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Overview of Cryptorchidism with Emphasis on the Human
Published in Tom O. Abney, Brooks A. Keel, The Cryptorchid Testis, 2020
David R. Roth, Larry I. Lipshultz
Differentiation of the primordial gonads into either ovaries or testes begins after arrival of the gonocytes at the genital ridge. Differentiation into a testis is regulated by the expression of the H-Y antigen as determined by the Y chromosome. This surface antigen promotes the organization of the gonadal blastema into a recognizable testis.
Anatomy & Embryology
Published in Manit Arya, Taimur T. Shah, Jas S. Kalsi, Herman S. Fernando, Iqbal S. Shergill, Asif Muneer, Hashim U. Ahmed, MCQs for the FRCS(Urol) and Postgraduate Urology Examinations, 2020
Embryology of the gonads. Which one of the following is TRUE?The genital ridges develop during the 12th week.In female embryos, Müllerian Inhibiting Substance causes regression of the paramesonephric duct.Sertoli cells secrete testosterone that plays a role in embryogenesis.Hydatid of Morgagni is a remnant of the paramesonephric duct.The testes reach the inguinal region by the 24th week.
Primordial germ cells: Origin, migration and testicular development
Published in Rajender Singh, Molecular Signaling in Spermatogenesis and Male Infertility, 2019
The gonads initially develop from the mesothelial layer of the peritoneum and are a part of the prenatal development of the reproductive system that eventually forms the testes in males and the ovaries in females. Although the testis and ovary arise from a common primordial structure, the genital ridge, they are remarkably analogous to each other, with distinct mechanisms of gene regulation and cellular organization for their development. Here we focus only on the development procedure of the testis. After migration, the germ cells get covered by surrounding somatic cells, which eventually become the testicular cord by the process of testicular differentiation. This process has to be perfectly regulated and synchronized so that this happens only after the germ cell localization to the gonadal ridge but not before that. Few studies have pointed out that the initiation of testicular development is not entirely dependent on the localization of gonocytes, as many germ cell–deficient mouse models have successfully developed normal testis with adequate endocrine function (52–55). The exact mechanism behind the commencement of testicular development is still elusive in nature. However, the process of transformation of a group of cells to a specific organ in a very short span of time is known to involve three major steps: (a) Sertoli cell specification and expansion, (b) testis cord formation and compartmentalization, and (c) formation of seminiferous tubules from testis cords.
Premature ovarian insufficiency – the need for a genomic map
Published in Climacteric, 2021
During ovarian development, PGCs emerge in the wall of the yolk sac on day 18 as a small cluster of cells. Simultaneously, the genital ridges develop from the intermediate mesoderm. Between days 28 and 36, the PGCs migrate to the genital ridge. Subsequently, the oogonia undergo mitosis and increase up to 600,000 in number by 8 weeks. These oogonia then either continue multiplying through mitosis up until 28 weeks or continue down a path of meiosis for the generation of non-dividing PGCs, or undergo oogonial atresia. As a result, up to 7 million PGCs are present by the 20th week; however, after this time, atresia dominates, resulting in 1–2 million germ cells at the time of birth [62]. The majority of the primordial follicles will undergo atresia, occurring from birth through to the menopause. Therefore, inadequate in utero production of the PGC pool can result in POI [8,63].
Could Aberrant Migration Explain Metachronous Germ Cell Tumors?
Published in Cancer Investigation, 2021
Pierre Kubicek, Tanguy Fenouil, Julien Jacquemus, Olivia Chapuis, Aude Fléchon, Cécile Dumesnil, Cécile Faure-Conter
The physiopathology of such rare presentations is not clear. Biological analysis including methylation profiles and epidemiologic data have provided new insights into the biology of GCTs, with the description of seven distinct subtypes (1). Type-I GCTs are mainly yolk sac tumors and teratomas that occur in infancy, whereas type-II GCTs (either seminomatous or nonseminomatous) develop in postpubertal individuals. Extragonadal GCTs have been described in both types. Mismigrated human PGCs have been identified in the sacrococcygeal region, the anterior mediastinum, the retroperitoneum, the suprasellar region, and the pineal gland (16). Their failure to undergo apoptosis is thought to give rise to extragonadal GCTs (1). Indeed, in a GCT type I mouse model, germ cells that are unable to reach the genital ridges (precursor of the gonads) undergo apoptosis by activation of the protein BAX (proapoptotic BCL-2-associated X). In Bax-null mouse embryos, PGCs fail to die and are thus identified at extragonadal sites (17). It is likely that the present three cases are type II GCTs, based on age and histology. Exploration of this latter subgroup has been hampered by the lack of a reliable animal model, which precludes experimental documentation of mismigration.
Differential Activation of Immune Effector Processes in Mature Compared to Immature Sacrococcygeal Teratomas
Published in Fetal and Pediatric Pathology, 2022
Mette Hambraeus, Jenny Karlsson, Ioanna Kasselaki, Catharina Hagerling, Lars Hagander, David Gisselsson
It has been suggested that SCTs derive from primordial germ cells (PGCs), which are thought to arise in the fetal epiblast during the second week of gestation [7,20]. From week 3-4 of gestation, PGCs have been observed in the yolk sac wall, and from here they migrate through the hindgut to the genital ridges, which marks the end of the PGC stage [20]. In line with previous studies [9], our results show a high expression of certain genes involved in early germ cell differentiation and pluripotency. The transcription profile was found across all histological subtypes. Compared to the reference group of tumors, SCTs showed a high expression of SOX2, which encodes a protein required for stem-cell maintenance in central nervous tissue. This protein combines with OCT4 to form a transcription factor that controls a number of genes required for embryological development [21]. We also found increased expression of genes normally active in early germ cell development, i.e. PRMD1, TFAP2C, and KIT [19]. SOX2 regulates KIT-expression in PGCs and is essential for survival and continued proliferation [22]. The transcriptional regulator PRMD1 (BLIMP1) is a signature gene for germ cell-commitment in active migratory and gonadal PGCs [20]. It induces TFAP2C, which further regulates germ cell specific genes and inhibits somatic differentiation [23]. PRDM1, TFAP2C and KIT are regulators of hematopoietic stem cells, antibody secreting plasma cells and formation of the placenta, and may therefore be expressed throughout fetal development [24–26]. However, the combined expression is generally considered to reflect a germ cell profile and the expression decreases during the initial primordial germ cell stage [19,27].