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Teenage and young adult cancer risk factors statistics

Lifestyle-related risk factors for cancer in adults are in general unlikely to apply in the same way to the teenage and young adult age-group, as periods of exposure will have been relatively short, and due to the latency between exposure to risk factors and development of related cancer. This section will instead focus on factors that have a shorter latency, and genetic factors likely to be relevant to development of certain cancers in teenagers and young adults.

Meta-analyses and systematic reviews are cited where available, as they provide the best overview of all available research and most take study quality into account. Individual case-control and cohort studies are reported where such aggregated data are lacking.

Previous cancer diagnosis

Treatment for cancer in childhood increases risk of being diagnosed with a second primary cancer in teenagers and young adults. There is a ten-fold risk increase for those aged between 5 and 19 who have been diagnosed with cancer at least five years previously, according to the British Childhood Cancer Survivor Study.1 The risk ratio falls with age, with a five-fold risk increase of being diagnosed with a second primary cancer in those aged 20-29.1 The risk of second primary bone cancer is especially high, with 38-fold and 25-fold risk increases at the ages of 5-19 and 20-29, respectively.1

section reviewed 25/03/13
section updated 25/03/13

Infections

Infection with the Epstein-Barr virus (EBV) is estimated to be associated with 45% of cases of Hodgkin lymphoma in the UK, although this proportion varies by age and is lowest (20%) between the ages of 15 and 44.2 Between the ages of 15 and 49, males are twice as likely as females to have EBV-positive tumours.3 It has been suggested that the aetiology of Hodgkin lymphoma is different in young and middle-aged adults from older adults, and that delayed exposure to common childhood infections is involved in the development of Hodgkin lymphomas diagnosed before or in middle age, but not in cases of the disease in older age. 

Studies have shown that risk of Hodgkin lymphoma is higher in children and young adults with small family size, single-family housing, and relatively high maternal education, and lower in those aged between 15 and 42 with at least three older siblings compared with first-born individuals (risk ratios of 0.3 and 0.7 reported), or who attended pre-school daycare (risk ratio of 0.6).4-6 Evidence is less consistent for non-Hodgkin lymphoma (NHL), but higher birth order has also been associated with a lower risk of NHL before the age of 38 (risk ratio of 0.9 for an increment of one birth).7

Infection with the human papillomavirus (HPV) is a necessary cause of cervical cancer and is also a risk factor for anal, vaginal, vulval, penile and oral cancers.8 HPV 16 is found in more than 60% of invasive cervical cancers, and HPV 18 in 16%, according to a recent meta-analysis.9 Between 1996 and 2006, incidence of cervical cancer increased in women aged 20–29 in most English regions, whereas incidence rates in those aged 40–79 decreased markedly.10 This may be linked to HPV infection rates, which may have increased as the proportion of women having sexual intercourse before the age of 16 has risen in recent decades.11 HPV vaccination has been offered to 12-13-year-old girls in the UK since 2008, and currently uses the Gardasil vaccine, which protects against HPV types 6, 11, 16 and 18.12 The quadrivalent HPV vaccine against these types has been shown to prevent between 94% and 100% of cervical intraepithelial neoplasia (CIN) related to HPV 16/18/6/11 when given to women aged 15-26 uninfected with HPV, over up to five years of follow-up.13,14

section reviewed 25/03/13
section updated 25/03/13

Genes and family history

Li Fraumeni syndrome (LFS) – associated with germ-line mutations on the TP53 gene – is a rare genetic condition that carries a high risk of multiple primary tumours in childhood and young adulthood. Carriers are especially susceptible to carcinomas of the breast and adrenal cortex, soft tissue sarcomas, bone tumours, and brain and CNS tumours. It is diagnosed based on a patient’s personal and family history of cancers.15

The breast cancer predisposition genes BRCA1 and BRCA2 carry an estimated cumulative risk of breast cancer by the age of 30 of 3.6% and 0.6%, respectively.16 Cowden syndrome, which is associated with mutations on the PTEN gene, also carries a higher risk of breast cancer in young adults.17

Individuals with Down syndrome have an increased risk of leukaemia before the age of 40, with the highest risk in childhood. Risk of testicular cancer is also increased in this group, according to a Finnish cohort study and earlier studies.18

Lynch syndrome (or hereditary nonpolyoposis colorectal cancer, caused by mutations in one of the four MMR genes) is responsible for 2–4% of all bowel cancers, and is associated with bowel cancer in teenagers and young adults, although risk is higher for those aged over 40.19 Familial adenomatous polyposis (FAP), caused by germ-line mutations in the APC gene, leads to colon cancer in most patients before the age of 40. Annual or biennial colonic surveillance is recommended from the age of 10–12 for typical FAP, and biennial colonoscopy from the age of 18–20 for those with an attenuated FAP phenotype.20

Germ-line mutations in neurofibromatosis type 1 carry an increased risk of brain and CNS tumours, malignant peripheral nerve sheath tumours, gastro-intestinal stromal tumours and early breast cancer.17

section reviewed 25/03/13
section updated 25/03/13

Puberty and adolescent growth

Osteosarcomas occur much more frequently in the long bones of the arms and legs in teenagers and young adults, and it has been suggested that this is evidence of a link with the adolescent growth spurt, as these are the bones which have the greatest increase in length during that period.21 Young osteosarcoma patients are on average taller than those in the general population.22

section reviewed 25/03/13
section updated 25/03/13

UV radiation

Unlike most other lifestyle factors, exposure to ultraviolet radiation (UVR) is an established factor in development of melanoma in teenagers and young adults. Level of ambient UVR was shown to be linked to risk of melanoma in children, teenagers and young adults in the US, and while white and black children have a similar incidence of melanoma in the first year of life, by the age of 20-24, incidence is 40 times higher in whites.23

Sunbed use, which increases risk of melanoma at all ages, has a particularly marked effect on risk of melanoma diagnosed before the of 30, with ever-use associated with a four-fold increase in risk in this age-group, and more than ten previous sessions of use associated with almost a seven-fold risk increase.24 Although sunbed use in under-18s is now banned across the UK, in 2008-2009, 6% of 11-17 year-olds surveyed in England had already used a sunbed, with higher prevalence among females (8.6%).25 Use is higher among female than male adolescents in other countries, and is a likely factor in the higher incidence of melanoma in young women than young men.26,27

section reviewed 25/03/13
section updated 25/03/13

Hormones

It has been suggested that the higher incidence of melanoma in female than male teenagers and young adults – which is not apparent at all ages – may be linked partly to hormonal exposures, for example from oral contraceptives or pregnancy, but evidence remains limited.28

section reviewed 25/03/13
section updated 25/03/13

Smoking

Smoking doubles risk of developing cervical pre-cancerous lesions in young women, after controlling for HPV infection.29

section reviewed 25/03/13
section updated 25/03/13

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References for teenage and young adult cancer risk factors

  1. Reulen RC, Frobisher C, Winter DL, et al. Long-term risks of subsequent primary neoplasms among survivors of childhood cancer. JAMA 2011;305:2311-9.
  2. Parkin DM. 11. Cancers attributable to infection in the UK in 2010. Br J Cancer 2011;105 Suppl 2:S49-56.
  3. Glaser SL, Lin RJ, Stewart SL, et al. Epstein-Barr virus-associated Hodgkin's disease: epidemiologic characteristics in international data. Int J Cancer 1997;70:375-82.
  4. Chang ET, Zheng T, Weir EG, et al. Childhood social environment and Hodgkin's lymphoma: new findings from a population-based case-control study. Cancer Epidemiol Biomarkers Prev 2004;13:1361-70.
  5. Westergaard T, Melbye M, Pedersen JB, et al. Birth order, sibship size and risk of Hodgkin's disease in children and young adults: a population-based study of 31 million person-years. Int J Cancer 1997;72:977-81.
  6. Chang ET, Montgomery SM, Richiardi L, et al. Number of siblings and risk of Hodgkin's lymphoma. Cancer Epidemiol Biomarkers Prev 2004;13:1236-43.
  7. Crump C, Sundquist K, Sieh W, et al. Perinatal and family risk factors for non-Hodgkin lymphoma in early life: a Swedish national cohort study. J Natl Cancer Inst 2012;104:923-30.
  8. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. J Natl Cancer Inst 2011;103:1827-39.
  9. Guan P, Howell-Jones R, Li N, et al. Human papillomavirus types in 115,789 HPV-positive women: A meta-analysis from cervical infection to cancer. Int J Cancer 2012;131:2349-59.
  10. Foley G, Alston R, Geraci M, et al. Increasing rates of cervical cancer in young women in England: an analysis of national data 1982-2006. Br J Cancer 2011;105:177-84.
  11. Tripp J, Viner R. Sexual health, contraception, and teenage pregnancy. BMJ 2005;330:590-3.
  12. NHS Choices. Human papilloma virus (HPV) cervical cancer vaccine. Accessed February 2013.
  13. Dillner J, Kjaer SK, Wheeler CM, et al. Four year efficacy of prophylactic human papillomavirus quadrivalent vaccine against low grade cervical, vulvar, and vaginal intraepithelial neoplasia and anogenital warts: randomised controlled trial. BMJ 2010;341:c3493.
  14. Munoz N, Kjaer SK, Sigurdsson K, et al. Impact of human papillomavirus (HPV)-6/11/16/18 vaccine on all HPV-associated genital diseases in young women. J Natl Cancer Inst 2010;102:325-39.
  15. International Agency for Research on Cancer. Li-Fraumeni syndrome. Accessed February 2013.
  16. Ford D, Easton DF, Stratton M, et al. Genetic heterogeneity and penetrance analysis of the BRCA1 and BRCA2 genes in breast cancer families. The Breast Cancer Linkage Consortium. Am J Hum Genet 1998;62:676-89.
  17. Coccia PF, Altman J, Bhatia S, et al. Adolescent and young adult oncology. J Natl Compr Canc Netw 2012;10:1112-50.
  18. Patja K, Pukkala E, Sund R, et al. Cancer incidence of persons with Down syndrome in Finland: a population-based study. Int J Cancer 2006;118:1769-72.
  19. Vasen HF, Abdirahman M, Brohet R, et al. One to 2-year surveillance intervals reduce risk of colorectal cancer in families with Lynch syndrome. Gastroenterology 2010;138:2300-6.
  20. Mallinson EK, Newton KF, Bowen J, et al. The impact of screening and genetic registration on mortality and colorectal cancer incidence in familial adenomatous polyposis. Gut 2010;59:1378-82.
  21. Arora RS, Alston RD, Eden TO, et al. The contrasting age-incidence patterns of bone tumours in teenagers and young adults: Implications for aetiology. Int J Cancer 2012;131:1678-85.
  22. Arora RS, Kontopantelis E, Alston RD, et al. Relationship between height at diagnosis and bone tumours in young people: a meta-analysis. Cancer Causes Control 2011;22:681-8.
  23. Strouse JJ, Fears TR, Tucker MA, et al. Pediatric melanoma: risk factor and survival analysis of the surveillance, epidemiology and end results database. J Clin Oncol 2005;23:4735-41.
  24. Cust AE, Armstrong BK, Goumas C, et al. Sunbed use during adolescence and early adulthood is associated with increased risk of early-onset melanoma. Int J Cancer 2011;128:2425-35.
  25. Thomson CS, Woolnough S, Wickenden M, et al. Sunbed use in children aged 11-17 in England: face to face quota sampling surveys in the National Prevalence Study and Six Cities Study. BMJ 2010;340:c877.
  26. Cokkinides V, Weinstock M, Lazovich D, et al. Indoor tanning use among adolescents in the US, 1998 to 2004. Cancer 2009;115:190-8.
  27. Coelho SG, Hearing VJ. UVA tanning is involved in the increased incidence of skin cancers in fair-skinned young women. Pigment Cell Melanoma Res 2010;23:57-63.
  28. Weir HK, Marrett LD, Cokkinides V, et al. Melanoma in adolescents and young adults (ages 15-39 years): United States, 1999-2006. J Am Acad Dermatol 2011;65:S38-49.
  29. Collins S, Rollason TP, Young LS, et al. Cigarette smoking is an independent risk factor for cervical intraepithelial neoplasia in young women: a longitudinal study. Eur J Cancer 2010;46:405-11.
Updated: 25 March 2013