A survey of etiologic hypotheses among testicular cancer researchers

Abstract

Basic research results can provide new ideas and hypotheses to be examined in epidemiological studies. We conducted a survey among testicular cancer researchers on hypotheses concerning the etiology of this malignancy. All researchers on the mailing list of Copenhagen Testis Cancer Workshops and corresponding authors of PubMed-indexed articles identified by the search term “testicular cancer” and published within 10 years (in total 2750 recipients) were invited to respond to an e-mail based survey. Participants of the 8th Copenhagen Testis Cancer Workshop in May 2014 were subsequently asked to rate the plausibility of the suggested etiologic hypotheses on a scale of 1 (very implausible) to 10 (very plausible). This report describes the methodology of the survey, the score distributions by individual hypotheses, hypothesis group and the participants’ major research fields, and discuss the hypotheses that scored as most plausible. We also present plans for improving the survey that may be repeated at a next international meeting of experts in testicular cancer. Overall 52 out of 99 (53%) registered participants of the 8th Copenhagen Testis Cancer Workshop submitted the plausibility rating form. Fourteen out of 27 hypotheses were related to exposures during pregnancy. Hypotheses with the highest mean plausibility ratings were either related to prenatal exposures or exposures that might have an effect during pregnancy and in post-natal life. The results of the survey may be helpful for triggering more specific etiologic hypotheses that include factors related to endocrine disruption, DNA damage, inflammation, and nutrition during pregnancy. The survey results may stimulate a multidisciplinary discussion about new etiologic hypotheses of testicular cancer.

Annual Report to the Nation on the Status of Cancer, Featuring Cancer in Men and Women Age 20–49 Years

“…This cancer shows wide variability in incidence rates by race, with higher incidence among white (12.5) and AI/AN (10.5) men and the lowest incidence among black (2.8) and API (3.6) men, as has been noted in previous studies (77). Primary prevention approaches do not exist for well-known testicular cancer risk factors, which include a family history of testicular cancer, reduced fertility, cryptorchidism, hypospadias, a personal history of testicular cancer, and adult height (78). With the introduction of effective cisplatin-based therapies in the 1970s, testicular cancer is highly curable, with a 10-year relative survival approaching 95% (79).…”

Reappraising the exteriorization of the mammalian testes through evolutionary physiology

“…It is clear that there is no common agreement among researchers as to the cause of testicular cancers [154]. However, an accumulating weight of evidence suggests that the teratogenic effects of cryptochidism can be ascribed to ecological imbalance of innate testicular cells with their companion microbes as a generalized ecological dysbiosis which has reverberations at multiple system levels.…”

Parental occupations at birth and risk of adult testicular germ cell tumors in offspring: a French nationwide case–control study

“…Such exposures could induce downregulation of androgen and oestrogen receptor signaling (25,26), oxidative damage and apoptosis in testes observed in animal and in vitro studies (27), inhibition of DNA synthesis in testes seen in animal studies (28,29) or act as a tumor promoter through the inhibition of intercellular communication (30), which may contribute to GCNIS development in the early stages of pregnancy (13,14,16,31,32). The hypothesis of prenatal and/or early-life exposures is now widely accepted (33)(34)(35), including parental exposures before birth as risk factor candidates for TGCT in the offspring.…”