MESOTHELIOMA CANCER INFORMATION

Prostate cancer screening is an attempt to find unsuspected cancers. Screening tests may lead to more specific follow-up tests such as a biopsy, where small cores of the prostate are removed for closer study. Prostate cancer screening options include the digital rectal exam and the prostate specific antigen (PSA) blood test. Screening for prostate cancer is controversial because it is not clear if the benefits of screening outweigh the risks of follow-up diagnostic tests and cancer treatments.

Prostate cancer is usually a slow-growing cancer, very common among older men. In fact, most prostate cancers never grow to the point where they cause symptoms, and most men with prostate cancer die of other causes before prostate cancer has an impact on their lives. The PSA screening test may detect these small cancers that would never become life threatening. Doing the PSA test in these men may lead to overdiagnosis, including additional testing and treatment. Follow-up tests, such as prostate biopsy, may cause pain, bleeding and infection. Prostate cancer treatments may cause urinary incontinence and erectile dysfunction. Therefore, it is essential that the risks and benefits of diagnostic procedures and treatment be carefully considered before PSA screening.

Several medical societies have not found sufficient evidence to support routine screening for prostate cancer. The American Urological Association, however, does support routine screening.

* In 2002, the U.S. Preventive Services Task Force (USPSTF) concluded that the evidence was insufficient to recommend for or against routine screening for prostate cancer using PSA testing or digital rectal examination (DRE). The previous 1995 USPSTF recommendation was against routine screening.
* In 1997, American Cancer Society (ACS) guidelines began recommending that beginning at age 50 (age 45 for African-American men and men with a family history of prostate cancer, and since 2001, age 40 for men with a very strong family history of prostate cancer), PSA testing and DRE be offered annually to men who have a life-expectancy of 10 or more years (average life expectancy is 10 years or more for U.S. men under age 76) along with information on the risks and benefits of screening. The previous ACS recommendations since 1980 had been for routine screening for prostate cancer with DRE annually beginning at age 40, and since 1992 had been for routine screening with DRE and PSA testing annually beginning at age 50.
* The 2007 National Comprehensive Cancer Network (NCCN) guideline recommends offering a baseline PSA test and DRE at ages 40 and 45 and annual PSA testing and DRE beginning at age 50 (with annual PSA testing and DRE beginning at age 40 for African-American men, men with a family history of prostate cancer, and men with a PSA ≥ 0.6 ng/mL at age 40 or PSA > 0.6 ng/mL at age 45) through age 80, along with information on the risks and benefits of screening. Biopsy is recommended if DRE is positive or PSA ≥ 4 ng/mL, and biopsy considered if PSA > 2.5 ng/mL or PSA velocity ≥ 0.35 ng/mL/year when PSA ≤ 2.5 ng/mL.
* Some U.S. radiation oncologists and medical oncologists who specialize in treating prostate cancer recommend obtaining a baseline PSA in all men at age 35 or beginning annual PSA testing in high risk men at age 35.
* The American Urological Association Patient Guide to Prostate Cancer.

Since there is no general agreement that the benefits of PSA screening outweigh the harms, the consensus is that clinicians use a process of shared decision-making that includes discussing with patients the risks of prostate cancer, the potential benefits and harms of screening, and involving the patients in the decision.

However, because PSA screening is widespread in the United States, following the recommendations of major scientific and medical organizations to use shared decision-making is legally perilous in some U.S. states. In 2003, a Virginia jury found a family practice residency program guilty of malpractice and liable for $1 million for following national guidelines and using shared decision-making, thereby allowing a patient (subsequently found to have a high PSA and incurable advanced prostate cancer) to decline a screening PSA test, instead of routinely ordering without discussion PSA tests in all men ≥ 50 years of age as four local physicians testified was their practice, and was accepted by the jury as the local standard of care.

An estimated 20 million PSA tests are done per year in North America and possibly 20 million more outside of North America.

* In 2000, 34.1% of all U.S. men age ≥ 50 had a screening PSA test within the past year and 56.8% reported ever having a PSA test.
* In 2000, 33.6% of all U.S. men age 50–64 and 51.3% of men age ≥ 65 had a PSA test within the past year.
* In 2005, 33.5% of all U.S. men age 50–64 had a PSA test in the past year.
o 37.5% of men with private health insurance, 20.8% of men with Medicaid insurance, 14.0% of currently uninsured men, and 11.5% of men uninsured for > 12 months.
* In 2000–2001, 34.1% of all Canadian men age ≥ 50 had a screening PSA test within the past year and 47.5% reported ever having a screening PSA test.
* Canadian men in Ontario were most likely to have had a PSA test within the past year and men in Alberta were least likely to have had a PSA test with the past year or ever.

-References From Wikipedia-

Prostate cancer is a disease in which cancer develops in the prostate, a gland in the male reproductive system. It occurs when cells of the prostate mutate and begin to multiply out of control. These cells may spread (metastasize) from the prostate to other parts of the body, especially the bones and lymph nodes. Prostate cancer may cause pain, difficulty in urinating, erectile dysfunction and other symptoms.

Rates of prostate cancer vary widely across the world. Although the rates vary widely between countries, it is least common in South and East Asia, more common in Europe, and most common in the United States. Prostate cancer develops most frequently in men over fifty. This cancer can occur only in men, as the prostate is exclusively of the male reproductive tract. It is one of the most common types of cancer in men. However, many men who develop prostate cancer never have symptoms, undergo no therapy, and eventually die of other causes. That is because malignant neoplasms of the prostate are, in most cases, slow-growing, and because most of those affected are over 60. Hence they often die of causes unrelated to the prostate cancer, such as heart/circulatory disease, pneumonia, other unconnected cancers or old age. Many factors, including genetics and diet, have been implicated in the development of prostate cancer.

Prostate cancer is most often discovered by PSA (prostate specific antigen) screening and less commonly by physical examination or by symptoms. There is some current concern about the accuracy of the PSA test and its usefulness. Suspected prostate cancer is typically confirmed by taking a biopsy of the prostate and examining it under a microscope. Further tests, such as CT scans and bone scans, may be performed to determine whether prostate cancer has spread.

Treatment options for prostate cancer with intent to cure are primarily surgery and radiation therapy. Other treatments such as hormonal therapy, chemotherapy, proton therapy, cryosurgery, high intensity focused ultrasound (HIFU) also exist depending on the clinical scenario and desired outcome. Abiraterone Acetate is showing promise in reducing Tumor Size and PSA levels in Aggressive end-stage prostate cancers. The age and underlying health of the man as well as the extent of spread, appearance under the microscope and response of the cancer to initial treatment are important in determining the outcome of the disease. The decision whether or not to treat localized prostate cancer (a tumor that is contained within the prostate) with curative intent is a patient trade-off between the expected beneficial and harmful effects in terms of patient survival and quality of life.

Prostate

The prostate is a part of the male reproductive organ which helps make and store seminal fluid. In adult men a typical prostate is about three centimeters long and weighs about twenty grams. It is located in the pelvis, under the urinary bladder and in front of the rectum. The prostate surrounds part of the urethra, the tube that carries urine from the bladder during urination and semen during ejaculation. Because of its location, prostate diseases often affect urination, ejaculation, and rarely defecation. The prostate contains many small glands which make about twenty percent of the fluid constituting semen. In prostate cancer the cells of these prostate glands mutate into cancer cells. The prostate glands require male hormones, known as androgens, to work properly. Androgens include testosterone, which is made in the testes; dehydroepiandrosterone, made in the adrenal glands; and dihydrotestosterone, which is converted from testosterone within the prostate itself. Androgens are also responsible for secondary sex characteristics such as facial hair and increased muscle mass.

Symptoms

Early prostate cancer usually causes no symptoms. Often it is diagnosed during the workup for an elevated PSA noticed during a routine checkup. Sometimes, however, prostate cancer does cause symptoms, often similar to those of diseases such as benign prostatic hypertrophy. These include frequent urination, increased urination at night, difficulty starting and maintaining a steady stream of urine, blood in the urine, and painful urination. Prostate cancer is associated with urinary dysfunction as the prostate gland surrounds the prostatic urethra. Changes within the gland therefore directly affect urinary function. Prostate cancer may also cause problems with sexual function, such as difficulty achieving erection or painful ejaculation. Because the vas deferens deposits seminal fluid into the prostatic urethra, and secretions from the prostate gland itself are included in semen content, prostate cancer can affect sexual performance and cause painful ejaculation.

Advanced prostate cancer can spread to other parts of the body and this may cause additional symptoms. The most common symptom is bone pain, often in the vertebrae (bones of the spine), pelvis or ribs. Spread of cancer into other bones such as the femur is usually to the proximal part of the bone. Prostate cancer in the spine can also compress the spinal cord, causing leg weakness and urinary and fecal incontinence.

Pathophysiology

Prostate cancer is classified as an adenocarcinoma, or glandular cancer, that begins when normal semen-secreting prostate gland cells mutate into cancer cells. The region of prostate gland where the adenocarcinoma is most common is the peripheral zone. Initially, small clumps of cancer cells remain confined to otherwise normal prostate glands, a condition known as carcinoma in situ or prostatic intraepithelial neoplasia (PIN). Although there is no proof that PIN is a cancer precursor, it is closely associated with cancer. Over time these cancer cells begin to multiply and spread to the surrounding prostate tissue (the stroma) forming a tumor. Eventually, the tumor may grow large enough to invade nearby organs such as the seminal vesicles or the rectum, or the tumor cells may develop the ability to travel in the bloodstream and lymphatic system. Prostate cancer is considered a malignant tumor because it is a mass of cells which can invade other parts of the body. This invasion of other organs is called metastasis. Prostate cancer most commonly metastasizes to the bones, lymph nodes, rectum, and bladder.

Etiology

The specific causes of prostate cancer remain unknown. A man's risk of developing prostate cancer is related to his age, genetics, race, diet, lifestyle, medications, and other factors. The primary risk factor is age. Prostate cancer is uncommon in men less than 45, but becomes more common with advancing age. The average age at the time of diagnosis is 70. However, many men never know they have prostate cancer. Autopsy studies of Chinese, German, Israeli, Jamaican, Swedish, and Ugandan men who died of other causes have found prostate cancer in thirty percent of men in their 50s, and in eighty percent of men in their 70s. In the year 2005 in the United States, there were an estimated 230,000 new cases of prostate cancer and 30,000 deaths due to prostate cancer.

A man's genetic background contributes to his risk of developing prostate cancer. This is suggested by an increased incidence of prostate cancer found in certain racial groups, in identical twins of men with prostate cancer, and in men with certain genes. In the United States, prostate cancer more commonly affects black men than white or Hispanic men, and is also more deadly in black men. Men who have a brother or father with prostate cancer have twice the usual risk of developing prostate cancer. Studies of twins in Scandinavia suggest that forty percent of prostate cancer risk can be explained by inherited factors. However, no single gene is responsible for prostate cancer; many different genes have been implicated. Two genes (BRCA1 and BRCA2) that are important risk factors for ovarian cancer and breast cancer in women have also been implicated in prostate cancer.

Dietary amounts of certain foods, vitamins, and minerals can contribute to prostate cancer risk. Men with higher serum levels of the short-chain ω-6 fatty acid linoleic acid have higher rates of prostate cancer. However, the same series of studies showed that men with elevated levels of long-chain ω-3 (EPA and DHA) had lowered incidence. A long-term study reports that "blood levels of trans fatty acids, in particular trans fats resulting from the hydrogenation of vegetable oils, are associated with an increased prostate cancer risk." Other dietary factors that may increase prostate cancer risk include low intake of vitamin E (Vitamin E is found in green, leafy vegetables), omega-3 fatty acids (found in fatty fishes like salmon), and the mineral selenium. A study in 2007 cast doubt on the effectiveness of lycopene (found in tomatoes) in reducing the risk of prostate cancer. Lower blood levels of vitamin D also may increase the risk of developing prostate cancer. This may be linked to lower exposure to ultraviolet (UV) light, since UV light exposure can increase vitamin D in the body.

There are also some links between prostate cancer and medications, medical procedures, and medical conditions. Daily use of anti-inflammatory medicines such as aspirin, ibuprofen, or naproxen may decrease prostate cancer risk. Use of the cholesterol-lowering drugs known as the statins may also decrease prostate cancer risk. More frequent ejaculation also may decrease a man's risk of prostate cancer. One study showed that men who ejaculated five times a week in their 20s had a decreased rate of prostate cancer, though others have shown no benefit. Infection or inflammation of the prostate (prostatitis) may increase the chance for prostate cancer. In particular, infection with the sexually transmitted infections chlamydia, gonorrhea, or syphilis seems to increase risk. Finally, obesity and elevated blood levels of testosterone may increase the risk for prostate cancer.

Research released in May 2007, found that US war veterans who had been exposed to Agent Orange had a 48% increased risk of prostate cancer recurrence following surgery.

Prostate cancer risk can be decreased by modifying known risk factors for prostate cancer, such as decreasing intake of animal fat.

One research study, by the Cancer Council Victoria, has shown that men who report that they regularly ("more than five times per week") masturbate have up to one third fewer occurrences of prostate cancer. The researchers hypothesize that this could be because regular ejaculation reduces the buildup of carcinogenic deposits such as 3-methylcholanthrene, produced from the breakdown of cholesterol, which could damage the cells lining the prostate. The researchers also speculated that frequent ejaculation may cause the prostate to mature fully, making it less susceptible to carcinogens. It is also possible that there is another factor (such as hormone levels) that is a common cause of both a reduced susceptibility to prostate cancer and a tendency toward frequent masturbation. There is also some evidence that frequent sexual intercourse is associated with reduced risk of prostate cancer, although contrarily the risks associated with STDs have been shown to increase the risk of prostate cancer. Once the lining of the prostate is affected with cancer, the only known treatments are surgery and radiation therapy. Both may limit the ability to have erections afterward.

Prevention

Vitamins and medication

Evidence from epidemiological studies supports protective roles in reducing prostate cancer for dietary selenium, vitamin E, lycopene, and soy foods. High plasma levels of Vitamin D may also have a protective effect. Estrogens from fermented soybeans and other plant sources (called phytoestrogens) may also help prevent prostate cancer. The selective estrogen receptor modulator drug toremifene has shown promise in early trials. Two medications which block the conversion of testosterone to dihydrotestosterone, finasteride and dutasteride, have also shown some promise. The use of these medications for primary prevention is still in the testing phase, and they are not widely used for this purpose. The initial problem with these medications is that they may preferentially block the development of lower-grade prostate tumors, leading to a relatively greater chance of higher grade cancers, and negating any overall survival improvement. More recent research found that finasteride did not increase the percentage of higher grade cancers. A 2008 study update found that finasteride reduces the incidence of prostate cancer by 30%. In the original study it turns that that the smaller prostate caused by finasteride means that a doctor is more likely to hit upon cancer nests and more likely to find aggressive-looking cells. Most of the men in the study who had cancer — aggressive or not — chose to be treated and many had their prostates removed. A pathologist then carefully examined every one of those 500 prostates and compared the kinds of cancers found at surgery to those initially diagnosed at biopsy. Finasteride did not increase the risk of High-Grade prostate cancer.

Green tea may be protective (due to its polyphenol content), although the most comprehensive clinical study indicates that it has no protective effect. A 2006 study of green tea derivatives demonstrated promising prostate cancer prevention in patients at high risk for the disease. Recent research published in the Journal of the National Cancer Institute suggests that taking multivitamins more than seven times a week can increase the risks of contracting the disease. This research was unable to highlight the exact vitamins responsible for this increase (almost double), although they suggest that vitamin A, vitamin E and beta-carotene may lie at its heart. It is advised that those taking multivitamins never exceed the stated daily dose on the label. Scientists recommend a healthy, well balanced diet rich in fiber, and to reduce intake of meat. A 2007 study published in the Journal of the National Cancer Institute found that men eating cauliflower, broccoli, or one of the other cruciferous vegetables, more than once a week were 40% less likely to develop prostate cancer than men who rarely ate those vegetables. The phytochemicals indole-3-carbinol and diindolylmethane, found in cruciferous vegetables, has antiandrogenic and immune modulating properties.

Ejaculation frequency

In 2003, an Australian research team led by Graham Giles of The Cancer Council Australia concluded that frequent masturbation by males appears to help prevent the development of prostate cancer. Australian research concluded that the more men ejaculate between the ages of 20 and 50, the less likely they are to develop prostate cancer. The protective effect is greatest while men are in their twenties: those who had ejaculated more than five times per week in their twenties, for instance, were one-third less likely to develop aggressive prostate cancer later in life. The results contradict those of previous studies, which have suggested that having had many sexual partners, or a high frequency of sexual activity, increases the risk of prostate cancer by up to 40 percent. The key difference is that these earlier studies defined sexual activity as sexual intercourse, whereas this study focused on the number of ejaculations, whether or not intercourse was involved. Another study completed in 2004 reported that "Most categories of ejaculation frequency were unrelated to risk of prostate cancer. However, high ejaculation frequency was related to decreased risk of total prostate cancer." The report abstract concluded, "Our results suggest that ejaculation frequency is not related to increased risk of prostate cancer."

-References From Wikipedia-

Lymphoma a type of neoplasm that originates in lymphocytes (a type of white blood cell in the vertebrate immune system). They often originate in lymph nodes, presenting as an enlargement of the node (a tumor). Lymphomas are closely related to lymphoid leukemias, which also originate in lymphocytes but do not form tumors.There are many types of lymphomas, and in turn, lymphomas are a part of the broad group of diseases called hematological neoplasms.

Thomas Hodgkin published in 1832 the first description of lymphoma, specifically of the form named after him, Hodgkin's lymphoma. Since, many other forms of lymphoma have been described and many classifications proposed. The 1982 Working formulation classification became very popular. It introduced the category Non-Hodgkin lymphoma (NHL), itself divided into 16 different diseases. However, since these different lymphomas have little in common with each other, the NHL label is of limited usefulness for doctors or patients and is slowly being abandoned. The latest classification by the WHO (2001) lists 43 different forms of lymphoma divided in four broad groups.

Some forms of Lymphoma are indolent (e.g. Small lymphocytic lymphoma), compatible with a long life even without treatment, whereas other forms are aggressive (e.g. Burkitt's lymphoma), causing rapid deterioration and death. The prognosis therefore depends on the correct classification of the disease, established by a pathologist after examination of a biopsy. Chemotherapy is prescribed by an oncologist, radiation therapy by a radiation oncologist.

Although older classifications referred to histiocytic lymphomas, these are recognized in newer classifications as of B, T or NK cell lineage. True Histiocytic malignancies are rare and are classified as sarcomas.

-References From Wikipedia-

Bladder cancer refers to any of several types of malignant growths of the urinary bladder. It is a disease in which abnormal cells multiply without control in the bladder. The bladder is a hollow, muscular organ that stores urine; it is located in the pelvis. The most common type of bladder cancer begins in cells lining the inside of the bladder and is called urothelial cell or transitional cell carcinoma (UCC or TCC).

Signs and symptoms

Bladder cancer characteristically causes blood in the urine; this may be visible to the naked eye (frank haematuria) or detectable only by microscope (microscopic hematuria). Other possible symptoms include pain during urination, frequent urination (Pollakiuria) or feeling the need to urinate without results. These signs and symptoms are not specific to bladder cancer, and are also caused by non-cancerous conditions, including prostate infections and cystitis.

CAUSES

Risk factors
Exposure to environmental carcinogens of various types is responsible for the development of most bladder cancers. Tobacco use (specifically cigarette smoking) is thought to cause 50% of bladder cancers discovered in male patients and 30% of those found in female patients.Thirty percent of bladder tumors probably result from occupational exposure in the workplace to carcinogens such as benzidine. Occupations at risk are metal industry workers, rubber industry workers, workers in the textile industry and people who work in printing. Some studies also suggest that auto mechanics have an elevated risk of bladder cancer due to their frequent exposure to hydrocarbons and petroleum-based chemicals.Hairdressers are thought to be at risk as well because of their frequent exposure to permanent hair dyes. It has been proposed that hair dyes are a risk factor, and some have shown an odds ratio of 2.1 to 3.3 for risk of developing bladder cancer among women who use permanent hair dyes, while others have shown no correlation between the use of hair dyes and bladder cancer. Certain drugs such as cyclophosphamide and phenacetin are known to predispose to bladder TCC. Chronic bladder irritation (infection, bladder stones, catheters, bilharzia) predisposes to squamous cell carcinoma of the bladder. Approximately 20% of bladder cancers occur in patients without predisposing risk factors.

Genetics
Like virtually all cancers, bladder cancer development involves the acquisition of mutations in various oncogenes and tumor supressor genes. Genes which may be altered in bladder cancer include H19, FGFR3, HRAS, RB1 and TP53. Several genes have been identified which play a role in regulating the cycle of cell division, preventing cells from dividing too rapidly or in an uncontrolled way. Alterations in these genes may help explain why some bladder cancers grow and spread more rapidly than others.
A family history of bladder cancer is also a risk factor for the disease. Many cancer experts assert that some people appear to inherit reduced ability to break down certain chemicals, which makes them more sensitive to the cancer-causing effects of tobacco smoke and certain industrial chemicals.

DIAGNOSIS

The gold standard of diagnosing bladder cancer is urine cytology and transurethral (through the urethra) cystoscopy. Urine cytology can be obtained in voided urine or at the time of the cystoscopy ("bladder washing"). Cytology is very specific (a positive result is highly indicative of bladder cancer) but suffers from low sensitivity (a negative result does not exclude the diagnosis of cancer). There are newer urine bound markers for the diagnosis of bladder cancer. These markers are more sensitive but not as specific as urine cytology. They are much more expensive as well. Many patients with a history, signs, and symptoms suspicious for bladder cancer are referred to a urologist or other physician trained in cystoscopy, a procedure in which a flexible tube bearing a camera and various instruments is introduced into the bladder through the urethra. Suspicious lesions may be biopsied and sent for pathologic analysis.

Pathological Classification
90% of bladder cancer are Transitional cell carcinomas (TCC) that arise from the inner lining of the bladder called the urothelium. The other 10% of tumours are squamous cell carcinoma, adenocarcinoma, sarcoma, small cell carcinoma and secondary deposits from cancers elsewhere in the body.
TCCs are often multifocal, with 30-40% of patients having more than one tumour at diagnosis. The pattern of growth of TCCs can be papillary, sessile (flat) or carcinoma-in-situ (CIS).

The 1973 WHO grading system for TCCs (papilloma, G1, G2 or G3) is most commonly used despite being superseded by the 2004 WHO grading (papillary neoplasm of low malignant potential (PNLMP), low grade and high grade papillary carcinoma.

CIS invariably consists of cytologically high grade tumour cells.

Bladder TCC is staged according to the 1997 TNM system:

• Ta Non-invasive papillary tumour
• T1 Invasive but not as far as the muscular bladder layer
• T2 Invasive into the muscular layer
• T3 Invasive beyond the muscle into the fat outside the bladder
• T4 Invasive into surrounding structures like the prostate, uterus or pelvic wall

Staging
The following stages are used to classify the location, size, and spread of the cancer, according to the TNM (tumor, lymph node, and metastasis) staging system:

• Stage 0: Cancer cells are found only on the inner lining of the bladder.
• Stage I: Cancer cells have proliferated to the layer beyond the inner lining of the urinary bladder but not to the muscles of the urinary bladder.
• Stage II: Cancer cells have proliferated to the muscles in the bladder wall but not to the fatty tissue that surrounds the urinary bladder.
• Stage III: Cancer cells have proliferated to the fatty tissue surrounding the urinary bladder and to the prostate gland, vagina, or uterus, but not to the lymph nodes or other organs.
• Stage IV: Cancer cells have proliferated to the lymph nodes, pelvic or abdominal wall, and/or other organs.
• Recurrent: Cancer has recurred in the urinary bladder or in another nearby organ after having been treated.

TREATMENT

The treatment of bladder cancer depends on how deep the tumor invades into the bladder wall. Superficial tumors (those not entering the muscle layer) can be "shaved off" using an electrocautery device attached to a cystoscope. Immunotherapy in the form of BCG instillation is also used to treat and prevent the recurrence of superficial tumors.BCG immunotherapy is effective in up to 2/3 of the cases at this stage. Instillations of chemotherapy into the bladder can also be used to treat superficial disease.

Untreated, superficial tumors may gradually begin to infiltrate the muscular wall of the bladder. Tumors that infiltrate the bladder require more radical surgery where part or all of the bladder is removed (a cystectomy) and the urinary stream is diverted. In some cases, skilled surgeons can create a substitute bladder (a neobladder) from a segment of intestinal tissue, but this largely depends upon patient preference, age of patient, renal function, and the site of the disease.

A combination of radiation and chemotherapy can also be used to treat invasive disease. It has not yet been determined how the effectiveness of this form of treatment compares to that of radical ablative surgery.

There is weak observational evidence from one very small study (84) to suggest that the concurrent use of statins is associated with failure of BCG immunotherapy.

The hemocyanin found in Concholepas concholepas blood has immunotherapeutic effects against bladder and prostate cancer. In a research made in 2006 mice were primed with C. concholepas before implantation of bladder tumor (MBT-2) cells. Mice treated with C. concholepas showed a significant antitumor effect as well. The effects included prolonged survival, decreased tumor growth and incidence and lack of toxic effects.

EPIDEMIOLOGY

In the United States, bladder cancer is the fourth most common type of cancer in men and the ninth most common cancer in women. More than 47,000 men and 16,000 women are diagnosed with bladder cancer each year. One reason for its higher incidence in men is that the androgen receptor, which is much more active in men than in women, plays a major part in the development of the cancer.

-References From Wikipedia-

Colorectal cancer is the third most common cancer in men and women. An estimated 131,000 Americans are diagnosed with this disease each year and some 55,000 die as a result of it. Certain genetic factors play a role in the development of this cancer. The specific cause of Colorectal cancer is unknown, however, environmental, genetic, familial factors and preexisting Ulcerative Colitis have been linked to the development of this cancer. It is more common among African-Americans.

Risk Factors

Age: Average age at the time of diagnosis is between 60-65, and the older we get the higher our risk of colorectal cancer.

Family History of colorectal cancer increases the risk of developing this illness in first- degree relatives. Certain familial conditions, like Familial Polyposis, is associated with a much higher risk.

Genetic factors clearly play a role in the development of colorectal cancers. Several genetic and inherited illnesses carry a very high risk of colorectal cancer: Familial Polyposis, Turcot syndrome, Gardner syndrome, Peutz-Jeghers syndrome, Juvenile Polyposis, Cowden's disease, Neurofibromatosis.

Ulcerative colitis , High Dietary Fat and Low Dietary Fiber can each increase the risk of this cancer.

Signs and Symptoms

This cancer may exhibit no signs in its early stages. Gradually, as the disease progresses, any of the following may be seen;

* Blood in the stool
* Diarrhea
* Constipation
* Bowel obstruction, causing nausea, vomiting and abdominal distention
* Abdominal pain
* Pelvic pain
* Anemia due to blood Loss
* Weight loss
* Loss of appetite
* Fatigue

Screening and Diagnosis

This cancer may be detected in its very early stages by any of the following screening tests:

Stool Occult Blood Test. Annual screening for colorectal cancer with a stool occult blood test for adults over age 50 is a must. Incidence of this cancer rises with age. This test is a rather simple test. Small amounts of stool are placed on a paper card and delivered to the physician's office for testing. A positive test mandates a complete work-up, including a Colonoscopy.

Flexible Sigmoidoscopy is a simple test that has a higher accuracy in detecting lower colon and rectal cancer. A tube is inserted inside the rectum and advanced into lower part of the large bowel. The performing physician can look for any abnormalities and take a biopsy from the abnormal area. Almost 50% of colorectal cancers are detected with this procedure.

Digital Rectal Examination is very simple to perform and can detect lesions in rectum and prostate. It should be done in a routine physical exam for adults. The physician examines the area by inserting his finger inside the rectum and feeling for abnormalities.

When colon cancer is suspected, a careful workup should be done to establish the diagnosis or to rule it out. It is empirical to visualize the entire colon and rectum. This is achieved by:

* Barium Enema - A radiological study wherein patients are given a barium enema followed by a series of x-rays of the abdomen.

* Colonoscopy -This is by far the best method for evaluating the colorectal area. Biopsies can be taken of any abnormal areas at the same time. A diagnosis is established by laboratory examination of the cancer tissue.

Staging:

What is the extent of cancer? How advanced is the cancer? What areas of the body are involved? Has the cancer spread to lymph glands, bones, liver, etc.? This step is referred to as staging. These important questions must be answered prior to treatment. The answers to these questions should be obtained by utilizing a minimal number of tests and least invasive methods.

Once the diagnosis is established, the next step is to determine the extent of the disease and to implement an appropriate treatment plan. A cancer specialist should be involved for proper planning of testing and studies. A chest x-ray is always a routine aspect of this workup. Further testing will rely on the findings of the physician and his intuition. Other x-rays, CT scans, Bone scan, MRI study , etc., will determine the extent of the cancer. CEA is a blood test which indicates the presence of the cancer.

Prognosis and treatment plans for colorectal cancer depend on the extent and pattern of spread of the cancer at the time of diagnosis. Staging workup is incomplete until the removed cancer is studied by a pathologist.

* Stage 1 or Duke A: When the cancer is limited to the inside of bowel
* Stage 2 or Duke B: When the cancer is larger and penetrates through the wall of the bowel to the outside layers
* Stage 3 or Duke C: When cancer has spread to the lymph glands in the abdomen
* Stage 4 or Duke D: When the cancer has spread to other organs -- liver, lungs, etc.

-References From Wikipedia-

Breast cancer is the most common cancer in women, being responsible for almost 20 percent of all cancer deaths in women. It ranks second after lung cancer. Roughly 180,000 women are diagnosed with this disease each year, of which 44,000 will die. With increased awareness and increased use of routine mammograms,more women are diagnosed in the earlier stages of this disease, at which time a cure may be possible. For every 100 women, one man is diagnosed with this disease. The disease is more common in women after age 40. It is also more frequent in women of a higher social-economic class.

Causes and risk factors:

Many factors are known to increase the risk of development of breast cancer:



* Genetic predisposition. A few genetic markers have been linked to development
of breast cancer.
* History of breast cancer in a first-degree relative
* History of breast cancer in the same patient, in the opposite breast
* Onset of menstruation in early ages
* Late onset of menopause
* Radiation exposure
* Heavy alcohol consumption
* High fat diet
* Obesity
* First pregnancy after age of 30
* Very tall women

Signs and Symptoms:

More women are now being diagnosed by means of a routine mammogram. Others may feel a lump in the breast or notice abnormal discharge from the nipple, or feel thickness or swelling of the skin or nipple. It is frequently diagnosed by a physician during a routine breast examination.

Any lump in the breast and any mammogram abnormality must be studied very carefully. If any degree of suspicion exists as to the nature of the lump, it should be

biopsied. This may be accomplished by Fine Needle Aspiration, a Core Biopsy or Surgical Biopsy.

Staging:

What is the extent of cancer? How advanced is the cancer? What areas of the body are involved? Has the cancer spread to lymph glands, bones, liver, etc.? Resolving these questions is referred to as staging. These are the most important questions to be answered prior to an effective treatment plan being implemented. The answers to these questions should be obtained by a minimal amount of tests and by least invasive methods. Sentinel Node biopsy is a newer method of evaluating lymph node involvement.

Once the diagnosis is established, the next step is determination of the extent of the disease and appropriate treatment planning. A cancer specialist should be engaged to plan for proper testing and studies. A chest x-ray is always a routine part of workup. Further tests will depend on the findings by the physician and his intuition. Other x-rays, CT scans, Bone scan, MRI study, etc. are performed to determine the extent of the cancer.

-References From Wikipedia-

A brain tumor is any intracranial tumor created by abnormal and uncontrolled cell division, normally either in the brain itself (neurons, glial cells (astrocytes, oligodendrocytes, ependymal cells), lymphatic tissue, blood vessels), in the cranial nerves (myelin-producing Schwann cells), in the brain envelopes (meninges), skull, pituitary and pineal gland, or spread from cancers primarily located in other organs (metastatic tumors). Primary (true) brain tumors are commonly located in the posterior cranial fossa in children and in the anterior two-thirds of the cerebral hemispheres in adults, although they can affect any part of the brain. In the United States in the year 2005, it was estimated that there were 43,800 new cases of brain tumors (Central Brain Tumor Registry of the United States, Primary Brain Tumors in the United States, Statistical Report, 2005 - 2006),which accounted for 1.4 percent of all cancers, 2.4 percent of all cancer deaths,and 20–25 percent of pediatric cancers.Ultimately, it is estimated that there are 13,000 deaths/year as a result of brain tumors.

Primary tumors

Tumors occurring in the brain include: astrocytoma, pilocytic astrocytoma, dysembryoplastic neuroepithelial tumor, oligodendrogliomas, ependymoma, glioblastoma multiforme, mixed gliomas, oligoastrocytomas, medulloblastoma, retinoblastoma, neuroblastoma, germinoma and teratoma.

Most primary brain tumors originate from glia (gliomas) such as astrocytes (astrocytomas), oligodendrocytes (oligodendrogliomas), or ependymal cells (ependymoma). There are also mixed forms, with both an astrocytic and an oligodendroglial cell component. These are called mixed gliomas or oligoastrocytomas. Plus, mixed glio-neuronal tumors (tumors displaying a neuronal, as well as a glial component, e.g. gangliogliomas, disembryoplastic neuroepithelial tumors) and tumors originating from neuronal cells (e.g. gangliocytoma, central gangliocytoma) can also be encountered.

Other varieties of primary brain tumors include: primitive neuroectodermal tumors (PNET, e.g. medulloblastoma, medulloepithelioma, neuroblastoma, retinoblastoma, ependymoblastoma), tumors of the pineal parenchyma (e.g. pineocytoma, pineoblastoma), ependymal cell tumors, choroid plexus tumors, neuroepithelial tumors of uncertain origin (e.g. gliomatosis cerebri, astroblastoma), etc.

From a histological perspective, astrocytomas, oligondedrogliomas, oligoastrocytomas, and teratomas may be benign or malignant. Glioblastoma multiforme represents the most aggressive variety of malignant glioma. At the opposite end of the spectrum, there are so-called pilocytic astrocytomas, a distinct variety of astrocytic tumors. The majority of them are located in the posterior cranial fossa, affect mainly children and young adults, and have a clinically favorable course and prognosis. Teratomas and other germ cell tumors also may have a favorable prognosis, although they have the capacity to grow very large.

Another type of primary intracranial tumor is primary cerebral lymphoma, also known as primary CNS lymphoma, which is a type of non-Hodgkin's lymphoma that is much more prevalent in those with severe immunosuppression, e.g. AIDS.

In contrast to other types of cancer, primary brain tumors rarely metastasize, and in this rare event, the tumor cells spread within the skull and spinal canal through the cerebrospinal fluid, rather than via bloodstream to other organs.

There are various classification systems currently in use for primary brain tumors, the most common being the World Health Organization (WHO) brain tumor classification, introduced in 1993.

Secondary tumors and non-tumor lesions

Secondary or metastatic brain tumors originate from malignant tumors (cancers) located primarily in other organs. Their incidence is higher than that of primary brain tumors. The most frequent types of metastatic brain tumors originate in the lung, skin (malignant melanoma), kidney (hypernephroma), breast (breast carcinoma), and colon (colon carcinoma). These tumor cells reach the brain via the blood-stream.

Some non-tumoral masses and lesions can mimic tumors of the central nervous system. These include tuberculosis of the brain, cerebral abscess (commonly in toxoplasmosis), and hamartomas (for example, in tuberous sclerosis and von Recklinghausen neurofibromatosis).

Symptoms of brain tumors may depend on two factors: tumor size (volume) and tumor location. The time point of symptom onset in the course of disease correlates in many cases with the nature of the tumor ("benign", i.e. slow-growing/late symptom onset, or malignant (fast growing/early symptom onset).

Many low-grade (benign) tumors can remain asymptomatic (symptom-free) for years and they may accidentally be discovered by imaging exams for unrelated reasons (such as a minor trauma).

New onset of epilepsy is a frequent reason for seeking medical attention in brain tumor cases.

Large tumors or tumors with extensive perifocal swelling edema inevitably lead to elevated intracranial pressure (intracranial hypertension), which translates clinically into headaches, vomiting (sometimes without nausea), altered state of consciousness (somnolence, coma), dilatation of the pupil on the side of the lesion (anisocoria), papilledema (prominent optic disc at the funduscopic examination). However, even small tumors obstructing the passage of cerebrospinal fluid (CSF) may cause early signs of increased intracranial pressure. Increased intracranial pressure may result in herniation (i.e. displacement) of certain parts of the brain, such as the cerebellar tonsils or the temporal uncus, resulting in lethal brainstem compression. In young children, elevated intracranial pressure may cause an increase in the diameter of the skull and bulging of the fontanelles.

Depending on the tumor location and the damage it may have caused to surrounding brain structures, either through compression or infiltration, any type of focal neurologic symptoms may occur, such as cognitive and behavioral impairment, personality changes, hemiparesis, (hemi) hypesthesia, aphasia, ataxia, visual field impairment, facial paralysis, double vision, tremor etc. These symptoms are not specific for brain tumors - they may be caused by a large variety of neurologic conditions (e.g. stroke, traumatic brain injury). What counts, however, is the location of the lesion and the functional systems (e.g. motor, sensory, visual, etc.) it affects.

A bilateral temporal visual field defect (bitemporal hemianopia—due to compression of the optic chiasm), often associated with endocrine disfunction—either hypopituitarism or hyperproduction of pituitary hormones and hyperprolactinemia is suggestive of a pituitary tumor.

Brain tumors in infants and children

In 2000 approximately 2.76 children per 100,000 were affected by a CNS tumor in the United States. This rate has been increasing and by 2005 was 3.0 children per 100,000. This is approximately 2,500-3,000 pediatric brain tumors occurring each year in the US. The tumor incidence is increasing by about 2.7% per year. The CNS Cancer survival rate in children is approximately 60%. However, this rate varies with the age of onset (younger has higher mortality) and cancer type.

In children under 2, about 70% of brain tumors are medulloblastoma, ependymoma, and low-grade glioma. Less commonly, and seen usually in infants, are teratoma and atypical teratoid rhabdoid tumor.

Signs and symptoms

Diagnosis

Although there is no specific clinical symptom or sign for brain tumours, slowly progressive focal neurologic signs and signs of elevated intracranial pressure, as well as epilepsy in a patient with a negative history for epilepsy should raise red flags. However, a sudden onset of symptoms, such as an epileptic seizure in a patient with no prior history of epilepsy, sudden intracranial hypertension (this may be due to bleeding within the tumour, brain swelling or obstruction of cerebrospinal fluid's passage) is also possible.

Symptoms include phantom odours and tastes. Often, in the case of metastatic tumours, the smell of vulcanized rubber is prevalent.[citation needed]

Imaging plays a central role in the diagnosis of brain tumours. Early imaging methods—invasive and sometimes dangerous—such as pneumoencephalography and cerebral angiography, have been abandoned in recent times in favour of non-invasive, high-resolution modalities, such as computed tomography (CT) and especially magnetic resonance imaging (MRI). Benign brain tumours often show up as hypodense (darker than brain tissue) mass lesions on cranial CT-scans. On MRI, they appear either hypo- (darker than brain tissue) or isointense (same intensity as brain tissue) on T1-weighted scans, or hyperintense (brighter than brain tissue) on T2-weighted MRI. Perifocal edema also appears hyperintense on T2-weighted MRI. Contrast agent uptake, sometimes in characteristic patterns, can be demonstrated on either CT or MRI-scans in most malignant primary and metastatic brain tumours. This is due to the fact that these tumours disrupt the normal functioning of the blood-brain barrier and lead to an increase in its permeability.

Electrophysiological exams, such as electroencephalography (EEG) play a marginal role in the diagnosis of brain tumours.

The definitive diagnosis of brain tumour can only be confirmed by histological examination of tumour tissue samples obtained either by means of brain biopsy or open surgery. The histologic examination is essential for determining the appropriate treatment and the correct prognosis. This examination, performed by a pathologist, typically has three stages: interoperative examination of fresh tissue, preliminary microscopic examination of prepared tissues, and followup examination of prepared tissues after immunohistochemical staining or genetic analysis.

Treatment and prognosis

Many meningiomas, with the exception of some tumors located at the skull base, can be successfully removed surgically. In more difficult cases, stereotactic radiosurgery, such as Gamma Knife radiosurgery, remains a viable option.

Most pituitary adenomas can be removed surgically, often using a minimally invasive approach through the nasal cavity and skull base (trans-nasal, trans-sphenoidal approach). Large pituitary adenomas require a craniotomy (opening of the skull) for their removal. Radiotherapy, including stereotactic approaches, is reserved for the inoperable cases.

Although there is no generally accepted therapeutic management for primary brain tumors, a surgical attempt at tumor removal or at least cytoreduction (that is, removal of as much tumor as possible, in order to reduce the number of tumor cells available for proliferation) is considered in most cases. However, due to the infiltrative nature of these lesions, tumor recurrence, even following an apparently complete surgical removal, is not uncommon. Postoperative radiotherapy and chemotherapy are integral parts of the therapeutic standard for malignant tumors. Radiotherapy may also be administered in cases of "low-grade" gliomas, when a significant tumor burden reduction could not be achieved surgically.

Survival rates in primary brain tumors depend on the type of tumor, age, functional status of the patient, the extent of surgical tumor removal, to mention just a few factors.

Patients with benign gliomas may survive for many years, while survival in most cases of glioblastoma multiforme is limited to a few months after diagnosis.

The main treatment option for single metastatic tumors is surgical removal, followed by radiotherapy and/or chemotherapy. Multiple metastatic tumors are generally treated with radiotherapy and chemotherapy. Stereotactic radiosurgery, such as Gamma Knife radiosurgery, remains a viable option. However, the prognosis in such cases is determined by the primary tumor, and it is generally poor.

A shunt operation is used not as a cure but to relieve the symptoms. The hydrocephalus caused by the blocking drainage of the cerebrospinal fluid can be removed with this operation.

Research to treatment with the VSV-virus

In 2008, Researchers of the Yale University, led by Dr. Anthony van den Pol, have discovered that the Vesicular stomatitis virus, or VSV-virus, can infect and kill brain tumors, without affecting the other brain cells. The oncolytic properties of the virus, which normally applies to cancer cells, have shown to apply to brain tumors as well.

In the research, a human brain tumor was implanted into mice brains. The VSV-virus was injected via its tail and within 3 days all tumor cells were either killed or dying. On the 10,000 infected tumor cells, only one healthy brain cell was affected 'on accident'.

Research to virus-treatment like this has been some years old, but no other viruses have shown to be as efficient or specific as the VSV-virus. Future research will focus on the risks of this treatment, before it can be applied to humans.

-References From Wikipedia-

Lung cancer is a disease of uncontrolled cell growth in tissues of the lung. This growth may lead to metastasis, invasion of adjacent tissue and infiltration beyond the lungs. The vast majority of primary lung cancers are carcinomas of the lung, derived from epithelial cells. Lung cancer, the most common cause of cancer-related death in men and the second most common in women, is responsible for 1.3 million deaths worldwide annually.In the UK, it is the most common site of fatal cancer in both men and women. The most common symptoms are shortness of breath, coughing (including coughing up blood), and weight loss.

The main types of lung cancer are small cell lung carcinoma and non-small cell lung carcinoma. This distinction is important because the treatment varies; non-small cell lung carcinoma (NSCLC) is sometimes treated with surgery, while small cell lung carcinoma (SCLC) usually responds better to chemotherapy and radiation.The most common cause of lung cancer is long term exposure to tobacco smoke. The occurrence of lung cancer in non-smokers, who account for fewer than 10% of cases, appears to be due to a combination of genetic factors,radon gas,asbestos, and air pollution, including second-hand smoke.

Lung cancer may be seen on chest x-ray and computed tomography (CT scan). The diagnosis is confirmed with a biopsy. This is usually performed via bronchoscopy or CT-guided biopsy. Treatment and prognosis depend upon the histological type of cancer, the stage (degree of spread), and the patient's performance status. Possible treatments include surgery, chemotherapy, and radiotherapy. With treatment, the five-year survival rate is 14%

-References From Wikipedia-

The cancer of the mesothelium is known as Mesothelioma. Mesothelioma damages the tissues and other organs of the body and can also affect the cells and spread throughout the body.

Asbestos is the main factor for this disease. People in factories or offices who work under the asbestos roof or people who manufacture asbestos sheets or asbestos related products tend to get this disease. Around 70-80 percent cases for mesothelioma are because of asbestos. However, there are some cases where the person with mesotheliioma has no exposure to asbestos. The tiny particles or asbestos dust float in the air, and when they are inhaled, it leads to health problems. Exposure to asbestos also increases the possibility of lung cancer, and other types of cancers. Smoking as well as exposure to asbestos could lead to cancer in the air passageways.

Before the Internet era it was hard to find any information on mesothelioma. Now, with the advent of Internet, information about the causes, diagnosis, treatments etc can be gained with a click of a mouse. Around 2000 mesothelioma cases are diagnosed in the United States alone every year. In the past 20 years mesothelioma cases have shot up. Mesothilioma mainly affects men rather than women.

Some symptoms of mesothelioma are shortness of breath and chest pain. Mesothelioma is treated by surgery, radiation therapy, chemotherapy etc.

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