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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

Testicular temperature in humans and rodents. (A) Human gonocytes mature in the first year when the testicular temperature is 33°C. Congenital UDT have abnormal temperature early, which interferes with gonocyte development. By contrast, acquired UDT only interferes with subsequent survival of stem cells. (B) In rodents, gonocytes mature before a change in temperature occurs, so that gonocyte development is unaffected, similar to acquired UDT in humans.
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Figure 8: Testicular temperature in humans and rodents. (A) Human gonocytes mature in the first year when the testicular temperature is 33°C. Congenital UDT have abnormal temperature early, which interferes with gonocyte development. By contrast, acquired UDT only interferes with subsequent survival of stem cells. (B) In rodents, gonocytes mature before a change in temperature occurs, so that gonocyte development is unaffected, similar to acquired UDT in humans.

Mentions: Investigators have puzzled over why UDT in rodents caused infertility but not cancer, as in humans. We propose that this is the result of differences in timing in when the testis reaches the low-temperature scrotal environment. In humans, the testis is at 33°C from birth, so that congenital UDT has the potential to damage neonatal gonocytes by high temperature. By contrast, rodent testes only reach the scrotum after 12 days of age (Bergh, 1991), which is well after normal gonocyte transformation and/or apoptosis is complete (Figure 8).


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)

Testicular temperature in humans and rodents. (A) Human gonocytes mature in the first year when the testicular temperature is 33°C. Congenital UDT have abnormal temperature early, which interferes with gonocyte development. By contrast, acquired UDT only interferes with subsequent survival of stem cells. (B) In rodents, gonocytes mature before a change in temperature occurs, so that gonocyte development is unaffected, similar to acquired UDT in humans.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 8: Testicular temperature in humans and rodents. (A) Human gonocytes mature in the first year when the testicular temperature is 33°C. Congenital UDT have abnormal temperature early, which interferes with gonocyte development. By contrast, acquired UDT only interferes with subsequent survival of stem cells. (B) In rodents, gonocytes mature before a change in temperature occurs, so that gonocyte development is unaffected, similar to acquired UDT in humans.
Mentions: Investigators have puzzled over why UDT in rodents caused infertility but not cancer, as in humans. We propose that this is the result of differences in timing in when the testis reaches the low-temperature scrotal environment. In humans, the testis is at 33°C from birth, so that congenital UDT has the potential to damage neonatal gonocytes by high temperature. By contrast, rodent testes only reach the scrotum after 12 days of age (Bergh, 1991), which is well after normal gonocyte transformation and/or apoptosis is complete (Figure 8).

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