Testicular cancer is a type of cancer that develops in the testicles (singular testis), a part of the male reproductive system. In the United States, about 8,000 to 9,000 diagnoses of testicular cancer are made each year. Over his lifetime, a man's chance of getting testicular cancer is roughly 1 in 250 (four tenths of one percent, or 0.4%). It is most common among males aged 15?40 years. Testicular cancer has one of the highest cure rates of all cancers: in excess of 90%; essentially 100% if it has not spread. Even for the relatively few cases in which the cancer has spread widely, chemotherapy offers a cure rate of at least 50%.
Symptoms and early detection
Because testicular cancer is curable (stage I can have a success rate of >95%) when detected early, experts recommend regular monthly testicular self-examination after a hot shower or bath, when the scrotum is looser. Men should examine each testicle, feeling for pea-shaped lumps. Symptoms may include one or more of the following:
a lump in one testis or a hardening of one of the testicles
pain and tenderness in the testicles
build-up of fluid in the scrotum
a dull ache in the lower abdomen or groin
an increase, or significant decrease, in the size of one testis
Men should report any of these to a doctor as soon as possible.
The extent of testicular cancer and whether the cancer is present are ascertained by ultrasound (of the testicles), X-rays, and/or CT scans, which are used to locate tumors. Blood tests are also used to identify and measure tumor markers that are specific to testicular cancer. A biopsy should not be performed, as it raises the risk of migrating cancer cells into the scrotum.
 Differential Diagnosis
An incorrect diagnosis is made at the initial examination in up to 25% of patients with testicular tumors and may result in delay in treatment or a suboptimal surgical approach (scrotal incision) for exploration.
Epididymitis or epididymoorchitis
Prevalence and distribution
Testicular cancer is most common among white males and rare among African Americans. Worldwide incidence has doubled since the 1960s, with the highest rates of prevalence in Scandinavia, Germany, and New Zealand. Testicular cancer is uncommon in Asia and Africa.
Incidence among African Americans doubled from 1988 to 2001 with a bias towards seminoma. The lack of any significant increase in the incidence of early-stage testicular cancer during this timeframe suggests that the overall increase was not due to heightened awareness of the disease.
Although testicular cancer is most common among men aged 15?40 years, it has three peaks: infancy, ages 25?40 years, and age 60 years.
Pathology, staging, and genetics
Testicular cancer can be caused by any type of cell found in the testes, but more than 95% of all testicular cancers originate in germ cells. (Germ cells produce sperm. They are not pathogenic; i.e., they are not to be confused with the "germs" (viruses, bacteria) that cause illness.) In general, the remainder of this article discusses germ-cell testicular cancer.
Germ-cell tumors are classified as either seminomas or nonseminomas (which may be called teratomas in the UK). Seminomas are slow-growing. Seminomas, when found, tend to be localized (i.e., only in the testicles), simply because they spread relatively slowly. Nonseminomas, on the other hand, tend to spread more quickly. Nonseminomas are further classified into four subtypes; embryonal carcinomas, choriocarcinomas, yolk sac tumors, teratomas and mixed tumors. Their appearance under the microscope and also their gene expression is rather distinguished from each other, their rate of spread varies somewhat, but they are nevertheless treated similarly. When seminomas and nonseminomas are both present (which is not unusual), the cancer is classified as nonseminoma
 Tumor markers
Blood markers for testicular tumors include the beta subunit of human chorionic gonadotropin (?hCG), lactate dehydrogenase (LDH), and alpha-fetoprotein (AFP). Seminomatous tumors never present elevated AFP levels. Placental alkaline phosphatase and other markers are sometimes used by the pathologist to differentiate between seminoma and nonseminomatous tumors.
After removal, a testicular tumor is staged by a pathologist according to the TNM Classification of Malignant Tumors as published in the AJCC Cancer Staging Manual. Testicular cancer is categorized as being in one of three stages (which have subclassifications). The size of the tumor in the testis is irrelevant to staging.  In broad terms, tesicular cancer is staged as follows:
Stage I: the cancer remains localized to the testis.
Stage II: the cancer involves the testis and metastasis to retroperitoneal and/or Paraaortic lymph nodes (lymph nodes below the diaphragm).
Stage III: the cancer involves the testis and metastasis beyond the retroperitoneal and Paraaortic lymph nodes. Stage III is further subdivided into nonbulky stage III and bulky stage III. 
There are alternative therapies favored by some to help fight testicular cancer. Studies have found that epigallocatechin gallate, found in green tea, has beneficial effects. It can bind to a protein on a tumor cell and slow its growth. Other active ingredients, quercetin and gallic acid, have also shown effectiveness, as well as the aqueous solutions of ardisia and yerba mate teas, as chemopreventative agents. http://www.ncbi.nlm.nih.gov/entrez/query...
The diallyl sulfide component in garlic may be an effective inhibitor in the development of carcinogenic tumors, according to a number of studies which showed some preventative effect. http://www.krysalis.net/cancer2.htm
Finally the maitake mushroom appears to both inhibit the growth of tumors as well as stimulate immunity. The particular active ingredient is a beta-glucan called D-fraction, which stimulates immune cells. In some cases extracts need to be injected, but the mushroom is effective orally and can be bought as a supplement. It?s also been posited that the maitake might make chemotherapeutic drugs more effective, which means lower does of chemotherapy can be used.