| disease | Testicular Tumor |
Testicular tumors are not common, accounting for only 1% of all malignant tumors in the body. According to statistical data from around the world, the incidence of testicular tumors varies by region and ethnicity, with higher rates in Europe and America and lower rates in China. However, testicular tumors are given special attention for the following reasons: ① Breakthroughs in treatment since the 1970s have reduced the mortality rate from 50% to around 10%. ② It is the most common cancer among young people aged 15 to 35, as they can withstand rigorous comprehensive treatments such as surgery, radiotherapy, and chemotherapy. ③ There is a tendency for differentiation, either spontaneously or after treatment, where malignant tumors can turn benign, such as metastatic cancer becoming benign teratoma after chemotherapy. Understanding this mechanism could potentially lead to the differentiation of malignant tumors into benign ones. ④ The tumors secrete marker substances that can be detected in the blood, which is uncommon in other tumors.
bubble_chart Etiology
Cryptorchidism is considered a risk factor for testicular tumors, with the chance of developing tumors being 3 to 4 times higher than in normal testes. About 7-10% of testicular tumors occur in cryptorchid testes. It has been observed that surgery after the age of 10 cannot prevent tumors, while surgery before the age of 10 can significantly reduce the risk, and surgery before the age of 3 can prevent the occurrence of tumors.
Additionally, testicular tumors are also related to genetics, polythelia, testicular atrophy due to trauma, hormones, and other factors.
bubble_chart Pathological Changes
Testicular tumors have various classification methods. By 1986, Morse et al. summarized and categorized the commonly used classification methods (Table 25-1). According to this classification, testicular tumors can be divided into two major categories: primary and secondary. Among primary tumors, they can be further classified into germ cell tumors and non-germ cell tumors, with seminoma, the most common type of germ cell tumor, being specifically listed separately. This has unique implications for guiding treatment and elucidating prognosis.Testicular germ cell tumors all originate from the same source and, influenced by different carcinogenic factors, can develop into seminomas or tumors of embryonic and extraembryonic tissues such as embryonal carcinoma, teratocarcinoma, choriocarcinoma, and yolk sac tumors. See the table below (Table 25-1).
Table 25-1 Histological Classification of Testicular Tumors
| (I) Primary Tumors 1. Germ Cell Tumors (1) Seminoma Classic Seminoma Stromal Type Seminoma Spermatocytic Seminoma (2) Embryonal Carcinoma (3) Teratoma (with or without malignant transformation) Mature Type Immature Type (4) Choriocarcinoma (5) Yolk Sac Tumor (Endodermal Sinus Tumor, Embryonal Adenocarcinoma) 2. Non-Germ Cell Tumors (1) Gonadal Stromal Tumors (2) Leydig Cell Tumor Sertoli Cell Tumor (3) Gonadoblastoma (4) Other Types of Tumors Testicular Adenocarcinoma Stromal Tumors Carcinoid Tumor Adrenal Rest Tumor (II) Secondary Tumors 1. Reticuloendothelial Tumors 2. Metastatic Tumors (III) Paratesticular Tumors 1. Adenomatoid Tumor 2. Epididymal Cystadenoma 3. Stromal Tumors 4. Cortical Tumor 5. Metastatic Tumors |
bubble_chart Clinical Manifestations
Testicular tumors are often discovered incidentally as a mass within the scrotum, and there may also be a sensation of local dull pain and heaviness. Cryptorchidism may present with masses in the groin or lower abdomen. A sudden increase in the size of an atrophied testis should raise suspicion of a tumor. Acute pain is uncommon, but 10% of cases may present with symptoms similar to orchitis or epididymitis. Approximately 10% of patients primarily exhibit symptoms of metastatic cancer, such as enlarged supraclavicular lymph nodes, lung metastases causing cough and dyspnea, etc.
Testicular examination should begin with the healthy side for comparison of size, hardness, and contour. Tumors are generally not sensitive and do not feel like normal tissue. The epididymis is clearly separated, and the tunica vaginalis and scrotum are not adherent, often without fluid accumulation. The size of the tumor and the presence of metastatic cancer often manifest as irregular masses within the normal testicular tissue. Spread to the epididymis and spermatic cord occurs in 10-15% of cases, indicating a poor prognosis.
(1) Tumor Markers (Tumor Markers) The most widely used currently are Alpha-fetoprotein (AFP) and Human Chorionic Gonadotropin (HCG).
AFP: Normal value <40ng/ml, half-life 4 to 5 days. Elevated in all yolk sac tumors, 50-70% of embryonal carcinomas, and teratocarcinomas in testicular tumors; not elevated in pure choriocarcinomas and pure seminomas.
HCG: Normal value <1ng/ml, positive in all choriocarcinomas and 40-60% of embryonal carcinomas, "pure" seminomas are 5-10% positive.
Using the above two tumor markers, 90% of non-seminomas are positive for one or both. Pure seminomas are HCG positive in 5-10% of cases, meaning over 90% of pure seminomas do not produce tumor markers, and 10% of non-seminomas do not produce tumor markers. Therefore, once a clinical diagnosis of testicular tumor is made, an orchiectomy should be performed immediately without waiting for tumor marker results.
Tumor markers can serve as indicators for observing treatment efficacy. A rapid decline after surgery, chemotherapy, or radiotherapy indicates a better prognosis, while a slow or no decline may suggest residual tumor.
(2) B-ultrasound Can be used to determine the presence of tumors within the testis and whether there are metastatic lymph nodes in the inguinal region.
(3) CT and MRI Can detect retroperitoneal lymph node metastases <2cm.
Additionally, there are dorsal foot lymphography and urography.
bubble_chart Treatment Measures
The treatment of testicular tumors depends on their pathological nature and staging, and can be divided into surgery, radiotherapy, and chemotherapy. First, a radical orchiectomy via the inguinal approach should be performed. The specimen should be thoroughly examined, preferably with segmental sections, to understand the nature of the tumor, especially whether the seminoma is pure or mixed, as there is a significant difference in treatment. Generally, statistics show that 65-70% of seminomas have already metastasized. If a pure seminoma has no retroperitoneal lymph node metastasis but has lung or liver metastases, the possibility of non-seminomatous components should be considered. The treatment plans are discussed separately below.
(1) Seminoma: After orchiectomy, radiotherapy is administered, with 25-35GY (2500-3500rad) over 3 weeks to the para-aortic and ipsilateral iliac and inguinal lymph nodes. For stage I, 90-95% can survive for 5 years. If clinical findings indicate retroperitoneal disease, i.e., stage II, then the mediastinum and supraclavicular areas are also irradiated with 20-35GY (2000-3500rad) over 2-4 weeks, with a 5-year survival rate of over 80%. Large intra-abdominal metastases and distant lesions have a poor prognosis, with a survival rate of only 20-30%. In recent years, chemotherapy containing cisplatin has been used, significantly improving survival rates, with 60-100% effectiveness (PVB or DDP + GY). The chemotherapy regimen is introduced in the following section.
If there is a lesion in the spermatic cord during orchiectomy, the ipsilateral scrotum should also be included in the irradiation area. Abdominal tumors larger than 10cm and pulmonary metastases have significant radiotherapy effects.
(2) Non-seminoma: Includes embryonal carcinoma, teratocarcinoma, choriocarcinoma, yolk sac tumor, or various mixed tumors. Retroperitoneal lymph node metastasis is very common. Since they are less sensitive to radiation than seminomas, in addition to orchiectomy, retroperitoneal lymph node dissection should be performed. In stage I cases, surgery proves that about 10-20% have already metastasized, i.e., pathological stage II. Orchiectomy plus retroperitoneal lymph node dissection results in a 5-year survival rate of about 90% for pathological stage I, dropping to about 50% for pathological stage II. In stage III, distant metastases were found in 144 cases: lung 89%, liver 73%, brain 31%, bone 30%, kidney 30%, adrenal gland 29%, gastrointestinal tract 27%, spleen 13%, and vena cava 11%. Chemotherapy is the main treatment. In non-seminomas, choriocarcinoma often metastasizes first to distant sites like the lungs. During treatment, close observation of tumor markers HCG and AFP changes is necessary.
In infants under 3 years old, the malignancy of embryonal carcinoma is lower than in adults, and tolerance to surgery, chemotherapy, and radiotherapy is poor. Retroperitoneal lymph node metastasis is also lower than in adults, about 4%, so retroperitoneal lymph node dissection is generally not considered. The treatment of pediatric teratoma and yolk sac tumor is the same as for embryonal carcinoma. Death is mostly due to hematogenous metastasis. Chemotherapy is necessary when indicated.
Chemotherapy: Chemotherapy has a certain role in non-seminomas, mainly indicated for: ① Poor prognosis stage I non-seminoma, with invasion of the spermatic cord or testis, and persistent elevation of tumor markers after resection. ② Stage IIA-IV non-seminoma. ③ Advanced stage refractory tumor recurrence or ineffective medication, using salvage chemotherapy regimens.
The PVB chemotherapy regimen is the most widely used, consisting of cisplatin, vinblastine, and bleomycin. Common regimen: cisplatin 20mg/m2/day on days 1, 2, 3, 4, and 5; vinblastine 0.2mg/kg on day 2; bleomycin 30mg/week on days 2, 9, and 16, with a 3-week cycle for a total of 12 weeks.
The combined treatment of the above three drugs can achieve partial remission in 100% of cases and complete remission in 70%. Stage I testicular tumors without lymph node metastasis may not require chemotherapy, and some advocate for re-chemotherapy in stage II cases when multiple occurrences are present, to reduce unnecessary impact on the patient.
Large retroperitoneal tumors that do not exceed the diaphragm can also be treated with chemotherapy, followed by retroperitoneal lymph node dissection after tumor shrinkage. Stage III patients are mainly treated with chemotherapy.
Testicular tumors have a short natural history, and the 2-year survival rate is commonly used to evaluate treatment efficacy. Since survival does not necessarily indicate a cure, the 5-year survival rate has been adopted as the standard for assessing treatment effectiveness in recent years.
(1) Rarely completely spontaneous regression.
(2) All adult genital tumors should be considered malignant; so-called "benign teratomas" show ductal invasion under the microscope, and ultimately 29% of those who undergo simple orchiectomy die from the tumor. Pediatric teratomas are benign.
(3) The white membrane serves as a natural barrier; tumor breakthrough often occurs at the tumor mediastinum, where blood vessels, lymphatic vessels, nerves, and small ducts pass through. The risk of lymphatic and hematogenous metastasis increases in 10-15% of cases that extend to the epididymis and spermatic cord.
(4) All testicular tumors are prone to lymphatic metastasis, although pure choriocarcinoma can also spread through the bloodstream. The 4 to 8 lymphatic vessels of the spermatic cord fan out upward to the retroperitoneal lymphatic chain. The initial lymph nodes reached by the right testicle are the lymph nodes in the L3 vertebral body region near the main artery, while the first-tier lymph nodes for the left testicle are located near the left ureter, renal vein, and the origin of the inferior mesenteric artery adjacent to the main artery. Upward spread can reach the cisterna chyli, thoracic duct, and supraclavicular lymph nodes (mainly on the left side), and downward retrograde metastasis can occur to the iliac and inguinal lymph nodes. Inguinal disease can also result from metastasis of scrotal lesions.
(5) Metastasis outside lymph nodes can directly invade blood vessels or spread through tumor emboli from lymphatic-venous anastomoses. Most hematogenous metastases occur after lymphatic metastasis. If stage A non-seminomatous tumors are treated only with orchiectomy, 20% will spread, with 80% of these cases involving retroperitoneal lymph node metastasis and 20% unrelated. Pure seminoma metastases are usually seminomas, with less than 10% being other components, and those with other component metastases account for 30-45% of deaths from pure seminoma.
Non-seminomatous tumors develop rapidly, with a doubling time of only 10 to 30 days; 85% of those who do not respond to treatment die within two years, and the rest within three years. Seminomas can recur 2 to 10 years after effective treatment.
