterectomy and removal of ovaries.

This is generally true, but only for early disease – stage 1 disease has a five year survival of 85%.

(You need to know the different staging definitions for the MRCOG, but not the DRCOG.)

But stage 1 means the disease is confined to the body of the uterus and has not reached the cervix.

It is almost as if there were two different disorders.

A small number of cases will have poorly differentiated tumours with deep myometrial invasion and cervical extension.

These patients have a high incidence of secondary disease in the pelvic and para-aortic lymph nodes.

Their prognosis is poor, with five-year survival rates of 10% being quoted.

The "investigation" section mentions the degree of spread as a major risk factor.

The prognosis in endometrial cancer worsens if:

    the tumour is poorly differentiated,

    has extended to the outer third of the myometrium,

    has extended down to the cervix, whence it may spread fairly readily via the cervical lymphatics,

    has spread outside the uterus.

Distant spread is more common with poorly differentiated tumours and is obviously bad news.

Spread may be along the round ligaments to the groin nodes.

Though this is rare, it is one of those stupid questions favoured by those who set examinations.

The other big risk factor is the histology.

Well-differentiated tumours are less aggressive and respond best to treatment.

Poorly-differentiated and anaplastic tumours are very bad news.

They invade and metastasise early and are less amenable to treatment.

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Treatment.

Remember to do your Pavlovian responses for essays in the exam.

Get in all the relevant buzz words: multidisciplinary team (MDT), oncology nurse, protocols, audit,  etc.

This is particularly an issue for EC.

There remains a lot of debate about the best treatment for the different types, stages and grades of the disease.

There is even debate about investigation.

If you are going to:

 use only the histological grade for determining whether or not to do lymphaenectomy

 and not the presence or absence of nodes

or depth of myometrial invasion

you don't need to do MR or CT scanning to look for depth of myometrial invasion or lymphadenopathy.

So, you would be wise to include a phrase like the following in any essay:

"the investigation and management of EC has become more evidence-based with the results of trials such as ASTEC, PORTEC and PORTEC-2.

But debate remains about

the most appropriate means of investigation

which patients should have lymphadenectomy and whether this should include PAL

and which patients would benefit from adjuvant radiotherapy.

This makes discussion by the experts of the MDT essential so that the woman's care can be individualised and based on best, up-to-date research evidence.

Treatment is usually by hysterectomy and removal of ovaries.

In the more advanced case, the addition of removal of pelvic and para-aortic nodes is appropriate.

There is debate about whether pelvic lymphadenectomy should be done in apparently early disease.

The argument is based on the fact that ~ 10% of women with stage 1 disease have spread to lymph nodes.

But there is no evidence that lymphadenectomy improves prognosis.

Traditionally surgery was combined with pre- or post-operative radiotherapy in more advanced cases in the belief that this improves the prognosis.

Pre-operative radiotherapy is now out of fashion.

Radiotherapy is not often used on its own, except in very advanced disease or patients who are not fit for surgery.

Other unresolved questions have been how to cut down the percentage of patients having radiotherapy after hysterectomy and how to reduce complications.

If more had lymph node dissection and more accurate staging, might some be spared radiotherapy?

Research is gradually throwing light on which patients might benefit from radiotherapy and which would not.

And the relative merits or EBRT and VBT.

A study called ASTEC was set up to look at these questions for patients with cancer confined to the uterus.

One group had hysterectomy + removal of ovaries.

The next had hysterectomy + removal of ovaries + lymphadenectomy.

Another had hysterectomy + removal of ovaries + external beam radiotherapy.

A fourth group had hysterectomy + removal of ovaries + radiotherapy if clinically indicated.

Preliminary results were presented to the British Congress in 2007.

These suggested no early benefit from lymphadenectomy and radiotherapy.

The results were subsequently published in the Lancet

The PORTEC trial indicated benefit from radiotherapy in early disease.

But Johnson & Cornes concluded that it was of benefit only in advanced disease.

Kong et al reached similar conclusions. 

PORTEC-2 (Postoperative Radiation Therapy for Endometrial Carcinoma) completed recruitment in 2006. 

It is a Dutch trial and will compare external beam radiotherapy with local vaginal brachytherapy in endometrial cancer.

Women will be followed up for five years to see the recurrence rates.

Full results should be available in 2011 or soon after.

Some patients will benefit from post-operative radiotherapy.

In the past some believed that progestagens improved the outlook, but this is no longer believed.

Regimes such as medroxyprogesterone 100 mg. t.d.s. were used (enormous dose!), 

However, most gynaecologists will recall cases where elderly patients with recurrence and not suitable for radiotherapy.

Some seemed to have the recurrence kept under control for a reasonable time using progestagens.                       

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HRT used after treatment.

Most women will be terrified of hormone therapy after what they have been through.

But the limited research that has been done shows no evidence that it worsens the prognosis.                       

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