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Germ cell development in the postnatal testis: the key to prevent malignancy in cryptorchidism?

Hutson JM, Li R, Southwell BR, Petersen BL, Thorup J, Cortes D - Front Endocrinol (Lausanne) (2013)

Bottom Line: Failure of any part of this process leads to congenital cryptorchidism, wherein the malpositioned testis finds itself at the wrong temperature after birth, which leads to secondary germ cell loss and later infertility and risk of cancer.Recent studies suggest that neonatal gonocytes transform into the putative spermatogenic stem cells between 3 and 9 months, and this initial postnatal step is deranged in cryptorchid testes.In addition, it is thought the abnormality high temperature may also impair apoptosis of remaining gonocytes, allowing some to persist to become the possible source of carcinoma in situ and malignancy after puberty.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, Royal Children's Hospital Parkville, VIC, Australia.

ABSTRACT
To permit normal postnatal germ cell development, the mammalian testis undergoes a complex, multi-staged process of descent to the scrotum. Failure of any part of this process leads to congenital cryptorchidism, wherein the malpositioned testis finds itself at the wrong temperature after birth, which leads to secondary germ cell loss and later infertility and risk of cancer. Recent studies suggest that neonatal gonocytes transform into the putative spermatogenic stem cells between 3 and 9 months, and this initial postnatal step is deranged in cryptorchid testes. In addition, it is thought the abnormality high temperature may also impair apoptosis of remaining gonocytes, allowing some to persist to become the possible source of carcinoma in situ and malignancy after puberty. The biology of postnatal germ cell development is of intense interest, as it is likely to be the key to the optimal timing for orchidopexy.

No MeSH data available.


Related in: MedlinePlus

“Mini-puberty,” with testosterone (T) and MIS/AMH secreted after birth. Neonatal gonocytes mature into adult dark spermatogonia between 3 and 9 months of age, and primary spermatocytes form about 3–4 years. After a period of quiescence, spermatids form about 10 years of age, with the onset on spermatogenesis. Undescended testis (UDT) interferes with the first step.
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Figure 2: “Mini-puberty,” with testosterone (T) and MIS/AMH secreted after birth. Neonatal gonocytes mature into adult dark spermatogonia between 3 and 9 months of age, and primary spermatocytes form about 3–4 years. After a period of quiescence, spermatids form about 10 years of age, with the onset on spermatogenesis. Undescended testis (UDT) interferes with the first step.

Mentions: In baby boys, the temperature of the intra-scrotal testes drops to 33°C at birth, with all the testicular enzyme systems readjusting presumably within a few weeks to this new environment (Zorgniotti, 1991). Between 2 and 4 months of age pituitary gonadotropins stimulate a sudden increase in testosterone production which peaks at about 3–6 months, before it wanes and becomes almost negligible until the onset of puberty. This brief surge of gonadotropins and androgens is known as “mini-puberty” (Job et al., 1988; Hadziselimovic and Zivkovic, 2007). As androgen levels subside there is a surge in production of MIS/AMH by Sertoli cells, which peaks at 6–12 months, but remains high then until puberty when serum levels fall (Baker et al., 1990; Yamanaka et al., 1991; Aksglaede et al., 2010; Figure 2).


Germ cell development in the postnatal testis: the key to prevent malignancy in cryptorchidism?

Hutson JM, Li R, Southwell BR, Petersen BL, Thorup J, Cortes D - Front Endocrinol (Lausanne) (2013)

“Mini-puberty,” with testosterone (T) and MIS/AMH secreted after birth. Neonatal gonocytes mature into adult dark spermatogonia between 3 and 9 months of age, and primary spermatocytes form about 3–4 years. After a period of quiescence, spermatids form about 10 years of age, with the onset on spermatogenesis. Undescended testis (UDT) interferes with the first step.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3539691&req=5

Figure 2: “Mini-puberty,” with testosterone (T) and MIS/AMH secreted after birth. Neonatal gonocytes mature into adult dark spermatogonia between 3 and 9 months of age, and primary spermatocytes form about 3–4 years. After a period of quiescence, spermatids form about 10 years of age, with the onset on spermatogenesis. Undescended testis (UDT) interferes with the first step.
Mentions: In baby boys, the temperature of the intra-scrotal testes drops to 33°C at birth, with all the testicular enzyme systems readjusting presumably within a few weeks to this new environment (Zorgniotti, 1991). Between 2 and 4 months of age pituitary gonadotropins stimulate a sudden increase in testosterone production which peaks at about 3–6 months, before it wanes and becomes almost negligible until the onset of puberty. This brief surge of gonadotropins and androgens is known as “mini-puberty” (Job et al., 1988; Hadziselimovic and Zivkovic, 2007). As androgen levels subside there is a surge in production of MIS/AMH by Sertoli cells, which peaks at 6–12 months, but remains high then until puberty when serum levels fall (Baker et al., 1990; Yamanaka et al., 1991; Aksglaede et al., 2010; Figure 2).

Bottom Line: Failure of any part of this process leads to congenital cryptorchidism, wherein the malpositioned testis finds itself at the wrong temperature after birth, which leads to secondary germ cell loss and later infertility and risk of cancer.Recent studies suggest that neonatal gonocytes transform into the putative spermatogenic stem cells between 3 and 9 months, and this initial postnatal step is deranged in cryptorchid testes.In addition, it is thought the abnormality high temperature may also impair apoptosis of remaining gonocytes, allowing some to persist to become the possible source of carcinoma in situ and malignancy after puberty.

View Article: PubMed Central - PubMed

Affiliation: Department of Urology, Royal Children's Hospital Parkville, VIC, Australia.

ABSTRACT
To permit normal postnatal germ cell development, the mammalian testis undergoes a complex, multi-staged process of descent to the scrotum. Failure of any part of this process leads to congenital cryptorchidism, wherein the malpositioned testis finds itself at the wrong temperature after birth, which leads to secondary germ cell loss and later infertility and risk of cancer. Recent studies suggest that neonatal gonocytes transform into the putative spermatogenic stem cells between 3 and 9 months, and this initial postnatal step is deranged in cryptorchid testes. In addition, it is thought the abnormality high temperature may also impair apoptosis of remaining gonocytes, allowing some to persist to become the possible source of carcinoma in situ and malignancy after puberty. The biology of postnatal germ cell development is of intense interest, as it is likely to be the key to the optimal timing for orchidopexy.

No MeSH data available.


Related in: MedlinePlus