Epidemiology and Aetiology of Testicular Cancers



Fig 17.1
Tumour of an undescended right testis (Courtesy of Kurian George, Urology, Royal Hospital, Muscat, Oman)




 


2.

ITGCN or carcinoma in situ of the testis or testicular intraepithelial neoplasia (TIN): This is a noninvasive premalignant precursor of germ cell tumours. It is commonly found in patients with pre-existing ipsilateral testicular GCT (80 % of patients), but may even be encountered in the contralateral “normal” one (5–10 %) [15]. ITGCN has also been found in association with cryptorchidism, atrophic testis, infertility and hermaphroditism. The progression risk into invasive GCTs increases with time and has been evaluated to be 50 % within 5 years and 70 % within 7 years [1618].

 

3.

Past history of a testicular cancer: This exposes the patient to an increased risk of developing a synchronous or metachronous GCT in the contralateral testis. This risk is reported to be higher in patients who are younger at the time of the diagnosis and in those with seminoma [19, 20].

 

4.

Family history of testicular tumour: Having a first-degree relative with testicular cancer increases the risk of developing this tumour. The median age at diagnosis in such patients with a positive family history is 2–3 years younger than in the general population [21]. Family-linked testicular cancers have been extensively studied by Scandinavian authors who found the individual’s risks for testicular cancer increased by 8- and 4-folds with an affected brother and father [2224]. A recessive mode of inheritance was proposed as an explanation for the higher correlation between brothers than between a father and his son [25]. The combination of shared childhood environment and heritable causes were suggested as an explanation of this high familial risk. There are few genetic changes described in association with testicular cancer. The most commonly encountered is an isochromosome of the short arm of chromosome 12i(12p) which was reported in almost all histological types of germ cell tumours [26, 27]. However, a study has shown that the overrepresentation of 12p is more related to invasive growth and is not an early event in the development of testicular GCTs [28]. Alterations in the p53 locus have been described in 66 % of cases of ITGCN.

 

5.

Other possible risk factors: These include Klinefelter’s syndrome, HIV infection [29], testicular atrophy, infertility, testicular feminization, trauma and hormones. Testicular regression syndrome or vanishing testis syndrome is believed to carry a potential for malignant degeneration in the long term, and it is a common practice to remove such remnants as a preventive measure. However, a recent literature review failed to identify any report of a GCT arising from this condition [30]. This phenomenon should not be confused with the so-called burntout germ cell tumour, a yet unexplained regression of the primary testicular lesion in metastatic germ cell tumour which could be due to immunological reactions.

 



Note: Testicular tumour has also been described as a causative factor for other pathologies:



  • A small population study in Mayo Clinic has shown that sarcoidosis has a 100-fold increased association with testicular cancer patients compared with the general population of young white men [31]. The onset of sarcoidosis was shown to occur after an average of 5 years following the diagnosis of testicular cancer. This appears to be the strongest association between any solid tumours and sarcoidosis.


  • Testicular sarcoma with fatal outcome was reported to arise in association with spermatocytic seminomas [32].


Take-Home Message: Epidemiology and Aetiology















Testicular cancer is the most common malignancy encountered in younger men aged 20–40 years.

Higher incidence is observed in Western countries with an estimated incidence of 3–10 new cases/100,000 males.

There are 4 established aetiological factors: cryptorchidism, presence of ITGCN, personal history and family history of testicular cancer.

Associated genetic findings are consistent with an isochromosome of the short arm of chromosome 12-i(12p) and alterations in the p53 locus.



References



1.

Horner MJ, Ries LA, et al. SEER cancer statistics review, 1975–2006. Bethesda: National Cancer Institute; 2009.


2.

Jemal A, Siegel R, Ward E, Hao Y, Xu J, Thun MJ. Cancer statistics, 2009. CA Cancer J Clin. 2009;59(4):225–49.CrossRefPubMed


3.

Huyghe E, Matsuda T, Thonneau P. Increasing incidence of testicular cancer worldwide: a review. J Urol. 2003;170:5–11.CrossRefPubMed


4.

Jacobsen R, Moller H, Thoresen SO, Pukkala E, Kjaer SK, Johansen C. Trends in testicular cancer incidence in the Nordic countries, focusing on the recent decrease in Denmark. Int J Androl. 2006;29:199–204.CrossRefPubMed


5.
< div class='tao-gold-member'>

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Jul 4, 2016 | Posted by in UROLOGY | Comments Off on Epidemiology and Aetiology of Testicular Cancers

Full access? Get Clinical Tree

Get Clinical Tree app for offline access