Carcinoma in situ (CIS) of the testis
Testicular cancer is the most common malignancy in 20- to 34-years-old males. It has been stated that testicular cancer derives from a precocious lesion, the carcinoma in situ of the testis, also known as Intratubular Germ Cell Neoplasia (IGCN) or Testicular Intraepithelial Neoplasia (TIN). This lesion deserves great attention, because the diagnosis of CIS may lead to a precocious diagnosis of testicular cancer. Generally, the diagnosis of CIS is incidental. Every physician should know the management of this precocious lesion, as the correct management of CIS can lead to a decrease of the incidence of overt testicular cancer (the most frequent malignancy in young men). Moreover, the correct diagnosis and management of CIS can shorten the hospital stay, reduce the cost, and improve the social impact of the testicular cancer.
Available from: Fabiano Nino
- "It is known that undescended testes, if untreated, lead to an increased risk of TC, usually seminomas (10), arising from mutant germ cells. TC is a solid neoplasm that has an incidence of 1% of all cancers in men and is the most common between 20 and 30 years of life (11, 12). Boys with an undescended testis have a 20-fold higher risk to develop a TC and about 10% of the cases of TC develop in men with a history of cryptorchidism (13). "
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ABSTRACT: Cryptorchidism represents the most common endocrine disease in boys, with infertility more frequently observed in bilateral forms. It is also known that undescended testes, if untreated, lead to an increased risk of testicular tumors, usually seminomas, arising from mutant germ cells. In normal testes, germ cell development is an active process starting in the first months of life when the neonatal gonocytes transform into adult dark (AD) spermatogonia. These cells are now thought to be the stem cells useful to support spermatogenesis. Several researches suggest that AD spermatogonia form between 3 and 9 months of age. Not all the neonatal gonocytes transform into AD spermatogonia; indeed, the residual gonocytes undergo involution by apoptosis. In the undescended testes, these transformations are inhibited leading to a deficient pool of stem cells for post pubertal spermatogenesis. Early surgical intervention in infancy may allow the normal development of stem cells for spermatogenesis. Moreover, it is very interesting to note that intra-tubular carcinoma in situ in the second and third decades have enzymatic markers similar to neonatal gonocytes suggesting that these cells fail transformation into AD spermatogonia and likely generate testicular cancer (TC) in cryptorchid men. Orchidopexy between 6 and 12 months of age is recommended to maximize the future fertility potential and decrease the TC risk in adulthood.
Frontiers in Endocrinology 05/2014; 5:63. DOI:10.3389/fendo.2014.00063
Available from: David H Volle
- "It also supports a model of differentiation from IGCN to seminomas or embryonal carcinomas. Gene expression patterns and genomic imprinting analyses in TGCC show similarity to PGCs and gonocytes (Ziglioli et al., 2011). "
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ABSTRACT: In the last decades, studies in rodents have highlighted links between in utero and/or neonatal exposures to molecules that alter endocrine functions and the development of genital tract abnormalities, such as cryptorchidism, hypospadias, and impaired spermatogenesis. Most of these molecules, called endocrine disrupters exert estrogenic and/or antiandrogenic activities. These data led to the hypothesis of the testicular dysgenesis syndrome which postulates that these disorders are one clinical entity and are linked by epidemiological and pathophysiological relations. Furthermore, infertility has been stated as a risk factor for testicular cancer (TC). The incidence of TC has been increasing over the past decade. Most of testicular germ cell cancers develop through a pre-invasive carcinoma in situ from fetal germ cells (primordial germ cell or gonocyte). During their development, fetal germ cells undergo epigenetic modifications. Interestingly, several lines of evidence have shown that gene regulation through epigenetic mechanisms (DNA and histone modifications) plays an important role in normal development as well as in various diseases, including TC. Here we will review chromatin modifications which can affect testicular physiology leading to the development of TC; and highlight potential molecular pathways involved in these alterations in the context of environmental exposures.
Frontiers in Endocrinology 11/2012; 3:150. DOI:10.3389/fendo.2012.00150
Available from: Silvère Baron
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ABSTRACT: The link between cholesterol homeostasis and male fertility has been clearly suggested in patients who suffer from hyperlipidemia and metabolic syndrome. This has been confirmed by the generation of several transgenic mouse models or in animals fed with high cholesterol diet. Next to the alteration of the endocrine signaling pathways through steroid receptors (androgen and estrogen receptors); "orphan" and "adopted" nuclear receptors, such as the Liver X Receptors (LXRs), the Proliferating Peroxisomal Activated Receptors (PPARs) or the Liver Receptor Homolog-1 (LRH-1), have been involved in this cross-talk. These transcription factors show distinct expression patterns in the male genital tract, explaining the large panel of phenotypes observed in transgenic male mice and highlighting the importance of lipid homesostasis and the complexity of the molecular pathways involved. Increasing our knowledge of the roles of these nuclear receptors in male germ cell differentiation could help in proposing new approaches to either treat infertile men or define new strategies for contraception.
Molecular and Cellular Endocrinology 07/2012; 368(1-2). DOI:10.1016/j.mce.2012.06.011 · 4.41 Impact Factor
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