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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

Postnatal germ cell development in humans. (A) Gonocytes migrate from the center of the cords to the basement membrane around 6 months, and become type-A spermatogonia. By 3–4 years of age the center of the cords becomes recolonized with primary spermatocytes. (B) Numbers of germ cells/tubule in a normal testis and undescended testis (UDT) relative to age in years. Note the normal fall in total numbers between birth and 2 years, but failure of this to recover in UDT. The shaded area shows the normal range and the dotted lines show the average numbers.
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Figure 4: Postnatal germ cell development in humans. (A) Gonocytes migrate from the center of the cords to the basement membrane around 6 months, and become type-A spermatogonia. By 3–4 years of age the center of the cords becomes recolonized with primary spermatocytes. (B) Numbers of germ cells/tubule in a normal testis and undescended testis (UDT) relative to age in years. Note the normal fall in total numbers between birth and 2 years, but failure of this to recover in UDT. The shaded area shows the normal range and the dotted lines show the average numbers.

Mentions: Huckins and Oakberg have proposed a widely accepted model for spermatogenic development which is useful to describe here (Huckins, 1971; Oakberg, 1971; de Rooij and Russell, 2000). In this model, single type-A spermatogonia are the putative SSCs, which can self-renew, while paired type-A spermatogonia are differentiating paired daughter cells connected by an intercellular bridge. Paired type-A spermatogonia divide into chains of aligned cells, which then become type A1, A2, A3, and then A4 spermatogonia. The latter cells (A4) divide to form intermediate spermatogonia and the type-B spermatogonia. Type-B cells then divide to form primary spermatocytes that enter meiosis (Figure 4). All these steps are regulated by growth factors from Sertoli and possibly the peritubular myoid cells (Skinner, 1991; Jegou, 1993). A recent morphological study (Drumond et al., 2001) showed that postnatal development of type-A spermatogonia may occur more rapidly than in mature spermatogenesis.


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)

Postnatal germ cell development in humans. (A) Gonocytes migrate from the center of the cords to the basement membrane around 6 months, and become type-A spermatogonia. By 3–4 years of age the center of the cords becomes recolonized with primary spermatocytes. (B) Numbers of germ cells/tubule in a normal testis and undescended testis (UDT) relative to age in years. Note the normal fall in total numbers between birth and 2 years, but failure of this to recover in UDT. The shaded area shows the normal range and the dotted lines show the average numbers.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 4: Postnatal germ cell development in humans. (A) Gonocytes migrate from the center of the cords to the basement membrane around 6 months, and become type-A spermatogonia. By 3–4 years of age the center of the cords becomes recolonized with primary spermatocytes. (B) Numbers of germ cells/tubule in a normal testis and undescended testis (UDT) relative to age in years. Note the normal fall in total numbers between birth and 2 years, but failure of this to recover in UDT. The shaded area shows the normal range and the dotted lines show the average numbers.
Mentions: Huckins and Oakberg have proposed a widely accepted model for spermatogenic development which is useful to describe here (Huckins, 1971; Oakberg, 1971; de Rooij and Russell, 2000). In this model, single type-A spermatogonia are the putative SSCs, which can self-renew, while paired type-A spermatogonia are differentiating paired daughter cells connected by an intercellular bridge. Paired type-A spermatogonia divide into chains of aligned cells, which then become type A1, A2, A3, and then A4 spermatogonia. The latter cells (A4) divide to form intermediate spermatogonia and the type-B spermatogonia. Type-B cells then divide to form primary spermatocytes that enter meiosis (Figure 4). All these steps are regulated by growth factors from Sertoli and possibly the peritubular myoid cells (Skinner, 1991; Jegou, 1993). A recent morphological study (Drumond et al., 2001) showed that postnatal development of type-A spermatogonia may occur more rapidly than in mature spermatogenesis.

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