Testicular Cancer (The Biology of Cancer)

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The technique is familiar to many people as the method used to view a fetus in utero, or in the uterus. Ultrasound is relatively inexpensive and there is no radiation involved. A small handheld instrument called a transducer produces high frequency sounds as it passes back and forth over the structures to be studied, in this case the testis and surrounding tissues in the scrotum.

A gel is applied to the transducer to help make a good connection between the instrument and the body. When the sound waves hit body structures, 38 testicular Cancer they bounce back, or echo. These echoes are then picked up by the transducer and sent to a computer, which converts the sounds into images. Different tissues produce different echoes, and the combination of these echoes produces a meaningful image. The ultrasound technician captures the best images, which are then evaluated by a radiologist, a specialist who analyzes medical images. A testicular tumor will produce different echoes than the surrounding healthy testicular tissue and will therefore stand out against a background of normal tissue.

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Many testicular tumors produce weaker echoes than healthy tissue, and therefore appear lighter than their surroundings. In addition to showing the size of the mass, ultrasound allows the assessment of two features that are key to a cancer diagnosis: 1 whether the mass is within the testis intratesticular or outside of it extratesticular , and 2 whether it is a mass of cells solid or a sac filled with fluid or semisolid material cystic.

If the mass is extratesticular and cystic, it is almost always benign not cancerous. Most extratesticular solid masses and intratesticular cystic masses are benign, but a testicular mass that is intratesticular and solid is usually malignant. Therefore, if a testicular ultrasound shows that a mass is within the testicle and solid, the next step will almost certainly be removal of the testicle for laboratory analysis of the tumor. Tumor Markers in the Blood In addition to having an ultrasound to evaluate a testicular mass, the patient will visit a lab to have blood drawn so it can be analyzed for the presence of tumor markers.

These are molecules produced by certain cancer cells that can be detected in bodily fluids. Removal of the testicle Diagnosis of Testicular Cancer Figure 3. Ultrasound images are made by the varying reflections of high-frequency sound waves. Cancerous tissue reflects these waves differently than noncancerous tissue. Because some testicular cancers do not produce a tumor marker and tumor marker concentration may be low in the early stages of testicular cancer, the absence of a tumor marker does not rule out testicular cancer.

Conversely, because some cells that are not testicular cancer cells can also produce these molecules, the presence of a testicular cancer tumor marker does not confirm testicular cancer. Nonetheless, the presence—and concentration—of one or more of these markers can aid in making a diagnosis of testicular cancer. The type of tumor marker found, or the absence of 39 40 testicular Cancer a tumor marker, is also important in determining the type of testicular cancer an essential part of the diagnosis.

If a tumor marker is found, its concentration indicates the degree to which the disease has advanced. Later, tumor marker concentration can also be used to monitor treatment success. The tumor markers for testicular cancer are alpha-fetoprotein, human chorionic gonadotropin, and lactate dehydrogenase. Alpha-Fetoprotein Alpha-fetoprotein AFP is a protein normally produced by an embryo the developmental stage that encompasses the first eight weeks of pregnancy and, later, the fetus the developmental stage after the eighth week of pregnancy.

The protein is first produced by cells of the yolk sac, a sac attached to the embryo that produces the first blood cells as well as the cells that will eventually develop into gametes cells that unite during sexual reproduction, sperm in males and ova in females. Later in development, AFP is produced by liver cells of the fetus. Scientists are not sure of the function of AFP in the developing baby. From the age of about 8 to 12 months through adulthood, AFP concentrations in the blood are normally low. Like its role in the developing embryo or fetus, the role of AFP in adults—if there is one—is unknown.

Many people are familiar with AFP because of its role as a marker for some birth defects. Diagnosis of Testicular Cancer Although all individuals have small amounts of AFP in their blood serum, in some diseases, such as liver disease and some cancers, AFP concentrations become elevated. Among the few cancers that cause AFP to rise are some forms of testicular cancer. Testicular cancer can occur at any age, and so doctors who are working with a testicular cancer patient who is younger than one year must remember that an elevated AFP concentration is normal in this age group.

Human Chorionic Gonadotropin Human chorionic gonadotropin hCG is a protein that is made by cells of the developing embryo that are known as trophoblasts, and later by cells that develop from trophoblasts: cytotrophoblasts and syncytiotrophoblasts. These cells are part of an embryo-associated membrane known as the chorion, which forms the fetal part of the placenta.

The placenta is the structure made of both fetal and maternal tissue that allows materials to pass between maternal and fetal blood. The alpha subunit is not unique to hCG, but the beta subunit only occurs in the molecule hCG. Its concentration can become elevated in certain diseases, including certain types of testicular cancer. The production of hCG by certain testicular cancers is one reason why some testicular cancers cause enlargement of breast tissue, a condition known as gynecomastia. The presence of this protein in men is a sign of disease, often testicular cancer.

This protein functions as an enzyme, which is a protein that speeds up a particular chemical reaction. LDH is involved in the process by which body cells produce energy from foods. Therefore, the presence of this enzyme in the blood is normal. Its concentration, however, can be elevated when tissue is damaged for example following a heart attack or in certain diseases, such as liver disease and in many types of cancers, including some testicular cancers.

The Orchiectomy and Analysis Often, one or both testes are surgically removed in order to evaluate the tissue. The procedure is called a radical inguinal orchiectomy. To perform an orchiectomy, a small, shallow incision is made in an area of the lower abdomen known as the inguinal region.

This exposes the spermatic cord, which connects the testicle to important structures in the abdomen. The testicle is pulled up from the scrotum into the incision area. The spermatic cord is then tied and cut. The testicle is then analyzed by a pathologist. Histology Testicular tumors are classified by the pathologist largely by gross appearance what the tumor looks like with the naked eye and by histology what the tumor cells, and the tissue[s] into which those cells are organized, look like when the tumor is sliced, stained, and viewed under a microscope.

Pieces of a tumor are thinly sliced and placed on a microscope slide. Because testicular tumors can be made of more than one cell 44 testicular Cancer type, pathologists have to systematically examine tissue from different areas of the tumor to be sure that it has been thoroughly analyzed. The slices are stained with a general tissue stain, usually hematoxylin-eosin. Stains enable the cells—which would not normally stand out from the clear background of the microscope slide—to pick up color so they can be seen.

In a hematoxylin-eosin stain, the cells are first stained with a blue dye hematoxylin and then with a red dye eosin. The two dyes differ chemically, and therefore bind differently to separate cell parts. For example, the nucleus becomes stained a bluish purple color by the hematoxylin, while the cytoplasm becomes stained pink by the eosin. Pathologists are well trained in how normal—and abnormal—testicular cells and tissues stained by hematoxylin-eosin look under a microscope.

As researchers have become aware of specific molecules that are present in some cell types but absent in others, pathologists have been able to use a newer histology method—immunohistochemistry—that uses chemicals that specifically stain, or label, the many copies of a particular molecule in a cell. Only cells with that particular molecule are stained, and the stain occurs in the parts of the cell where those molecules are located. This technique is especially useful for pathologists in evaluating tumors, because cancer cells can often be identified by the molecules they have as well as the molecules they lack.

The staining specificity for immunohistochemistry can be achieved by looking for the molecule in question with a type of molecule known as an antibody. Antibodies are proteins that normally play a part in the immune defense system by binding to molecules on cells and viruses that are not normally found in the body, triggering complex reactions that help to destroy them.

The body has many thousands of different antibodies, and each antibody type is remarkably specific. For example, Diagnosis of Testicular Cancer an antibody that can bind to a molecule unique to the measles virus will not be able to bind to a molecule unique to the chicken pox virus. The immuno in immunohistochemistry refers to antibodies used to probe for the molecule in question, histo refers to the histology technique, and chemistry acknowledges the chemical nature of the molecules and their interactions in the test. For immunohistochemistry, scientists use lab animals, such as mice, to produce antibodies that will bind exclusively to the copies of a specific molecule they want to be able to look for in a cell.

Instead of staining the tissue slices with a stain such as hematoxylin-eosin that will dye most parts of the cell, the tissue slices will be coated with a solution containing these antibody molecules. The antibodies will stick to the tissue only if the tissue contains the appropriate molecule. The cell molecules may have antibodies attached to them, but there is no way to know this because the attached antibodies cannot be seen. Making the antibodies visible can be accomplished in several ways. In the simplest method, before the antibody is added to the tissue slices it is modified by attaching conjugating an enzyme to it.

Once an antibody-enzyme has been allowed to attach to the cells, the tissue is treated with a molecule that the enzyme can break down. It is the breakdown product of this molecule that acts as a dye. As a result, dye is only deposited on cells near the molecule in question. Once a physician suspects testicular cancer, the next steps involve analyzing the testicular mass through ultrasound and the blood for tumor markers AFP, hCG, and LDH that are made by some types of testicular cancer cells.

Once this is determined, the next step is removal of the entire testicle and attached spermatic cord in a surgery known as a radical inguinal orchiectomy. The testicle is then sent to a pathologist where it is analyzed. These procedures will not only confirm a testicular cancer diagnosis, but will determine the type of testicular cancer a patient has. They later move into the scrotum.

Blood, tissue fluid, and sperm move in tubes through the spermatic cords. Leydig cells are found in the interstitium; Sertoli cells and germ cells are in the seminiferous tubules. The patient is also advised about the different types of testicular cancer, either germ cell cancer, the most common type, or non—germ cell cancer. The latter is formed when cells that are not germ cells, such as Sertoli and Leydig cells, develop into cancer cells and form tumors. The physician also talks with the patient about the possibility that his cancer has metastasized to parts of his body outside of the testicle.

Most testicular cancers that spread from their site of origin do so by way of the lymphatic system to lymph nodes, most commonly those that are located in an area at the back of the abdomen known as the retroperitoneum. The physician might also mention that some cases of testicular cancer spread by way of the circulatory system. Understanding the anatomy and workings of the testes, as well as the circulatory and lymphatic systems to which they connect, is essential in order to grasp the complexities of testicular cancer. The Testes, the Scrotum, and the Inguinal Canal The testes are the male reproductive glands, or gonads.

They are key structures in sexual reproduction. These paired, egg-shaped organs produce spermatozoa, commonly known as sperm. Each of these male gametes has the ability to fertilize a female gamete egg cell, ovum to create a zygote, the first cell of the offspring. Testes also produce certain hormones, which are chemicals made by cells that travel through blood The Testes to affect the function of other cells.

The testes are also referred to as male sex glands. The term gland implies that these organs secrete materials. Testes are exocrine glands, which means that they secrete materials in this case sperm through a duct to the outside of the body. They are also endocrine glands, because they secrete materials hormones directly into the bloodstream. Each testis is suspended by its spermatic cord in the scrotum scrotal sac , a skin-covered sac that lies just below the abdomen and behind the penis.

Each also has a piece of tissue—the gubernaculum—that connects it to the inside of the scrotum. These tissues expand to form a pocket-like extension of the abdominal cavity, which becomes the scrotum. The fetal scrotum is connected to the abdominal cavity by tissues that are arranged to form two tubelike passageways known as the inguinal canals.

These connections play an essential role in development: The testes of the fetus develop at the back of the abdominal cavity near the kidneys, outside of and behind a membrane that lines much of the abdominal cavity, known as the peritoneum. This area is known as the retroperitoneum. To move from their location in this retroperitoneal space to the scrotum, the testes must pass through the inguinal canals.

The descent of each testis into the scrotum normally occurs before birth. Each testis moves from the retroperitoneum, through the abdominal opening of the inguinal canal the internal inguinal ring , through the inguinal canal, and out the scrotal opening of that inguinal canal the external inguinal ring to the scrotum. Connective tissue then closes the inguinal canal, separating the abdominal cavity from the scrotum.

Although closure of the inguinal canal prevents materials from moving freely between the abdominal cavity and the scrotum, connections 49 50 testicular Cancer between the two areas of the body must be maintained. With regard to the testes, the following connections are necessary: 1 blood must be able to flow back and forth between the abdominal cavity and the testes; 2 sperm made in the testes must be able to travel to the abdominal cavity where it enters the urethra, a tube that carries it from the body during ejaculation; and 3 excess tissue fluid of the testes, which originates from the fluid part of the blood in the circulatory system, must be able to travel to the abdominal cavity on its journey back to the circulatory system.

The connections between the testes and the abdominal cavity of the body are made by blood vessels, lymph vessels the tissue fluid-carrying tubes of the lymphatic system , and the vas deferens, a sperm-carrying duct. These tubes are tethered together by muscle and connective tissue in a structure known as the spermatic cord, which carries these tubes through the connective tissue of the inguinal canal. Nerves also run between the abdomen and the testes through the spermatic cord. The spermatic cord thus does much more than suspend the testes in the scrotum: It allows for the testes to connect to essential structures in the abdominal cavity.

The spermatic cord is also the conduit for testicular cancer cells to move from the testes to the abdomen and, at times, beyond the abdomen to other body areas. The Anatomy of the Testis The surface of the testis Figure 4. This tough, fibrous layer of connective tissue supportive tissue made primarily of the protein collagen contains embedded muscle cells.

The Testes In the area of the hilus, the tunica albuginea penetrates to the inside of the testis, forming an area rich in connective tissue known as the mediastinum testis. Strands of connective tissue fan out from the mediastinum across the testis to the inside of the tunica albuginea. These provide structural support and divide the inside of the testis into regions known as lobules.


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It is estimated that there are about lobules per testis. To the outside scrotal side of the tunica albuginea is another covering, the tunica vaginalis, a flattened sac with two layers that wrap around much of the testis. The tunica vaginalis partially covers but does not penetrate the testis. This closed sac is actually a remnant of a section of the peritoneum that moves into the scrotum during fetal development. Recall that a condition known as hydrocele can cause scrotal swelling.

In hydroceles, it is the tunica vaginalis that fills with fluid. Each testis lobule contains one to about four sperm-producing tubules known as seminiferous tubules. These are separated by the interstitium, an area of connective tissue with embedded cells: defense cells, connective-tissue making cells, and hormone-producing Leydig cells. Testosterone, the predominant hormone made by the Leydig cell, is required for many aspects of male development especially during fetal development and puberty and function, including sperm production by the seminiferous tubules.

The seminiferous tubules make up approximately 70 to 80 percent of the volume of a testis; the interstitium makes up an estimated 20 to 30 percent of the volume. The interstitium is an important exchange area of the testis: Here, fluid and key molecules enter and leave the blood vessels, and excess tissue fluid enters the lymphatic vessels. Exchange is not limited to liquids. Certain blood cells also have the ability to move from the circulatory system to the tissue fluid to the lymphatic system in the interstitium.

Because a Leydig cell is not a germ cell i. Sperm Production in the Testes Each testis of a male who has gone through puberty has many hundreds estimates range from to more than 1, of U-shaped seminiferous tubules actively engaged in spermatogenesis, the The Testes process by which millions of sperm cells are produced each day. The looped tubules are also coiled; looping and coiling enables more of these important structures to fit into the confined space of the testis.

If stretched out, each tubule would be about a foot or two in length; if the many hundreds of seminiferous tubules from a testis were stretched out and placed end to end, they would cover the length of at least two football fields! Sperm production occurs along the entire length of a seminiferous tubule.

Seminiferous tubules have walls that surround the open area in the center, called the lumen. Sperm made in the wall, along with fluid that enables these cells to be moved through the tubule, are released into the lumen of the tubules. The walls of the seminiferous tubules are made of cells dedicated to sperm production the germinal epithelium and underlying supportive tissue.

The cells of the germinal epithelium of the seminiferous tubule walls are of two types: germ cells cells in various stages of sperm development and Sertoli cells cells that aid developing germ cells.

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The rest of the seminiferous tubule is made of supportive tissues that surround the germinal epithelium. Immediately underlying the germinal epithelium is the basement membrane. The tissue layer is made of structural molecules, such as the protein collagen, that physically support the germinal epithelium and also connect it to the underlying loose connective tissue, the peritubular tissue literally, tissue around the tube.

This tissue, which is also composed of molecules such as collagen, plays a structural role. Cells that can produce connective tissue molecules are present in the peritubular tissue, and researchers are learning that these cells also communicate with—and influence—cells of the germinal epithelium. These testis cells and the many other non—germ cells have a variety of functions, all of which are directed at assisting in the primary function 53 54 testicular Cancer Figure 4.

The center of each seminiferous tubule is filled with developing sperm, of which the tails can be seen blue. Spermatozoa, or sperm cells Some of these germ cells develop into germ cell tumors. Evidence gathered by researchers indicates that cells early in the germ cell developmental pathway are the ones that become cancer cells, but this remains an active area of investigation.

One of the challenges faced by scientists is that there is still much to be learned about the many changes that occur as these cells proceed along the normal development pathway: from primordial germ cell formation to mature sperm. The process of spermatogenesis begins in puberty as spermatogonia divide by a process known as mitosis to produce two cell types: 1 cells that are copies of the original cell which ensure that the supply of stem cells will not be depleted and 2 cells that will develop into primary spermatocytes.

A primary spermatocyte undergoes two rounds of a special type of cell division called meiosis. The first division of the primary spermatocyte produces two secondary spermatocytes. Each secondary spermatocyte undergoes division to produce two cells called spermatids. Thus, each primary spermatocyte ultimately produces a total of four spermatids. The arrangement of germ cells in the germinal epithelium reflects the stages of their development: spermatogonia lie in the outer region of the germinal epithelium farthest from the lumen and closest 55 56 testicular Cancer to the basement membrane , the spermatocytes are closer to the lumen, and the spermatids are closest to the lumen.

Meiosis is the type of cell division that produces gametes, sperm in males and eggs in females. The result of division by meiosis rather than by mitosis is that the spermatids have half the number of chromosomes as the primary spermatocytes, 23 instead of This halving of the number of chromosomes is essential for successful sexual reproduction; if it did not occur, the amount of chromosomal DNA would double in each successive generation.

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The process of meiosis is precise, and the number of chromosomes is not randomly cut in half. Like all of the body, or somatic cells, each primary spermatocyte is diploid, meaning it has two copies of each chromosome, one from the mother maternal and the other from the father paternal. Imagine that there are 23 pairs of chromosomes, each carrying a sign with a numeral from 1 to The cell would have two chromosomes marked 1, two chromosomes labeled 2, and so on through chromosome pair Meiosis ensures that each cell will get one of each chromosome 1 through Meiosis reduces the chromosome number so that each spermatid is haploid, having only one copy of each chromosome.

It is in the zygote stage, after the maternal and paternal DNA have come together, that the diploid number is restored.

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Each spermatid develops into a sperm cell by a process known as spermiogenesis, a process of cell differentiation i. The entire process—from primary spermatocyte to mature sperm— takes about 60 days. The Testes 57 Sertoli Cells Sertoli cells assist in many ways with the development of sperm cells. These large cells span the germinal epithelium, from the basement membrane to the lumen, and lie side by side, forming a continuous layer of cells around the tubule.

The sides of the Sertoli cells are attached tightly to each other by specialized connections, preventing fluid, dissolved molecules, and cells from moving between the Sertoli cells. As a result, molecules must pass through the cytoplasm of Sertoli cells to move from the lumen-side of Sertoli cells to the basement membrane-side of Sertoli cells. This lack of free movement of materials between cells is an important contributor to the blood-testis barrier, a system that restricts access to the developing sperm cells by molecules and immune cells from the blood and prevents sperm cells from gaining access to immune cells.

Germ cells develop in pocketlike projections of the Sertoli cells, moving closer to the lumen as they mature. This requires breaking and reforming of the connections between Sertoli cells. Sertoli cells secrete a variety of molecules, including androgen-binding protein that concentrates testosterone, and hormones; they also engulf spermatid cytoplasm and secrete the fluid that helps carry sperm through the seminiferous tubule. Sertoli cells are capable of developing into cancer cells. Because a Sertoli cell is not a germ cell, a Sertoli cell cancer is considered a non—germ cell cancer.

This collects sperm and fluid from all of the seminiferous tubules and is located in the mediastinum testis. Although rare, cells of the rete testis can become cancer cells, resulting in cancer of the rete testis. The Testes Sperm leave the rete testis and the testis itself at the hilus by way of 6 to 12 small tubes known as efferent ductules.

These carry the sperm to the epididymis, a collection tube that lies just outside the testis. The highly coiled epididymis which would be about 16 feet if stretched out runs along the back of the testis. In the first section, much of the fluid produced in the seminiferous tubules is reabsorbed, concentrating the sperm. The rest of the epididymis serves as more than a simple conduit for sperm: It is where the sperm mature to the point at which they are able to successfully fertilize an ovum.

Sperm are also stored in the epididymis until they leave the scrotal area to be released from the penis through ejaculation. Sperm leave the epididymis by way of the vas deferens, which carries sperm from the scrotum, through the inguinal canal, and into the abdominal cavity. In the male sterilization procedure known as a vasectomy, the vasa deferentia—one vas deferens on each side of the body—are cut. In the abdominal cavity, the vas deferens loops up and over the bladder, the structure that stores urine. Sperm are propelled through the vas deferens by contractions of the muscles that surround the tube.

Just near its end, the vas deferens is renamed the ejaculatory duct. The short ejaculatory ducts on each side of the body join with the urethra—the tube that carries urine from the bladder. The urethra serves two important functions: It delivers sperm and urine at separate times to the outside of the body through the penis. The urethra is the first—and only—tube where sperm traveling from the right testicle and sperm traveling from the left testicle join. All the other tubes through which sperm travel are present on both sides of the body. From there the sperm will finish developing and be stored in the epididymis.

Fluid, known as seminal fluid, is added to the sperm in the vas deferens and the urethra by specialized glands. The combination of sperm and seminal fluid, the material released from the urethra during ejaculation, is known as semen. The Testes 61 The Circulatory System and the Testis The circulatory system carries blood through blood vessels arteries, arterioles, veins, venules, and capillaries that are distributed throughout the body. Blood consists of fluid plasma , red and white blood cells, and platelets. Important molecules, such as nutrients and hormones, are carried in the plasma.

Under pressure from the pumping heart, blood is pushed through arteries and the smaller arterioles, tubes that carry blood away from the heart, eventually reaching the capillaries, the vessels of the body that exchange materials with body tissues. This exchange is possible because capillaries have thin walls, made only of a single layer of cells known as endothelial cells.

Plasma and at times white blood cells leaves the blood by passing between endothelial cells, allowing the fluid now referred to as tissue fluid to bathe body tissues. Molecules can then be exchanged between the cells of the body tissues and the tissue fluid. Much of the tissue fluid is eventually returned to the circulatory system, moving back into the capillaries.

From capillaries, the fluid travels in venules to larger veins back to the heart. The blood supply for the testes comes largely from the testicular arteries. They are then routed through the spermatic cord; the right testicular artery delivers blood to the right testis and the left testicular artery delivers blood to the left testis. Once at the testis, the artery branches, supplying all areas of the testis.

Many of the branches travel along connective tissue to the individual lobules. Capillaries in the interstitium exchange with the local tissue fluid. Although some of these 62 testicular Cancer capillaries are near the seminiferous tubules, the seminiferous tubules do not have their own capillary supply: Exchange occurs with the capillaries of the interstitium. Fluid and molecules reenter the capillaries and move to venules, then to larger veins.

The veins that leave the testis join other veins to form a network of veins in the spermatic cord known as the pampiniform plexus. From the plexus, two testicular veins enter the retroperitoneum where they return blood to the inferior vena cava—the main vessel that returns blood to the heart from the lower part of the body—or to a branch of the inferior vena cava. The Lymphatic System and the Testis Although most tissue fluid eventually returns to the circulatory system through capillaries, about 1 percent does not.

This excess fluid enters another system of the body: the lymphatic system. Like the circulatory system, the lymphatic system has vessels through which fluid moves. But unlike the circulatory system, these vessels do not form a continuous loop. Rather, lymph capillaries of this one-way system pick up fluid which at this point is referred to as lymph from tissues. They then join progressively larger vessels lymph veins and ultimately a large vessel—a duct—through which the fluid is returned to the circulatory system.

In the lymphatic system, there is no heart that pumps, there are no arteries or arterioles, and capillaries only collect fluid from the tissues. The lymphatic system contributes to this defense in two important ways: The Testes 1. Lymph vessels empty lymph into one end of a lymph node. The lymph moves slowly through the meshlike node, eventually leaving through a lymph vessel on the opposite side. The lymph node is more than a mechanical filter. Cells in a lymph node trap, destroy, and become activated to destroy microbes and cancer cells.

Some cancer cells trapped by lymph nodes survive and multiply within the node, but without the lymph nodes, these cancer cells would enter the bloodstream unchecked. In the testis, many lymph capillaries, like the blood capillaries, are located in the interstitium.

They join others, leaving the testis as larger lymphatic vessels at the hilus. They enter the spermatic cord, then travel to the retroperitoneal cavity. From there, vessels join a long and much larger vessel, the thoracic duct, which returns lymph to the left subclavian vein, located near the heart. Testicular cancer cells that are picked up by lymphatic capillaries in the testes first encounter lymph nodes in the retroperitoneal cavity.

These retroperitoneal lymph nodes are therefore usually the first landing sites for testicular cancer metastases. As development proceeds, they move through the inguinal canals into the scrotum. Each remains connected to the abdomen through its spermatic cord. The spermatic cord contains blood vessels, lymph vessels, and a tube that carries sperm from the 63 64 testicular Cancer testes. Sperm are made in the testes in long tubes known as seminiferous tubules.

Production of sperm takes many weeks, and is a stepwise process that involves cell division and cell changes. Sertoli cells, located in seminiferous tubules, help in the process of sperm development. Leydig cells, located in tissue between seminiferous tubules, produce the hormone testosterone. They are classified with the nonseminomatous germ cell cancers because of the way they respond to available treatments.

There are many different types of testicular cancer. Most testicular cancers are germ cell cancers; in males who have gone through puberty, more than 90 percent of testicular cancers fall into this category. There are many different types of germ cell cancer. The type of germ cell tumor GCT a patient has is determined in the laboratory. The pathologist determines the way the tumor looks to the eye as well as histologically, when stained slices are examined under a microscope.

Immunohistochemistry can add important diagnostic clues by showing whether certain cell-specific molecules are present. Serum tumor marker information can also assist in tumor identification. Germ cell tumor classification has changed over time, and there is variation in how GCTs are classified from one part of the world to another. In the WHO system, GCTs are classified as either pure composed of one histological—or tissue—type or mixed composed of more than one histological type. The pure histological types of GCTs are seminoma, spermatocytic seminoma, embryonal carcinoma, yolk sac tumor, trophoblastic tumors, and teratoma.

Mixed GCTs are made up of varying combinations of these types. Germ Cell Cancers For testicular cancers other than seminoma and spermatocytic seminoma, the transformed cell types become very different from germ cells. They change to take on some properties that are similar to cells of early embryos as in embryonal carcinoma ; more developed embryos, fetuses, and adults as in teratoma ; or extraembryonic membranes, structures that are attached to an embryo and assist in its development as in yolk sac tumor and trophoblastic tumors. As the blastocyst implants into the lining of the uterus, the chorion develops to form two placenta-producing layers the cytotrophoblast and the synctiotrophoblast.

The inner cell mass forms two layers: the endoderm and the ectoderm. Later, a third layer, the mesoderm, will form. Trophoblasts, cytotrophoblasts, and synctiotrophoblasts secrete hCG. Later in embryonic development, a well-developed yolk sac appears. The placenta, the structure that connects and exchanges materials between the fetus and the mother, is also well developed.

The yolk sac and chorion are both extraembryonic membranes, structures that are attached to a developing embryo and assist in its development.

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Physicians and researchers group these different tumor types into two categories: seminomatous GCTs seminomas and nonseminomatous GCTs nonseminomas. Seminomas respond to radiation and chemotherapy, while nonseminomas respond only to chemotherapy and often require more aggressive treatment.

Seminomatous Germ Cell Cancers 69 GCTs include seminoma sometimes referred to as classic seminoma and the less common and quite different spermatocytic seminoma. Because spermatocytic seminoma is so different, often the term seminomatous GCT is used to refer only to seminoma. Some mixed GCTs have seminoma as a component. Funded projects. Men's Health Partners. We monitor this through report cards which detail what we seek to achieve, key measures and the impact.

Prostate Cancer. Our disruptive funding approach identifies revolutionary ways to accelerate health outcomes by creating strong, global collaborative teams. Colleen Nelson, Global Scientific Chair. Men's Health. Mental health and suicide prevention. Testicular Cancer. Australia AUD 1,, Australia AUD , United Kingdom GBP 98, Advanced Prostate Cancer Consensus Conference. Sertoli cells, located in seminiferous tubules, help in the process of sperm development. Leydig cells, located in tissue between seminiferous tubules, produce the hormone testosterone.

They are classified with the nonseminomatous germ cell cancers because of the way they respond to available treatments. There are many different types of testicular cancer. Most testicular cancers are germ cell cancers; in males who have gone through puberty, more than 90 percent of testicular cancers fall into this category. There are many different types of germ cell cancer. The type of germ cell tumor GCT a patient has is determined in the laboratory. The pathologist determines the way the tumor looks to the eye as well as histologically, when stained slices are examined under a microscope.

Immunohistochemistry can add important diagnostic clues by showing whether certain cell-specific molecules are present. Serum tumor marker information can also assist in tumor identification. Germ cell tumor classification has changed over time, and there is variation in how GCTs are classified from one part of the world to another. In the WHO system, GCTs are classified as either pure composed of one histological—or tissue—type or mixed composed of more than one histological type. The pure histological types of GCTs are seminoma, spermatocytic seminoma, embryonal carcinoma, yolk sac tumor, trophoblastic tumors, and teratoma.

Mixed GCTs are made up of varying combinations of these types. Germ Cell Cancers For testicular cancers other than seminoma and spermatocytic seminoma, the transformed cell types become very different from germ cells. They change to take on some properties that are similar to cells of early embryos as in embryonal carcinoma ; more developed embryos, fetuses, and adults as in teratoma ; or extraembryonic membranes, structures that are attached to an embryo and assist in its development as in yolk sac tumor and trophoblastic tumors.

As the blastocyst implants into the lining of the uterus, the chorion develops to form two placenta-producing layers the cytotrophoblast and the synctiotrophoblast. The inner cell mass forms two layers: the endoderm and the ectoderm. Later, a third layer, the mesoderm, will form. Trophoblasts, cytotrophoblasts, and synctiotrophoblasts secrete hCG.

Later in embryonic development, a well-developed yolk sac appears. The placenta, the structure that connects and exchanges materials between the fetus and the mother, is also well developed. The yolk sac and chorion are both extraembryonic membranes, structures that are attached to a developing embryo and assist in its development.

Physicians and researchers group these different tumor types into two categories: seminomatous GCTs seminomas and nonseminomatous GCTs nonseminomas. Seminomas respond to radiation and chemotherapy, while nonseminomas respond only to chemotherapy and often require more aggressive treatment. Seminomatous Germ Cell Cancers 69 GCTs include seminoma sometimes referred to as classic seminoma and the less common and quite different spermatocytic seminoma. Because spermatocytic seminoma is so different, often the term seminomatous GCT is used to refer only to seminoma.

Some mixed GCTs have seminoma as a component. Why, then, are all mixed GCTs—regardless of the presence of seminoma—classified as nonseminomas? The reason is related to treatment: If the tumor is treated as a nonseminoma, both the seminoma and the nonseminomatous component will respond; if the tumor is treated as a seminoma, only the seminoma component will respond.

Germ Cell Tumors in Boys and Older Men Most individuals who develop testicular cancer do so between the onset of puberty and their mid-forties. But testicular cancer can also occur in boys males before puberty and older men. For all age groups, the most common type of tumor is a GCT, although these represent a smaller fraction—only about two-thirds—of the testicular tumors in boys.

The distribution of GCT types differs among age groups. Spermatocytic seminoma occurs mostly in men older than 50, and it never occurs in men younger than In adults, the most common GCTs are seminoma about 50 percent of the cases , mixed GCT a little less than 50 percent , and embryonal carcinoma less than 10 percent. In boys, yolk sac tumor and teratoma are the most common GCT types, while seminoma and embryonal carcinoma occur only rarely.

The differences are not just in tumor incidence. Scientists have discovered that there are genetic differences between GCT cells that occur in boys, those that occur in men, and spermatocytic seminoma. The term extragonadal implies that these primary tumors tumors that have developed in—rather than metastasized to—a location occur outside the gonad.

At times, a physician may discover that the mass is not a true EGGCT because a small mass can actually be found in the testicle. A commonly accepted explanation for the presence of these tumors is that an error occurred during migration of primordial germ cells in the fetus; instead of migrating from the yolk sac to the primitive testis developing in the abdomen, the germ cells traveled to a different area, such as the mediastinum.

But researchers are exploring other hypotheses. One is that cells in a testis that have started to, but not yet, become cancer cells migrate from the testes to other areas; only when they reach these other areas do they become cancer cells. Brian Piccolo, football player for the Chicago Bears, died in at the age of 26 of embryonal carcinoma that originated in the mediastinum. Thankfully, advancements in the treatment of this type of cancer have been made since the s. Germ Cell Cancers 71 It appears that GCTs in these three categories have different causes and pathways of development.

There are also interesting differences between teratomas that occur before and after puberty. Teratoma in children is always benign—it does not invade neighboring tissues or spread to other parts of the body by metastasis. In adults, teratoma can be benign but it can also be malignant, spreading to nearby tissues and capable of spreading to distant sites. An additional age-related difference is that teratoma in children is almost always a pure tumor, while in adults it is usually found as a component of a mixed GCT.

The reasons for these differences are not understood. Seminoma Seminoma classic seminoma is the most common type of GCT found in adults. Seminoma is rarely found in boys, and occurs mostly in men in their mid-thirties to mid-forties. This is later in life than adult nonseminomas tend to occur. The main symptom for most seminoma patients is an enlarged but pain-free testicle. A small percentage of seminoma patients may also have enlarged breast tissue gynecomastia. If the tumor has metastasized, symptoms may be felt in parts of the body to which the cancer has spread, most commonly the abdomen.

For most patients, however, the tumor has not metastasized at the time of diagnosis. Sometimes the tumor will spread locally to nearby structures such as the epididymis or spermatic cord. Seminoma spreads to distant areas through the lymphatic system: first to retroperitoneal lymph nodes, and later to lymph nodes in the middle of the chest mediastinal and 72 testicular Cancer above the collarbone.

The disease can spread further still by way of the circulatory system, to sites such as the liver, lung, and bones. In some cases, seminoma cells secrete hCG, which is detectable in low concentration in the blood. Seminoma cells never secrete AFP, which is an important factor in certain diagnoses. For example, if the histology shows pure seminoma but blood tests show elevated concentrations of AFP, a doctor will know that the tumor is not seminoma, but actually a mixed GCT nonseminoma that will require different treatment.

When a pathologist cuts into a seminoma tumor, it appears light in color. There is no significant necrosis dead tissue or hemorrhage bleeding. The tumor is homogeneous, meaning that different areas of the tumor are similar in appearance. After staining the sample with hematoxylin-eosin, microscopic examination shows that the cells are organized to form sheets of neatly arranged cells, commonly in clusters that are separated by connective tissue in which many white blood cells, especially lymphocytes, have gathered.

Neighboring cells do not overlap. The cells are fairly uniform in appearance, and cell features such as a cell membrane, cytoplasm, and nucleus with one or more nucleoli are easily seen. A challenge for pathologists is the existence of forms of seminoma that vary in cell characteristics and cell arrangement and differ from the normal microscopic appearance. Some variants may look like other tumor types. In one variant, syncytiotrophoblasts, large cells with many nuclei per cell, are found among the typical cells.

Spermatocytic Seminomas Spermatocytic seminoma is not a variant of seminoma; it is a unique type of GCT. It accounts for only a small percentage of testicular Germ Cell Cancers 73 cancers. Most commonly, the disease occurs in men older than It occasionally occurs in younger men, but not in those under Unlike other histological types, spermatocytic seminoma is never a component of GCTs.

Feelings for Testicular Cancer

The primary symptom is a painless mass in the testis. The tumor may invade local tissues such as the epididymis, but it rarely metastasizes. The cut surface of the tumor is light in color, and some tumors may have small areas of necrosis or hemorrhage. Microscopically, one characteristic of spermatocytic seminoma is the presence of three cell types that differ in size: small, intermediate the predominant cell type , and large. These cells are not arranged in well-organized sheets as in seminoma. Groups of cells are often separated by areas that have only a small amount of connective tissue and may be filled with fluid.

Even though prognosis is usually excellent, on occasion, parts of the tumor change to form a sarcoma, a connective-tissue-like tumor. The sarcoma may metastasize to the retroperitoneum and organs. Currently, prognosis for these patients is poor. Embryonal Carcinoma Embryonal carcinoma is the most common nonseminomatous, pure GCT in adults, but it is much less common than seminoma and mixed GCTs, accounting for less than 10 percent of adult GCTs. It tends to occur in men between their mid-twenties and mid-thirties, about 10 years earlier than seminoma.

It rarely occurs before puberty and is a component of more than 80 percent of mixed GCTs. Embryonal carcinoma is usually noticed because of a mass in the testis. Often, but not always, the mass is painless. Gynecomastia may 74 testicular Cancer occur. Many patients have metastases at the time of diagnosis and may have symptoms resulting from the spread to lymph nodes or organs. Sometimes the cancer invades local structures such as the epididymis and spermatic cord.

It metastasizes via the lymphatics to the retroperitoneal and mediastinal lymph nodes. At times, it may spread through the blood, often to the lungs. Some tumors make hCG, which can be detected in the blood serum. When a tumor of this type is examined in the lab, large areas of necrosis and hemorrhage are typically seen. Microscopically, the cells are large and have different shapes and they tend to overlap.

Many cells appear to be in the process of division, and abnormalities in the division process can be seen. Syncytiotrophoblasts may be present. Embryonal carcinoma cells are undifferentiated—they are not mature cells with a set function. Many of the cells look like epithelial cells, which cover surfaces of the body; in some areas, they are even arranged like epithelial cells around cavities, forming structures that look roughly like glands. Embryonal carcinoma cells can be arranged in many different patterns, and a pathologist must be able to recognize them all.

Yolk Sac Tumor Yolk sac tumor is the most common testicular cancer in children. The name comes from the fact that the tumor has characteristics—such as AFP production—that are similar to the embryonic yolk sac. It occurs in boys from infancy to age 11; the median age is about 16 months. Yolk sac tumor also appears in adults, but almost always as a component of mixed GCTs.

About 40 percent of mixed GCTs contain yolk sac tumor. For example, what if the pathologist wants to determine if a tumor is seminoma or embryonal carcinoma? Cells of these two cancers have many molecules in common, including a surface protein known as placental alkaline phosphatase PLAP. Detection of such molecules cannot help tell the two cancer types apart. However, the cells of the two cancers differ in the presence of other surface molecules, such as c-Kit, Ki-1, and podopladin. The difference in the presence of these proteins can help tell the two cancers apart: Seminoma cells, but not those of embryonal carcinoma, have c-Kit and podopladin on the surface; embryonal carcinoma cells, but not those of seminoma, have Ki Scientists continue to look for cellular molecules that can identify particular cancer cells.

They are also interested in gaining a better understanding of the normal roles of these proteins, as well as their relationship to the development of particular cancers. PLAP is an enzyme that is normally made by trophoblasts of the chorion. The normal function of podopladin is unclear, but it has been found in fetal germ cells, and has been suggested to play a role in fetal germ cell development.

Ki-1 and c-Kit are receptor molecules; each allows the cell to detect and respond to a particular outside chemical signal. These are normally made by certain blood cells. In about 10 to 20 percent of children, the tumor has metastasized at time of diagnosis. Metastasis may occur via the lymphatics to the retroperitoneal lymph nodes.

Often, however, spread is through the blood only; for these patients, the first site of metastasis is often the lungs. When the tumors are large, necrosis and hemorrhage are often present. Two tumor features that can be seen microscopically are crucial to diagnosis: the presence of multiple histological patterns characteristic cell arrangements in a single tumor, and the presence of structures known as Schiller-Duval bodies, collections of cancer cells that surround fingerlike, blood-vessel containing projections of connective tissue.

Commonly, hyaline globules, collections of AFP or another protein normally produced by the yolk sac, are also present. Choriocarcinoma Almost all trophoblastic tumors fall into the category of choriocarcinoma. The name comes from its similarity to the chorion, which forms the fetal part of the placenta. Choriocarcinoma occurs only very rarely less than 1 percent of cases in pure form.

Most men diagnosed with this form of cancer are in their teens and twenties. Choriocarcinoma occurs in about 8 percent of mixed GCTs. Choriocarcinoma spreads rapidly and widely, and has the worst prognosis of all the germ cell cancers. Germ Cell Cancers 77 Choriocarcinoma differs from other germ cell cancers in presentation: Most patients seek medical help from the symptoms of metastasis and not the tumor itself.

Often, by the time of diagnosis, the tumor has regressed shrunk. Choriocarcinoma spreads through the blood to the lungs and often to the liver, gastrointestinal tract, brain, and other organs. It also spreads through the lymphatic system to the retroperitoneal lymph nodes. Symptoms include shortness of breath, coughing up or vomiting blood, and dark stools due to gastrointestinal bleeding.

Bleeding can occur in many areas of the body, causing anemia too few red blood cells. Neurological problems that result from spread to the brain can also occur. The high concentrations of hCG may cause gynecomastia and an underactive thyroid a gland that controls metabolism. Microscopically, choriocarcinoma has two main cell types: syncytiotrophoblasts and cytotrophoblasts. These cells are arranged in varying patterns. The two cell types normally compose the placentaforming extraembryonic membrane known as the chorion. Like trophoblast cells of the chorion, these cells produce large quantities of hCG.

While hCG is sometimes produced in other types of testicular cancer, it is always secreted in large concentrations in choriocarcinoma. Teratoma The word teratoma comes from the Greek word for monster teraton and reflects the fact that the tumor is an odd conglomeration of recognizable tissues. Although not in testicular cancer, other types of teratomas can actually have hair and teeth.

Teratoma occurs frequently as part of mixed GCTs in adults; about half of these tumors contain teratoma. Pure teratoma occurs more commonly in children. Some feel that the pediatric percentage is underreported because teratoma is benign in this population. Most teratomas in children occur in those younger than four years of age, and most often in one- and two-year-olds. There are two types of teratoma: mature and immature. A mature teratoma has adultlike, differentiated cells only. Usually several types of tissue are present in one tumor. For example, tumors might have neural tissue, bone, and cartilage.

An immature teratoma may also have adultlike differentiated cells, but less differentiated cells more embryonic, or fetal-like are also present. These less-differentiated cells, however, are more differentiated than those seen in embryonal carcinoma. Some teratomas have tissues from only a single germ layer monodermal teratoma , while others have tissues from two, or all three, germ layers. What is a germ layer? As normal embryonic development proceeds, cells of the inner cell mass begin to differentiate, taking on specific structures and roles. As part of this process, three layers of tissue germ layers form in the embryo: the ectoderm, the endoderm, and the mesoderm.

The ectoderm is on the outside and will eventually develop into adult structures such as the epidermis outer skin layer and nervous system. The endoderm is on the inside and will develop into adult tissues that line body cavities such as the lungs and digestive tract. The mesoderm, in the middle, will develop into tissues such as muscle and bone. The difference between pre- and postpuberty teratomas is that most teratomas that occur before puberty are mature, while most that occur after puberty are immature.

Both immature and mature adult teratomas can metastasize. Germ Cell Cancers Figure 5. Each teratoma cell shown here has a large, irregular-shaped nucleus brown. In children, because there is never metastasis, the only symptom is a testicular mass. Adults may present with a mass or symptoms of metastasis. The pathologist will note that the cut tumor surface is not homogenous—different tissue types can be seen in different areas of the tumor. Cysts filled with fluid of different consistencies are commonly found. At times, these different tissues can be seen arranged to form primitive organlike structures, such as skin.

Synctiotrophoblasts may be present. Any of the different GCT types, with the exception of spermatocytic seminoma, may be present in a single tumor. More than 80 percent of mixed GCTs have embryonal carcinoma as one of the components, and about half contain teratoma. Yolk sac tumor and seminoma occur less frequently, but are still commonly found.


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Choriocarcinoma is found in less than 10 percent of the mixed GCTs. The different tumor types vary in aggressiveness, metastasis locations, and treatment sensitivity, and so it is important for the pathologist to list the different tumor types and to estimate the percentage of each. This information will affect treatment decisions. The type of GCT a patient has is determined by analysis of the tumor in the pathology lab and by the presence or absence of certain tumor markers in the blood. It is important to diagnose the type of GCT accurately because they may require different treatment.

Seminomatous GCTs are of two types: seminoma classic Germ Cell Cancers seminoma and spermatocytic seminoma, which occurs in older men. Nonseminomatous GCTs include embryonal carcinoma, yolk sac tumor, trophoblastic tumors primarily choriocarcinoma , and teratoma. These tumors some of which may contain seminoma are classified as nonseminomatous for treatment purposes. In boys, yolk sac tumor and teratoma are prevalent. Many of the malignant forms carry a poor prognosis.

Testicular tumors that arise from cells that support germ cells or play other roles in testicular function—non-germ cell testicular tumors—occur much less frequently than their germ cell tumor counterparts. Testicular tumors that do not arise from germ cells represent a greater 82 Non-Germ Cell Testicular Cancers 83 proportion of testicular tumors in children than in adults. Some of these tumors are benign, but others are malignant. Unfortunately, the great success in the treatment of germ cell tumors has not been replicated for non-germ cell tumors, and many still carry a poor prognosis.

There are many different types of non-germ cell tumors; in this chapter, Leydig cell tumors, Sertoli cell tumors, carcinoma of the rete testis, and testicular lymphoma are described. About 25 percent of LCTs occur in children, generally between the ages of 5 and 10, and are benign.

About 10 percent of adult LCTs are malignant. Malignant LCTs respond poorly to existing treatments, so prognosis is poor. LCTs produce sex hormones predominately testosterone, and at times estrogen , which in many cases cause body changes. These changes may appear when the tumor is small, before it can be felt in the testis. If a testosterone-producing tumor occurs in someone who has not yet gone through puberty, it will most likely cause precocious, or early, puberty. The hormonal effects of such a tumor are usually not noticed postpuberty because of background testosterone.

If an estrogen-producing tumor occurs before puberty, symptoms such as gynecomastia and poor development of the gonads and genitals may occur. Postpuberty, symptoms include gynecomastia, decreased libido, and erectile dysfunction. Even after tumor removal, these effects from estrogen may persist.

The most common type is 84 testicular Cancer Figure 6. Some testicular tumors produce excess amounts of this hormone. In some cases, LCCSCT occurs as part of a syndrome, such as Peutz-Jeghers, a rare genetic disorder in which patients develop intestinal polyps and have a greatly increased risk of developing various cancers. Non-Germ Cell Testicular Cancers 85 Rete Testis Carcinoma Rete testis carcinoma is a rare tumor that arises in the sperm-collecting ducts of the testis. These tumors most commonly occur in elderly men, but are not restricted to this age group.

Prognosis is poor. When the initial site is the testis, the lymphoma is referred to as primary testicular lymphoma. In adults, the most common form that occurs in the testis involves a type of lymphocyte known as a B cell—a cell that normally matures to secrete defensive proteins known as antibodies. Most primary testicular lymphomas are unilateral, meaning that one testicle is affected, but some are bilateral, meaning that both testes are affected. Primary testicular lymphoma accounts for 3 to 5 percent of testicular tumors; as with GCTs, however, the incidence of this disease appears to be increasing and it is not known why.

Testicular lymphoma is the most common type of testicular cancer in older men. Prognosis is usually poor. SUMMA RY Cells of the testis that are not germ cells, but rather support germ cells or have other functions in the testis, can also form tumors. These are referred to as non-germ cell tumors. They are much less common than GCTs, but they make up a greater proportion of testicular tumors in children than in adults. Non-germ cell cancers have not shared the treatment success 86 testicular Cancer Figure 6. Lymphomas, or cancers of the lymphocytes, can occur in the testes and are known as primary testicular lymphomas.

Non-germ cell tumors include Leydig tumors, Sertoli cell tumors, carcinoma of the rete testis, and primary testicular lymphoma. He also underwent chemotherapy. The treatments of all of these individuals began with an orchiectomy. Why was there such variation in the treatments that followed? The initial step in the treatment and diagnosis of testicular cancer is the orchiectomy.

Once this has been done, the decision about which additional procedures to use for a given patient is based on the type of cancer the patient has and the cancer stage—the extent to which the cancer has advanced and the locations to which it has spread. There is some variation among physicians in treatment preferences; variation also arises as a result of patient decisions about their treatment options.

Because his disease was not advanced at the time of diagnosis, he did not need additional surgery or chemotherapy. Follow-up treatment for Scott Hamilton and Lance Armstrong did not involve radiation because they were diagnosed with nonseminoma, which is not sensitive to radiation.

Because of the extent to which their cancers had spread, both chemotherapy and surgery were needed. Variation in the body locations to which their cancers had spread the result of differences in the composition of their tumors meant different follow-up surgeries.

Hence, he did not need retroperitoneal lymph node removal, but he did require surgery to remove cancer that had spread to his brain. Each of the three stages is broken down further into subcategories i. The process of determining the cancer stage is referred to as cancer staging. In cancer staging, information about serum blood fluid tumor marker concentration is gathered, as well as information about whether the tumor has spread to tissues near the testis, to the regional lymph nodes, or to more distant sites.

The staging system used to determine the extent of cancer spread is known as the TNM tumor-node-metastasis system. In this system, T stands for the spread of the tumor to nearby structures, such as the tunica vaginalis and the spermatic cord; N stands for metastasis to regional usually retroperitoneal lymph nodes; and M stands for metastasis of the cancer to nonregional distant lymph nodes or organs, such as the lungs and brain.

Cancer staging requires blood work to determine tumor marker concentration; analysis in the pathology lab of the testicle and structures near it e. In addition to using the CT scan to determine whether there is metastasis to retroperitoneal lymph nodes, the determination is at times based on analysis in the pathology lab of surgically removed lymph nodes. Table 7. In stage I, the cancer is restricted to the testis or surrounding tissues. In stage II, the cancer has spread to the regional usually retroperitoneal lymph nodes, but no further. In stage III, the cancer has spread beyond the regional lymph nodes or tumor marker information suggests that it might have.

When the cancer stage is determined by information gained by tissue analysis in the pathology lab, the term pathologic stage is used. Otherwise, the term clinical stage is used. The pathologic stage is more accurate. Retroperitoneal Lymph Node Dissection Testicular cancers spread in a predictable manner. In most cases, the first site of metastasis is the lymph nodes in the retroperitoneum. This predictability is good news for testicular cancer treatment, because it means that if the cancer has spread only as far as the retroperitoneum, orchiectomy followed by surgery to remove the retroperitoneal lymph nodes—a retroperitoneal lymph node dissection RPLND —can often cure the disease.

Lymph nodes in the retroperitoneum are grouped according to location within the retroperitoneum. The surgeon decides which groups of retroperitoneal lymph nodes to remove and all of the lymph nodes in those groups are removed, even if some of the individual lymph nodes do not appear to be affected. RPLND is a treatment option for patients in clinical stage I imaging studies show no spread to the retroperitoneum or clinical stage II Treatment of Testicular Cancer 91 imaging studies show spread to the retroperitoneum who have nonseminomatous germ cell tumors NSGCTs.

The answer lies in the limitations of the CT scan used to determine spread to the retroperitoneal lymph nodes. Clinical stage I does not mean that the cancer has not spread to the retroperitoneum; rather, it means that imaging studies do not show that it has spread to the retroperitoneum. Physicians have found that it is not uncommon for the pathology lab to find metastasis to one or more nodes of clinical stage I patients. These patients were understaged by the CT scan; they were actually in pathologic stage II and not clinical stage I.

Staging errors can occur in the opposite direction as well. Some patients who are placed in clinical stage II based on the CT scan are found to have no metastasis to the retroperitoneal lymph nodes on laboratory examination of the nodes. As more physicians began to use the technique and scientists learned more about which lymph nodes could become involved by metastasis, the procedure evolved to increase the number of lymph nodes removed. By the late s, the procedure involved removing lymph nodes from both sides of the retroperitoneum bilateral RPLND , including those 92 testicular Cancer Table 7.

The tumor may have invaded the tunica albuginea. Bahrami, J. Ro, and A. Treatment of Testicular Cancer Figure 7. In addition, a surgical technique used to reach lymph tissue from behind the aorta and the vena cava was introduced. One problem with the RPLND surgeries being done at that time was that removal of the suprahilar nodes led to some added surgical complications. Another problem was that, in the process of removing retroperitoneal lymph nodes, nerves that controlled ejaculation were often damaged.

This resulted in sperm being ejaculated into the bladder rather than through the urethra retrograde ejaculation , which rendered the patient infertile. In the s, physician John Donohue and his colleagues at Indiana University began to investigate whether they could safely reduce the number of lymph nodes removed in a RPLND in order to minimize surgical complications, including the nerve damage that caused retrograde ejaculation.

To do this, they evaluated lymph nodes of many patients so they could map the common pathways of spread to the retroperitoneal nodes. As part of this study, they compared the metastasis patterns of right-sided and left-sided tumors. They found that for early stage testicular cancer, right-sided tumors metastasized to different sets of lymph nodes than left-sided tumors. The surgically complex removal of suprahilar lymph nodes could often be eliminated without increased risk of death from cancer.

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