Testicular Tumor

Testicular tumors account for 1%-2% of male malignancies, divided into primary and secondary. The vast majority are primary, divided into germ-cell and non-germ-cell tumors. Germ-cell tumors arise from the germinal epithelium of seminiferous tubules, accounting for 90%-95% of testicular tumors; seminoma is most common, grows slowly and generally has good prognosis; non-seminomatous tumors such as embryonal carcinoma, teratocarcinoma and choriocarcinoma are relatively rare but highly malignant, with early lymphatic and hematogenous metastasis and poorer prognosis. Non-germ-cell tumors arise from testicular interstitial cells, accounting for 5%-10%, derived from fibrous tissue, smooth muscle, blood vessels and lymphatic tissue. Secondary testicular tumors are quite rare.

Common Symptoms

Cough; dyspnea; nodule; on-duty physician

Causes and Pathogenesis

(A) Etiology: The cause remains incompletely clear; possibly related to viral infection, environmental pollution, endocrine abnormalities, trauma and heredity. Five proven factors promote testicular tumors: cryptorchidism, prior testicular germ-cell tumor, family history, true hermaphroditism and infertility. Malignant-transformation rate of cryptorchid testes is 30-50 times higher than normally descended testes; literature reports 1 testicular tumor per 20 abdominal-type or per 80 inguinal-type cryptorchid testes. (B) Pathogenesis: Testicular tumors by tissue origin fall into 4 categories: ① germ-cell tumors; ② stromal tumors; ③ mixed germ-cell and stromal tumors; ④ rete testis tumors. Histogenesis of testicular germ-cell tumors has been controversial; recent understanding holds that all types except spermatocytic seminoma originate from a common precursor — testicular carcinoma in situ, pathologically called intratubular germ-cell neoplasia of unclassified type (IGCNU). IGCNU cells resemble seminoma cells in morphology and DNA content, and are the precursor of other germ-cell tumors; pure seminoma can differentiate into non-seminomatous germ-cell tumors (NSGCT). WHO (1994) classification: 1. Germ-cell tumors: Precursor lesion — intratubular germ-cell neoplasia (carcinoma in situ). (1) Single histologic type: ① spermatocytic seminoma; ② variant with sarcomatous component; ③ seminoma (may have syncytiotrophoblasts); ④ embryonal carcinoma; ⑤ yolk-sac tumor (endodermal sinus tumor); ⑥ choriocarcinoma; ⑦ teratoma: A mature teratoma, B dermoid cyst, C immature teratoma, D teratoma with obvious malignant component, E carcinoid (pure or with teratomatous component), F primitive neuroectodermal tumor. (2) More than one histologic type: ① mixed germ-cell tumor; ② polyembryoma. 2. Sex-cord stromal tumors: (1) Leydig-cell tumor; (2) Sertoli-cell tumor: ① typical, ② sclerosing, ③ large-cell calcifying; (3) granulosa-cell tumor (adult type C, juvenile); (4) mixed sex-cord stromal tumor; (5) undifferentiated sex-cord stromal tumor. 3. Mixed germ-cell and sex-cord stromal tumors: (1) gonadoblastoma; (2) others. 4. Rete testis tumors: (1) adenoma; (2) adenocarcinoma; (3) adenomatous hyperplasia. 5. Other testicular-tissue tumors: (1) epidermoid cyst; (2) mesenchymal tumors. 6. Metastatic tumors of hematopoietic origin: (1) lymphoma; (2) plasmacytoma; (3) leukemia. Testicular tumors spread mainly via lymphatics; half of patients already have metastasis at first visit. Testicular lymphatic drainage originates from the genital ridge near the 2nd lumbar vertebra, forming in the retroperitoneum; as the testis descends it carries lymphatics and vessels through the inguinal internal ring into the scrotum. Thus the first lymphatic station is para-lumbar at renal-pedicle level; bilateral lymphatics cross the midline; upper boundary 2 cm above renal pedicle, lateral boundaries medial borders of both kidneys and upper ureters, lower boundary aortic bifurcation and upper 1/3 of iliac vessels. Inguinal-node metastasis occurs when tumor penetrates tunica albuginea to involve epididymis, spermatic cord and scrotal skin. Trans-scrotal orchiectomy and testicular biopsy may cause local implantation. Distant metastasis most commonly to lung and liver, then intra-abdominal. Another key issue is clinical staging since local/systemic spread affects treatment and prognosis; at least 9 staging systems exist. Traditional Boden-Gibb (1951): ① tumor limited to testis = Stage I (A); ② regional (retroperitoneal) node metastasis without supra-diaphragmatic/visceral spread = Stage II (B); ③ spread beyond retroperitoneal nodes (mediastinum, lung, other viscera) = Stage III (C). UICC (1992) recommends TNM: T primary tumor; N subdiaphragmatic regional nodes; M distant organs or supra-diaphragmatic nodes. Simplified TNM stages I-III: Stage I no metastasis; IA tumor limited to testis/epididymis; IB tumor involves spermatic cord or arises in undescended testis; IC tumor involves scrotum or post inguinal/scrotal surgery; ID primary extent indeterminate. Stage II subdiaphragmatic node metastasis: IIA nodes <2 cm; IIB at least one node 2-5 cm; IIC retroperitoneal nodes >5 cm; IID palpable abdominal mass or fixed inguinal nodes. Stage III mediastinal/supraclavicular nodes and/or distant metastasis: IIIA mediastinal/supraclavicular nodes only; IIIB distant metastasis limited to lung: 'few pulmonary mets' <5 per side with lesions >2 cm; 'late pulmonary mets' >5 per side with lesions >2 cm; IIIC any hematogenous metastasis outside lung; IIID no obvious residual after radical surgery but tumor marker positive. Tumor markers are used early in testicular tumor management and are important for early diagnosis, classification, treatment planning, monitoring and long-term follow-up. High-specificity/sensitivity markers are alpha-fetoprotein (AFP) and human chorionic gonadotropin (HCG), both glycoproteins; 70%-80% of NSGCT patients have elevated AFP and/or HCG. AFP elevation indicates embryonal-carcinoma component → surgery-oriented; HCG elevation suggests choriocarcinoma or embryonal-carcinoma component. Other non-specific markers may also rise: CEA, LDH isoenzymes, placental alkaline phosphatase (PALP).

Treatment

Drug therapy, surgery, rehabilitation, radiotherapy

Preventive Measures

Daily prevention: Tobacco contains carcinogens such as arsenic and smoking alters sex hormones; scientists long suspected smoking as a risk factor, and current research confirms it increases testicular-cancer risk. High dairy intake also raises risk; especially high cheese intake raises risk by 87% vs average. Thus smoking cessation and improved diet are key to prevention.

Department to Visit

It is recommended to visit the Surgical Oncology department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.