Testicular cancer

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Shanshan Cen, M.D. [3]

Testicular cancer is cancer that develops in the testicles, a part of the male reproductive system. According to World Health Organization, testicular cancer may be classified into six subtypes based on the histopathology.Testicular cancer is a rare type cancer accounting about 0.5% of all new cancer cases in U.S. with germ cell tumor being the most common.Testicular cancer must be differentiated from epididymitis, hematocele, hydrocele, spermatocele, granulomatous orchitis, and varicocele. The prevalence of testicular cancer is approximately approximately 9,310 new cases of testicular cancers in the United States.The incidence of testicular cancer is approximately 5.88 per 100,000 males in the United States. Common risk factors in the development of testicular cancer are undescended testicle, family history, personal history of testicular cancer, Klinefelter syndrome.The most common symptoms of testicular cancer include a painless lump in the testicle, swelling of the testicle, and weight loss. An elevated concentration of blood tumor marker such as human chorionic gonadothrophin (HCG), alpha fetoprotein (AFP) tests is diagnostic of testicular cancer. The diagnostic test of choice is scrotal ultrasound along with biopsy. The predominant therapy for testicular cancer is surgical resection. Adjunctive chemotherapy and radiation therapy may be required. Prognosis of testicular cancer is generally good but it depends on the subtype. 5-year survival rate is approximately 96.6%.

There is a limited information about the historical perspective of testicular germ cell tumors. Leydig cells were first discovered by Franz Leydig who was a German anatomist in 1870.

Testicular cancer is a very rare type of cancer. Based on the histopathological features, testicular cancer may be classified into six subtypes: germ cell tumors, sex–cord stromal tumors, tumors containing both germ cell and sex–cord stromal elements, miscellaneous tumors of the testis, hematolymphoid tumors, and tumors of collecting duct and rete testis.

The pathophysiology of testicular cancer depends on the histological cell subtypes and findings. Most testicular cancers derived from the lack of differentiation of primordial germ cell into spermatogonia. Germ cells testicular tumor have some genetic component while most sex cord stromal testicular cancer are hormonal dependent. Most gross pathology of testicular tumors look similar on the physical appearance. On microscopic histopathological analysis of testicular cancer, fried-egg appearance is the characteristic finding of seminoma; marked nuclear atypia is the characteristic finding of embryonal carcinoma; hyaline-type globules, and Schiller-Duval bodies are characteristic findings of yolk sac tumor  ; syncytiotrophoblasts and cytotrophoblast cells are the characteristic findings of choriocarcinoma, Polymorphism with”spirene” chromatin for spermatocytic.

There are no direct causes for testicular cancer. However, there are some common risk factors that may lead to gene mutations and cause the testicular cancer.

Testicular cancer must be differentiated from epididymitis, hematocele, hydrocele, spermatocele, granulomatous orchitis, and varicocele.

Testicular cancer is a rare type cancer accounting about 0.5% of all new cancer cases in U.S. In 2018, the estimate prevalence of testicular cancer is approximately 9,310 new cases of testicular cancers in the United States. The incidence of testicular cancer is approximately 5.7 per 100,000 men per year based on 2011-2015 report in the United States. The majority of cases are reported in New Zealand. Testicular cancer commonly affects more white males than any other races and black males are less affected by it. Testicular cancer is commonly affects men aged 20-44 years old and median age depends on the subtype.

Common risk factors in the development of testicular germ cells cancer are undescended testicle, family history, personal history of testicular cancer, and Klinefelter syndrome. There are no known risk factors for testicular sex cord stromal tumors.

According to the the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for testicular cancer.

Prognosis of testicular cancer is generally good, and the 5-year survival rate is approximately 96.6% (2004-2010). Common complications of testicular cancer include metastasis, bleeding, infection, and infertility.

The diagnostic study of choice for testicular cancer is scrotal ultrasound.

The most common symptoms of testicular cancer include a painless lump in the testicle, swelling of the testicle, and weight loss.

Common physical examination findings of testicular cancer include weight loss, swelling of the testicle , and a painless mass in the testicle.

An elevated concentration of blood tumor marker tests is diagnostic of testicular cancer.

There are no X-ray findings associated with testicular cancer. Chest X-ray may be required in case of testicular tumor metastases into the lungs and mediastinum.

CT scan may be helpful in the diagnosis of testicular cancer.

MRI may be helpful in the diagnosis of testicular cancer for Extension of the metastasis and differentiating the seminomas from the nonseminomatous germ cells tumors.

Ultrasound may be helpful in the diagnosis of testicular cancer. Findings on ultrasound suggestive of testicular cancer mass include well defined well circumscribed hypoechoic lesion for seminoma; calcification, cystic spaces, and heterogeneous for nonseminomatous germ cell tumors. Ultrasound may be helpful in the diagnosis of testicular cancer.

There are no other imaging findings associated with testicular cancer.

There are no other diagnostic findings associated with testicular cancer.

Biopsy is rarely done in the diagnosis of testicular cancer. However, Inguinal biopsy may be done in the contralateral testis if the ultrasound showed the intratesticular mass, cryptorchid testis, marked atrophy, and suspicious mass. Other indications for testicular biopsy are obstructive azoospermia, testicular sperm extraction and diagnosis of carcinoma in situ of the testis.

The predominant therapy for testicular cancer is surgical resection. Adjunctive chemotherapy and radiation therapy may be required.

Surgery is the mainstay of treatment for testicular cancer. Radical inguinal orchiectomy is recommended for every patient with testicular cancer for cure and histology.

There are no established measures for the primary prevention of testicular cancer.

There are no secondary preventive measures available for testicular cancer.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2]

There is a limited information about the historical perspective of testicular germ cell tumors. Leydig cells were first discovered by Franz Leydig who was a German anatomist in 1870.

• There is a limited information about the historical perspective of testicular tumors. Leydig cells were first discovered by Franz Leydig who was a German anatomist in 1870.^[1]

• In 1965, Dr. Barnett Rosenberg, a biophysics research at Michigan State University, discovered cisplatin drug which affects the cells division. The blockage of cell division was from the platinum found in the electrodes. The experiment was tested in the mice at low dose of cisplatin since cisplatin at high doses might cause renal toxicities.^[2][3]
• In 1972, National Cancer Institute stepped in and participated in the funding of the clinical trials in human patients with advanced testicular cancers under the supervision of Dr. lawrence Einhorn at Indiana University.
• In 1978, Food and Drugs Administration (FDA) approved cisplatin drug for the treatment of testicular cancer based on successful clinical trials. Cisplatin has improved the lives of many patients diagnosed with testicular cancers and others when combining with others drugs.^[4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Shanshan Cen, M.D. [3]

Testicular cancer is a very rare type of cancer. Based on the histopathological features, testicular cancer may be classified into six subtypes: germ cell tumors, sex–cord stromal tumors, tumors containing both germ cell and sex–cord stromal elements, miscellaneous tumors of the testis, hematolymphoid tumors, and tumors of collecting duct and rete testis.

WHO classifies testicular tumors as follows:^[1][2]

Testicular Cancer
Germ cell tumors	Sex-cord stromal tumors	Miscellaneous tumors of the testis	Hematolymphoid tumors	Tumors of collecting duct and rete testis	Tumors containing both germ cell and sex-cord stromal elements
Germ cell tumors derived from germ cell neoplasia in situ: Non-invasive germ cell neoplasia Germ cell neoplasia in situ Specific forms of intratubular germ cell tumor neoplasia Tumors of a single histological type (pure forms) Seminoma Seminoma with syncytiotrophoblast cells Non-seminomatous germ cell tumors Embryonal carcinoma Yolk sac tumor, postpubertal-type Trophoblastic tumors Choriocarcinoma Non-choriocarcinomatous trophoblastic tumors Placental site trophoblastic tumor Epitheliol trophoblastic tumor Cystic trophoblastic tumor Teratoma, postpubertal-type Teratoma with somatic-type Non-seminomatous germ cell type tumor of more than one histological type Mixed germ cell tumors Germ cell tumors of unknown type Regressed germ cell tumors Germ cell tumors unrelated to germ cell neoplasia in situ: Spermatocytic tumor Teratoma, prepubertal-type Dermoid cyst Epidermoid cyst Well-differentiated neuroendocrine tumor (monodermal teratoma) Mixed teratoma and yolk sac tumor, prepubertal-type Yolk sac tumor, prepubertal-type	Pure tumors Leydig cell tumor Malignant leydig cell tumor Sertoli cell tumor Malignant Sertoli cell tumor Large cell calcifying Sertoli cell tumor Intratubular large cell hyalinizing Sertoli cell neoplasia Granulosa cell tumor Adult granulosa cell tumor Juvenile granulosa cell tumor Tumors in the fibroma–thecoma group Mixed and unclassified sex-stromal tumors Mixed sex cord-stromal tumor Unclassified sex cord-stromal tumor	Ovarian epithelial-type tumors Serous cystadenoma Serous tumor of borderline malignancy Serous cystadenocarcinoma Mucinous borderline tumor Mucinous cystadenocarcinoma Endometrioid adenocarcinoma Clear cell adenocarcinoma Brenner tumor Juvenile Xanthogranuloma Hemangioma	Diffuse large B-cell lymphoma Follicular lymphoma, NOS Extranodal NK/T-cell lymphoma, nasal type Plasmacytoma Myeloid sarcoma Rosai-Dorfman disease	Adenoma Adenocarcinoma	Gonadoblastoma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Shanshan Cen, M.D. [3]

The pathophysiology of testicular cancer depends on the histological cell subtypes and findings. Most testicular cancers derived from the lack of differentiation of primordial germ cell into spermatogonia. Germ cells testicular tumor have some genetic component while most sex cord stromal testicular cancer are hormonal dependent. Most gross pathology of testicular tumors look similar on the physical appearance. On microscopic histopathological analysis of testicular cancer, fried-egg appearance is the characteristic finding of seminoma; marked nuclear atypia is the characteristic finding of embryonal carcinoma; hyaline-type globules, and Schiller-Duval bodies are characteristic findings of yolk sac tumor  ; syncytiotrophoblasts and cytotrophoblast cells are the characteristic findings of choriocarcinoma, Polymorphism with”spirene” chromatin for spermatocytic.

• Normal inner cell mass leads to primordial germ cell mass^[1][2]

• Primordial germ cell mass leads to gonocytes through cell proliferation
• Gonocytes differentiate into spermatogonia

• Leydig cells are found in the seminiferous tubules of the testis.^[3][4]
• Leydig cells secrete testosterone hormone under the signal of luteinizing hormone.
• Leydig cells are involved in the development of male secondary sexual characteristics and spermatogenesis.

• Lack of primordial germ cell to differentiate into spermatogonia leads to germ cell neoplasia in Situ^[2]
• Germ cell neoplasia in Situ may gain some abnormal chromosome(12), then it leads to seminomas and nonseminomas cancers.
• Seminomas and non seminotous germ cell tumors have similar pathogenesis.^[5][6]
  • Aneuploid
  • Loss of chromosomes 4,5,11,13,18, and Y
  • Gain of chromosomes 7,8,12, and X
• More than 90% of all testicular cancers are germ cell tumors. This type of cancer starts in germ cells, which are the cells that develop into sperms.
• About 50% of all germ cell tumors are seminomas, or seminomatous germ cell tumours. They grow slower than non-seminomas.
• Overrepresentation of short arm of chromosomes 12p may be related to invasive growth of seminomas and nonseminomatous testicular cancer.^[7]
• Seminomas tumors may have both genetic and immune components due to lymphocytes infiltration in HIV patients.^[8]
• Histological of seminomas tumor in HIV patients: tumor infiltrated by lymphocytes which may lead to weak immune system response.^[8]
• Familial contribution:^[9]
  • Gene on chromosome Xq27 may be related to testicular germ cell tumors
• Some proteins such as C-kit (receptor) and placental-like alkaline phosphatase (PLAP) may be excessively expressed^[10]

• Mutations from the proteins that may be involved in the maturation of the spermatogonia.^[11]
• Mostly located in the testis and rarely metastases.
• Mutated proteins involved: SAGE1 and SSX2-4.
• Hypothesis of gain of chromosome 9 may be involved in the process.^[12]

• The pathogenesis of leydig cells tumors is not well understood.^[3][13]
• It is hypothesized that there is a disturbance of hypothalamic-pituitary-testicular axis which lead to excess of hormone productions.
• The G proteins in the leydig cells and the structure alteration of Luteinizing hormone receptors may play role in leydig cells tumors.

• Sertoli cell arise from testicular supporting cells which regulate the spermatogenesis.
• It may due to excess production of androgen hormone.^[14]

• It involved in hyperestrogenism due to an unregulated aromatase enzyme activity that leads to excessive production of hormones.^[15]

The gross and microscopic features of the most common tumors are described below:^{[16][17][18][19][20][21][22][19][23][24][25][26][27][3][28][29][15]}

Types	Gross pathology	Microscopic pathology	Images
Germ cell neoplasia in situ	Solid, fleshy nodules Similar to seminoma in appearance Well-circumscribed with hemorraghic and necrotic areas	Hyperchromatic nuclei Prominent nucleoli and clear cytoplasm Thickened basement menbrane Proliferation of tumor germ cell in the seminiferous tubules
Seminoma	Solid, firm without cross section Solid fleshy tan to yellow mass in homogeneous appearance Well-circumscribed with small hemorraghic and necrotic areas	Large nucleoli with clear to pale to eosinophilic cytoplasm due to the presence of glycogen Clonal proliferation of neoplastic germ cells Fried-egg appearance Prominent mitotic figures Nests and sheets of cancer cells with “squared-off” nuclei Granulomatous inflammation
Embryonal carcinoma	Poorly demarcated mass Soft gray on cut surface Large hemorraghic and necrotic foci.	Presents with mixed histological features (solid, papular, glandular) Marked nuclear atypia Marked epithelial cells with polymorphism Large nuclei with abundant amphophilic cytoplasm Prominent mitotic activities
Yolk sac tumor	Solid, lobulated, soft, mucinous on cut surface Gray and grayish yellow mass May have small hemorrhagic and necrotic foci Heterogenous mass	Hyaline-type globules Schiller-Duval bodies Multiple histological patterns such as recticular, microcystic, glandular, papillary, hepatoid, and solid Associated with myxoid stroma Variable cytologic atypia
Choriocarcinoma	Hemorrhagic and necrotic nodules May appear more cystic and calcified in homogeneous	More Hemorrhagic and necrotic Made up of mononucleated trophoblast and multinucleated syncytiotrophoblast cells Hyperchomatic cytoplasm
Teratoma, postpubertal-type	Hetereogenous, cystic and irregular calcification on appearance Solid, firm mass	Arrange in disorder fashion Cytologic atypia High mitotic activities Presence of 3 germ cells layers Presence of immature elements with primitive nuclei
Mixed germ cell tumors	Solid and cystic mass More hemorhragic and necrotic.	Microscopic findings are variable depending on the tumor type May have the component of yolk sac and choriocarcinoma
Spermatocytic tumor	Soft, gray, and gelatinous mass Well circumscribed with small hemorrhagic and necrotic foci.	Atyical mitoses activities Eosinophilic cytoplasm without glycogen Tumors cells with three different sizes (small, intermediate, and large) Polymorphism with”spirene” chromatin find in the giant cells Frequent apoptosis
Teratoma, prepubertal-type, Desmoid cyst Epidermoid cyst	Solid and firm mass	Lack of cytologic atypia No mitotic activities Absence of immature elements Desmoid cyst has polosebaceous cells Epidermoist cyst is surrounded with squamous epithelial cells
Testicular lymphoma	Soft, gray, and gelatinous mass Well circumscribed with small hemorrhagic and necrotic foci.	Vascular invasion Pleomorphic tumor cells Large irregular nuclei
Leydig cells tumor	Homogeneous and well circumscribed mass Solitary and unilateral mass White to brown to yellow on cut surface	Cells are arranged in nest, sheets polygonal fahsion Cytoplasm is eosinophilic with round nuclei and prominent nucleoli Presence of lipofuscin pigment and reinke crystal intracytoplasmic
Sertoli tumor	Homogeneous and well circumscribed mass White to grey on cut surface	Cells are arranged in cords, nests and lobulated tubules Fibrous stroma ans septa with lymphocytes Elongated spaces and microscysts Pale lipid- rich cytoplasm No prominent nucleoli
Granulosa tumor	Adult type No distint feature Juvenile type Solid, nodule yellow-orange and cystic mass	Adult type Cells are arranged in elongated, microfollicular “call-Exner bodies” Juvenile type Cells are presented in solid sheets and nodules and form the estatic space Eosinophilic cytoplasm Hyperchromatic, round to oval nuclei High mitotic activities Follicles are located on the periphery

These are genes involved in the pathogenesis of testicular cancer:^[30][31]

• Chromosome 12p
• 12q22.2

• Germ cell neoplastic in situ:
  • +PLAP (Placenta like-alkaline phosphatase)^[32]
• Seminomas:^[21][33][34]
  • OCT3/4 transcription factors^[35]
  • C-kit
  • CD30
  • D2-40 monoclonal antibody
  • PLAP
  • NANOG transcription factor

• Embryonal carcinoma:^[33][34]
  • PLAP
  • OCT3/4^[35]
  • SOX2
  • CD30
  • +/-GpC3,keratin

• Yolk sac tumor:^[12][36]
  • +SALL4
  • +AFP
  • +GATA3
  • +Glypican3
  • +Keratin
  • +/-C-kit

• Choriocarcinoma:^[12]
  • +Ck7
  • +GATA3
  • +HCG
  • +/-SALL4

• Spermatocytic tumor:^[12]
  • +SALL4
  • +/-C-kit

• Teratoma:^[23][37][12]
  • +SALL4
  • +Cytokeratin
  • +HCG
  • +/-GATA3,SOX2,OCT4

• Testicular lymphoma:^[12]
  • +CD3
  • +CD20
  • +CD45

• Leydig cell tumor:^[3][38]
  • +Inhibin
  • +Calretinin
  • +Melan-A
  • +Vimentin

• Sertoli cell tumor:^[29][38][3]
  • +Inhibin
  • +Vimentin
  • +EMA (epithelial menbrane antigen)
  • +/-Cytokeratin

• Granulosa cell tumor:^[39][29][40]
  • +Inhibin
  • +Calretinin
  • +Vimentin

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Shanshan Cen, M.D. [3]

There are no direct causes for testicular cancer. However, there are some common risk factors that may lead to gene mutations and cause the testicular cancer.

There are no established direct causes for testicular cancer. Common risk factors can be found here.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shadan Mehraban, M.D.[2]

Testicular cancer must be differentiated from epididymitis, hematocele, hydrocele, spermatocele, granulomatous orchitis, and varicocele.

Abbreviations:

AFP: Alpha-fetoprotein, B-hCG: Beta-human chorionic gonadotropin, P-ALP: Placental– Alkaline phosphatase

Diseases	Benign/ Malignant	Unilateral/Bilateral	History/demography	Metastasis	Genetics	Clinical manifestations			Para-clinical findings
						Symptoms		Physical examination	Lab findings			Imaging	Histopathology
						Pain	Mass		AFP	Beta hCG	p-ALP
Germ Cell tumors
Seminoma[1][2]	Malignant	Unilateral	Cryptorchidism Most common among age of 15-35 years old	Late metastasis	Stains positively for: ALP C-KIT CD30 EMA Glycogen	–	+	Palpable, nontender unilateral testicular mass Usually homogeneous enlargement	N/A	N/A	↑	Ultrasound Homogeneous hypoechoic intratesticular mass Cysts and calcification are uncommon Inhomogenous feature in larger mass	Large cells wit watery cytoplasm Fried egg appearance
Embryonal carcinoma[3]	Malignant	Usually located in parenchyma of testis May be nonpalpable	Hemorrhagic mass with necrosis Rare type Peak incidence at the age of 30 years old	Early metastasis to: Retroperitoneum Lung Liver	Stains positively for: CD30 HCG May stain positively for : AFP, when mixed with other tumors	+	±	Unremarkable May present with abdominal/ pelvic mass Abdominal pain may be present Metastatic findings	↑*	↑	N/A	Ultrasound Usually hypoechoic mass Invasion to tunica albuginea Irregular calcification	Primitive epithelial cells with marked pleomorphism Often mixed histopathological features (solid, papillary, tubular, pseudoglandular)
Yolk sac tumor[4][5]	Malignant	Unilateral	Known as a endodermal sinus tumor Undescended testes in youth Most common prepubertal testicular cancer in children < 3 years of age	Uncommon	Stains positively for: AFP Alpha-1-antitrypsin PAS diastase	+	+	Palpable mass Nontender mass Unilateral mass	↑	N/A	N/A	Ultrasound Diffuse enlargement of the testis with a heterogeneous appearance MRI Areas of hemorrhage and necrosis	Yellow, mucinous, encapsulated mass Schiller-Duval bodies (perivascular structures) Hyaline-type globules
Teratoma[6][7]	Benign Malignant	Unilateral	May present in both prepubertal and adult men Benign form in children under 4 years oldCongenital disease such as: Klinefelter’s syndrome Down syndrome Spina bifida	Uncommon in benign ones among prepubertal men Common in malignant ones among postpubertal ones Metastasis may be teratomatous	Chromosome 12 mutations Stains positively for: Cytokeratin HCG AFP	–	+	Palpable mass Nontender mass Unilateral mass	↑	↑	N/A	Ultrasound Heterogeneous, cystic appearance Irregular calcification	Large, heterogeneous appearance Presence of at least 2 germ layers
Choriocarcinoma[8][9]	Malignant	Testicular mass may be small/ asymptomatic	Cryptorchidism Abdominal undescended testes Most aggressive type	Early metastasis: Liver Brain Lung	Stains positively for: HCG Genetic changes of 12p11.2-p12.1 chromosomal region	+	±	Nonpalpable or small mass Painless or radiating pain to groin/ abdomen Metastatic findings Gynecomastia Hyperthyroidism symptoms	N/A	↑	N/A	Ultrasound Hemorrhage and necrosis May appear more cystic inhomogeneous, and calcified	Characterized by hemorrhagic and necrotic areas Disordered syncytiotrophoblastic and cytotrophoblastic elements
Mixed germ cell tumors[10][11]	Malignant	Unilateral	Two or more germ cell tumors present as a single mass Depends on underlying components Average age about 30 years old Rare in prepubertal age Include one-third of all testicular germ cell tumors	Metastasis depends on tumors types Metastasis to lung, liver, brain, skin	May stain positive based on underlying components	±	+	Physical exam findings based on underlying components	↑	↑	N/A	Imaging findings based on underlying components	Variable components depends on tumor Accompanied with necrosis and hemorrhages
Carcinoma in situ (intratubular germ cell neoplasia )[12][13][14]	Malignant	Unilateral Bilateral	Cryptorchid testes Previous testicular cancer Abnormal sexual differentiation A precursor of most testicular germ cell tumors Adjacent to a other testicular germ cell tumors > 90% of all	Common: Lymph nodes Any other organs	Stain positively for: Placental ALP Genetic changes in chromosome 12	–	–	N/A	N/A	N/A	↑	N/A	Proliferation of neoplastic germ cells in seminiferous tubules
Diseases	Benign/ Malignant	Unilateral/Bilateral	History/Demography	Metastasis	Genetics	Pain	Mass	Physical exam	AFP	Beta hCG	p-ALP	Imaging	Histopathology
Non-germ cell tumors
Leydig cell tumor[15]	Malignant in up to 20% of adult cases Benign among children	Unilateral	Based on large size, vascular invasion, and mitotic activity classify into benign / malignant Bimodal age distribution in both adults and children	Uncommon metastasis	Mutation in fumarate hydratase Stains positively for: Inhibin A Calretinin WT-1 SALL-4	–	+	Palpable mass Unilateral mass Nontender Gynecomastia	N/A	N/A	N/A	Ultrasound Well-defined, hypoechoic solid mass Cystic component Irregular calcification	Golden brown color May have cystic, hemorrhagic, or necrotic areas Eosinophilic crystals of Reinke
Sertoli cell tumor ( Androblastoma)[16][17][18]	Usually Benign	Unilateral Bilateral	Classified as large cell calcifying or sclerosing types History of peutz-Jeghers syndrome and Carney complex Occur in any ages (infancy to elderly) Average age of 45 years Mean age for large cell calcifying variant is 21 years old	Uncommon metastasis	Stain positively for: Inhibin Cytokeratin	–	+	Palpable and painless mass Hyperestrinism is noted in syndromic cases Gynecomastia	N/A	N/A	N/A	Ultrasound Large cell calcifying variant Hypoechoic	Solid or hollow tubules divided by basement membrane Pale eosinophilic cytoplasm
Testicular lymphoma[19][20][21]	Malignant	Unilateral Bilateral ( mostly up to 35% of cases)	Aggressive extranodal non-Hodgkin lymphoma The most common in men older than 50 years old	Common metastasis to : Skin Subcutaneous tissue Bone marrow Central nervous system Lung	Stains positively for: CD45 Depends on lymphoma subtype	–	+	Palpable mass Nontender mass	↑ or ↓	↑ or ↓	N/A	Ultrasound Diffuse testicular infiltration and enlargement Hypervascularity Hypoechoic and solid lesion	Pleomorphic malignant cells Large irregular nuclei Vascular invasion Seminiferous tubules
Granulosa cell tumors[22][23]	Malignant	Unilateral	Juvenile type in children less than 2 years old ( the most common infancy tumor) Adult type with average age of 44 years old ( rare) Juvenile type associated with: Sex chromosome abnormalities Ambiguous genitalia Cryptorchidism	Metastasis occur in 10%-20% of cases	Stains positively for: Calretinin Inhibin Vimentin Actin MIC2	–	+	Palpable mass Nontender mass	N/A	N/A	N/A	Ultrasound Hypoechoic mass Solid and cystic appearance	Common features are microfollicular and diffuse Call-Exner bodies in adult type ( eosinophillic material) In juvenile type: Solid sheets or nodules and form ectatic spaces

* May stain positively when mixed.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Rim Halaby, M.D. [3], Shanshan Cen, M.D. [4]

Testicular cancer is a rare type cancer accounting about 0.5% of all new cancer cases in U.S. In 2018, the estimate prevalence of testicular cancer is approximately 9,310 new cases of testicular cancers in the United States. The incidence of testicular cancer is approximately 5.7 per 100,000 men per year based on 2011-2015 report in the United States. The majority of cases are reported in New Zealand. Testicular cancer commonly affects more white males than any other races and black males are less affected by it. Testicular cancer is commonly affects men aged 20-44 years old and median age is 33 years old.

• Testicular cancer is the most common type of cancer in young males.^[1][2]
• Germ cell tumors are about 98% of testicular cancer.^[3]
  • About 55% of germ cell tumors are seminomas
  • About 44% of germ cell tumors are non-seminomas
  • About 1-2% of germ cell tumors are spermatocytic
• In the United States, the estimate prevalence of testicular cancer is approximately 9,310 new cases in 2018.^[4]
• Sex cord stromal testicular tumors are about less than 5%.

• The incidence of testicular cancer is approximately 5.7 per 100,000 men per year based on 2011-2015 report in the United States.^[4]

• Testicular cancer is more common among men aged 20-44 years old.^[2]
• Median age is 33 years old.^[2]
• Germ cell tumors of the testis are the most common cancer in young adults.^[1]
• Median age is 33-39 years old for seminomas germ cell type of testicular cancer^[3]
• Median age is 25-29 years old for non-seminoma germ cell type of testicular cancer^[3]
• Median age is 50-54 years old for spermatocytic germ cell type of testicular cancer^[3]

• The 5 years of survival rate for patients with testicular cancer are 95.3% in 2008-2014.^[4]

• Testicular cancer is more common in white males compared to other races.^[4]
• The incidence of testicular cancer in African American is lower than that among white people;^[5] however, African American subjects tend to present at later stages of the disease due to a delayed presentation.^[5]

• Shown below is a table depicting the age-adjusted incidence of testicular cancer by race in 2011-2015 in the United States.^[4]

	All Races	White	Black	Asian/Pacific Islander	Hispanic
Age-adjusted incidence	5.7 per 100,000	6.8 per 100,000	1.5 per 100,000	2.3 per 100,000	5.3 per 100,000

• The highest rates of incidence in New Zealand, followed by United Kingdom, Australia, Sweden, United States, Poland, and Spain.^[1]

• Testicular cancer is uncommon in Asia and Africa.^[3]
• The lowest incidence of testicular cancer is in India.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Shanshan Cen, M.D. [3]

Common risk factors in the development of testicular germ cells cancer are undescended testicle, family history, personal history of testicular cancer, and Klinefelter syndrome. There are no known risk factors for testicular sex cord stromal tumors.

Common risk factors for testicular germ cells tumors include:^[1][2][3]

• Undescended testicle
• Family history of testicular cancer
• Personal history of testicular cancer
• Klinefelter syndrome
• Impaired spermatogenesis^[4]
• Hypospadias

Less common risk factors include:^[1][5]

• Testicular microlithiasis
• HIV infection or AIDS^[6]
• Occupational exposures:^[2]
  • Aircraft maintenance
  • Firefighting
• Early puberty
• Higher maternal age seen in seminomas type^[7]
• Tall height
• Decreased fertility
• Pesticides
• Marijuana
• Prenatal exposure to estrogens
• Vasectomy
• Trauma or injury
• Tobacco
• Alcohol

• There are no known risk factors for testicular sex cord stromal tumors.^[8][9][10]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2], Shanshan Cen, M.D. [3]

According to the the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for testicular cancer.

According to the the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for testicular cancer.^[1][2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Gertrude Djouka, M.D.[2],Rim Halaby, M.D. [3] Shanshan Cen, M.D. [4]

Prognosis of testicular cancer is generally good, and the 5-year survival rate is approximately 96.6% (2004-2010). Common complications of testicular cancer include metastasis, bleeding, infection, and infertility.

• Seminoma tends to occur in middle aged people.
• Rarely metastasize.^[1]
• Affects people in their 15 and 35 years old

• Median age is 30 years old^[1]
• Has most of the component of mixed non seminoma germ tumor^[1]
• Tend to metastasize early to lungs, retroperitoneum, and liver^[2]

• Patient presents with early symptoms if there are metastatic lesions.^[3]
• Early metastasis through hematogenous route
• Tends to metastasize to lungs, brain, liver, peritoneum, and others.
• Affects most male patients in the second and third decade of their life.^[4]

• Mostly seen in children less than 2 years old^[5]
• Patients are usually asymptomatic at onset^[6]
• Tends to have elevated alpha fetoproteins (AFP)

• Seen in old men
• Barely metastasize^[7]

• Seen mostly in any age
• Benign in boys aged 5 to 10 years old and malignant in adults aged 30 to 60 years old^[8][9]
• It metastasizes in the regional lymph nodes such as iliac, inguinal and retroperitonial nodes^[10]

• It affects both infants and older adults
• Malignancy is seen in infants in presence of metastasis^[9]
• Sertoli cell tumor is associated with Peutz-Jeghers syndrome and Carney complex.
• large cell calcifying sertoli cell tumor is associated with Carney’s complex (syndrome of myxoma, spotty pigmentation and endocrine overactivity).^[11][12]

• It is rare type of testicular cancer.
• Seen mostly in the ovary

Adult type:

• It rarely metastasizes.
• Seen in the 4th decade of life.^[13]

Juvenile type

• It is seen mostly in infants.^[14]
• It is mostly benign
• It has an underlined association with sex chromosome abnormalities, ambiguous genitalia, and ipsilateral cryptorchidism.^[15]

Common complications of testicular cancer include:

• Metastasis

• Abdomen
• Lungs
• Retroperitoneal area
• Brain

• Post-surgery complications

• Bleeding
• Infection
• Infertility

• Between 2004 and 2010, the 5-year relative survival of patients with testicular cancer was 96.6%.^[16]

• When stratified by age, the 5-year relative survival of patients with testicular cancer was 95.4% and 86.4% for patients <65 and ≥ 65 years of age respectively.^[16]

• The survival of patients with testicular cancer varies with the stage of the disease. Shown below is a table depicting the 5-year relative survival by the stage of testicular cancer:^[16]

Stage	5-year relative survival (%), (2004-2010)
All stages	95.3%
Localized	99.2%
Regional	96%
Distant	73.1%
Unstaged	78.8%

• Shown below is an image depicting the 5-year conditional relative survival (probability of surviving in the next 5-years given the cohort has already survived 0, 1, 3 years) between 1998 and 2010 of testicular cancer by stage at diagnosis according to SEER. These graphs are adapted from SEER: The Surveillance, Epidemiology, and End Results Program of the National Cancer Institute.^[16]

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