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Embryology, Anatomy, and Physiology of the Male Reproductive System
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Male: the Y chromosome short arm (Yp11) carries the sex-determining region Y gene (SRY, also known as testis determining factor).Signals differentiation of primitive sex cords to form the testis/medullary cords.The SRY and SOX9 genes are responsible for testes differentiation.
Ovarian, Fallopian Tube, and Primary Peritoneal Cancer
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Robert D. Morgan, Andrew R. Clamp, Gordon C. Jayson
Sex cord-stromal tumors of the ovary account for <5% of all ovarian tumors, and their clinical presentation is often characterized by their ability to secrete sex hormones.143 They are classified as pure stromal tumors (e.g., fibroma, thecoma, and Leydig cell tumor), pure sex cord tumors (e.g., granulosa cell tumor [GCT] and Sertoli cell tumor), or mixed sex cord-stromal tumors (e.g., Sertoli-Leydig cell tumor). GCTs are the commonest sex cord-stromal tumors, accounting for approximately 70%. Genetic studies have revealed somatic mutations in FOXL2 as well as the promoter region of TERT, which have been linked to the pathogenesis of GCTs,144,145 as well as mutations in DICER1, which has been linked to Sertoli-Leydig cell tumours.146,147
Summation of Basic Endocrine Data
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
At the time of birth in males, germ cells have developed in the sex cords of the testes, surrounded by supporting cells which become the Sertoli cells. The sex cords also develop a lumen and become the seminiferous tubules.
From diagnosis to treatment of androgen-secreting ovarian tumors: a practical approach
Published in Gynecological Endocrinology, 2022
Patrycja Rojewska, Blazej Meczekalski, Grzegorz Bala, Stefano Luisi, Agnieszka Podfigurna
Androgen-secreting ovarian tumors constitute approximately 1% of all primary ovarian neoplasms. Most of these, arise from the stroma or sex cord of female gonads. Sex cord-stromal tumors (SCSTs) may produce estrogens, androgens, progesterone, and corticoids. Granulosa Cell Tumors are most common type of SCST accounting for about 70% of all cases, they are also the most frequent tumor causing hyperestrogenism [8]. Androgen-secreting tumors are less common than those producing estrogens but may occur in females of all ages. The incidence of various tumor histopathology is age dependent. Among women of reproductive age, Sertoli-Leydig Cell Tumors are the most common and account for approximately 0.5% of all primary ovarian neoplasms [9]. Pure Leydig Cell Tumors have a higher incidence in postmenopausal patients presenting with hyperandrogenism but overall account for 0.1% of all ovarian neoplasms [10]. Beyond SCSTs, a small number of other neoplasms have been found to secrete androgens, notably metastases (mostly of gastric origin), primary mucinous cystic tumors, teratomas, carcinoids, and Brenner tumors.
Sex-Cord Tumor with Annular Tubules with Unusual Morphology in an Infant with Peutz-Jeghers Syndrome
Published in Fetal and Pediatric Pathology, 2022
Priyanka Maity, Nandini Das, Uttara Chatterjee, Dhananjay Basak
Immunostaining patterns of the sex-cord stromal tumors are not distinctive enough and show considerable overlap. They show positivity for SF1, FOXL2, alpha inhibin, calretinin and WT 1. The similarity of the morphological patterns and immunohistochemical staining between SCTAT and Sertoli cell tumor makes it difficult to precisely classify these cases. However, these tumors appear to be more closely related to Sertoli cell neoplasia, rather than granulosa cell neoplasia. Unclassified sex-cord tumors associated with sexual precocity have been reported in association with PJS, which again highlight the diagnostic difficulty [11]. Yet, distinction is important as malignancy is more often reported in Sertoli cell tumors, especially in those larger than 5 cm and mitosis more than 5/10HPF [13].
Hyperthecosis: an underestimated nontumorous cause of hyperandrogenism
Published in Gynecological Endocrinology, 2021
Blazej Meczekalski, Anna Szeliga, Marzena Maciejewska-Jeske, Agnieszka Podfigurna, Paulina Cornetti, Gregory Bala, Eli Y. Adashi
One of the most common causes of virilization in postmenopausal woman beyond ovarian hyperthecosis are virilizing ovarian tumors (VOTs). These tumors account for approximately 1% of all ovarian neoplasms [41]. There are numerous distinct ovarian tumor types that can lead to hyperandrogenism; Sertoli-Leydig Cell Tumor (SLCT), Steroid Cell Tumor Not Otherwise Specified (SCT NOS), and Leydig cell tumor (LCT) are classed as the most frequent VOTs. Sertoli-Leydig cell tumors belong to the group of sex-cord stromal tumors. They account for 0.5% of all ovarian neoplasm and usually occur in early adulthood. SLCTs are characterized by the presence of hormonally active testicular structures. They are usually benign and found unilaterally [42]. Steroid cell tumors NOS represent around 0.1% of all ovarian tumors and usually affect women in the 5th or 6th decade of life. SCT NOS are mostly unilateral and can be either benign or malignant [43]. Leydig cell tumors are very rare, with most being hormonally active. 95% of LCTs unilaterally affect the ovaries and are mostly found in postmenopausal women.