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Testicular cancer

CISS relies strongly in its evaluations below on impartial analyses by the International Cochrane Collaboration and the British Medical Journal’s Clinical Evidence Group – two groups of researchers who specialise in Evidence Based Medicine.

Conventional medicine supports the paradigm that the tumour is the first stage of cancer, therefore, treating and removing the cancer should cure the cancer. Unfortunately statistics will show this is rarely the case. Conventional medicine also advocates treatment should only be used if supported by appropriate clinical trials showing efficacy. Evidence based medicine suggests that the only reliable evidence needs to come from properly run randomised controlled trials (RCTS). Again, with conventional cancer treatment, this is generally not the case.

Much of the following descriptions are based on the conventional cancer paradigm with comments from CISS inserted where claims have not been established.

 

The testicles (also called the testes; a single testicle is called a testis) are two small, oval-shaped organs located behind the penis in a skin sack called the scrotum. They are part of the male reproductive system. Testicles have 2 main functions:

  • They make male hormones (androgens) such as testosterone.
  • They make sperm, the male cells needed to fertilize a female egg cell to start a pregnancy.

Testicular cancer starts as an abnormal growth or tumour that develops in one or both testicles.

More than 90% of testicular cancers develop in germ cells, which are responsible for the production of sperm. Secondary testicular tumours are caused by cancerous cells that have spread to the testicles from other parts of the body (metastasis). These cancers are much rarer than the previous forms of testicular cancer. ) (There is little evidence for the claim that cancer spreads to other parts of the body – See below- CISS)

 

A cancer will usually appear as a painless lump in a testis. If a man sees a doctor as soon as a lump, swelling or pain in a testis is noticed, the cancer can remain localised (remain within the testis). However, if not treated, the cancer typically spreads to other parts of the body via the blood or lymphatic system.

A hard lump in either testis is the usual symptom of testicular cancer. The lump is usually painless but in about one in 10 men it is painful or tender. In a few men, constant backache, coughing or breathlessness, and enlarged or tender nipples may mean that the cancer has spread. However, there may be many other reasons for these symptoms.

Young men (about 20 to 40 years of age) are most at risk of developing testicular cancer.

 

Due to the higher risk of testicular cancer in men with a history of undescended testes, it is important for families to share details of medical history with boys in early adolescence so they are aware of the need to regularly check their testes.

 

Men with a history of undescended testes have about ten times the chance of testicular cancer; the risk may be lower if surgery to fix the problem happened before one year of age. Where there has been a single undescended testis, the risk of cancer is usually only in that testis.

 

Pre-cancer cells (ITGCN) are sometimes found in testicular biopsies from infertile men (Not all pre-cancer cells will develop into cancer). (Andrology Australia)

There is no known link between testicular cancer and injury to the testicles, sporting strains, hot baths or wearing tight clothes.

 

Testicular cancer may cause no symptoms. The most common symptom is a painless swelling or a lump in a testicle.

 

Less common symptoms include:

 

  • feeling of heaviness in the scrotum
  • change in the size or shape of the testicle
  • feeling of unevenness
  • pain or ache in the lower abdomen, the testicle or scrotum
  • enlargement or tenderness of the breast.

In 2012 768 new cases of testicular cancer were diagnosed in Australia. For Australian men, the risk of being diagnosed with testicular cancer by age 85 is 1 in 201. The rate of men diagnosed with testicular cancer has grown by more than 50% over the past 30 years. However the reason for this is not known.

  • Most testicular cancers are successfully treated. In 2013, there were 15 deaths from testicular cancer.

(From: Cancer Council Australia)

 

More than 90% of cancers of the testicle develop in special cells known as germ cells. These are the cells that make sperm. The 2 main types of germ cell tumours (GCTs) in men are:

 

  • Seminomas
  • Non-seminomas, which are made up of embryonal carcinoma, yolk sac carcinoma, choriocarcinoma, and/or teratoma

 

Doctors can tell what type of testicular cancer you have by looking at the cells under a microscope.

 

These 2 types occur about equally. Many testicular cancers contain both seminoma and non-seminoma cells. These mixed germ cell tumours are treated as non-seminomas because they grow and spread like non-seminomas.

 

Seminomas

Seminomas tend to grow and spread more slowly than non-seminomas. The two main subtypes of these tumours are classical (or typical) seminomas and spermatocytic seminomas. Doctors can tell them apart by how they look under the microscope.

 

Classical seminoma: More than 95% of seminomas are classical. These usually occur in men between 25 and 45.

 

Spermatocytic seminoma: This rare type of seminoma tends to occur in older men. The average age of men diagnosed with spermatocytic seminoma is about 65. Spermatocytic tumours tend to grow more slowly and are less likely to spread to other parts of the body than classical seminomas.

 

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 tumour marker for certain types of testicular cancer. It can be used for diagnosis and to check how the patient is responding to treatment.

Non-seminomas

These types of germ cell tumours usually occur in men between their late teens and early 30s. The 4 main types of non-seminoma tumours are:

  • Embryonal carcinoma
  • Yolk sac carcinoma
  • Choriocarcinoma
  • Teratoma

 

Most tumours are a mix of different types (sometimes with a seminoma component as well), but this doesn’t change the general approach to treatment of most non-seminoma cancers.

Embryonal carcinoma: This type of non-seminoma is present to some degree in about 40% of testicular tumours, but pure embryonal carcinomas occur only 3% to 4% of the time.

 

When seen under a microscope these tumours can look like tissues of very early embryos. This type of non-seminoma tends to grow rapidly and spread outside the testicle.

Embryonal carcinoma can increase blood levels of a tumour marker protein called alpha-fetoprotein (AFP) as well as human chorionic gonadotropin (HCG).

Yolk sac carcinoma: These tumours are so named because their cells look like the yolk sac of an early human embryo. Other names for this cancer include yolk sac tumour, endodermal sinus tumour, infantile embryonal carcinoma, or orchidoblastoma. This is the most common form of testicular cancer in children (especially in infants), but pure yolk sac carcinomas (tumours that do not have other types of non-seminoma cells) are rare in adults. When they occur in children, these tumours usually are treated successfully. But they are of more concern when they occur in adults, especially if they are pure. Yolk sac carcinomas respond very well to chemotherapy, even if they have spread.

 

This type of tumour almost always increases blood levels of AFP (alpha-fetoprotein).

 

Choriocarcinoma: This is a very rare and aggressive type of testicular cancer in adults. Pure choriocarcinoma is likely to spread rapidly to distant organs of the body, including the lungs, bones, and brain. More often, choriocarcinoma cells are present with other types of non-seminoma cells in a mixed germ cell tumour. These mixed tumours tend to have a somewhat better outlook than pure choriocarcinomas, although the presence of choriocarcinoma is always a worrisome finding.

 

This type of tumour increases blood levels of HCG (human chorionic gonadotropin).

 

Teratoma: Teratomas are germ cell tumours with areas that, under a microscope, look like each of the 3 layers of a developing embryo: the endoderm (innermost layer), mesoderm (middle layer), and ectoderm (outer layer).

 

Pure teratomas of the testicles are rare and do not increase AFP (alpha-fetoprotein) or HCG (human chorionic gonadotropin) levels. More often teratomas are seen as parts of mixed germ cell tumours.

 

There are 3 main types of teratomas:

 

  • Mature teratomas are tumours formed by cells similar to cells of adult tissues. They rarely spread to nearby tissues and distant parts of the body. They can usually be cured with surgery, but some come back (recur) after treatment.
  • Immature teratomas are less well-developed cancers with cells that look like those of an early embryo. This type is more likely than a mature teratoma to grow into (invade) surrounding tissues, to spread (metastasize) outside the testicle, and to come back (recur) years after treatment.
  • Teratomas with somatic type malignancy are very rare cancers. These cancers have some areas that look like mature teratomas but have other areas where the cells have become a type of cancer that normally develops outside the testicle (such as a sarcoma, adenocarcinoma, or even leukemia).

Carcinoma in situ of the testicle

Testicular germ cell cancers can begin as a non-invasive form of the disease called carcinoma in situ (CIS) or intratubular germ cell neoplasia. In testicular CIS, the cells look abnormal under the microscope, but they have not yet spread outside the walls of the seminiferous tubules (where sperm cells are formed). Carcinoma in situ doesn’t always progress to invasive cancer.

 

It is hard to find CIS before it does become an invasive cancer because it generally does not cause symptoms and often does not form a lump that you or the doctor can feel. The only way to diagnose testicular CIS is to have a biopsy (a procedure that removes a tissue sample and looks at it under a microscope). Some cases are found incidentally (by accident) when a testicular biopsy is done for another reason, such as infertility.

 

Experts don’t agree about the best treatment for CIS. Since CIS doesn’t always become an invasive cancer, many doctors in the United States consider observation (watchful waiting) to be the best treatment option.

 

When CIS of the testicle becomes invasive, its cells are no longer just in the seminiferous tubules but have grown into other structures of the testicle. These cancer cells can then spread either to the lymph nodes (small, bean-shaped collections of white blood cells) through lymphatic channels (fluid-filled vessels that connect the lymph nodes), or through the blood to other parts of the body.

Stromal tumours

Tumours can also develop in the supportive and hormone-producing tissues, or stroma, of the testicles. These tumours are known as gonadal stromal tumours. They make up less than 5% of adult testicular tumours but up to 20% of childhood testicular tumours. The 2 main types are Leydig cell tumours and Sertoli cell tumours.

 

· Leydig cell tumours

  • These tumours develop from the Leydig cells in the testicle that normally make male sex hormones (androgens like testosterone). Leydig cell tumours can develop in both adults and children. These tumours often make androgens (male hormones) but sometimes produce estrogens (female sex hormones).
  • Most Leydig cell tumours are benign. They usually do not spread beyond the testicle and are cured with surgery. But a small portion of Leydig cell tumours spread to other parts of the body and tend to have a poor outlook because they usually do not respond well to chemotherapy or radiation therapy.

 

· Sertoli cell tumours

  • These tumours develop from normal Sertoli cells that support and nourish the sperm-making germ cells. Like the Leydig cell tumours, these tumours are usually benign. But if they spread they usually don’t respond well to chemotherapy and radiation therapy.

Secondary testicular cancers

 

Cancers that start in another organ and then spread to the testicle are called secondary testicular cancers. These are not true testicular cancers – they are named and treated based on where they started.

 

Lymphoma is the most common secondary testicular cancer. Testicular lymphoma occurs more often than primary testicular tumours in men older than 50. The outlook depends on the type and stage of lymphoma. The usual treatment is surgical removal, followed by radiation and/or chemotherapy.

 

In boys with acute leukemia, the leukemia cells can sometimes form a tumour in the testicle. Along with chemotherapy to treat the leukemia, this might require treatment with radiation or surgery to remove the testicle.

 

Cancers of the prostate, lung, skin (melanoma), kidney, and other organs also can spread to the testicles. The prognosis for these cancers tends to be poor because these cancers have usually spread widely to other organs as well. Treatment depends on the specific type of cancer.

From: American Cancer Society

Risks:

Testicular cancer is a relatively rare disease in Australia. The exact cause remains unknown, but there are several factors that may increase a man’s risk of developing testicular cancer.

These risk factors include:

  • Undescended testes (cryptorchidism) – men born with undescended testes are more likely to develop testicular cancer. Surgical correction of the undescended testes can reduce but not completely offset this risk.
  • A family history – is important if you have a father or brother who has had testicular cancer.
  • An abnormality of the penis and urethra, known as hypospadias, means you are twice as likely to develop testicular cancer, compared to other men in the general population.
  • Infertility (having difficulty conceiving a baby) – infertility shares a number of risk factors with testicular cancer.
  • Human immunodeficiency virus (HIV) – there is some evidence that men with HIV have an increased risk of testicular cancer.
  • Personal history – men who have previously had testicular cancer in one testicle are more likely to develop cancer in the other testicle.

 

There is no known link between testicular cancer and testicular injury. However, injury can often cause swelling and lumps, which can then make detecting testicular cancer difficult. If you have testicular swelling due to an injury, see your doctor for advice.

 

The two main types of testicular cancer are non-seminoma and seminoma.

Diagnosing testicular cancer involves a number of tests, including:

 

  • examination – a physical examination of the testicles
  • ultrasound scan – to help distinguish between cancers and lumps due to other causes
  • blood tests – many testicular cancers produce a hormone that can be measured in the blood. Doctors call them ‘markers’. There are three different types of markers for testicular cancer.

 

If the ultrasound results suggest cancer, the affected testicle will need to be surgically removed. The cells from the lump will be examined under a microscope. Unfortunately, this is the only way to confirm testicular cancer. Doctors will only do this operation if they are fairly sure it is cancer.

If your doctor suspects the cancer has spread to other parts of the body, they will do other tests such a chest x-ray and scans – either magnetic resonance imaging (MRI) scan or a

computed tomography (CT) scan.

 

Treatment

 

Treatments include:

Surgery

  • Orchiectomy (surgical removal of the affected testis), done under general anesthetic.

 

Testicular cancer and the removal of one testicle should not alter sexual function or fertility. The effect on fertility following removal of one of the testicles is minimal as a single testicle produces such large numbers of sperm.

 

Please note: there is little evidence that cancer with surgery has any benefit on increased 5 year survival except in cases where the tumour is in a life threatening position (The Efficacy of Cancer Surgery, D.Benjamin) or very early stage.

  • Chemotherapy or radiotherapy, often prescribed after surgery to treat any remaining cancer cells that may have spread to other parts of the body, such as lymph nodes.

Men with testicular cancer should talk to their oncologist about sperm banking before commencing chemotherapy or radiation therapy.

 

For those men who require further treatment, fertility is likely to be affected, at least temporarily.

(From: CCA & Andrology Australia)

Further treatment for testicular cancer may include:

 

  • Radiotherapy – this involves the use of x-rays to kill cancer cells, while doing as little harm as possible to the normal cells. Radiotherapy may be given to prevent the cancer coming back after surgery or to treat any cancer cells that have spread. Testicular cancer most commonly spreads to the lymph nodes in the pelvis and lower abdominal region. Radiotherapy does not make you radioactive, so it is safe for you to be with other people, including children, after your treatment.

 

  • Chemotherapy – this involves the use of anti-cancer medications to kill cancer cells by circulating in the bloodstream and reaching cancer cells anywhere in the body. This treatment may be given:

 

  • if the cancer has spread outside your testicle
  • together with surgery, or less commonly, with radiotherapy (adjuvant treatment) if there is moderate risk of the cancer spreading or returning
  • as the primary treatment, if the cancer has spread to other parts of your body.

 

  • Further surgery – if the cancer has spread to the lymph nodes in your abdomen and remained after chemotherapy or radiotherapy, the lymph nodes may be surgically removed. This may cause infertility by preventing the ejaculation of sperm through the penis. However, sexual function and the ability to orgasm remain intact.

 

From: Better Health Victoria (www.betterhealth.vic.gov.au/health/conditionsandtreatments/testicular-cancer)

 

(Note: There is little evidence that surgery for testicular cancer has any benefit on increased percentage 5 year survival or reduced mortality. (The Efficacy of surgical treatment of cancer – 20 years later, DJ Benjamin) Screening for testicular cancer may reduce both morbidity and mortality, yet the effectiveness of any method is unknown. Equally, screening may also promote treatment procedures that are unwarranted or may adversely affect the health outcomes of the patient with no net benefit. Additionally, many organisations recommend against screening for testicular cancer due to the low incidence of testicular cancer and favourable outcomes in the absence of screening. (Ilic, D and Misso ML. Screening for testicular cancer. Cochrane Database of Systematic Reviews,16 February 2011) All of these comments come from peer-reviewed research. CISS)

 

 

 

 

  1. Radiotherapy – uses high energy rays to destroy or damage cancer cells. May be given before surgery to help make surgery safer and easier, or after surgery, to reduce the chance of the cancer cells regrowing (Australian Cancer Cancer).

Please note: radiation has been shown to reduce recurrence with many types of cancer but this rarely results in increased survival. (The efficacy of radiotherapy, DJ Benjamin).

  1. Chemotherapy – the use of toxic drugs to kill the cancer cell or stop them from growing. For certain types of bone cancer, chemotherapy can be used in combination with surgery to either shrink the tumour before surgery, or after surgery to kill any cancer cells left behind (Australian Cancer Council).

 

Note 🙂 Research by Morgan et al conclude that chemotherapy in soft tissue sarcoma gives a zero percent five year survival benefit.

 

The above therapies all come with risks and side effects which should be discussed in detail by your treating physician. For a complete comprehensive overview of conventional treatments used for sarcoma cancer with up to date information on % effectiveness of each treatment on mortality and morbidity, please follow this link to The Ralph Moss Reports.

High-dose chemotherapy and stem cell transplant for testicular cancer

 

In general, testicular cancers respond well to chemotherapy (chemo), but not all cancers are cured. Even though higher doses of chemo might be more effective, they are not given because they could severely damage the bone marrow, which is where new blood cells are formed. This could lead to life-threatening infections, bleeding, and other problems because of low blood cell counts.

 

A stem cell transplant allows doctors to use higher doses of chemo. Blood-forming stem cells are collected from the bloodstream in the weeks before treatment using a special machine. In the past the stem cells were taken from the bone marrow, but this is done less often now. The stem cells are frozen, and then the patient receives high-doses of chemo.

After the chemo the patient gets his stem cells back again. This is called a transplant, but it doesn’t involve surgery – the cells are infused into a vein much like a blood transfusion. The stem cells settle in the bone marrow and start making new blood cells over the next few weeks.

For testicular cancer, stem cell transplant is most often used to treat cancers that have come back after treatment with chemo. Current studies are exploring whether a stem cell transplant may be valuable in treating some patients with advanced germ cell cancers as part of their first treatment.

 

A stem cell transplant is a complex treatment that can cause life-threatening side effects because of the high doses of chemotherapy used. Be sure you understand the possible benefits and risks. If the doctors think you might benefit from a transplant, it should be done at a hospital where the staff has experience with the procedure and with managing the recovery phase.

 

Stem cell transplants often require a long hospital stay and can be very expensive. Even if the transplant is covered by your insurance, your co-pays or other costs could add up to a lot of money. It is important to find out what your insurer will cover before deciding on a transplant to get an idea of what you might have to pay.

From: American Cancer Society

Treatments for Testicular Cancer may include (but are not limited to) the following which has been proven to kill cancer cells:

  1. Sono-Photo Dynamic Therapy: SPDT involves getting an “activator” agent, which reacts with light and/or sound, into the cancer cells of the body. The agent that is inside of cancer cells adheres to cancer cells. When this agent comes in contact with the correct frequency of light or sound, the agent “explodes” into free radical oxygen, instantly killing the cancer cells, which cannot survive in oxygen.

 

  1. Hyperthermia: Hyperthermia is a natural, non-toxic treatment in which body tissue is exposed to high temperatures (up to 104ºF), to damage and kill cancer cells, or make cancer cells more sensitive to the effects of certain anticancer drugs.

 

  1. AARSOTA Vaccine: A protein extracted from cancer cells is used to develop a customized biological vaccine for each individual patient. This vaccine is administered at specific intervals to promote antigen-antibody response. The antibodies generated are specific to the cancer type in the body.

 

  1. Virotherapy: The cancer is introduced to a virous programmed with seek and destroy properties. It enters cancer cells and divides until the cell explodes. The virus then moves into other tumour cells and continues to divide. This treatment is gaining traction as a serious tumour killer.

 

  1. Oxygen Therapy: Hydrogen peroxide, Hyperbaric chamber, Ozone, UVB… Different varieties of oxygen therapy are promoted as alternative treatments for dozens of diseases, including cancer, asthma, emphysema, arthritis, heart and vascular diseases, multiple sclerosis, and Alzheimer’s disease. Cancer cells thrive in low-oxygen environments, adding oxygen to the body creates an oxygen-rich condition in which cancer cells cannot survive

(Mexican Cancer Clinics)

 

Signs and Symptoms:

Bone cancer:

  • pain in the bones and joints, may be worse at night
  • swelling over the affected part of the bone
  • problems with movement
  • unexplained weight loss
  • loss of feeling in the affected limb
  • tiredness

Bone cancer is diagnosed using x-rays, CT or MRI scans and/or biopsy.

Soft tissue sarcoma:

  • You may develop a painless lump. You may begin to have pain as the lump grows and presses on nerves and muscles.

Please note, most painless lumps are not sarcoma.

Soft tissue sarcoma is diagnosed with blood tests, x-rays and scans. You may require a biopsy (Victorian Cancer Council).

Treatment:

Conventional medicine supports the paradigm that the tumour is the first stage of cancer, therefore, treating and removing the cancer should cure the cancer. Unfortunately statistics will show this is rarely the case. Conventional medicine also advocates treatment should only be used if supported by appropriate clinical trials showing efficacy, again, with conventional cancer treatment, this is generally not the case.

Other paradigms believe cancer is a systemic disease and the tumour is in fact a late stage symptom of that disease. Therefore; treating the disease should be systemic and wholistic (meaning treating the whole body) and should include the following components:

  1. Cause no harm
  2. Wholistic (whole body)
  3. Look after our health. This latter paradigm is supported by CISS (See Introduction to CISS)

Alternative cancer therapies generally support the above 3 components. There are approximately 200 alternative cancer therapies that have been shown or anecdotally reported to help a person with cancer have better morbidity and longer mortality. What is important in any cancer treatment is to both understand and believe in your chosen therapy.

In Sarcoma cancer, Ralph Moss (Cancer Therapy, The Independent Consumers Guide to Non-Toxic Treatment and Prevention) reports the following alternative therapies have been shown to benefit.

  1. Sulindac – is a common prescription drug (NSAID). While it was originally marketed to fight arthritis, gout and other rheumatic disorders, it is now believed to exercise a beneficial role against precancerous conditions and possibly against cancer itself.

 

Desmoid tumours are slow growing sarcomas that sometimes invade local tissue but rarely spread to distant parts of the body, according to William R. Waddell and Wolff M, Kirsch of the department of surgery, University of Arizona. Sometimes these occur spontaneously, but more often they are associated with Gardner’s syndrome, in which about 55 percent of the patients develop such growths.

 

Smaller growths can be removed but large tumours – for example those found in the abdomen, neck, pelvis, thigh or shoulder – often cannot be excised. These scientists have spent 17 years treating this king of tumour with various agents. Their conclusion is that almost all cases can now be controlled by a combination of sulindac and other drugs such as indomethacin (another NSAID), warfarin with vitamin K1, tamoxifen and the hormone testolactone. Sulindac may work by inhibiting the hormone prostaglandin, Tucson scientists said.

References. Huskisson E and Franchimont P. Clinoril in the treatment of rheumatic disorders. New York: Raven Press, 1976.

Waddell W and Loughry R. Sulindac for polyposis of the colon. J Surg Oncol.1983;24:83-7.

 

  1. Urea – urine has been used in medicine almost since the beginning of history. Today, it is employed in diagnosis, prevention and even therapy. Urea is the most abundant chemical found in urine other than water.

Eight patients with cancer of the eye were successfully treated with urea, Danopoulos reported in 1975. One of them had a malignant melanoma, one Kaposi’s sarcoma, and six had squamous cell carcinomas. At least 4 of these 8 would have been subjected to removal of their eyeball as the standard treatment.

References. Danaopoulos ED, et al. Urea in the treatment of epibulbar malignancies. Br J Ophthalmol.1975;1:341-50.

  1. Heat therapy – is the scientific use of heat for the treatment of cancer. Some doctors believe that fever is a natural healing mechanism of the body, stimulating the immune system, while disarming microbes and cancer cells.

 

Hyperthermia is another term for heat therapy. It is a very promising aspect of sarcoma treatment. Rolf Issels, MD, PhD, professor of medical oncology at the Klinikum Grosshadern Medical Center, University of Munich, presented the results of regional hyperthermia (RHT) at a press conference in Berlin on September 23, 2009. This was part of Europe’s largest cancer congress.

 

The final results were surprisingly robust. Issels reported on 341 patients with high-risk sarcomas who received a standard chemotherapy regimen consisting of three drugs: etoposide, ifosfamide and adriamycin. Half of the patients were then randomized to receive hyperthermia before and after their chemotherapy. The median follow-up time was 34 months. Adding regional hyperthermia to chemotherapy reduced the risk for recurrence or death by 42 percent. Patients who were assigned to the combination treatment survived an estimated 120 months before progressing compared to 75 months for those who were assigned to chemotherapy alone.

 

There were other signs of the benefit of adding heat to conventional treatment. After two years, 76 percent of patients assigned to the combination therapy were alive without local progression compared with 61 percent of those assigned to chemotherapy alone. Tumour shrinkage occurred in just 12.7 percent of patients assigned to chemotherapy alone vs. 28.8 percent assigned to combination therapy. In addition, tumour growth occurred in 6.8 percent of those assigned to combination therapy vs. 20 percent of those assigned to chemotherapy alone.

 

Issels described this as “the first—and the only completed—randomized study on neoadjuvant chemotherapy in high-risk soft tissue sarcoma showing that the addition of regional hyperthermia significantly improves the overall response rate, time to progression, local progression free survival, and disease free survival.”

 

References: (Lindner LH, Issels RD. Hyperthermia in soft tissue sarcoma. Curr Treat Options Oncol. 2011;12:12-20)

 

If you or someone close to you have just been diagnosed with sarcoma cancer, it is important you research and understand your chosen treatment, whether that be conventional, alternative or a mixture of both. For the best results your treatment should include physical treatment, mental treatment and psychological treatment.

For more information on some more common evidenced based alternative treatments please go to the alternative treatment tab. If you don’t know where to begin in your journey to wellness then we suggest you read where to start.

Testis Cancer

ICD-9: 186; incidence: 529 (Australia), 989 (SEER).

 

Seminoma of testis

Incidence: 529 X 50% of total = 265 (Australia); 989 X 59% of total = 584 (SEER).

A review article [71] concluded that chemotherapy only has a role in bulky disease with para-aortic masses over 5 cm diameter or in those who relapse after definitive radiotherapy. These patients are in the minority of those with seminoma of testis d maximum 20%.

 

Non-seminomatous testicular cancer

Incidence: 529 x 50% of total = 265 (Australia); 989 x 41% of totalZ405 (SEER).

The outcome was changed dramatically by the use of cisplatinum [4]. The introduction of effective chemotherapy was not due to an RCT, but the results were a major improvement on previous treatment. Nowadays, up to 95% are long-term disease-free survivors, although this is less in those presenting with poor prognostic grouping. In stage I non-seminomatous testicular cancer (NSTC) (40% total), a ‘surveillance’ policy is standard practice, and only the 20% of this group who relapse will receive chemotherapy.

 

Number benefiting from chemotherapy

Australia: seminoma: 265 (incidence) x 20% (relapse) x 95% (benefit from chemotherapy) = 50; NSTC: stage I = 265 (incidence) x 40% (subgroup)x 20% (relapse) x 95% (benefit from chemotherapy) = 20; stage II-IV = 265 (incidence) x 60% (subgroup)x x 95% (benefit from chemotherapy) =151; total = 221 (41.8%). SEER: seminoma: 584 x 20% x 95% = 111; NSTC: stage I-IV = 405 x 40% x 20% x 95% = 31; stage II-IV =405 x 60% x 95% = 231; total = 373 (37.7%).

 

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