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Uterine cancer

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2]

Synonyms and keywords: Endometrial adenocarcinoma; uterine adenocarcinoma; Endometrial cancer; adenocarcinoma – endometrium; adenocarcinoma – uterus; cancer – uterine; cancer – endometrial; uterine corpus cancer

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2]Roukoz A. Karam, M.D.[3]


Overview

In the United States, endometrial cancer is the fourth most common type of cancer among women. Development of endometrial cancer is the result of multiple genetic mutations. Genes involved in the pathogenesis of endometrial cancer include TP53, KRAS, and PTEN. Approximately 8–30% of patients with atypical endometrial hyperplasia may progress to develop endometrial cancer. The pathophysiology of endometrial cancer depends on the 7 histological subtypes: endometrioid, uterine papillary serous, mucinous, clear cell, squamous cell, mixed and undifferentiated. Common risk factors in the development of endometrial cancer are estrogen exposure, tamoxifen, obesity, diabetes, high blood pressure and genetic disorders. The hallmark of endometrial cancer is abnormal vaginal bleeding. A positive history of bleeding between normal periods in premenopausal women and vaginal bleeding and/or spotting in postmenopausal women is suggestive of endometrial cancer. Pelvic MRI and endometrial biopsy may be diagnostic of endometrial cancer. Depending on the extent of the tumor at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good. The optimal therapy for endometrial cancer depends on the stage at diagnosis and comprises total hysterectomy and bilateral salpingo-oophorectomy to most patients if they are surgical candidates.

Historical Perspective

The earliest descriptions of endometrial cancer were reported in the early 1900s. The association between estrogen and development of endometrial cancer was first reported in the 1970s when the incidence of endometrial cancer significantly increased between 1970 and 1975 following the introduction of estrogen replacement therapy.

Classification

Endometrial cancer may be classified according to histology into either type I comprising 80% of endometrial cancers or type II accounting for around 20%.

Pathophysiology

Development of endometrial cancer is the result of multiple genetic mutations. Genes involved in the pathogenesis of endometrial cancer include TP53, KRAS, and PTEN. The pathophysiology of endometrial cancer depends on the histological subtype.

Causes

Causes of endometrial cancer include genetic mutations of the KRAS gene, TP53 gene, TP16 gene, and/or PTEN gene. Other genetic mutations have also been described.

Differential Diagnosis

Endometrial cancer in early stage must be differentiated from diseases that cause abnormal uterine bleeding and endometrial thickening on ultrasound, such as endometrial hyperplasia, endometrial polyp, and submucosal uterine leiomyoma. In advanced stages endometrial cancer must be differentiated from uterine sarcoma and uterine lymphoma.

Epidemiology and Demographics

In the United States, endometrial cancer is the fourth most common type of cancer among women. In 2011, the age-adjusted prevalence was approximately 232 per 100,000 and the age-adjusted incidence was approximately 27 per 100,000 in the USA.

Risk Factors

Common risk factors in the development of endometrial cancer are estrogen exposure, tamoxifen use, obesity, diabetes, high blood pressure and genetic disorders.

Screening

There is insufficient evidence to recommend routine screening for endometrial cancer.

Natural History, Complications and Prognosis

If left untreated, approximately 8–30% of patients with atypical endometrial hyperplasia may progress to develop endometrial cancer. Common complications of endometrial cancer include menorrhagia and metastasis. Depending on the extent of the tumor at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as good.

Diagnosis

Staging

According to the FIGO Staging System, there are 4 stages of endometrial cancer.

History and Symptoms

The hallmark of endometrial cancer is abnormal vaginal bleeding. A positive history of bleeding between normal periods in premenopausal women and vaginal bleeding and/or spotting in postmenopausal women is suggestive of endometrial cancer.

MRI

The MRI is not needed for the diagnosis of endometrial cancer. However, an MRI may be helpful in staging of the disease.

Ultrasound

On transvaginal ultrasound, endometrial cancer is characterized by thickening of the endometrium and disruption of a subendometrial halo.

Other Diagnostic Studies

Other diagnostic studies for endometrial cancer include endometrial biopsy

Treatment

Medical therapy

The optimal therapy for endometrial cancer depends on the stage at diagnosis. A combination of chemotherapy and radiation therapy is indicated in stages IIIB- IV.

Surgery

Surgery is the mainstay of treatment for endometrial cancer stage I-III.

Primary Prevention

Effective measures for the primary prevention of endometrial cancer include administration of combination oral contraceptives.

References


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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.

Overview

The earliest descriptions of endometrial cancer were reported in the early 1900s. The association between estrogen and development of endometrial cancer was first reported in the 1970s when the incidence of endometrial cancer significantly increased between 1970 and 1975 following the introduction of estrogen replacement therapy.

Historical Perspective

  • The earliest descriptions of endometrial cancer were reported in the early 1900s.
  • The association between estrogen and development of endometrial cancer was first reported in the 1970s when the incidence of endometrial cancer significantly increased between 1970 and 1975 following the introduction of estrogen replacement therapy.[1]
  • Surgical staging of endometrial cancer was first suggested in 1988 and was later revised in 2009.[2]
  • The first laparoscopic hysterectomy was reported in 1992.[3]

References

  1. ↑ Jick H, Walker AM, Rothman KJ (1980). “The epidemic of endometrial cancer: a commentary”. Am J Public Health. 70 (3): 264–7. PMC 1619376. PMID 7356090.
  2. ↑ Creasman W (2009). “Revised FIGO staging for carcinoma of the endometrium”. Int J Gynaecol Obstet. 105 (2): 109. doi:10.1016/j.ijgo.2009.02.010. PMID 19345353.
  3. ↑ Childers JM, Surwit EA (1992). “Combined laparoscopic and vaginal surgery for the management of two cases of stage I endometrial cancer”. Gynecol Oncol. 45 (1): 46–51. PMID 1534780.

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Pathophysiology

Pathophysiology


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2]

Overview

Development of endometrial cancer is the result of multiple genetic mutations. Genes involved in the pathogenesis of endometrial cancer include TP53, KRAS, and PTEN. The pathophysiology of endometrial cancer depends on the histological subtype.

Pathogenesis

  • Endometrial cancer forms when there are errors in normal endometrial cell growth.[1][2]
  • Development of an endometrial hyperplasia (overgrowth of endometrial cells) is a significant risk factor because hyperplasia can and often do develop into adenocarcinoma, though cancer can develop without the presence of a hyperplasia. Within ten years, 8–30% of atypical endometrial hyperplasias develop into cancer, whereas 1–3% of non-atypical hyperplasias do so.[3]
  • Mutations in the KRAS gene can cause endometrial hyperplasia and therefore type I endometrial cancer. Endometrial hyperplasia typically occurs after the age of 40. Endometrial glandular dysplasia occurs with an overexpression of TP53, and develops into a serous carcinoma (type II endometrial cancer).[4]
  • Endometrial cancer frequently metastasizes to the ovaries and fallopian tubes when the cancer is located in the upper part of the uterus and the cervix when the cancer is in the lower part of the uterus.
  • The cancer usually first spreads into the myometrium and the serosa, then into other reproductive and pelvic structures. When the lymphatic system is involved, the pelvic lymph nodes and para-aortic lymph nodes are usually first to become involved, but in no specific pattern, unlike cervical cancer.
  • More distant metastases are spread by the blood and often occur in the lungs, as well as the liver, brain, and bone.[5]

Genetics

Mutations found in Type I and Type II endometrial cancers[6]
Gene mutated Mutation type Type I prevalence Type II prevalence
ARID1A point mutation 40% unknown
CTNNB1 point mutation 14–44% unknown
FGFR2 point mutation 16% unknown
KRAS point mutation 10–20% unknown
PIK3R1 point mutation 43% unknown
TP53 point mutation 10–20% 90%
PTEN point mutation 37–61% unknown
MLH1 epigenetic silencing 30% unknown
RASSF1A epigenetic silencing 48% unknown
SPRY2 epigenetic silencing 20% unknown
PPP2R1A point mutation unknown 17–41%
CDH1 loss of heterozygosity unknown 80–90%
CDKN2A loss of heterozygosity and/or
epigenetic silencing 		20% 40%
PIK3CA (oncogene) amplification 24–39% 20–30%
PIK3R1 (oncogene) point mutation unknown 12%
STK15 (oncogene) amplification unknown 60%
CCNE1 (oncogene) amplification unknown 55%
ERBB2 (oncogene) amplification unknown 30%
CCND1 (oncogene) amplification unknown 26%

Genes involved in pathogenesis of endometrial cancer involve:

  • In 10–20% of endometrial cancers, mostly grade 3 (the highest histologic grade), mutations are found in a tumor suppressor gene, commonly TP53 or PTEN.
  • In 20% of endometrial hyperplasias and 50% of endometrioid cancers, PTEN suffers a loss-of-function mutation or a null mutation, making it less effective or completely ineffective.[7] Loss of PTEN function leads to up-regulation of the PI3k/Akt/mTOR pathway, which causes cell growth.[8]
  • The TP53 pathway can either be suppressed or highly activated in endometrial cancer. When a mutant version of TP53 is overexpressed, the cancer tends to be particularly aggressive. TP53 mutations and chromosome instability are associated with serous carcinomas, which tend to resemble ovarian and fallopian carcinomas. Serous carcinomas are thought to develop from endometrial intraepithelial carcinoma.[8]
  • PTEN and p27 loss of function mutations are associated with a good prognosis, particularly in obese women. The Her2/neu oncogene, which indicates a poor prognosis, is expressed in 20% of endometrioid and serous carcinomas. CTNNB1 (beta-catenin; a transcription gene) mutations are found in 14–44% of endometrial cancers and may indicate a good prognosis, but the data is unclear. Beta-catenin mutations are commonly found in endometrial cancers with squamous cells.[8]
  • FGFR2 mutations are found in approximately 10% of endometrial cancers, and their prognostic significance is unclear.[7]
  • SPOP is another tumor suppressor gene found to be mutated in some cases of endometrial cancer: 9% of clear cell endometrial carcinomas and 8% of serous endometrial carcinomas have mutations in this gene.[9]
  • Type I and type II cancers (explained below) tend to have different mutations involved. ARID1A, which often carries a point mutation in type I endometrial cancer, is also mutated in 26% of clear cell carcinomas of the endometrium, and 18% of serous carcinomas. Epigenetic silencing and point mutations of several genes are commonly found in type I endometrial cancer.[10]
  • Mutations in tumor suppressor genes are common in type II endometrial cancer. PIK3CA is commonly mutated in both type I and type II cancers. In women with Lynch syndrome-associated endometrial cancer, microsatellite instability is common.[8]
  • The genetic mutations most commonly associated with endometrioid adenocarcinoma are in the genes PTEN, a tumor suppressor gene, PIK3CA (expresses a kinase), KRAS (expresses GTPase that functions in signal transduction), and CTNNB1 that expresses a protein involved in adhesion and cell signaling. The CTNNB1 (beta-catenin) gene is most commonly mutated in the squamous subtype of endometrioid adenocarcinoma.[11]
  • The genetic mutations seen in serous carcinoma are chromosomal instability and mutations in TP53, an important tumor suppressor gene.[12]
  • The p53 cell signaling system is not active in endometrial clear cell carcinoma.[13]

Microscopic Pathology

On microscopic histopathological analysis, endometrial cancer is characterized by:[14]

1. Endometrioid (most common; 75%–80%)

  • Ciliated adenocarcinoma
  • Secretory adenocarcinoma
  • Papillary or villoglandular
  • Adenocarcinoma with squamous differentiation
  • Adenoacanthoma
  • Adenosquamous (Adenosquamous tumors contain malignant elements of both glandular and squamous epithelium)

2. Uterine papillary serous (<10%)

3. Mucinous (1%)

4. Clear cell (4%)

5. Squamous cell (<1%)

6. Mixed (10%)

7. Undifferentiated

Characteristic/Parameter Type I endometrial cancers Type II endometrial cancers
Time of onset Occur most commonly before and around the time of menopause Occur in older, post-menopausal
Race White Black
Grade of tumor Low-grade High-grade
Invasive Minimally invasive into the underlying uterine wall myometrium Deep invasion into the underlying myometrium
Estrogen Dependent Independent
Type Endometrioid Uterine papillary serous carcinoma, clear cell carcinoma
Prognosis. Good Poor
Types of endometrial cancer Histopathological features

Endometrioid adenocarcinoma

1. Cancer cells grow in patterns reminiscent of normal endometrium
2. Glands formed from columnar epithelium with abnormal nuclei
3. Low-grade endometrioid adenocarcinomas
  • Well differentiated cells
  • No invasion to the myometrium
  • Observed alongside endometrial hyperplasia
  • Glands without the stromal tissue that separates them.

Serous carcinoma

1. Cancer cells appears with many atypical nuclei, papillary structures, rounded cells
2. Aggressive and often invades the myometrium and metastasizes within the peritoneum seen as omental cake or the lymphatic system.
3. They can spread outside the uterus without invading the myometrium.

Clear cell carcinoma

1. Common to all clear cells visible
2. Distinct cell membranes

Mucinous carcinoma

Well-differentiated columnar cells organized into glands with the characteristic mucin in the cytoplasm.

Mixed or undifferentiated carcinoma

Sheets of identical epithelial cells with no identifiable pattern

References

  1. ↑ Kong A, Johnson N, Kitchener HC, Lawrie TA (2012). “Adjuvant radiotherapy for stage I endometrial cancer”. Cochrane Database Syst Rev. 4: CD003916. doi:10.1002/14651858.CD003916.pub4. PMC 4164955. PMID 22513918.
  2. ↑ What You Need To Know: Endometrial Cancer”.NCI. National Cancer Institute. Retrieved 6 August 2014.
  3. ↑ Luo, L; Luo, B; Zheng, Y; Zhang, H; Li, J; Sidell, N (5 June 2013). “Levonorgestrel-releasing intrauterine system for atypical endometrial hyperplasia”. The Cochrane database of systematic reviews. 6: CD009458. doi:10.1002/14651858.CD009458.pub2. PMID 23737032.
  4. ↑ Saso, S; Chatterjee, J; Georgiou, E; Ditri, AM; Smith, JR; Ghaem-Maghami, S (2011). “Endometrial cancer”. BMJ. 343: d3954–d3954. doi:10.1136/bmj.d3954. PMID 21734165.
  5. ↑ Kurra V, Krajewski KM, Jagannathan J, Giardino A, Berlin S, Ramaiya N (2013). “Typical and atypical metastatic sites of recurrent endometrial carcinoma”. Cancer Imaging. 13: 113–22. doi:10.1102/1470-7330.2013.0011. PMC 3613792. PMID 23545091.
  6. ↑ International Agency for Research on Cancer (2014). World Cancer Report 2014. World Health Organization. Chapter 5.12. ISBN 978-92-832-0429-9.
  7. ↑ 7.0 7.1 Thaker, PH; Sood, AK. “Molecular Oncology in Gynecologic Cancer”. In Lentz, GM; Lobo, RA; Gershenson, DM; Katz, VL. Comprehensive Gynecology (6th ed.). Mosby. ISBN 978-0-323-06986-1.
  8. ↑ 8.0 8.1 8.2 8.3 Colombo N, Preti E, Landoni F, Carinelli S, Colombo A, Marini C; et al. (2013). “Endometrial cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up”. Ann Oncol. 24 Suppl 6: vi33–8. doi:10.1093/annonc/mdt353. PMID 24078661.
  9. ↑ Mani, RS (September 2014). “The emerging role of speckle-type POZ protein (SPOP) in cancer development”. Drug Discovery Today. 19 (9): 1498–1502. doi:10.1016/j.drudis.2014.07.009. PMID 25058385. A recent exome-sequencing study revealed that 8% of serious endometrial cancers and 9% of clear cell endometrial cancers have SPOP mutations
  10. ↑ International Agency for Research on Cancer (2014). World Cancer Report 2014. World Health Organization. Chapter 5.12. ISBN 978-92-832-0429-9.
  11. ↑ Colombo, N; Preti, E; Landoni, F; Carinelli, S; Colombo, A; Marini, C; Sessa, C (2011). “Endometrial cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up”. Annals of Oncology. 22 (Supplement 6): vi35–vi39. doi:10.1093/annonc/mdr374. PMID 21908501.
  12. ↑ Johnson N, Bryant A, Miles T, Hogberg T, Cornes P (2011). “Adjuvant chemotherapy for endometrial cancer after hysterectomy”. Cochrane Database Syst Rev (10): CD003175. doi:10.1002/14651858.CD003175.pub2. PMC 4164379. PMID 21975736.
  13. ↑ Saso S, Chatterjee J, Georgiou E, Ditri AM, Smith JR, Ghaem-Maghami S (2011). “Endometrial cancer”. BMJ. 343: d3954. doi:10.1136/bmj.d3954. PMID 21734165.
  14. ↑ Hoffman, Barbara (2012). Williams gynecology. New York: McGraw-Hill Medical. ISBN 9780071716727.


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Differentiating Endometrial cancer from other Diseases

Differentiating Endometrial cancer from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qurrat-ul-ain Abid, M.D.[2]; Monalisa Dmello, M.B,B.S., M.D. [3]Roukoz A. Karam, M.D.[4]

Overview

In early stages endometrial cancer must be differentiated from diseases that cause abnormal uterine bleeding and endometrial thickening on ultrasound, such as endometrial hyperplasia, endometrial polyp, and submucosal uterine leiomyoma. In advanced stages endometrial cancer must be differentiated from uterine sarcoma and uterine lymphoma.

Differentiating Endometrial Cancer From Other Diseases

Diseases Clinical manifestations Para-clinical findings Gold standard
Symptoms Physical examination
Lab Findings Imaging Pap Smear Histopathology
Bleeding Pelvic Pain/pressure/

discomfort

Other Abdomino-pelvic examination Hb B-HCG CA-125 Ultrasound MRI
Endometrial cancer[2][3][4][5] ± ↓ – +
  • Atypical glandular cells
 Endometrial malignant cells
  • Low grade Type I
  • High grade Type II
Uterine

leiomyosarcoma[6][7][8][9]

± ↓ – +
  • Shows details of uterine mass boundaries, extent and spread
  • Negative
Diseases Bleeding Pelvic Pain/pressure/

discomfort

Other Pelvic examination Hb B-HCG CA-125 Ultrasound MRI Pap Smear Histopathology Gold standard
Uterine leiomyoma[10][11][12] + ↓ or Nl – –
  • Hypoechoic, well-circumscribed round masses
  • Location of fibroid: Submucosal, intramural, subserosal, and cervical fibroids
  • Normal
  • Imaging and histologic analysis
Uterine carcinosarcomas (Malignant mixed mullerian tumour (MMMT) of the uterus)[13][14][15][16] ± ↓ – +
  • Heterogenous bulky polypoid mass with intense enhancement
  • Biphasic:
Cervical cancer[17][18] ±

Pressure-related bowel and bladder symptoms

↓ – ±
  • To evaluate tumor size, extent and parametrial invasion
  • Usually not needed for diagnosis
  • To evaluate tumor size, local extent and staging
  • Low-grade squamous intraepithelial lesions (LSILs)
  • High-grade squamous intraepithelial lesions (HSILs)
  • Atypical glandular cells (AGC)
  • Endocervical adenocarcinoma in situ (AIS)
Diseases Bleeding Pelvic Pain/pressure/

discomfort

Other Pelvic examination Hb B-HCG CA-125 Ultrasound MRI Pap Smear Histopathology Gold standard
Metastasis ± ↓ – –
  • Not recommended
  • It may show the malignant cells of the primary site
Endometrial polyp[19][20] –
  • Asymptomatic
  • Endometrial polyp prolapses (visible on speculum examination protruding through cervical os)
  • Normal sized uterus with smooth surface
 ↓ – + or Nl
  • MRI will show polyp size and dimension in detail
  • Not required for diagnosis
  • Normal
Endometrial hyperplasia[21][22][23][24] –
  • Asymptomatic
 ↓ – +
  • Determines endometrial thickness
  • Rules out other abnormalities
  • Non-neoplastic changes:
  • Disordered endometrial growth
  • Benign hyperplasia
  • Simple hyperplasia
  • Complex hyperplasia without atypia
  • Precancerous changes:
  • Endometrial intraepithelial neoplasms
  • Atypical complex hyperplasia
Uterine adenomyosis[25][26][27] – ±
  • Diffusely enlarged tender boggy uterus with smooth surface
  • Uterus may develop masses
 ↓ – +
Diseases Bleeding Pelvic Pain/pressure/

discomfort

Other Pelvic examination Hb B-HCG CA-125 Ultrasound MRI Pap Smear Histopathology Gold standard
Hematometra (blood within the uterine cavity)

[28][29]

– +

Cramping cyclic pain

↓ – –
  • Not required
  • Normal
  • Biopsy is not required for diagnosis
Gestational trophoblastic disease[30][31] + ↓ ± +
  • Dilated grape like structures
  • Diffuse hydropic swelling
  • Multiples echoes
  • Cystic spaces invading edometrium and myometrium (in case of invasive disease)
  • MRI defines the extent of primary lesion, invasion and distant metastasis
  • Trophoblastic cells
  • Dilated grape like villous structures
  • Invasive malignant lesions
  • Imaging
  • Histologic diagnosis
Incomplete abortion + N/↓ ± +↓
  • Not required for the diagnosis
  • Not required for the diagnosis
  • Imaging
  • Histologic diagnosis
Pregnancy
  • Absent menstrual cycle
  • May have intermenstrual bleeding
 + – + –
  • Normal or may show cervical cells
Uterine lymphoma[1][32][33][34] + ↓ – –
Diseases Bleeding Pelvic Pain/pressure/

discomfort

Other Pelvic examination Hb B-HCG CA-125 Ultrasound MRI Pap Smear Histopathology Gold standard

References

  1. ↑ 1.0 1.1 Hippisley-Cox J, Coupland C (2011). “Identifying women with suspected ovarian cancer in primary care: derivation and validation of algorithm”. BMJ. 344: d8009. doi:10.1136/bmj.d8009. PMC 3251328. PMID 22217630.
  2. ↑ “ACOG practice bulletin, clinical management guidelines for obstetrician-gynecologists, number 65, August 2005: management of endometrial cancer”. Obstet Gynecol. 106 (2): 413–25. August 2005. PMID 16055605.
  3. ↑ Boruta DM, Gehrig PA, Fader AN, Olawaiye AB (October 2009). “Management of women with uterine papillary serous cancer: a Society of Gynecologic Oncology (SGO) review”. Gynecol. Oncol. 115 (1): 142–153. doi:10.1016/j.ygyno.2009.06.011. PMID 19592079.
  4. ↑ Bokhman JV (February 1983). “Two pathogenetic types of endometrial carcinoma”. Gynecol. Oncol. 15 (1): 10–7. PMID 6822361.
  5. ↑ Felix AS, Weissfeld JL, Stone RA, Bowser R, Chivukula M, Edwards RP, Linkov F (November 2010). “Factors associated with Type I and Type II endometrial cancer”. Cancer Causes Control. 21 (11): 1851–6. doi:10.1007/s10552-010-9612-8. PMC 2962676. PMID 20628804.
  6. ↑ Nordal RR, Thoresen SO (May 1997). “Uterine sarcomas in Norway 1956-1992: incidence, survival and mortality”. Eur. J. Cancer. 33 (6): 907–11. PMID 9291814.
  7. ↑ Goto A, Takeuchi S, Sugimura K, Maruo T (2002). “Usefulness of Gd-DTPA contrast-enhanced dynamic MRI and serum determination of LDH and its isozymes in the differential diagnosis of leiomyosarcoma from degenerated leiomyoma of the uterus”. Int. J. Gynecol. Cancer. 12 (4): 354–61. PMID 12144683.
  8. ↑ Bell SW, Kempson RL, Hendrickson MR (June 1994). “Problematic uterine smooth muscle neoplasms. A clinicopathologic study of 213 cases”. Am. J. Surg. Pathol. 18 (6): 535–58. PMID 8179071.
  9. ↑ Karpathiou G, Sivridis E, Giatromanolaki A (2010). “Myxoid leiomyosarcoma of the uterus: a diagnostic challenge”. Eur. J. Gynaecol. Oncol. 31 (4): 446–8. PMID 20882892.
  10. ↑ Stewart EA (April 2015). “Clinical practice. Uterine fibroids”. N. Engl. J. Med. 372 (17): 1646–55. doi:10.1056/NEJMcp1411029. PMID 25901428.
  11. ↑ Dueholm M, Lundorf E, Hansen ES, Ledertoug S, Olesen F (March 2002). “Accuracy of magnetic resonance imaging and transvaginal ultrasonography in the diagnosis, mapping, and measurement of uterine myomas”. Am. J. Obstet. Gynecol. 186 (3): 409–15. PMID 11904599.
  12. ↑ Omary RA, Vasireddy S, Chrisman HB, Ryu RK, Pereles FS, Carr JC, Resnick SA, Nemcek AA, Vogelzang RL (November 2002). “The effect of pelvic MR imaging on the diagnosis and treatment of women with presumed symptomatic uterine fibroids”. J Vasc Interv Radiol. 13 (11): 1149–53. PMID 12427815.
  13. ↑ Chaffer CL, San Juan BP, Lim E, Weinberg RA (December 2016). “EMT, cell plasticity and metastasis”. Cancer Metastasis Rev. 35 (4): 645–654. doi:10.1007/s10555-016-9648-7. PMID 27878502.
  14. ↑ Zhao S, Bellone S, Lopez S, Thakral D, Schwab C, English DP, Black J, Cocco E, Choi J, Zammataro L, Predolini F, Bonazzoli E, Bi M, Buza N, Hui P, Wong S, Abu-Khalaf M, Ravaggi A, Bignotti E, Bandiera E, Romani C, Todeschini P, Tassi R, Zanotti L, Odicino F, Pecorelli S, Donzelli C, Ardighieri L, Facchetti F, Falchetti M, Silasi DA, Ratner E, Azodi M, Schwartz PE, Mane S, Angioli R, Terranova C, Quick CM, Edraki B, Bilgüvar K, Lee M, Choi M, Stiegler AL, Boggon TJ, Schlessinger J, Lifton RP, Santin AD (October 2016). “Mutational landscape of uterine and ovarian carcinosarcomas implicates histone genes in epithelial-mesenchymal transition”. Proc. Natl. Acad. Sci. U.S.A. 113 (43): 12238–12243. doi:10.1073/pnas.1614120113. PMC 5087050. PMID 27791010.
  15. ↑ Callister M, Ramondetta LM, Jhingran A, Burke TW, Eifel PJ (March 2004). “Malignant mixed Müllerian tumors of the uterus: analysis of patterns of failure, prognostic factors, and treatment outcome”. Int. J. Radiat. Oncol. Biol. Phys. 58 (3): 786–96. doi:10.1016/S0360-3016(03)01561-X. PMID 14967435.
  16. ↑ Teo SY, Babagbemi KT, Peters HE, Mortele KJ (July 2008). “Primary malignant mixed mullerian tumor of the uterus: findings on sonography, CT, and gadolinium-enhanced MRI”. AJR Am J Roentgenol. 191 (1): 278–83. doi:10.2214/AJR.07.3281. PMID 18562759.
  17. ↑ “Pap and HPV Testing – National Cancer Institute”.
  18. ↑ Benedet JL, Bender H, Jones H, Ngan HY, Pecorelli S (August 2000). “FIGO staging classifications and clinical practice guidelines in the management of gynecologic cancers. FIGO Committee on Gynecologic Oncology”. Int J Gynaecol Obstet. 70 (2): 209–62. PMID 11041682.
  19. ↑ Kim KR, Peng R, Ro JY, Robboy SJ (August 2004). “A diagnostically useful histopathologic feature of endometrial polyp: the long axis of endometrial glands arranged parallel to surface epithelium”. Am. J. Surg. Pathol. 28 (8): 1057–62. PMID 15252313.
  20. ↑ Salim S, Won H, Nesbitt-Hawes E, Campbell N, Abbott J (2011). “Diagnosis and management of endometrial polyps: a critical review of the literature”. J Minim Invasive Gynecol. 18 (5): 569–81. doi:10.1016/j.jmig.2011.05.018. PMID 21783430.
  21. ↑ Emons G, Beckmann MW, Schmidt D, Mallmann P (February 2015). “New WHO Classification of Endometrial Hyperplasias”. Geburtshilfe Frauenheilkd. 75 (2): 135–136. doi:10.1055/s-0034-1396256. PMC 4361167. PMID 25797956.
  22. ↑ Wright TC, Massad LS, Dunton CJ, Spitzer M, Wilkinson EJ, Solomon D (October 2007). “2006 consensus guidelines for the management of women with abnormal cervical screening tests”. J Low Genit Tract Dis. 11 (4): 201–22. doi:10.1097/LGT.0b013e3181585870. PMID 17917566.
  23. ↑ Espindola D, Kennedy KA, Fischer EG (December 2007). “Management of abnormal uterine bleeding and the pathology of endometrial hyperplasia”. Obstet. Gynecol. Clin. North Am. 34 (4): 717–37, ix. doi:10.1016/j.ogc.2007.09.001. PMID 18061866.
  24. ↑ Montgomery BE, Daum GS, Dunton CJ (May 2004). “Endometrial hyperplasia: a review”. Obstet Gynecol Surv. 59 (5): 368–78. PMID 15097798.
  25. ↑ McElin TW, Bird CC (1974). “Adenomyosis of the uterus”. Obstet Gynecol Annu. 3: 425–41. PMID 4608783.
  26. ↑ Maheshwari A, Gurunath S, Fatima F, Bhattacharya S (July 2012). “Adenomyosis and subfertility: a systematic review of prevalence, diagnosis, treatment and fertility outcomes”. Hum. Reprod. Update. 18 (4): 374–92. doi:10.1093/humupd/dms006. PMID 22442261.
  27. ↑ Byun JY, Kim SE, Choi BG, Ko GY, Jung SE, Choi KH (October 1999). “Diffuse and focal adenomyosis: MR imaging findings”. Radiographics. 19 Spec No: S161–70. doi:10.1148/radiographics.19.suppl_1.g99oc03s161. PMID 10517452.
  28. ↑ McCausland AM, McCausland VM (2007). “Long-term complications of endometrial ablation: cause, diagnosis, treatment, and prevention”. J Minim Invasive Gynecol. 14 (4): 399–406. doi:10.1016/j.jmig.2007.04.004. PMID 17630156.
  29. ↑ U Nayak A, Swarup A, G S J, N S (April 2010). “Hematometra and acute abdomen”. J Emerg Trauma Shock. 3 (2): 191–2. doi:10.4103/0974-2700.62117. PMC 2884455. PMID 20606801. Vancouver style error: name (help)
  30. ↑ Bakri YN, Berkowitz RS, Khan J, Goldstein DP, von Sinner W, Jabbar FA (March 1994). “Pulmonary metastases of gestational trophoblastic tumor. Risk factors for early respiratory failure”. J Reprod Med. 39 (3): 175–8. PMID 8035373.
  31. ↑ Lurain JR (December 2010). “Gestational trophoblastic disease I: epidemiology, pathology, clinical presentation and diagnosis of gestational trophoblastic disease, and management of hydatidiform mole”. Am. J. Obstet. Gynecol. 203 (6): 531–9. doi:10.1016/j.ajog.2010.06.073. PMID 20728069.
  32. ↑ Samama M, van Poelgeest M (September 2011). “Primary malignant lymphoma of the uterus: a case report and review of the literature”. Case Rep Oncol. 4 (3): 560–3. doi:10.1159/000334852. PMC 3251245. PMID 22220150.
  33. ↑ Shen CJ, Tsai EM, Tsai KB, Wu CH, Hsu SC (March 2007). “Primary T-cell lymphoma of the uterine corpus”. Kaohsiung J. Med. Sci. 23 (3): 138–41. doi:10.1016/S1607-551X(09)70388-2. PMID 17389178.
  34. ↑ Heeren JH, Croonen AM, Pijnenborg JM (April 2008). “Primary extranodal marginal zone B-cell lymphoma of the female genital tract: a case report and literature review”. Int. J. Gynecol. Pathol. 27 (2): 243–6. doi:10.1097/PGP.0b013e3181569a0a. PMID 18317217.
Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

In the United States, endometrial cancer is the fourth most common type of cancer among women.[1] In 2011, the age-adjusted prevalence was approximately 232 per 100,000 and the age-adjusted incidence was approximately 27 per 100,000 in the USA.[2]

Epidemiology and Demographics

Prevalence

  • In 2011, the age-adjusted prevalence of endometrial cancer was 232 per 100,000 in the United States.[2]

Incidence

  • In 2011, the age-adjusted incidence of endometrial cancer was 27 per 100,000 persons in the United States.[2]

Age

  • While the overall age-adjusted incidence of endometrial cancer in the United States between 2007 and 2011 is 24 per 100,000.
  • The age-adjusted incidence of endometrial cancer by age category is:[2]
    • Under 65 years: 16 per 100,000
    • 65 and over: 84 per 100,000

Race

  • Endometrial cancer is more prevalent among White patients.
  • Shown below is a table depicting the age-adjusted prevalence of endometrial cancer by race in 2011 in the United States.[2]
All Races White Black Asian/Pacific Islander Hispanic
Age-adjusted prevalence 232 per 100,000 252.5 per 100,000 145 per 100,000 167.6 per 100,000 166 per 100,000

References

  1. ↑ endometrial cancer statistics. CDC.gov
  2. ↑ 2.0 2.1 2.2 2.3 2.4 Howlader N, Noone AM, Krapcho M, Garshell J, Miller D, Altekruse SF, Kosary CL, Yu M, Ruhl J, Tatalovich Z,Mariotto A, Lewis DR, Chen HS, Feuer EJ, Cronin KA (eds). SEER Cancer Statistics Review, 1975-2011, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2011/, based on November 2013 SEER data submission, posted to the SEER web site, April 2014.


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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Roukoz A. Karam, M.D.[2]

Overview

Common risk factors in the development of endometrial cancer are estrogen exposure, tamoxifen use, obesity, diabetes, high blood pressure and genetic disorders.

Risk Factors

Some of the risk factors for endometrial cancer are:

1. Estrogen exposure
  • Women who have received higher doses or longer periods of estrogen therapy have higher risks of endometrial cancer.[1]
2. Early menarche
  • Women who have menstrual periods at an early age also increases the number of years the body is exposed to estrogen and increases a woman’s risk of endometrial cancer.[2]
3.Late menopause
  • Women who reach menopause at an older age are exposed to estrogen for a longer time and have an increased risk of endometrial cancer.[2]
4. Nulliparity
  • Never being pregnant is also a risk factor for endometrial cancer. Because estrogen levels are lower during pregnancy, women who have never been pregnant are exposed to estrogen for a longer time than women who have been pregnant. This increases the risk of endometrial cancer.[3]
5. Tamoxifen
  • Tamoxifen is one of a group of drugs called selective estrogen receptor modulators, or SERMs. Tamoxifen is used to prevent breast cancer in women who are at high risk for the disease, but it increases the risk of endometrial cancer. This risk is greater in postmenopausal women.[4]
6. Family history
  • Hereditary nonpolyposis colon cancer (HNPCC) syndrome (Lynch syndrome): Women with Lynch syndrome have a 40–60% risk of developing endometrial cancer, higher than their risk of developing colorectal (bowel) or ovarian cancer.[5] Carcinogenesis in Lynch syndrome comes from a mutation in MLH1 and/or MLH2: genes that participate in the process of mismatch repair, which allows a cell to correct mistakes in the DNA.[6] Other genes mutated in Lynch syndrome include MSH2, MSH6, and PMS2, which are also mismatch repair genes.
  • Cowden syndrome: Women with Cowden syndrome have a 5–10% lifetime risk of developing endometrial cancer, compared to the 2–3% risk for unaffected women.[7][8] Cowden syndrome is associated with mutations in PTEN, a tumor suppressor gene, that cause the PTEN protein not to work properly leading to hyperactivity of the mTOR pathway.
7. Polycystic ovary syndrome
  • Women who have polycystic ovary syndrome have an increased risk of endometrial cancer.
8. Obesity
  • Obesity increases the risk of endometrial cancer. This may be because obesity is related to other risk factors such as estrogen levels, polycystic ovary syndrome, lack of physical activity, and a diet that is high in saturated fats.[9]
11. Diabetes and hypertension
  • Women suffering from hypertension or diabetes are at increased risk for developing endometrial cancer.[10]

References

  1. ↑ Vern L. Katz, Gretchen M. Lentz (2012). Comprehensive gynecology. Philadelphia, PA, USA: Elsevier/ Mosby. ISBN 978-0-323-06986-1.
  2. ↑ 2.0 2.1 Brinton LA, Berman ML, Mortel R, Twiggs LB, Barrett RJ, Wilbanks GD; et al. (1992). “Reproductive, menstrual, and medical risk factors for endometrial cancer: results from a case-control study”. Am J Obstet Gynecol. 167 (5): 1317–25. PMID 1442985.
  3. ↑ Vale CL, Tierney J, Bull SJ, Symonds PR (2012). “Chemotherapy for advanced, recurrent or metastatic endometrial carcinoma”. Cochrane Database Syst Rev. 8: CD003915. doi:10.1002/14651858.CD003915.pub4. PMID 22895938.
  4. ↑ Staley H, McCallum I, Bruce J (2012). “Postoperative tamoxifen for ductal carcinoma in situ”. Cochrane Database Syst Rev. 10: CD007847. doi:10.1002/14651858.CD007847.pub2. PMID 23076938.
  5. ↑ Hoffman, Barbara (2012). Williams gynecology. New York: McGraw-Hill Medical. ISBN 9780071716727. Check |isbn= value: invalid character (help).
  6. ↑ Hoffman, Barbara (2012). Williams gynecology. New York: McGraw-Hill Medical. ISBN 9780071716727. Check |isbn= value: invalid character (help).
  7. ↑ Kumar (2009). Robbins and Cotran Pathologic Basis of DiseaseProfessional Edition, 8th ed. Saunders, An Imprint of Elsevier.
  8. ↑ Cotran, Robbins (2009). Pathologic Basis of Disease. Jacksonville, FL, U.S.A: Saunders//Elsevier. ISBN 978-1-4160-3121-5.
  9. ↑ SGO Clinical Practice Endometrial Cancer Working Group. Burke WM, Orr J, Leitao M, Salom E, Gehrig P; et al. (2014). “Endometrial cancer: a review and current management strategies: part I.” Gynecol Oncol. 134 (2): 385–92. doi:10.1016/j.ygyno.2014.05.018. PMID 24905773.
  10. ↑ Furberg AS, Thune I (2003). “Metabolic abnormalities (hypertension, hyperglycemia and overweight), lifestyle (high energy intake and physical inactivity) and endometrial cancer risk in a Norwegian cohort”. Int J Cancer. 104 (6): 669–76. doi:10.1002/ijc.10974. PMID 12640672.


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Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2]Roukoz A. Karam, M.D.[3]

Overview

There is insufficient evidence to recommend routine screening for endometrial cancer.[1]

Endometrial Cancer Screening

There is insufficient evidence to recommend routine screening for endometrial cancer.[1]

Women with Lynch syndrome have a risk of developing endometrial cancer up to 50% higher than the general population.

  • Screening for endometrial cancer in women with Lynch syndrome by annual endometrial sampling is recommended starting at age 30 to 35 (or 5 to 10 years prior to the first diagnosed Lynch syndrome-associated cancer in a family member).[2]

References

  1. ↑ 1.0 1.1 “Endometrial Cancer Screening”.
  2. ↑ Lindor NM, Petersen GM, Hadley DW, Kinney AY, Miesfeldt S, Lu KH; et al. (2006). “Recommendations for the care of individuals with an inherited predisposition to Lynch syndrome: a systematic review”. JAMA. 296 (12): 1507–17. doi:10.1001/jama.296.12.1507. PMID 17003399.


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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shankar Kumar, M.B.B.S. [2]]


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Overview

Natural History

Complications

Complications are usually due to the therapy. They can be classified as –

  • Intra-operative-
  • Post-operative- typically common as many females have comorbid conditions like obesity, increased age, etc when they develop endometrial cancer. Of note is thromboembolism.

Prognosis

Of all prognostic factors to consider in endometrial cancer, staging is the most important one. Surgical histopathology contributes to it. Clear cell and papillary serous types are associated with a poor prognosis and are included in the histological category of poorly differentiated variety. As far as squamous types are concerned, it is just the adeno component which plays a key role in prognosis. More the adeno component, worse the prognosis.

It is the depth and not the grade of myometrial invasion that is important, as with increasing depth, there are high chances of extra-uterine spread. Lymph node metastasis is equally important and must be correlated with other prognostic factors. A positive peritoneal cytology needs only to be reported but it does not change the stage.

Because endometrial cancer is usually diagnosed in the early stages (70 % to 75 % of cases are in stage 1 at diagnosis; 10 % to 15 % of cases are in stage 2; 10 % to 15 % of cases are in stage 3 or 4), there is a better probable outcome associated with it than with other types of gynecological cancers such as cervical or ovarian cancer. While endometrial cancers are 40% more common in Caucasian women, an African American woman who is diagnosed with uterine cancer is twice as likely to die, possibly due to the higher frequency of aggressive subtypes in that population.

Survival rates

The 5-year survival rate for endometrial cancer following appropriate treatment is:

  • 75% to 95% for stage 1
  • 50% for stage 2
  • 30% for stage 3
  • less than 5% for stage 4

References


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 complications and prognosis
Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Staging | Laboratory Findings | Chest X Rays | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical therapy | Surgical options | Primary prevention | Secondary prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies


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