Testicular cancer
From Felipedia
A case report
In cats, testicular neoplasms are extremely rare and only a few cases have been reported. Rosen and Carpenter reported a 12-year-old, castrated, male cat with an interstitial cell tumour of the spermatic cord. In this retrospective study, we report on 5 cats that spontaneously developed neoplasms of testicular origin after castration. Immunohistochemistry was performed on a sample of these tumors to exclude other possibilities and for additional information[1].
All 5 cats had interstitial cell tumors located extratesticularly within the scrotal skin (n = 2) or the spermatic cord. The mean age at castration, for those with a known age, was 10 mo (range, 6 to 12 mo). The mean age at identification of an extratesticular tumour was 9.6 y (range, 9 to 14 y). The tumors were identified after a mean time period of 8 y (range, 5 to 13 y) following castration, for those of known age. The size of the tumors varied: the smallest tumour was 1 cm3 and the largest 1.5 cm3. All 5 cats demonstrated male, tomcat behaviour, such as spraying and aggressiveness. Two of the cats had penile barbs and 1 of these had a serum testosterone concentration of 1.09 μg/mL that dropped to less than 0.2 μg/mL after surgical removal. All animals lost secondary sexual characteristics after surgery[2].
Most masses were discovered upon routine physical examination or following investigation of feminization (1 dog) or male behaviour (5 cats). The referring veterinarians described the Sertoli cell tumors as firm, non-painful, encapsulated nodules within the scrotum/prescrotal regions of previously castrated males. None of the neoplasms reoccurred after surgery, nor had metastases been found[3].
The neoplasms may have arisen from an embryological testicular remnant. Extragonadal migration of the Sertoli and interstitial cell primordia may seed microscopic foci of these cells in a paratesticular location that could later progress to a hyperplastic colony. Nistal and Paniagua suggest that ectopic interstitial cells originate from undifferentiated precursor cells located beside or inside testicular nerves. Under hormonal influences, these precursor cells develop into mature interstitial cells in an ectopic location. Given the rarity of finding ectopic tissue and the cutaneous location of the masses, we consider this explanation unlikely[4].
Another possibility is the presence of an ectopic testis-like structure. Although there is no evidence that any of the animals were cryptorchid, the phenomenon of polyorchidism could not be excluded. Polyorchidism is an extremely rare anomaly that involves the presence of more than 2 testes. It has been reported to occur in dogs and cats. The exact mechanism of polyorchidism is unknown; however, several hypotheses, including anomalous appropriation of cells and possible longitudinal duplication or transverse division of the genital ridge, have been suggested and could account for its rare occurrence. A third possibility is that injury or excessive pressure to the testis may transplant parenchymal cells to an extratesticular location. Trauma or inappropriate pressure on the testis can result in embolization of testicular parenchymal cells to the veins of the pampiniform plexus. Finally, seeding of neoplastic cells to incision sites is a recognized phenomenon.
The location of many of the tumors described in this report makes the inadvertent transplantation of parenchymal tissue at initial surgery most likely. The textbook castration technique of dogs states that the tunica albuginea is not to be incised; however, in practice, unintentional incision of the testis occurs. This exposes the testicular parenchyma to the scrotal skin and areas around the incision site, enhancing the potential of transplanting Sertoli or interstitial cells to these locations. Furthermore, there is evidence to suggest that Sertoli cells survive transplantation. In several studies by Dufour et al, genetically engineered Sertoli cells survived transplantation and continued to thrive, suggesting that Sertoli cells could be used for transgenic technology to produce proteins for therapy of certain diseases. Additionally, in 1998, Ueyama induced gonadal stromal tumors by transplanting testicular tissue into the spleen. The results showed that intrasplenic testicular cells can develop into both Sertoli and interstitial cell tumors. We propose that transplantation of testicular parenchymal cells occurs at the time of castration. The transplanted cells then survive as a microscopic focus that may eventually progress to neoplasia. As our cases had been submitted from 15 different clinics (and surgeons), this proposal suggests that transplantation of testicular cells is a widespread occurrence and is not related to the technique of a small number of individuals[5].
Pathogenesis of testicular carcinogenesis is unclear; however, recent work in molecular genetic engineering has attempted to decipher the roles of endocrine signalling pathways and other cell cycle regulators in tumor development. Recently, gene knockout technology has shown that inhibin-deficient mice develop Sertoli cell tumors and, therefore, that inhibin is implicated as a potent tumor suppressor. Previously castrated animals are inhibin (and testosterone) deficient and presumably have high concentrations of gonadotropin-releasing hormone and follicle stimulating hormone, increasing the potential for carcinogenesis due to unregulated gonadotrophins. This stimulus would enhance cell proliferation of any residual testicular tissue in castrated animals and could lead to neoplasia.
We suggest that practitioners be particularly careful during castration to avoid placing pressure on the testis and to avoid incising the tunica albuginea, as this may lead to transplantation of small amounts of testicular tissue and subsequent development of extratesticular Sertoli or interstitial cell neoplasms.
References
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