Sex Cord-Stromal Tumors
Leydig cell tumor
Sertoli cell tumor
Most tumors in this group originate from intratubular germ cell neoplasia (ITGCN).  ITGCN is seen adjacent to all germ cell tumors in adults except for spermatocytic seminoma
and epidermoid and dermoid cysts. With rare exceptions, it is also not seen in pediatric tumors (teratomas, yolk sac tumors). ITCGN is encountered with a high frequency in the following
conditions, listed in order of increasing risk: cryptorchidism, prior germ cell tumors, strong family history of germ cell tumor, androgen insensitivity syndrome, and gonadal dysgenesis
syndrome. Untreated ITGCN progresses to invasive germ cell tumor in approximately 50% of cases over 5 years of follow-up. Thus its significance is similar to carcinoma in situ in other
organs. If ITGCN is identified, it is treated by low-dose radiotherapy, which destroys the germ cells yet maintains the androgen production of the Leydig cells.
Neoplastic germ cells may differentiate along gonadal lines to give rise to seminoma or transform into a totipotential cell population that gives rise to nonseminomatous tumors. Such
totipotential cells may remain largely undifferentiated to form embryonal carcinoma or may differentiate along extraembryonic lines to form yolk sac tumors or choriocarcinomas.
Teratoma results from differentiation of the embryonic carcinoma cells along the lines of all three germ cell layers. Some studies suggest that seminomas are not end-stage neoplasms.
Similar to embryonal carcinomas, seminomas may also act as precursors from which other forms of testicular germ cell tumors originate. This view is supported by the fact that cells that
form intratubular germ cell neoplasias (the presumed precursors of all types of germ cell tumors) share morphologic and molecular characteristics with tumor cells in seminomas. Despite
the fascination of pathologists with the heterogeneity of testicular tumors, from a clinical standpoint the most important distinction in germ cell tumors is between seminomas and
nonseminomatous tumors. As will be discussed later, this clinical distinction has important bearings on treatment and prognosis.
As with all neoplasms, little is known about the ultimate cause of germ cell tumors. Several predisposing influences, however, are important: (1) cryptorchidism, (2) testicular dysgenesis,
and (3) genetic factors, all of which may contribute to a common denominator: germ cell maldevelopment. Reference has already been made to the increased incidence of neoplasms in
undescended testes. In most large series of testicular tumors, approximately 10% are associated with cryptorchidism. The higher the location of the undescended testicle (intra-abdominal
versus inguinal), the greater is the risk of developing cancer.
Patients with disorders of testicular development (testicular dysgenesis), including testicular feminization and Klinefelter syndrome, harbor an increased risk of developing germ cell
tumors. The risk is highest in patients with testicular feminization. In cryptorchid and dysgenetic testes, foci of intratubular germ cell neoplasms can be detected at a high frequency before
the development of invasive tumors.
Genetic predisposition also seems to be important, although no well-defined pattern of inheritance has been identified. In support, striking racial differences in the incidence of testicular
tumors can be cited. Blacks in Africa have an extremely low incidence of these neoplasms, which is unaffected by migration to the United States. Familial clustering has been reported, and
according to one study, sibs of affected individuals have a tenfold higher risk of developing testicular cancer than does the general population.
As with all tumors, genomic changes are undoubtedly important in the pathogenesis of testicular cancers. An isochromosome of the short arm of chromosome 12, i(12p), is found in
virtually all germ cell tumors, regardless of their histologic type. In the approximately 10% of cases in which i(12p) is not detected, extra genetic material derived from 12p is found on
other chromosomes. Obviously, dosage of genes located on 12p is critical for the pathogenesis of germ cell tumors, and several candidate genes have been identified, including a novel
gene, called DAD-R, that prevents apoptosis.  It is of interest that i(12p) is also noted in ovarian germ cell neoplasms, suggesting that the events leading to this alteration may be
critical to the molecular pathogenesis of all germ cell neoplasms.
With this background of pathogenesis, we can discuss the morphologic patterns of germ cell tumors, followed by the clinical features that are common to most germinal tumors.
Seminomas are the most common type of germinal tumor (50%) and the type most likely to produce a uniform population of cells. They almost never occur in infants; they peak in the
thirties. An identical tumor arises in the ovary, where it is called dysgerminoma ( Chapter 22 ).
If not otherwise specified, the term "seminoma" refers to "classic" or "typical" seminoma. Spermatocytic seminoma, despite its nosologic similarity, is actually a distinct tumor; it has been
segregated into a separate category and will be discussed later.
Seminomas produce bulky masses, sometimes 10 times the size of the normal testis. The typical seminoma has a homogeneous, gray-white, lobulated cut surface, usually devoid of
hemorrhage or necrosis ( Fig. 21-23 ). In more than half of cases, the entire testis is replaced. Generally, the tunica albuginea is not penetrated, but occasionally, extension to the
epididymis, spermatic cord, or scrotal sac occurs.
Microscopically, the typical seminoma presents sheets of uniform cells divided into poorly demarcated lobules by delicate septa of fibrous tissue ( Fig. 21-24A ). The classic seminoma
cell is large and round to polyhedral and has a distinct cell membrane; a clear or watery-appearing cytoplasm; and a large,
Figure 21-23Seminoma of the testis appears as a fairly well circumscribed, pale, fleshy, homogeneous mass.
Figure 21-24Seminoma. A, Low magnification shows clear seminoma cells divided into poorly demarcated lobules by delicate septa. B, Microscopic examination reveals large cells with
distinct cell borders, pale nuclei, prominent nucleoli, and a sparse lymphocytic infiltrate.
Figure 21-25Embryonal carcinoma. In contrast to the seminoma illustrated in Figure 21-23 , the embryonal carcinoma is a hemorrhagic mass.
Figure 21-26Embryonal carcinoma shows sheets of undifferentiated cells as well as primitive glandular differentiation. The nuclei are large and hyperchromatic.
Figure 21-27Choriocarcinoma shows clear cytotrophoblastic cells with central nuclei and syncytiotrophoblastic cells with multiple dark nuclei embedded in eosinophilic cytoplasm.
Hemorrhage and necrosis are prominent.
Figure 21-28Teratoma of the testis. The variegated cut surface with cysts reflects the multiplicity of tissue found histologically.
Figure 21-29Teratoma of the testis consisting of a disorganized collection of glands, cartilage, smooth muscle, and immature stroma.
Figure 21-30Adult prostate. The normal prostate contains several distinct regions, including a central zone (CZ), a peripheral zone (PZ), a transitional zone (TZ), and a periurethral zone.
Most carcinomas arise from the peripheral glands of the organ and may be palpable during digital examination of the rectum. Nodular hyperplasia, in contrast, arises from more centrally
situated glands and is more likely to produce urinary obstruction early on than is carcinoma.
Figure 21-31Benign prostate gland with basal cell and secretory cell layer.
Figure 21-32Simplified scheme of the pathogenesis of prostatic hyperplasia. The central role of the stromal cells in generating dihydrotestosterone should be noted.
Figure 21-33Nodular prostatic hyperplasia. A, Well-defined nodules of BPH compress the urethra into a slitlike lumen. B, A microscopic view of a whole mount of the prostate shows
nodules of hyperplastic glands on both sides of the urethra.
Figure 21-34Adenocarcinoma of the prostate. Carcinomatous tissue is seen on the posterior aspect (lower left). Note the solid whiter tissue of cancer in contrast to the spongy appearance
of the benign peripheral zone on the contralateral side.
Figure 21-36 A, Photomicrograph of a small focus of adenocarcinoma of the prostate demonstrating small glands crowded in between larger benign glands. B, Higher magnification shows
several small malignant glands with enlarged nuclei, prominent nucleoli, and dark cytoplasm, compared to the larger benign gland (top).
Figure 21-35Metastatic osteoblastic prostatic carcinoma within vertebral bodies.
Figure 21-37Carcinoma of the prostate showing perineural invasion by malignant glands. Compare to a benign gland (left).
Figure 21-38 A, Low-grade (Gleason score 1 + 1 = 2) prostate cancer consisting of back to back, uniformly sized malignant glands. Glands contain eosinophilic intraluminal prostatic
crystalloids, a feature that is more commonly seen in cancer than in benign glands and more frequently seen in lower grade than in higher grade prostate cancer. B, Needle biopsy of the
prostate with variably sized, more widely dispersed glands of moderately differentiated (Gleason score 3 + 3 = 6) adenocarcinoma. C, Poorly differentiated Gleason score (5 + 5 = 10)
adenocarcinoma composed of sheets of malignant cells.
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