Uterine cancer risk factors

Prevention

Preventable cases of uterine cancer, UK

Excess bodyweight

Uterine cancer cases linked to excess bodyweight, UK

Physical inactivity

Uterine cancer cases linked to too little physical activity, UK

Hormone replacement

Uterine cancer cases linked to the use of hormone replacement therapy (HRT), UK

37% of uterine cancer cases each year in the UK are linked to major lifestyle and other risk factors.[1]

Uterine cancer is associated with a number of risk factors.[2,3,4]

Uterine Cancer Risk Factors

Increases risk (‘sufficient’ or ‘convincing’ evidence) May increase risk (‘limited’ or ‘probable’ evidence) Decreases risk (‘sufficient’ or ‘convincing’ evidence) May decrease risk (‘limited’ or ‘probable’ evidence)
  • Post-menopausal hormone therapy (oestrogen-only and  oestrogen-progestogen
  • Tamoxifen
  • Body fatness
  • Diethylstilbestrol (exposure in pregnancy)
  • Abdominal fatness
  • Combined oestrogen–progestogen contraceptives
  • Physical activity

International Agency for Research on Cancer (IARC) and The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) classifications. Find out more about IARC and WCRF/AICR classifications.

All classifications are for endometrium.

References

  1. Parkin DM, Boyd L, Walker LC. The fraction of cancer attributable to lifestyle and environmental factors in the UK in 2010. Summary and conclusions. Br J Cancer 2011; 105 (S2):S77-S81.
  2. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 105*. Available fromhttp://monographs.iarc.fr/ENG/Classification/index.php. Accessed October 2013.
  3. Cogliano VJ, Baan R, Straif K et al. Preventable exposures associated with human cancers. J Natl Cancer Inst. 2011 Dec 21;103(24):1827-39.
  4. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. Washington DC: AICR; 2007.
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The majority of endometrial cancers are oestrogen Open a glossary item-driven.[1,2] Oestrogen and progesterone Open a glossary item work in balance to regulate the female reproductive system, with oestrogen stimulating endometrial cell growth. But oestrogen unopposed by progesterone (e.g. after menopause, or during use of oestrogen-only hormone replacement therapy) increases endometrial cancer risk. Endometrial cancer Open a glossary item risk is 2.1-2.7 times higher in women with the highest circulating oestrogen levels, a cohort study showed.[3]

Many factors associated with uterine cancer risk are causes or markers of higher/lower oestrogen exposure, e.g. hormone replacement therapy (HRT) Open a glossary item, higher parity and longer menstrual lifespan are linked with higher oestrogen exposure, and use of oral contraceptives is linked with lower exposure. This is probably their mechanism of association with uterine cancer risk.

Irregular, infrequent, absent or anovulatory menstrual cycles may reflect exposure to oestrogen unopposed by progesterone, and so may be associated with increased uterine cancer risk.[4]

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Postmenopausal hormone therapy Open a glossary item (HRT; oestrogen-only and combined oestrogen-progestogen) is classified by the International Agency for Research on Cancer (IARC) as a cause of endometrial cancer.[2] An estimated 1% of uterine cancers each year in the UK are linked to HRT use.[2]

References

  1. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 105*. Available fromhttp://monographs.iarc.fr/ENG/Classification/index.php. Accessed October 2013.
  2. Parkin DM. Cancers attributable to exposure to hormones in the UK in 2010. Br J Cancer 2011; 105 (S2):S42-S48.
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Endometrial cancer Open a glossary item risk is 2.3 times higher in oestrogen-only hormone replacement therapy (HRT) Open a glossary item ever-users versus non users, a meta-analysis showed.[1] Studies with endometrial cancer as the endpoint are now rare, because the risks of oestrogen-only HRT users are now well-known, so users are closely monitored and their treatment stopped or changed if endometrial hyperplasia develops.[2]

Endometrial hyperplasia risk is not associated with use of low-dose oestrogen-only HRT for a year, a meta-analysis of randomised controlled trials (RCT) Open a glossary item showed.[3] At moderate and high doses, and at low-dose but 18-24 months use, endometrial hyperplasia risk is markedly higher in oestrogen-only HRT users versus placebo users.[3]

Endometrial cancer risk increases with duration of oestrogen-only HRT use.[1] Endometrial cancer risk decreases after cessation of oestrogen-only HRT use, though risk is still higher in ex-users than never users some years after cessation.[1] Endometrial cancer risk may only be associated with oestrogen-only HRT use in healthy-weight women, perhaps because endogenous oestrogen levels are already so high in women with excess body weight, that exogenous oestrogen has limited additional impact.[4,5]

Endometrial cancer risk is 79% higher in HRT ever-users whose last-used HRT type was tibolone (synthetic oestrogen), versus HRT non-users, a cohort study showed.[4] No association was found in a meta-analysis of randomised controlled trials (RCTs), but this included only 15 cancer cases.[6]

References

  1. Grady D, Gebretsadik T, Kerlikowske K, Ernster V, Petitti D. Hormone replacement therapy and endometrial cancer risk: a meta-analysis 1995 Feb;85(2):304-13.
  2. Marjoribanks J, Farquhar C, Roberts H, Lethaby A. Long term hormone therapy for perimenopausal and postmenopausal women. 2012 Jul 11;7:CD004143.
  3. Furness S, Roberts H, Marjoribanks J, Lethaby A. Hormone therapy in postmenopausal women and risk of endometrial hyperplasia. 2012 Aug 15;8:CD000402.
  4. Beral V, Bull D, Reeves G. Endometrial cancer and hormone-replacement therapy in the Million Women Study. Lancet, 2005. 365(9470): 1543-51.
  5. Crosbie EJ, Zwahlen M, Kitchener HC, et al. Body mass index, hormone replacement therapy, and endometrial cancer risk: a meta-analysis. Cancer Epidemiol Biomarkers Prev. 2010 Dec;19(12):3119-30.
  6. Formoso G, Perrone E, Maltoni S et al. Short and long term effects of tibolone in postmenopausal women. 2012 Feb 15;2:CD008536.
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Endometrial cancer Open a glossary item risk is 22% lower in ever-users of continuous combined HRT (oestrogen and progesterone taken together daily), versus non-users, a meta-analysis of observational studies showed.[1]

Endometrial hyperplasia and endometrial cancer risk is not associated with use of continuous combined HRT, a meta-analysis of Randomised Controlled Trials (RCTs) showed.[2]

The association between endometrial cancer and cyclic/sequential combined HRT (oestrogen taken daily with progesterone added for part of the menstrual cycle) varies with the proportion of the cycle where progesterone is used. Endometrial cancer risk is not associated with ever-use of cyclic/sequential combined HRT with 10-24 days progesterone per month, a meta-analysis of observational studies showed; but is 76% higher in ever-users of cyclic/sequential combined HRT with less than 10 days of progesterone per month, versus non-users.[1]

Endometrial hyperplasia risk is not associated with use of combined sequential/cyclic HRT overall, a meta-analysis of RCTs showed.[1]

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Endometrial cancer Open a glossary item risk is 35-42% higher in nulliparous women (those who have had no children), compared with parous women (those who have had children), a cohort study and pooled analysis showed.[1,2] Endometrial cancer risk decreases with greater number of full-term pregnancies.[2]

Endometrial cancer risk is 44% higher in women who were aged 25 or younger when they gave birth to their last child, compared with women who did so aged 40+, a pooled analysis showed.[3]

Increased progesterone levels during pregnancy and physical changes to the uterus during and after childbirth may explain the link between parity and endometrial cancer risk.[1,2]

References

  1. Schonfield SJ, Hartge P, Pfeiffer RM et al. An aggregated analysis of hormonal factors and endometrial cancer risk by parity. Cancer. 2013 Apr 1;119(7):1393-401.
  2. Dossus L, Allen N, Kaaks R et al. Reproductive risk factors and endometrial cancer: the European Prospective Investigation into Cancer and Nutrition. Int J Cancer. 2010 Jul 15;127(2):442-51.
  3. Setiawan VW, Pike MC, Karageorgi S et al. Age at last birth in relation to risk of endometrial cancer: pooled analysis in the epidemiology of endometrial cancer consortium. Am J Epidemiol. 2012 Aug 15;176(4):269-78. Epub 2012 Jul 23.
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Endometrial cancer Open a glossary item risk among parous women is 11% higher in those aged under 13 at menarche (first menstrual period), compared with those aged 13+ at menarche, a pooled analysis showed.[1] Endometrial cancer risk among nulliparous women is not associated with age at menarche.[1]

Endometrial cancer risk among parous women is 22% higher in those aged 50-54 at menopause, compared with those aged under 45 at menopause, a pooled analysis showed.[1] Endometrial cancer risk among nulliparous women is 34% higher in those aged 50-54 at menopause, compared with those aged under 45 at menopause.[1]

Longer menstrual lifespan results in greater cumulative oestrogen exposure, which may explain the link between parity and endometrial cancer risk.[2]

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Body fatness is classified by the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) as a cause of endometrial cancer Open a glossary item, and abdominal fatness as a probable cause of endometrial cancer.[1] An estimated 34% of uterine cancers each year in the UK are linked to overweight and obesity.[2]

Endometrial cancer risk is 32% higher in overweight (body mass index [BMI] 25-30) women, and 2.5 times higher in obese (BMI 30+ women), both compared with healthy-weight (BMI less than 25) women, a meta-analysis showed.[3] The association may be stronger in women who have never used Hormone replacement therapy (HRT).[4]

Endometrial cancer risk is 81% higher per 5-unit BMI gained during adulthood, a meta-analysis showed.[5]

Greater body fatness is associated with higher sex hormone levels (fatty tissue produces more oestrogen) and higher leptin levels, which may partly explain the link between body fatness and endometrial cancer risk.[6,7]

Endometrial cancer risk is 2.2 times higher in women with the highest waist circumference versus those with the lowest, a meta-analysis showed.[8]

References

  1. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. Washington DC: AICR; 2007.
  2. Parkin DM, Boyd L, Walker LC. The fraction of cancer attributable to lifestyle and environmental factors in the UK in 2010. Summary and conclusions. Br J Cancer 2011; 105 (S2):S77-S81.
  3. Zhang Y, Liu H, Yang S, et al. Overweight, obesity and endometrial cancer risk: results from a systematic review and meta-analysis. Int J Biol Markers. 2013 Sep 30:0
  4. Crosbie EJ, Zwahlen M, Kitchener HC, et al. Body mass index, hormone replacement therapy, and endometrial cancer risk: a meta-analysis. Cancer Epidemiol Biomarkers Prev. 2010 Dec;19(12):3119-30.
  5. Arem H, Gunter MJ, Cross AJ, et al. Body weight in early adulthood, adult weight gain, and risk of endometrial cancer in women not using postmenopausal hormones. Cancer Causes Control. 2014 Mar;25(3):321-8.
  6. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. Washington DC: AICR; 2007.
  7. Wang PP, He XY, Wang R, et al. High leptin level is an independent risk factor of endometrial cancer: a meta-analysis. Cell Physiol Biochem 2014;34(5):1477-84.
  8. Esposito K, Chiodini P, Capuano A, Bellastella G, Maiorino MI, Giugliano D.Metabolic syndrome and endometrial cancer: a meta-analysis. Endocrine. 2014 Feb;45(1):28-36.
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Uterine cancer risk is higher in breast and ovarian cancer survivors, cohort studies Open a glossary item have shown.[1-3]

This may reflect shared lifestyle or environmental factors (endometrial cancer risk among breast cancer survivors is higher in those with excess body weight, a meta-analysis showed[4]), the effect of treatment (e.g. tamoxifen) for the primary cancer, and/or increased diagnostic activity following the primary diagnosis.

References

  1. Jégu J, Colonna M, Daubisse-Marliac L, et al. The effect of patient characteristics on second primary cancer risk in France. BMC Cancer. 2014 Feb 15;14:94.
  2. Youlden DR, Baade PD. The relative risk of second primary cancers in Queensland, Australia: a retrospective cohort study. BMC Cancer. 2011 Feb 23;11:83.
  3. Hemminki K, Aaltonen L, Li X. Subsequent primary malignancies after endometrial carcinoma and ovarian carcinoma. Cancer. 2003 May 15;97(10):2432-9.
  4. Drusne-Pecollo N, Touvier M, Barrandon E, Chan DS et al. Excess body weight and second primary cancer risk after breast cancer: a systematic review and meta-analysis of prospective studies. Breast Cancer Res Treat. 2012 Oct;135(3):647-54.
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Endometrial cancer Open a glossary item risk is 40-81% higher in diabetics compared with non-diabetics, meta-analyses have shown,[1,2] however overweight/obesity in diabetics may largely explain this association.[3] Endometrial/uterine cancer risk among diabetics does not vary with diabetes treatment.[4,5]

Endometrial cancer risk is 39% higher in women with metabolic syndrome (characterised by overweight/obesity, ineffective insulin use, diabetes and hypertension), compared with the general population, a meta-analysis showed.[6]

References

  1. Starup-Linde J, Karlstad O, Eriksen SA, et al. CARING (CAncer Risk and INsulin analoGues): The Association of Diabetes Mellitus and Cancer Risk with Focus on Possible Determinants- a Systematic Review and a Meta-Analysis. Curr Drug Saf. 2013 Nov 7.
  2. Zhang ZH, Su PY, Hao JH, et al. The role of preexisting diabetes mellitus on incidence and mortality of endometrial cancer: a meta-analysis of prospective cohort studies. Int J Gynecol Cancer. 2013 Feb;23(2):294-303.
  3. Luo J, Beresford S, Chen C, et al. Association between diabetes, diabetes treatment and risk of developing endometrial cancer. Br J Cancer 2014 Sep;111(7):1432-9.
  4. Becker C, Jick SS, Meier CR, et al. Metformin and the risk of endometrial cancer: a case-control analysis. Gynecol Oncol. 2013 Jun;129(3):565-9.
  5. Ferrara A, Lewis JD, Quesenberry CP Jr, et al. Cohort study of pioglitazone and cancer incidence in patients with diabetes. Diabetes Care. 2011 Apr;34(4):923-9.
  6. Esposito K, Chiodini P, Capuano A, Bellastella G, Maiorino MI, Giugliano D.Metabolic syndrome and endometrial cancer: a meta-analysis. Endocrine. 2014 Feb;45(1):28-36.
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Endometrial cancer  risk is 2.8 times higher in women with polycystic ovary syndrome (PCOS) versus those without the condition, a meta-analysis showed.[1] Endometrial cancer risk is 4.1 times higher in women aged 54 and under (e.g. premenopausal), versus women of a similar age without PCOS.[1]

Increased endometrial cancer risk in PCOS probably reflects exposure to unopposed oestrogen. PCOS often coexists with metabolic syndrome so insulin pathways may also be implicated.[2]

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Among women with endometrial polyps, endometrial cancer occurs in 2-5% of cases, a meta-analysis showed.[1] Endometrial polyps are more likely to be malignant in postmenopausal than in premenopausal women.[1]

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Tamoxifen Open a glossary item is classified by The International Agency for Research on Cancer (IARC) as a cause of endometrial cancer.[1]

Uterine cancer risk among female breast cancer survivors is 3 times higher in those aged 55-69 who used tamoxifen for around 5 years, compared with non-users, a pooled analysis showed; it is not associated with first tamoxifen use at a younger age.[2]

References

  1. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 105*. Available fromhttp://monographs.iarc.fr/ENG/Classification/index.php. Accessed October 2013.
  2. Early Breast Cancer Trialists' Collaborative Group (EBCTCG), Davies C, Godwin J, et al. Relevance of breast cancer hormone receptors and other factors to the efficacy of adjuvant tamoxifen: patient-level meta-analysis of randomised trials. Lancet. 2011;378(9793):771-84
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Diethylstilbestrol (DES) exposure in pregnancy is classified by the International Agency for Research on Cancer (IARC) as a probable cause of endometrial cancer, based on limited evidence.[1]

Endometrial cancer risk is not associated with DES exposure in pregnancy or in utero, cohort studies have shown.[2,3]

References

  1. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 105*. Available fromhttp://monographs.iarc.fr/ENG/Classification/index.php. Accessed October 2013.
  2. Titus-Ernstoff L, Hatch EE, Hoover RN et al. Long-term cancer risk in women given diethylstilbestrol (DES) during pregnancy. Br J Cancer. 2001 Jan 5;84(1):126-33.
  3. Troisi R, Hatch EE, Titus-Ernstoff L et al. Cancer risk in women prenatally exposed to diethylstilbestrol. Int J Cancer. 2007 Jul 15;121(2):356-60.
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Red meat is classified by The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) as a possible cause of endometrial cancer, based on limited-suggestive evidence.[1]

Endometrial cancer risk is 51% higher per 100g/day of red meat consumed, a meta-analysis of case-control studies showed.[2]

Endometrial cancer risk is 40% higher in women with the highest dietary cadmium intake versus those with the lowest, a meta-analysis showed.[3]

References

  1. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. Washington DC: AICR; 2007.
  2. Bandera EV, Kushi LH, Moore DF, Gifkins DM, McCullough ML. Consumption of animal foods and endometrial cancer risk: a systematic literature review and meta-analysis. Cancer Causes Control. 2007 Nov;18(9):967-88. Epub 2007 Jul 19.
  3. Cho YA, Kim J, Woo HD, Kang M. Dietary cadmium intake and the risk of cancer: a meta-analysis. PLoS One. 2013 Sep 17;8(9):e75087.
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Greater adult attained height is classified by The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) as a possible cause of endometrial cancer Open a glossary item, based on limited-suggestive evidence; height is considered a marker of other factors rather than a cause in its own right.[1]

Endometrial cancer risk is 9-19% higher per 10cm height increment, some cohort studies have shown;[2,3] though others have shown no association.[4]

References

  1. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. Washington DC: AICR; 2007.
  2. Bjørge T, Engeland A, Tretli S, Weiderpass E. Body size in relation to cancer of the uterine corpus in 1 million Norwegian women. Int J Cancer. 2007 Jan 15;120(2):378-83.
  3. Green J, Cairns BJ, Casabonne D et al. Height and cancer incidence in the Million Women Study: prospective cohort, and meta-analysis of prospective studies of height and total cancer risk. Lancet Oncol. 2011 Aug;12(8):785-94.
  4. Wirén S, Häggström C, Ulmer H et al. Pooled cohort study on height and risk of cancer and cancer death. Cancer Causes Control. 2014 Feb;25(2):151-9.
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Oral contraceptives (OCs) Open a glossary item are classified by the International Agency for Research on Cancer (IARC) as protective against endometrial cancer Open a glossary item.[1] An estimated 17% of uterine cancers each year in the UK are prevented by OC use.[2]

Endometrial cancer risk is 26-43% lower in OC ever- versus never-users, meta-analyses have shown.[3,4] The lower risk may be limited to women with 5+ years OC use,[3] and may persist for 20 years after OC cessation.[5]

Physical activity of all types (occupational, household, transport, and recreational) is classified by The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) as probably protective against endometrial cancer.[6]An estimated 4% of uterine cancers in the UK are caused by women doing too little physical activity (less than 150 minutes per week).[2]

Endometrial cancer risk is 15-27% lower in the most physically active (recreational) women versus the least, meta-analyses have shown.[7,9] Endometrial cancer risk is 5% lower per 1 hour/week increment in leisure-time physical activity,[9] and 32% lower in women who spend the least time sitting versus those who spend the most.[10] Endometrial cancer risk is not associated with household physical activity, a meta-analysis showed. [11]

Non-starchy vegetables (not salted or pickled) are classified by WCRF/AICR as possibly protective against endometrial cancer, based on limited-suggestive evidence.[6]

Endometrial cancer risk is 10% lower per 100g /day intake of vegetables, and 21% lower per 100g/day intake of cruciferous vegetables, a meta-analysis of case-control studies showed.[12] However endometrial cancer risk is not associated with total vegetable intake in cohort studies.[13,14]

Endometrial cancer risk among postmenopausal women is 29% lower in ever-smokers versus never-smokers, a meta-analysis showed; the association may be stronger in HRT users.[15] Endometrial cancer risk among premenopausal women is not associated with smoking.[15]

Endometrial cancer risk is 29% lower in women with systemic lupus erythematosus, versus those without the condition, a meta-analysis showed.[16]

Endometrial cancer risk is lower in women with the highest intake of the following, versus those with the lowest intake meta- and pooled analyses or systematic reviews have shown:

  • Coffee – 21% lower risk.[17]
  • Tea – 25% lower risk (stronger effect for green than black tea).[18]

Endometrial cancer risk is lower in users of the following medications/medical devices, compared with non-users, meta- and pooled analyses or systematic reviews have shown:

  • Intrauterine device Open a glossary item – 19% lower risk [19]
  • Aspirin – 13% lower risk for any aspirin use versus none (may be limited to obese women).[20]

References

  1. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 105*. Available fromhttp://monographs.iarc.fr/ENG/Classification/index.php. Accessed October 2013.
  2. Parkin DM. Cancers attributable to exposure to hormones in the UK in 2010. Br J Cancer 2011; 105 (S2):S42-S48.
  3. Havrilesky LJ, Gierisch JM, Moorman PG, et al. Oral contraceptive use for the primary prevention of ovarian cancer. Evid Rep Technol Assess (Full Rep). 2013 Jun;(212):1-514.
  4. Setiawan VW, Yang HP, Pike MC, et al. Type I and II endometrial cancers: have they different risk factors? J Clin Oncol. 2013 Jul 10;31(20):2607-18.
  5. Mueck AO, Seeger H, Rabe T. Hormonal contraception and risk of endometrial cancer: a systematic review. Endocr Relat Cancer. 2010 Sep 23;17(4):R263-71.
  6. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. Washington DC: AICR; 2007.
  7. Voskuil DW, Monninkhof EM, Elias SG, et al. Physical activity and endometrial cancer risk, a systematic review of current evidence. Cancer Epidemiol Biomarkers Prev 2007; 16(4): 639-48.
  8. Moore SC, Gierach GL, Schatzkin A, et al. Physical activity, sedentary behaviours, and the prevention of endometrial cancer. Br J Cancer. 2010 Sep 28;103(7):933-8.
  9. Keum N, Ju W, Lee DH, et al. Leisure-time physical activity and endometrial cancer risk: Dose-response meta-analysis of epidemiological studies. Int J Cancer. 2013 Dec 20.
  10. Schmid D, Leitzmann MF. Television viewing and time spent sedentary in relation to cancer risk: a meta-analysis. J Natl Cancer Inst. 2014 Jun 16;106(7). pii: dju098.
  11. Shi Y, Li T, Wang Y, et al. Household physical activity and cancer risk: a systematic review and dose-response meta-analysis of epidemiological studies. Sci Rep. 2015;5:14901
  12. Bandera EV, Kushi LH, Moore DF< Gifkins DM, McCullough ML. Fruits and vegetables and endometrial cancer risk: a systematic literature review and meta-analysis. Nutr Cancer. 2007;58(1):6-21.
  13. Kabat GC, Park Y, Hollenbeck AR, Schatzkin A, Rohan TE. Intake of fruits and vegetables, and risk of endometrial cancer in the NIH-AARP Diet and Health Study. Cancer Epidemiol. 2010 Oct;34(5):568-73.
  14. McCullough ML, Bandera EV, Patel R, Patel AV et al. A prospective study of fruits, vegetables, and risk of endometrial cancer. Am J Epidemiol. 2007 Oct 15;166(8):902-11. Epub 2007 Aug 9.
  15. Zhou B, Yang L, Sun Q, Cong R, Gu H, Tang N, Zhu H, Wang B. Cigarette smoking and the risk of endometrial cancer: a meta-analysis. Am J Med. 2008 Jun;121(6):501-508.e3.
  16. Bernatsky S, Ramsey-Goldman R, Foulkes WD, Gordon C, Clarke AE. Breast, ovarian, and endometrial malignancies in systemic lupus erythematosus: a meta-analysis. Br J Cancer. 2011 Apr 26;104(9):1478-81.
  17. e Y, Giovannucci E Coffee consumption and risk of endometrial cancer: Findings from a large up-to-date meta-analysis. Int J Cancer 2011.
  18. Tang NP, Li H, Qiu YL, Zhou GM, Ma J. Tea consumption and risk of endometrial cancer: a meta analysis. Int J Cancer 2015;136(5):E410-22.
  19. Felix AS1, Gaudet MM, La Vecchia C, et al. Intrauterine devices and endometrial cancer risk: A pooled analysis of the Epidemiology of Endometrial Cancer Consortium.. Ann Epidemiol. 2008 Jun;18(6):492-9.
  20. Neill AS, Nagle CM, Protani MM, et al. Aspirin, nonsteroidal anti-inflammatory drugs, paracetamol and risk of endometrial cancer: A case-control study, systematic review and meta-analysis. Int J Cancer 2012.
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The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) make no judgment on the association between endometrial cancer risk and intake of cereals (grains) and their products; dietary fibre; fruits; pulses (legumes); soya and soya products; poultry; fish; eggs; milk and dairy products; total fat; animal fats; saturated fatty acids; cholesterol; coffee; alcohol; carbohydrates; protein; retinol; vitamin C; vitamin E; beta-carotene; lactation; or energy intake, due to limited evidence.[1]

Uterine cancer risk is not associated with the following factors, meta- and pooled analyses or systematic reviews have shown:

  • Alcohol.[2]
  • Fish consumption.[3-5]
  • Poultry consumption.[3-5]
  • Dairy consumption.[3]
  • Fruit and vegetable consumption.[6]
  • Human papillomavirus.[7]
  • Statins.[8]
  • Fertility treatment.[9-10]
  • Vitamin D (blood levels[11] or supplement[12]).
  • Dietary fatty acids.[13]

References

  1. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. Washington DC: AICR; 2007.
  2. Friberg E, Orsini N, Mantzoros CS, Wolk A. Alcohol intake and endometrial cancer risk: a meta-analysis of prospective studies. Br J Cancer. 2010 Jun 29;103(1):127-31.
  3. Bandera EV, Kushi LH, Moore DF, Gifkins DM, McCullough ML. Consumption of animal foods and endometrial cancer risk: a systematic literature review and meta-analysis. Cancer Causes Control. 2007 Nov;18(9):967-88. Epub 2007 Jul 19.
  4. Stevens VL, Jacobs EJ, Patel AV, et al. A prospective investigation of fish, meat and cooking-related carcinogens with endometrial cancer incidence. Br J Cancer. 2013 Aug 6;109(3):756-60.
  5. van Lonkhuijzen L, Kirsh VA, Kreiger N, et al. Endometrial cancer and meat consumption: a case-cohort study. Eur J Cancer Prev. 2011 Jul;20(4):334-9.
  6. Bandera EV, Kushi LH, Moore DF< Gifkins DM, McCullough ML. Fruits and vegetables and endometrial cancer risk: a systematic literature review and meta-analysis. Nutr Cancer. 2007;58(1):6-21.
  7. Olesen TB, Svahn MF, Faber MT, et al. Prevalence of Human Papillomavirus in endometrial cancer: A systematic review and meta-analysis. Gynecol Oncol. 2014;134(1):206-215.
  8. Liu Y, Qin A, Li T, Qin X, Li S. Effect of statin on risk of gynecologic cancers: a meta-analysis of observational studies and randomized controlled trials. Gynecol Oncol. 2014 Jun;133(3):647-55
  9. Saso S, Louis LS, Doctor F, et al. Does fertility treatment increase the risk of uterine cancer? A meta-analysis. Eur J Obstet Gynecol Reprod Biol. 2015;195:52-60
  10. Siristatidis C, Sergentanis TN, Kanavidis P et al. Controlled ovarian hyperstimulation for IVF: impact on ovarian, endometrial and cervical cancer--a systematic review and meta-analysis. Hum Reprod Update. 2013 Mar-Apr;19(2):105-23.
  11. Skaaby T, Husemoen LL, Thuesen BH et al. Prospective population-based study of the association between serum 25-hydroxyvitamin-D levels and the incidence of specific types of cancer. Cancer Epidemiol Biomarkers Prev. 2014 Jul;23(7):1220-9.
  12. Bjelakovic G, Gluud LL, Nikolova D, et al. Vitamin D supplementation for prevention of cancer in adults. Cochrane Database Syst Rev 2014;6:CD007469.
  13. Wu QJ, Gong TT, Wang YZ. Dietary fatty acids intake and endometrial cancer risk: a dose-response meta-analysis of epidemiological studies. Oncotarget. 2015;6(34):36081-97
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Cancer Statistics Explained

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