Pathology Notes

Testicular inflammation and injury   Updated: 01/28/2021 © Jun Wang, MD, PhD Infectious epididymitis and orchitis Sexually active men < 35 years of age: Commonly Chlamydia trachomatis and Neisseria gonorrhoeae > 35 years:   E. coli and Pseudomonas Gonorrhea : Extends from posterior urethra if untreated Mumps : 20 to 30% of postpubertal males one week after parotiditis, commonly unilateral, may cause infertility Tuberculosis : Begins in epididymis and spreads to testis Syphilis : Arises in testis before epididymis Granulomatous orchitis Rare Likely autoimmune process Tender testicular mass with sudden onset Need microbiology studies to rule out infection (AFB, fungal) Torsion May cause testicular infarct Usually occurs in first year of life May be caused by trauma or violent movement Associated with incomplete testicular descent, absent scrotal ligaments, absent gubernaculum testis or testicular atrophy causing testis to be abnormally mobile Treat

Testicle yolk sac tumor   Updated: 01/26/2021 © Jun Wang, MD, PhD General features Also called endodermal sinus tumor of Teilum Most common testicular tumor age 3 or less, often pure Adults: usually part of a mixed tumor, has prognosis of embryonal carcinoma May arise from seminoma Pathological findings Morphology same as ovarian yolk sac tumor Hemorrhage and necrosis Schiller-Duval body : central blood vessel enveloped by germ cells within a space similarly lined by germ cells, resembles glomerulus Marker Elevated serum AFP Positive: AFP , cytokeratin , variable PLAP Negative: hCG Management Orchiectomy with or without retroperitoneal lymph node dissection, chemo if with metastasis Good prognosis if < 3 years old Back to testicle tumors Back to pathology of male reproductive system Back to contents

Testicle teratoma   Updated: 01/28/2021 © Jun Wang,MD, PhD General features Tumors contain cellular components derived from 2 or 3 germ layers Second most common testicular tumor after yolk sac in children Most likely malignant if in adults More commonly as a component of mixed tumor Pathological findings Same microscopic morphology as ovarian teratoma Various differentiation, may have bone, cartilage , tooth or skin Management Orchiectomy Retroperitoneal lymph node dissection if positive for mets Chemotherapy Back to testicle tumors Back to pathology of male reproductive system Back to contents

Testicle sex cord-stromal tumor   Updated: 01/28/2021 © Jun Wang, MD, PhD Leydig cell tumor Most common sex cord stromal tumor Usually unilateral May be malignant Produce androgen May present with precocious puberty in children, or gynecomastia due to estrogen production Characteristic Reinke crystals : definitive feature, but present in only 30-40%; intracytoplasmic, nuclear or extracellular No respond to radiation or chemotherapy Treatment: surgery Sertoli cell tumor Rare Children or middle aged adults May be malignant May occur as part of androgen insensitivity syndrome, Carney’s complex and Peutz-Jegher’s syndrome May cause Feminization and gynecomastia Tumor cells have round to oval nuclei and moderate amount of pale, clear or eosinophilic cytoplasm Treatment: orchiectomy Gonadoblastoma Most before 30 Resembling immature granulosa cells and Sertolicells May be associated with disorders of sexual development, such as complete androgen insensit

Testicle choriocarcinoma   Updated: 01/28/2021 © Jun Wang, MD, PhD General features Most commonly a component of mixed tumor May present initially as metastasis to liver, lung, etc Pathological findings Morphology similar to ovarian or uterine choriocarcinoma Hemorrhage and necrosis Cytotrophoblast and syncytiotrophoblast Marker Elevated serum hCG Positive: hCG , cytokeratin , PLAP Negative: OCT ¾, AFP Management Orchiectomy with or without retroperitoneal lymph node dissection, chemo if with metastasis Back to testicle tumors Back to pathology of male reproductive system Back to contents

Testicle atrophy   Updated: 01/28/2021 © Jun Wang, MD, PhD General features Associated with various conditions, including Klinefelter syndrome, testicular regression syndrome, vasectomy, etc Testicular regression syndrome Possibly due to testicular infarct May be seen in cryptorchidism Testicular tissue replaced by fibrovascular nodule, calcification Rudimentary epididymis and spermatic cord with vas deferens Back to pathology of male reproductive system Back to contents

Spermatocytic tumor   Updated: 07/02/2023 © Jun Wang, MD, PhD General features Used to be called spermatocytic seminoma NOT related to classic seminoma NOT arise from intratubular germ cell neoplasia Most common in older population May occur in younger patients Only in descended testes Usually not part of mixed germ cell tumor Pathological findings Pale gray, mucoid, edematous 3 cell types ,  Small cells: scant eosinophilic cytoplasm, similar to lymphocytes Medium cells: Round nuclei, filamentous chromatin and eosinophilic cytoplasm, similar to spermatocyte Giant cells:One of more nuclei Marker Variable: KIT Negative: PLAP, OCT3/4, hCG, AFP  Management Orchiectomy Favorable prognosis unless presence of sarcomatoid components Back to testicle tumors Back to pathology of male reproductive system Back to contents

Intratubular germ cell neoplasia   Updated: 02/03/2022 © Jun Wang, MD, PhD General features AKA germ cell neoplasia in situ (GCNIS) Commonly in tissue adjacent to germ cell tumor Associated with gonadal dysgenesis, androgen insensitivity syndrome, infertility, cryptorchidism , contralateral testis in patients with prior testicular tumor May progress to germ cell tumor Usually incidental finding in biopsy for infertility evaluation Pathological findings Large cells (fried eggs, 3x normal) with clear cytoplasm Thickened tubular basement membrane Displaces Sertoli cells toward the lumen Spermatogenesis usually absent Marker PLAP Management Watchful waiting (clinical and ultrasound examination) Serum measurement of hCG, AFP, human placental lactogen (HPL) Back to testicle tumors Back to pathology of male reproductive system Back to contents

Embryonal carcinoma   Updated: 01/28/2021 © Jun Wang, MD, PhD General features Usually age 20-30's Most commonly a component of non seminoma germ cell tumor Aggressive Metastasis at diagnosis common May accompanied by gynecomastia May have elevated serum PLAP, LDH Pathological findings Tumor with hemorrhage and necrosis Solid, pseudoglandular, alveolar, tubular or papillary patterns Primitive epithelial type cells with minimal features of differentiation Marker Variable, likely AFP and hCG Positive: CD30 , cytokeratin , OCT ¾ Negative: EMA Management Orchiectomy with or without retroperitoneal lymph node dissection, chemo if with metastasis Back to testicle tumors Back to pathology of male reproductive system Back to contents

Seminoma   Updated: 02/03/2022 © Jun Wang, MD, PhD General features Counterpart of ovarian dysgerminoma Mean age 40 years vs. 25 years for nonseminomatous germ cell tumors (NSGCT) Rare in infants Also present in mediastinum, pineal gland (germinoma), retroperitoneum  Pathological findings Homogenous well demarcated gray-white with lobulated and bulging cut surface Uniform tumor cells with clear cytoplasm (glycogen contents), prominent cell border, and large nuclei with prominent nucleoli Marker Serum: PLAP, LDH (Less specific), hCG (probably) Tumor cells positive: KIT, OCT3/4, PLAP Tumor cells negative: cytokeratin Genetic abnormalities KRAS KIT OCT ¾ Others: CCND2, NANOG, etc Diagnosis Diagnosed if only seminomatous elements upon radical orchiectomy (Otherwise, mixed germ cell tumor) Normal AFP Management Orchiectomy Post operative radiation therapy if mets in regional lymph nodes (very radiosensitive) Cisplatin based chemotherapy, if di

Cryptorchidism   Updated: 01/28/2021 © Jun Wang, MD, PhD General features Permanent retention of testis outside scrotum, unilateral or bilateral May be associated with other GU malformations High risk for testicular carcinoma , usually seminoma (higher risk if abdominal vs. inguinal location) May have cancer in normal descended testes Risk for trauma, torsion , etc Spermatogenesis deficiency may persist after surgery Pathogenesis Failure of intra-abdominal testes to descend into scrotal sac Clinical features Most common location: Inguinal canal Pathological findings Small, firm, brown testes Increased fibrous tissue Prominent Leydig cells, often hyperplastic Sertoli cells with atrophy of other cells Treatment Orchiopexy Back to pathology of male reproductive system Back to contents

Testicle tumors   Updated: 09/14/2021 © Jun Wang, MD, PhD General features <1% of malignancies in male Most commonly seen solid tumor in male age 15-35 Predominantly germ cell tumors in young patients Most common malignant testicular neoplasm if > 60 years: Diffuse large B cell lymphoma Lymphatic spread to periaortic, iliac, mediastinal and supraclavicular nodes Inguinal nodes usually spared unless scrotal or inguinal surgery or invasion of scrotal wall Hematogenous spread to liver, lungs, brain, bones Germ Cell Tumors Most common tumor 25-29 years Either derived from intratubular germ cell neoplasia or not Highly curable even with advanced development Commonly mixed histologic types Higher risk for bilateral tumor if both testes undescended p53 mutations are common Risk factors: Cryptorchidism , family history, testicular dysgenesis, Li-Fraumeni syndrome , prior testicular germ cell tumor or intratubular germ cellneoplasia Prognosis: Depending on his