What can explain this increase?
There is one class of conditions that is overwhelmingly associated with the development of germ cell tumors of the testis: disorders of sex development of the testes.[1] Among the conditions within this general group are testicular dysgenesis, testicular feminization (insensitivity to androgens), and cryptorchidism. Disorders of sex development of the testis raise the incidence of intratubular germ cell neoplasia or of gonadoblastoma, both of which are testicular precancers.
As you might expect, along with the observed increase in testicular germ cell cancers in white males, there has been an observed increase in the incidence of disorders of sex development in the same population. [1,2] These disorders are characterized by a retardation in the maturation of primordial germ cells, along with an apparent mitotic over-stimulation of these same cells: leading to a proliferative, precancerous condition.
Though there is no proof at the moment, we might expect that males who develop testicular germ cell cancer who have clinically normal testes, may harbor small foci of [clinically unobserved] germ cell proliferative lesions.
What has caused the increased incidence of disorders of sex development in the testes? We don't know, but we have a candidate: the ubiquitous plasticizer and endocrine disruptor, Bisphenol A.
Bisphenol A is a synthetic estrogen used in the process of manufacturing plastics, and has been detected in the serum, milk, saliva, urine, and amniotic fluid of humans.[3] Because we get our daily dose of Bisphenol A from plastic bottles, one would expect that the levels of Bisphenol A in our blood would have increased steadily over the past several decades [coinciding with our increased dependence of plastic food and drink containers]. You might also expect that if Bisphenol A produced testicular cancers, you would see the largest increases in incidence among the wealthiest populations in the most industrialized nations [as we do].
Can we assume that Bisphenol A is causing the rise of incidence of testicular germ cell cancers? Absolutely not. All of the evidence, so far, is very weak (if it can be called evidence at all!). Still, nobody would suggest that Bisphenol A has much to recommend itself as a healthy addition to our diets. It seems prudent to try to limit our exposure to this compound when feasible, particularly among infants and pregnant women.
1. Pleskacova J, Hersmus R, Oosterhuis JW, Setyawati BA, Faradz SM, Cools M, Wolffenbuttel KP, Lebl J, Drop SL, Looijenga LH. Tumor Risk in Disorders of Sex Development. Sex Dev 4:259-269, 2010.
2. Skakkebaek NE, Rajpert-De Meyts E, Jorgensen N, Main KM, Leffers H, Andersson AM, Juul A, Jensen TK, Toppari J. Testicular cancer trends as 'whistle blowers' of testicular developmental problems in populations. Int J Androl 30:198-204, 2007.
3. Bouskine A, Nebout M, Brucker-Davis F, Benahmed M, Fenichel P. Low Doses of Bisphenol A Promote Human Seminoma Cell Proliferation by Activating PKA and PKG via a Membrane G-Protein-Coupled Estrogen Receptor. Environ Health Perspect 117:1053-1058, 2009.
This series of blogs has drawn heavily from the public use SEER data sets produced by the U.S. National Cancer Institute's Surveillance, Epidemiology and End Results project. In the next blog, I'll discuss how this data can be obtained and used by the science-minded public.
Jump to Tomorrow's blog
- © 2010 Jules Berman
key words: carcinogenesis, neoplasia, neoplasms, tumor development, tumour development, germ cell tumor, germ cell tumour, tumor epidemiology, increasing germ cell cancer rates, germ cell cancer, seminomas, seminomatous, non-seminomatous, non-germinomatous, embryonal carcinoma, choriocarcinoma, testis, testes, itgcn, intratubular germ cell neoplasm, plasticizers, endocrine disruptors
About my book, Precancer: The Beginning and the End of Cancer. Nearly every type of cancer passes through a precancer phase, during which it cannot metastasize or invade other tissues. While medicine is not always successful in treating or curing advanced stages of cancers, recent advances in our understanding of carcinogenesis have helped us to develop strategies to prevent, diagnose, and treat many cancers at the precancer stage. Research in this field is escalating rapidly as the evidence increasingly shows that the number of annual cancer deaths could be drastically reduced through the effective treatment and cure of precancer lesions. This book begins by explaining why it has been so difficult to cure cancers, followed by a review of precancer biology, with descriptions of the most common precancer lesions. The final chapters provide practical socio-political and medical goals for precancer treatment, including discussions of the economics and politics of treating precancers.
I urge you to read more about this important topic. Google Books has provided a generous preview of this book.
