Endometrial cancer causes: Difference between revisions

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{{Endometrial cancer}}
{{Endometrial cancer}}
{{CMG}}
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==Overview==
==Overview==
Causes of endometrial cancer include genetic mutations of the ''[[KRAS]]'' gene, ''[[TP53]]'' gene, ''[[P16 (gene)|TP16]]'' gene, and/or ''[[PTEN]]'' gene. Other genetic mutations have also been described.


==Causes==  
==Causes==
Most women with endometrial cancer have a history of unopposed and increased levels of [[estrogen]]. One of estrogen's normal functions is to stimulate the buildup of the [[endometrial]] lining of the uterus. Excess estrogen activity, especially in the setting of insufficient [[progesterone]], may produce [[endometrial hyperplasia]],  which can be a precursor for cancer.
Endometrial cancer arises following multiple genetic mutations. The following genes are involved in the development of endometrial cancer:
 
{| <!--Placing these in a table with no border will keep them together/aligned in any browser-->
Increased estrogen may be due to:
|-
* obesity (> 30 lb or 14 kg overweight)
|
* exogenous (medication)
{| class="wikitable sortable"
 
|+Mutations found in Type I and Type II endometrial cancers<ref>International Agency for Research on Cancer (2014). World Cancer Report 2014. World Health Organization. Chapter 5.12. ISBN 978-92-832-0429-9.</ref>
The incidence of endometrial cancer in women in the [[United States|U.S.]] is 1 % to 2 %. The incidence peaks between the ages of 60 and 70 years, but 2 % to 5 % of cases may occur before the age of 40 years. Increased risk of developing endometrial cancer has been noted in women with increased levels of natural estrogen.
|-
 
!Gene mutated
Associated conditions include the following:
!Mutation type
*[[obesity]]  
!Type I prevalence
*[[hypertension]]  
!Type II prevalence
*[[polycystic ovary syndrome]]  
|-
 
|''[[ARID1A]]''
Increased risk is also associated with the following:
|[[point mutation]]
*nulliparity (never having carried a pregnancy)
|40%
*[[infertility]] (inability to become pregnant)
|unknown
*early [[menarche]] (onset of menstruation)
|-
*late [[menopause]] (cessation of menstruation)
| ''CTNNB1''
 
|point mutation
Women who have a history of [[uterine polyp|endometrial polyp]]s or other benign growths of the uterine lining, postmenopausal women who use [[estrogen-replacement therapy]] (specifically if not given in conjunction with periodic [[progestin]]) and those with [[diabetes]] are also at increased risk.
|14–44%
 
|unknown
[[Tamoxifen]], a drug used to treat [[breast cancer]], can also increase the risk of developing endometrial cancer.
|-
 
|''[[FGFR2]]''
The same risk factors predisposes women to endometrial [[hyperplasia]], which is a precursor lesion for endometrial carcinoma. An atypical complex hyperplasia carries a 30% risk of developing endometrial carcinoma, while a typical simple hyperplasia only carries a 2-3% risk.
|point mutation
 
|16%
====Drug Side Effect====
|unknown
 
|-
*[[Drospirenone and Ethinyl estradiol]],
|''[[KRAS]]''
*[[Medroxyprogesterone]],
|point mutation
*[[Norethindrone acetate and Ethinyl estradiol]],
|10–20%
*[[Norgestimate and Ethinyl estradiol]]
|unknown
|-
| ''PIK3R1''
|point mutation
|43%
|unknown
|-
|''[[TP53]]''
|point mutation
|10–20%
|90%
|-
|''[[PTEN (gene)|PTEN]]''
|point mutation
|37–61%
|unknown
|-
|''[[MLH1]]''
|[[gene silencing|epigenetic silencing]]
|30%
|unknown
|-
| ''RASSF1A''
|epigenetic silencing
|48%
|unknown
|-
| ''SPRY2''
|epigenetic silencing
|20%
|unknown
|-
| ''PPP2R1A''
|point mutation
|unknown
|17–41%
|-
| ''CDH1 (gene)|CDH1''
|[[loss of heterozygosity]]
|unknown
|80–90%
|-
|''[[p16 (gene)|CDKN2A]]''
|loss of heterozygosity and/or<br />epigenetic silencing
|20%
|40%
|-
| ''PIK3CA'' ([[oncogene]])
|point mutation or amplification (molecular biology)|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%
|}
|}


==References==
==References==
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[[Category:Types of cancer]]
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Latest revision as of 22:15, 26 November 2017

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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]

Overview

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.

Causes

Endometrial cancer arises following multiple genetic mutations. The following genes are involved in the development of endometrial cancer:

Mutations found in Type I and Type II endometrial cancers[1]
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%

References

  1. ↑ International Agency for Research on Cancer (2014). World Cancer Report 2014. World Health Organization. Chapter 5.12. ISBN 978-92-832-0429-9.


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