Testicular Cancer


Definition/Description[edit | edit source]

Testicular cancer is cancer in mostly one and rarely both testicles[1]. It is most often found in young men. This type of cancer can be treated and very often cured;[2]with more than 95% survival rate.[1]

Testicles[edit | edit source]

Male reproductive system.png

The testicles (or testes) are part of the male reproductive system.  In adult men, each one is normally a little smaller than a golf ball.  They are held in a sack of skin called the scrotum.  The scrotum hangs beneath the base of the penis.[2]

The testicles make the male hormones testosterone.  They also make sperm.  Sperm cells are carried from the testicles through small tubes (the vas deferens) to the seminal vesicles.  Fluid from the vesicles and from the prostate gland is added.  During ejaculation (orgasm), this fluid, now called semen, travels through a tube (the urethra) in the center of the penis and out of the body.

The testicles have several kinds of cells.  The different cells may develop into one or more types of cancer.  It is important to know which kind of cell cancer started because these types of cancer are treated differently.  They also differ in the chance of survival for the patient (prognosis).

Main Types of Testicular Tumors[edit | edit source]

  • Germ cell tumors are the most common type of testicular tumours.  Germ cell tumors grow in the cells that make sperm.[2]
  • Stromal tumors grow in other parts of the testicles like the cells that make hormones.
  • Secondary testicular tumors are from cancer that has spread to the testicles from other parts of the body.

Each of the 3 types is explained in more detail below.

Germ Cell Tumors[edit | edit source]

  • More than 95% of testicular cancers start in the germ cells.[3] The 2 main types of germ cell tumors are seminomas and nonseminomas.[3] 
  • Some cancers contain both non-seminoma and seminoma cells.  These are treated as non-seminomas because they grow and spread like non-seminomas.

Seminomas[edit | edit source]

Seminomas start from germ cells of the testicle that make sperm.  The 2 main subtypes of these tumors are classical (or typical) seminomas and spermatocytic seminomas. Doctors can tell them apart by how they look under the microscope.[4]  

  1. Classical seminoma: More than 95% of seminomas are classical.  These usually occur in men when they are between their 30s and 40s.
  2. Spermatocytic seminoma: This rare type of seminoma tends to occur in older men.[3] The average age of men diagnosed with spermatocytic seminoma is about 55.  Spermatocytic tumors tend to grow more slowly and are less likely to spread to other parts of the body than classical seminomas[3].

Some seminomas can increase blood levels of a protein called human chorionic gonadotropin (HCG).  HCG can be detected by a simple blood test and is considered a tumor marker for certain types of testicular cancer.  It can be used for diagnosis and to check for response to therapy.

Non-seminomas[edit | edit source]

This type of germ cell tumor usually occurs in men between their late teens and early 40s. There are 4 main types of non-seminoma tumors:

  1. Embryonal carcinoma
  2. Yolk sac carcinoma
  3. Choriocarcinoma
  4. Teratoma

Most tumors are mixed with at least 2 different types, but this does not change treatment.  All non-seminoma germ cell cancers are treated the same way.

  1. Embryonal carcinomas: This type of non-seminoma is present to some degree in about 40% of testicular tumors, but pure embryonal carcinomas occur only 3% to 4% of the time. This type of non-seminoma tends to grow rapidly and spread outside the testicle. Embryonal carcinoma can increase blood levels of a tumor marker protein called alpha-fetoprotein (AFP), as well as HCG[3]
  2. Yolk sac carcinomas: These are so named because their cells look like the yolk sac of an early human embryo.  Other names for this cancer include yolk sac tumor, endodermal sinus tumor, infantile embryonal carcinoma, or orchidoblastoma. Yolk sac carcinoma is the most common form of testicular cancer in children.  When they occur in children, these tumors usually are treated successfully.  When yolk sac tumors develop in adults, however, they are of more concern, especially if they are "pure" (that is, the tumor does not contain other types of non-seminoma cells).  Yolk sac carcinomas respond very well to chemotherapy, even if they have spread.  This type of tumor almost always increases blood levels of AFP and/or hCG.[3]
  3. Choriocarcinomas: This is a very rare and aggressive type of testicular cancer that occurs in adults.  These cancers are likely to spread rapidly to distant organs of the body, including the lungs (most commonly)[3], bone, and brain. It has the worst prognosis of all [3]. This type of tumor increases blood levels of HCG.
  4. Teratomas: Teratomas are germ cell tumors with areas that, when seen under the microscope, look like each of the 3 layers of a developing embryo: the endoderm (innermost layer), mesoderm (middle layer), and ectoderm (outer layer)[3].  The 3 main types of these tumors are the mature teratoma, immature teratoma, and teratoma with malignant transformation. Pure teratomas do not increase AFP or HCG levels. Mature teratomas are tumors formed by cells similar to cells of adult tissues.  They are generally benign and rarely spread to nearby tissues and distant parts of the body. Immature teratomas are less well-developed cancers with cells that look like those of an early embryo.  Unlike mature teratomas, this type is more likely to grow into (invade) surrounding tissues and to spread (metastasize) outside the testicle.  Teratomas can usually be cured with surgery as they are resistant to chemotherapy and radiotherapy.[3]

Carcinoma in situ[edit | edit source]

All testicular germ cell cancers have the same precursor called carcinoma in situ (CIS)[5], intratubular germ cell neoplasia and recently, germ cell neoplasia in situ (GCNIS)[6]. Carcinoma in situ may not always progress to invasive cancer. CIS has an estimated risk of 50% in 5 years and 70% in 7 years to progress to the invasive form of germ cell cancer.[7] It is hard to find CIS before it develops into invasive cancer because it generally causes no symptoms and often does not form a lump that you or the doctor can feel.  The only way to diagnose testicular carcinoma in situ is to have a clinical examination, biopsy, and ultrasonography[8].

Stromal Tumors[edit | edit source]

Tumors can also develop in the supportive and hormone-producing tissues, or stroma, of the testicles.  These tumors are known as gonadal stromal tumors.  They make up less than 5% of adult testicular tumors but up to 20% of childhood testicular tumors.  The 2 main types are Leydig cell tumors and Sertoli cell tumors. About 10% of both types are malignant[3].

  • Leydig cell tumors: These generally benign tumors develop from the Leydig cells in the testicle that normally produce male sex hormones (androgens like testosterone).  Leydig cell tumors can develop in both adults (75% of cases) and children (25% of cases).  They often produce androgens but sometimes produce oestrogens (female sex hormones).
  • Most Leydig cell tumors do not spread beyond the testicle and are cured with surgery (orchiectomy)[3].  Sometimes, however, these tumors do spread to other parts of the body.  If they do metastasize, Leydig cell tumors have a poor prognosis because they usually do not respond well to chemotherapy or radiation therapy.
  • Sertoli cell tumors: These tumors develop from normal Sertoli cells, which support and nourish the sperm-producing germ cells.  Like the Leydig cell tumors, they are usually benign.  However, if they spread, they tend to be resistant to chemotherapy and radiation therapy.

Secondary Testicular Tumors[edit | edit source]

  • Secondary testicular tumors are those that start in another organ and then spread to the testicle.  Lymphoma is the most common secondary testicular cancer.  Testicular lymphoma is more common than primary testicular tumors in men older than 60[3].  Their prognosis depends on the type and stage of lymphoma.  The usual treatment is surgical removal, followed by radiation and/or chemotherapy. 
  • Cancers of the prostate, lung, skin (melanoma), kidney, and other organs also can spread to the testicles.  The prognosis for these cancers is usually poor because these cancers generally spread widely to other organs as well.  Treatment depends on the specific type of cancer.

[9]

The TNM Staging System[2][edit | edit source]

A staging system is a standardized way for the cancer care team to summarize and describe the extent of your cancer. Testicular cancer is staged using the TNM system created by the American Joint Committee on Cancer (AJCC).

Staging in Testicular Cancer is valuable for defining prognosis and treatment. Patients are classified as Stage I (limited to the testis), Stage II (lymph node involvement), and Stage III (metastasis to visceral organs). Factors are considered such as the degree of metastasis, elevation of tumor markers, and histology (seminoma or nonseminoma) are considered when staging.[10]

The staging system of testicular cancer contains 4 important pieces of information:

  • T refers to how much the primary tumor has spread to tissues next to the testicle.
  • N describes how much cancer has spread to regional (nearby) lymph nodes.
  • M indicates whether the cancer has metastasized (spread to distant lymph nodes or other organs of the body).
  • S indicates the serum levels of certain proteins (tumor markers) that are produced by some testicular cancers.

Detailed information on the TNM Staging System can be found at American Cancer Society

Epidemiology[edit | edit source]

Testicular cancer is relatively rare and occurs most often in young men (post pubertal) between the ages of 15 and 34 years old,[11] although any male can be affected at any time (including infants).[12] Testicular cancer is the most common solid organ tumour in young men. It is the second most common malignancy from age 35 to 39 years with a white-to-black incidence ratio of 5 to 1.[13]
The incidence of testicular cancer around the world has doubled in the past 40 years.[11]

There is an important global variability in mortality rates that are largely opposite in incidence rates. Testicular Cancer mortality is highest in low-income countries compared with higher-income countries. [10]

In recent years, the incidence of testicular cancer has increased globally with major increases observed in Western Europe, Northern Europe, and Australia/New Zealand. However, Japan, Switzerland, and China have all witnessed a stable incidence. Lowest incidence was observed in Middle Africa .[14]

Incidence rates were the same as mortality rates in Africa and Asia, ineffective diagnostic tools and treatment were the suggested reasons. Mortality rates in developed countries (95% survival rate)were lower than those in other countries. 80% of 10,351 deaths as a result of testicular cancer occurred in Africa, Asia, Central and South America, and the Caribbean[14].

About 50% of patients worldwide with Testicular Cancer are diagnosed with seminoma and the median ages at diagnosis 37 years.[10] Because treatment is so successful, the risk of dying from this cancer is very low: about 1 in 5,000.[2]

Testicular cancer is one of the most curable forms of cancer.[2] 

According to the National Cancer Institute, the 5-year relative survival rate for all men with this cancer is 95%.[2]

  • If cancer hasn't spread outside the testicle, the 5-year relative survival rate is 99%.  
  • Even if cancer has spread to nearby lymph nodes, the 5-year relative survival rate is 96%. 
  • If cancer has spread beyond the lymph nodes, the 5-year survival rate is around 71%. 
  • More than 170,000 men in the United States have survived testicular cancer.

There are considerable geographic and ethnic variations in the global incidence of testicular cancer. The disease mainly affects Western populations, with an increasing incidence since the middle of the twentieth century. Average rates in developed areas of the world are six times higher than those in developing areas. Approximately 79,200 new cases of testicular cancer were estimated to occur in the United States in 2007.[13]

Causes[edit | edit source]

The aetiology of testicular cancer is not well understood.[13] Although the cause is unknown, hormonal balance at various life stages appear to be related.[13]

  • Congenital and acquired factors have been associated with the development of testicular cancer; familial clustering has been observed particularly among siblings.[13]
  • The first susceptibility gene for testicular cancer has been located and named TGCT1 on the long arm of chromosome X, inherited from the mother; its presence increases a man’s risk of testicular cancer by up to 50 times.[13]
  • There is some evidence that cancer stem cells are derived from normal stem cells that have gradually accumulated various genetic defects; a group of tumour-specific antigens known as cancer/testis antigens (CTAs) may be expressed at early stages during embryogenesis in germ cell precursors eventually leading to testicular cancer.[13]
  • A great deal of research is being done to learn more about the causes. During the past few years, researchers have learned a lot about certain changes in chromosomes and DNA that may cause normal testicular germ cells to develop into germ cell tumours.[2] Testicular germ cell tumours may form when something abnormal happens during meiosis. Instead of forming normal sperm cells with 23 chromosomes, all 46 chromosomes remain. Usually, these chromosomes become unstable and progressively more abnormal in their shape and number (often between 69 and 82) as the cells continue to divide. Testicular cancer cells often have extra copies of a part of chromosome 12 (this is called isochromosome 12p). Scientists are studying DNA from this chromosome to learn more about exactly what goes wrong during meiosis and how this might be prevented or reversed. Several other abnormal chromosomes and changes in the factors that regulate cell division and the cell cycle have been associated with testicular cancer, both in animals and in humans.

Risk Factors[edit | edit source]

  • Cryptorchidism :The most significant factor in testicular cancer is the association of cryptorchidism (the testes not descending into the scrotum).[13] Although most cancers develop in the undescended testicle, about 1 out of 4 cases occur in the normally descended testicle.[2] The incidence of testicular cancer is 35 times higher in males with a cryptoid testis.[13] The cancer risk for boys with this condition is increased even if surgery is done to move the testicle to the scrotum. In the case of unilateral cryptorchidism, the risk of testicular cancer is increased in the normal testicle as well. This fact suggests testicular cancer is due to whatever caused the undescended testicle.[12]
  • History: A previous history of testicular cancer and a history of infertility and poor semen quality or infection have been associated with an increased risk of developing testicular cancer.[13] A causal relationship has not been established between infertility and infection and testicular cancer. Having a brother or father with testicular cancer also increases an individual’s risk.[12] If a man has the disease, there is an increased risk that one or more of his brothers or sons will also develop it. However, only about 3% of testicular cancer cases are actually found to occur in families. Most men with testicular cancer do not have a family history of the disease.[2] Within 15 years of initial diagnosis, cancer survivors are at 2% risk of developing cancer in the other testicle.[15]
  • Age: About 9 out of 10 testicular cancers occur in men between the ages of 20 and 54. But this cancer can affect males of any age, including infants and elderly men.[2]
  • Race and ethnicity: The risk of testicular cancer among white men is about 5 times that of black men and more than 3 times that of Asian-American and American Indian men.[2] The risk for Hispanics is between that of Asians and non-Hispanic whites.  The reason for this difference is unknown. The testicular cancer rate has more than doubled among white Americans in the past 40 years but has not changed for African Americans. Worldwide, the risk of developing this disease is highest among men living in the United States and Europe and lowest among African and Asian men.[12]
  • Other risk factors may include; occupation (e.g., miners, oil and gas workers, leather workers, food and beverage processing workers, janitors, firefighters, utility workers) and HIV infection.[12] Some evidence has shown that men infected with the Human Immunodeficiency Virus (HIV), particularly those with AIDS, are at increased risk. No other infections have been shown to increase testicular cancer risk.[2]
  • Men with Klinefelter’s syndrome (a sex chromosome disorder characterized by low levels of male hormones, sterility, breast enlargement, and small testes) are also at greater risk of developing testicular cancer.[13]
  • Lifestyle and occupational exposures occurring later in life may play a role in promoting the disease, but they are not likely involved in the initiation of cancer development.[13]
  • There is now strong evidence that prenatal or postnatal environmental oestrogen exposures (e.g., endocrine-mimicking environmental pollutants, pesticides, industrial chemicals, or chemical contaminants in drinking water) contribute to testicular cancer; this remains under further investigation.[13] Other risk factors still under investigation may include mothers who took exogenous oestrogen during pregnancy (diethylstilbestrol), scrotal trauma, exposure to high levels of radiofrequency/microwave radiation in radar technicians, first-born sons, and non-identical twins.[13]
  • Other risk factors in Testicular Cancer include vasectomy, scrotal trauma, inguinal hernia, diet, smoking and environment (such as heavy metals exposure and endocrine disruptors).[10]

Systemic Involvement[edit | edit source]

Musculoskeletal: Metastases occur via the blood or lymph system.[12] The most common place for the disease to spread is to the lymph nodes in the posterior part of the abdomen.[12]  Therefore, lower back pain is a frequent symptom of later-stage testicular cancer.[13] Referred pain from the male reproductive system to hip, groin, SI, and sacral areas. Back pain, changes in bladder function, and sexual dysfunction are the most common symptoms associated with male reproductive disorders.[13]

  • Back pain associated with cancer is usually constant, intense, and worse at night or with weight-bearing activities, although vague, diffuse back pain can be an early sign of non-Hodgkins lymphoma and multiple myeloma. Pain with metastasis to the spine may become quite severe before any radiologic manifestations appear. Back pain associated with malignant retroperitoneal lymphadenopathy or testicular cancers is characterized as persistent, poorly localized low back pain present at night but relieved by forward flexion. Pain may be so excruciating while lying down that the patient can sleep only while sitting in a chair hunched forward over a table. Typically systemic back pain is not relieved by recumbency.[12]
  • In fact, the bone pain of metastasis or myeloma tends to be more continuous, progressive, and prominent when the client is recumbent. Beware of the client with acute backache who is unable to lie still. Almost all clients with regional or nonspecific backache seek the most comfortable position (usually recumbency) and stay in that position. In contrast, individuals with systemic backache tend to keep moving trying to find a comfortable position. Back pain that is unrelieved by rest or change in position, or pain that does not fit the expected mechanical or neuromusculoskeletal pattern, should raise a red flag. When the symptoms cannot be reproduced, aggravated, or altered in any way during the examination, additional questions to screen for medical disease is indicated. Pain at night can signal a serious problem such as tumour, infection, or inflammation. Long-standing night pain unaltered by positional change suggests a space-occupying lesion, such as a tumour.[12]
  • Systemic back pain may get worse at night, especially when caused by vertebral osteomyelitis, septic discitis, Cushing’s disease, osteomalacia, primary and metastatic cancer, Paget’s disease, ankylosing spondylitis, or tuberculosis (of the spine).[12]

If cancer has spread to the lungs, persistent cough, chest pain, and/or shortness of breath can occur. Hemoptysis (sputum with blood) may also develop.[12]

Clinical Signs and Symptoms[12][edit | edit source]

  • A lump in either testicle
  • Any enlargement, swelling, or hardness of a testicle. The enlargement may be accompanied by an ache in the abdomen, testicle or scrotum or a sensation of heaviness in the scrotum.[13]
  • Significant loss of size in one of the testicles
  • Feeling of heaviness in the scrotum and/or lower abdomen
  • Dull ache in the lower abdomen or in the groin
  • Sudden collection of fluid in the scrotum
  • Pain may be the sole presenting symptom in metastasis to the retroperitoneal, cervical, and supraclavicular lymphatic chains.[13]
  • Approximately 20% of all cases have involved lymph nodes.[13]
  • Enlargement or tenderness of the breasts[12]This symptom occurs because certain types of germ cell tumors secrete high levels of a hormone called human chorionic gonadotropin (HCG), which stimulates breast development.[2]
  • Unexpected fatigue or malaise
  • Infertility
  • Metastasis, with little or no local change, is noted in the scrotum.[13]
  • Low back pain (metastases to retroperitoneal lymph nodes) in later stage testicular cancer. Up to 21% of men with testicular germ cell cancer have back pain as the primary presenting symptoms.[2] Retroperitoneal primary tumours may present with back pain and/or groin or pelvic pain (psoas muscle invasion). Metastatic testicular cancer can present as back pain (may be the primary presenting complaint), abdominal mass, haemoptysis, or neck or supraclavicular adenopathy.[13]
  • Bone metastasis is a late event, often combined with metastasis to the retroperitoneal lymph nodes, lung, and liver.[13] Even when testicular cancer has spread to other organs, only about 1 man in 4 may have symptoms. If cancer has spread to the lungs, persistent cough, chest pain, and/or shortness of breath can occur. Haemoptysis (sputum with blood) may also develop.[12] In rare cases, testicular cancer spreads to the brain and can cause headaches.[2]

Complications[edit | edit source]

The most serious long-term complications are as a result of chemotherapy or radiotherapy with cardiovascular toxicity and second malignancies; each has a 25-year risk of approximately 16%.

  • Some of the drugs used to treat testicular cancer can cause long-term side effects. Cisplatin can cause kidney damage. It can also damage nerves, causing hearing loss, numbness or tingling sensations in the hands or feet, and sensitivity to cold or heat. This is called peripheral neuropathy. In most cases this goes away once treatment is stopped, but it may last a long time in some people. Long-term sequelae of cisplatin use may include leukaemia, cardiovascular events, and reports that circulating cisplatin can be detected in the plasma as long as 20 years after treatment.[13]
  • There is an increased incidence of metabolic syndrome in long-term survivors that is most likely caused by the lower testosterone levels.[13]

Diagnostic Tests[edit | edit source]

Physical Exam[2][10][edit | edit source]

  • During a physical exam, the doctor will feel the testicles for swelling or tenderness and for the size and location of any lumps. The doctor also carefully examines the density of testes and palpates for any testicular masses.
  • The doctor will also examine the abdomen, lymph nodes, and other parts of the body carefully, looking for any signs of metastasis.

Ultrasound of the Testicles[2][edit | edit source]

An ultrasound can help doctors tell if a lump is solid or filled with fluid. Testicular ultrasound is used to differentiate a variety of scrotal disorders besides cancer (e.g., epididymitis, orchitis, hydrocele, or hematocele).[13]

Blood Tests for Tumor Markers[2][13][edit | edit source]

  • Serum tumor markers are increased by 40% to 60% of all cases and may be used to guide treatment and follow-up.
  • Many testicular cancers secrete high levels of certain proteins, such as alpha-fetoprotein (AFP) and human chorionic gonadotropin (HCG). When these proteins (called tumor markers) are in the blood, it suggests that there is a testicular tumor.
  • Non-seminomas often raise AFP and/or HCG levels.
  • Pure seminomas occasionally raise HCG levels but never AFP levels, so any increase in AFP means that the tumor has a non-seminoma component.[2]
  • The levels of these proteins may not be elevated if the tumor is small.

Imaging Tests[2][edit | edit source]

Chest x-ray

Computed tomography (CT) scan

Magnetic resonance imaging (MRI) scan

Lymphangiogram[edit | edit source]

  • Because of improvements in other imaging tests, lymphangiograms are rarely done today.
  • For a lymphangiogram, a special dye is injected into a lymph vessel in the foot or leg. The dye travels to the lymph nodes.
  • A special monitor displays x-ray images of the lymph system, which doctors can study to detect signs that cancer has spread to the lymph nodes.
  • CT scans are used to examine lymph nodes more frequently than lymphangiograms. However, the technique is sometimes used for patients with early-stage non-seminomas who are being watched for signs of progression before getting more chemotherapy or radiation.

Positron emission tomography (PET) scan[2][13][edit | edit source]

  • For a PET scan, radioactive glucose (sugar) is injected into the patient's vein. Cancer cells use sugar much faster than normal tissues, hence, the cancer cells in the body absorb large amounts of the radioactive substance. The amount of radioactivity is very low
  • A special camera can then be used to create a picture of areas of radioactivity in the body.
  • The picture is not finely detailed like a CT or MRI scan, but it can provide helpful information about the whole body.
  • This test can be helpful for spotting small collections of cancer cells.
  • It is sometimes useful for looking at enlarged lymph nodes that remain after chemotherapy.
  • Often the PET scan is combined with a CT scan. This helps decide if abnormalities seen on the CT scan are cancer or something else.

Differential Diagnosis[edit | edit source]

There are a number of non-cancerous conditions that have similar symptoms to testicular cancer, such as:

  • Testicle injury
  • Inflammation: inflammation of the testicle, known as orchitis, can cause painful swelling. The mumps virus causes orchitis in about 1 man in 5 who contracts mumps as an adult.

Other conditions are[2]:

  • Epididymitis (inflammation of the epididymis). This can also cause swelling and pain.
  • Both of these (orchitis, and epididymitis) can be caused by viral or bacterial infections.

Medical Management[edit | edit source]

The 3 main methods of treatment for testicular cancer are:[2]

  • Surgery
  • Radiation therapy: In general, radiotherapy is mainly used for patients with seminoma, which is very sensitive to radiation. It does not seem to work well for non-seminomas. Sometimes it is used after orchiectomy (the operation to remove the testicle) and is directed at the lymph nodes at the back of the abdomen (the retroperitoneal lymph nodes). This is to kill any tiny bits of cancer in those lymph nodes that can't be seen. Radiotherapy can also be used to treat small amounts of seminoma that are known to have spread to the nodes (based on changes seen on CT and PET scans).[2]
  • Chemotherapy: It is often used to cure testicular cancer when it has spread outside the testicle or to decrease the risk of cancer coming back after the testicle is removed. It is not used to treat cancer that is only in the testicle. [2]The main drugs used to treat testicular cancer are:[2]
    1. Cisplatin
    2. Vinblastine
    3. Bleomycin
    4. Cyclophosphamide
    5. Etoposide
    6. Paclitaxel
    7. Ifosfamide These drugs are used in various combinations. The chemotherapy regimens most commonly used as the initial treatment for testicular cancer are bleomycin, etoposide, and cisplatin (called BEP), or etoposide and cisplatin (also known as EP). New chemotherapeutic agents, including the taxanes gemcitabine and oxaliplatin, may also be used.[13] Management of testicular cancer has changed substantially in the last 20 years, primarily because of the ability of cisplatin-containing combination chemotherapy to cure advanced disease.[13]

Surgery[edit | edit source]

It is typically the first treatment for all testicular cancers.[2]

Radical inguinal orchiectomy[2][edit | edit source]

  • This type of surgery removes the testicle (or testicles) containing cancer.
  • An incision is made in the groin, and the testicle is taken from the scrotum through the opening.
  • A cut is made through the spermatic cord that attaches the testicle to the abdomen.
  • The surgeon takes special precautions to avoid spreading cancer cells into the surgical wound or dislodging them from the tumor into the bloodstream.
  • All stages of testicular cancer are typically treated with this type of surgery.
Orchiectomy

Retroperitoneal Lymph Node Dissection[2][edit | edit source]

Depending on the type and stage of cancer, some lymph nodes behind the abdomen may also be removed at the same time or during a second operation. Retroperitoneal lymph node dissection can be a major operation. A large incision is often made to remove these lymph nodes. About 5% to 10% of patients have temporary complications after surgery, such as bowel obstruction or wound infections. This is a difficult and long operation. In some cases, the surgeon can remove lymph nodes through very small skin incisions in the abdomen by using a laparoscope (a narrow, lighted tube, which lets doctors operate on the abdomen without making a large incision and scar).

Surgery to remove retroperitoneal lymph nodes may damage nearby nerves that control ejaculation. If these nerves are damaged, when a male ejaculates, the semen is not deposited outside the body but rather goes into the bladder. This is known as retrograde ejaculation. This type of surgery does not cause impotence; a man can still have erections and sexual intercourse, but retrograde ejaculation can make it harder to father children. Nerve-sparing retroperitoneal lymph node dissection is an integral part of testis cancer management strategies for both early and advanced-stage disease. Testicular-sparing management of testicular cancer is an alternative to radial orchiectomy and allows for the preservation of sperm and hormonal function without endangering survival rates. Sperm collection and cryopreservation before the initiation of therapy is available reproductive technology.[13] Men with testicular cancer often have lower than normal sperm counts, which may make it difficult to collect a good sperm sample.[2] Only a few sperms are needed for successful in vitro fertilization.[13]

Testicular Prosthesis[edit | edit source]

Men with testicular cancer are usually young and may be concerned that their appearance has changed.[2] They may be single and dating and worry about a partner's reaction, or they may be athletic and feel embarrassed by the missing testicle when in locker rooms. Since the operation also removes the cord above the testicle, that side of the scrotum can look and feel empty to them. To restore a more natural look, a man can have a testicular prosthesis surgically implanted in his scrotum. The prosthesis approved for use in the United States is filled with saline (salt water), and it comes in different sizes to match the remaining testicle.[2] When in place, it can look like a normal testicle.[2] There can be a scar after the operation, but it is often partly hidden by pubic hair.[2]

Physical Therapy Management[edit | edit source]

No known physical therapy management exists for testicular cancer.

Recommendations[edit | edit source]

  • The American Cancer Society recommends monthly self-exam of the testicles for adolescents and men, starting at age 15.
  • Testicular self-examination is an effective way of getting to know this area of the body and thus detecting testicular cancer at a very early, curable stage.
  • The self-exam is best performed once each month or after a warm bath or shower when the heat has relaxed the scrotum.

[16]


Additional resources that patients can find are in the Resources section. 

Resources[edit | edit source]

https://www.auajournals.org/doi/full/10.1097/JU.0000000000000318

https://www.aafp.org/afp/2018/0215/p261.html

References[edit | edit source]

  1. 1.0 1.1 Gaddam SJ, Chesnut GT. Testicle Cancer. StatPearls [Internet]. 2021 Oct 9.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 2.23 2.24 2.25 2.26 2.27 2.28 2.29 2.30 2.31 2.32 2.33 2.34 American Cancer Society. Overview: Testicular Cancer, What is Testicular Cancer? American Cancer Society, Inc.; 2009-08-28; 2010-02. Available from: http://www.cancer.org/docroot/CRI/content/CRI_2_2_1x_What_Is_Testicular_Cancer_41.asp?sitearea=
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 Brannigan RE. Urology, an Issue of Medical Clinics of North America, E-Book. Elsevier; 2018 Feb 9.
  4. Baroni T, Arato I, Mancuso F, Calafiore R, Luca G. On the origin of testicular germ cell tumors: from gonocytes to testicular cancer. Frontiers in endocrinology. 2019 Jun 6;10:343.
  5. Skakkebæk N. Possible carcinoma-in-situ of the testis. The Lancet. 1972 Sep 9;300(7776):516-7.
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  7. von der Maase H, Rørth M, Walbom-Jørgensen S, Sørensen BL, Christophersen IS, Hald T, Jacobsen GK, Berthelsen JG, Skakkebæk NE. Carcinoma in situ of contralateral testis in patients with testicular germ cell cancer: study of 27 cases in 500 patients. Br Med J (Clin Res Ed). 1986 Nov 29;293(6559):1398-401.
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