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Botulinum neurotoxin is produced by the gram-negative anaerobic bacterium Clostridium botulinum.

Eight serologically distinct botulinum neurotoxins exist, designated as A, B, C1, C2, D, E, F, and G. Seven are associated with paralysis. Types A, B, E and, rarely, F and G are associated with human botulism.

Botulism is a bilaterally symmetric descending neuroparalytic illness caused by botulinum neurotoxin. The German physician and poet Justinus Kerner published the first full description of clinical symptoms of food-borne botulism from 1817-1822. His observations followed an increase in food poisoning in Stuttgart from 1795-1813 caused by general economic hardship related to the Napoleonic wars and a decline in hygienic measures of food production and handling. The illness became known as “sausage poisoning” because it was observed to follow ingestion of spoiled sausage. The word botulism comes from the Latin botulus, meaning sausage.

Kerner deduced that the toxin acts by interrupting signal transmission within the peripheral and sympathetic nervous system, leaving sensory transmission intact. He also hypothesized possible therapeutic uses of the sausage toxin. In 1895, the microbiologist Emile-Pierre van Ermengen discovered the association with an anaerobic bacterium during an outbreak of botulism following a funeral ceremony in the Belgian village of Ellezelles.

When foods tainted with neurotoxin are ingested, the neurotoxin is absorbed and spread hematogenously to peripheral cholinergic nerve terminals, where it blocks the release of acetylcholine. The neurotoxin is heat labile and denatured by cooking. Sporadic outbreaks of botulism in the United States occur after ingestion of home-canned foods, meat products, and preserved fish. The incubation period following ingestion is 18-36 hours.

In contrast, infant botulism is caused by colonization of the gut by C botulinum, and subsequent production and absorption leads to absorption of the toxin. Honey consumption has been implicated in infant botulism, and microbiologic surveys have identified clostridial spores (mostly type B) in up to 25% of honey products.

Wound botulism may occur if the organism infects a wound and produces the toxin. The clinical syndrome of botulism is one of progressive muscle weakness, often beginning in the extraocular or pharyngeal muscles and becoming generalized. GI tract complaints may be prominent. Dilated unreactive pupils are common, and mucous membranes are often dry and erythematous. No sensory signs are associated, and alertness is maintained as long as respiration is adequate.

In 1946, Schantz helped isolate botulinum toxin type A in crystalline form. In the early 1970s, Scott experimented with botulinum toxin type A in monkeys for the treatment of strabismus. In 1977-1978, he performed trials in patients with strabismus. In the mid 1980s, he treated an individual with botulinum toxin for cosmetic reasons. Carruthers, Carruthers, Brin, and the Columbia University group noticed cosmetic improvement following botulinum toxin injection for facial dystonias and began pursuing this line of investigation in the late 1980s and early 1990s.

Botulinum toxins currently are used to treat a variety of disorders including strabismus, hemifacial spasms, focal dystonias (eg, blepharospasm, torticollis, spasmodic dysphonia, limb dystonia, writer’s cramp), spasticity, tremor, tics, synkinesis, hyperhidrosis, achalasia, and sphincter dysfunction. They are being evaluated to treat headaches and pain syndromes. BOTOX® (botulinum toxin type A) currently is approved by the Food and Drug Administration (FDA) for the treatment of blepharospasm and strabismus associated with dystonias, including benign essential blepharospasm or cranial nerve VII disorders in patients aged 12 years or older, and for the treatment of cervical dystonia in adults. Myobloc (botulinum toxin type B) is currently FDA approved for the treatment of cervical dystonia. Injection of botulinum toxins for cosmesis currently is considered off-label use but constitutes their most prevalent use.

Mechanism of action
Botulinum toxins block acetylcholine release, causing a chemical denervation. Neurotransmission at the neuromuscular junction involves the release of acetylcholine from the presynaptic nerve terminal. Acetylcholine release requires docking and binding of the neurotransmitter vesicles to the presynaptic membrane.

Several different proteins mediate this process. N-ethylmaleimide-sensitive fusion protein (NSF) is a cytoplasmic protein that is part of the fusion complex. Soluble N-ethylmaleimide-sensitive fusion–attachment proteins (SNAPs) are found in the cytoplasm and serve as attachment and stabilizing proteins for the NSF complex. SNAP receptors (SNAREs) are found on the vesicle and plasma membranes. SNAREs include vesicle-associated membrane protein (VAMP/synaptobrevin) and the plasma proteins SNAP-25 and syntaxin.

Botulinum toxin is a zinc-dependent endopeptidase made up of a light (50 kilodaltons [kDa]) and a heavy (100 kDa) chain linked by disulfide bonds.

The mechanism of action includes the following 4 key steps (see Image):

• The first step is binding of the toxin to specific receptors on the surface of the presynaptic cell surface, mediated by the C-terminal half of the heavy chain. This step occurs over approximately 30 minutes.
• The second step is internalization, an energy-dependent receptor-mediated endocytic process. In this step, the plasma membrane of the nerve cell invaginates around the toxin-receptor complex, forming a toxin-containing vesicle inside the nerve terminal.
• The third step is translocation. After internalization, the disulfide bond is cleaved, and the 50-kDa light chain of the toxin molecule is released across the endosomal membrane of the endocytic vesicle into the cytoplasm of the nerve terminal.
• The final step is blocking. The 50-kDa light chain of serotypes A and E inhibit acetylcholine release by cleaving a cytoplasmic protein (SNAP-25) required for the docking of acetylcholine vesicles on the inner side of the nerve terminal plasma membrane. Botulinum toxin type D is specific for VAMP/synaptobrevin. Botulinum toxin types B and F also affect the VAMP/synaptobrevin protein. These actions impede the release of acetylcholine into the synaptic cleft.

The clinical effect of botulinum toxin injections lasts 2-6 months and then resolves. Once chemical denervation begins, axon terminals form new unmyelinated sprouts, and the motor endplate regions expand (see Image).

After several months, the inactivated terminals slowly recover function, and the new sprouts and end plates regress. Recovery of inactivated terminals appears to be the basis of the loss of clinical effect several months after injection.

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Prostate Cancer Resource Books:

Here is a list of books that contain informations on prostate cancer, i know its such a big list but i had to cover any aspects of the prostate cancer, so this list will include absolute everything, you can start reading.

1. Albertsen PC, Fryback DG, Storer BE, et al: The impact of co-morbidity on life expectancy among men with localized prostate cancer. J Urol 1996 Jul; 156(1): 127-32[Medline].
2. Albertsen PC, Fryback DG, Storer BE, et al: Long-term survival among men with conservatively treated localized prostate cancer. JAMA 1995 Aug 23-30; 274(8): 626-31[Medline].
3. Amling CL, Kane CJ, Riffenburgh RH, et al: Relationship between obesity and race in predicting adverse pathologic variables in patients undergoing radical prostatectomy. Urology 2001 Nov; 58(5): 723-8[Medline].
4. Berthon P, Valeri A, Cohen-Akenine A, et al: Predisposing gene for early-onset prostate cancer, localized on chromosome 1q42.2-43. Am J Hum Genet 1998 Jun; 62(6): 1416-24[Medline].
5. Bostwick DG: Prostatic intraepithelial neoplasia (PIN): current concepts. J Cell Biochem Suppl 1992; 16H: 10-9[Medline].
6. Bostwick DG, Qian J: High-grade prostatic intraepithelial neoplasia. Mod Pathol 2004 Mar; 17(3): 360-79[Medline].
7. Bratt O, Kristoffersson U, Lundgren R, Olsson H: Familial and hereditary prostate cancer in southern Sweden. A population-based case-control study. Eur J Cancer 1999 Feb; 35(2): 272-7[Medline].
8. Carter BS, Bova GS, Beaty TH, et al: Hereditary prostate cancer: epidemiologic and clinical features. J Urol 1993 Sep; 150(3): 797-802[Medline].
9. Carter HB, Epstein JI, Chan DW, et al: Recommended prostate-specific antigen testing intervals for the detection of curable prostate cancer. JAMA 1997 May 14; 277(18): 1456-60[Medline].
10. Catalona WJ, Smith DS, Ornstein DK: Prostate cancer detection in men with serum PSA concentrations of 2.6 to 4.0 ng/mL and benign prostate examination. Enhancement of specificity with free PSA measurements. JAMA 1997 May 14; 277(18): 1452-5[Medline].
11. Chodak GW, Thisted RA, Gerber GS, et al: Results of conservative management of clinically localized prostate cancer. N Engl J Med 1994 Jan 27; 330(4): 242-8[Medline].
12. Djavan B, Susani M, Bursa B, et al: Predictability and significance of multifocal prostate cancer in the radical prostatectomy specimen. Tech Urol 1999 Sep; 5(3): 139-42[Medline].
13. Etzioni R, Legler JM, Feuer EJ, et al: Cancer surveillance series: interpreting trends in prostate cancer–part III: Quantifying the link between population prostate-specific antigen testing and recent declines in prostate cancer mortality. J Natl Cancer Inst 1999 Jun 16; 91(12): 1033-9[Medline].
14. Feuer EJ, Merrill RM, Hankey BF: Cancer surveillance series: interpreting trends in prostate cancer–part II: Cause of death misclassification and the recent rise and fall in prostate cancer mortality. J Natl Cancer Inst 1999 Jun 16; 91(12): 1025-32[Medline].
15. Gleason DF: Histologic grading of prostate cancer: a perspective. Hum Pathol 1992 Mar; 23(3): 273-9[Medline].
16. Graversen PH, Nielsen KT, Gasser TC, et al: Radical prostatectomy versus expectant primary treatment in stages I and II prostatic cancer. A fifteen-year follow-up. Urology 1990 Dec; 36(6): 493-8[Medline].
17. Greene FL, Sobin LH: The TNM system: our language for cancer care. J Surg Oncol 2002 Jul; 80(3): 119-20[Medline].
18. Hoffman RM, Gilliland FD, Eley JW, et al: Racial and ethnic differences in advanced-stage prostate cancer: the Prostate Cancer Outcomes Study. J Natl Cancer Inst 2001 Mar 7; 93(5): 388-95[Medline].
19. Holmberg L, Bill-Axelson A, Helgesen F, et al: A randomized trial comparing radical prostatectomy with watchful waiting in early prostate cancer. N Engl J Med 2002 Sep 12; 347(11): 781-9[Medline].
20. Hsing AW, Tsao L, Devesa SS: International trends and patterns of prostate cancer incidence and mortality. Int J Cancer 2000 Jan 1; 85(1): 60-7[Medline].
21. Hsing AW, Comstock GW: Serological precursors of cancer: serum hormones and risk of subsequent prostate cancer. Cancer Epidemiol Biomarkers Prev 1993 Jan-Feb; 2(1): 27-32[Medline].
22. Iczkowski KA, Chen HM, Yang XJ, Beach RA: Prostate cancer diagnosed after initial biopsy with atypical small acinar proliferation suspicious for malignancy is similar to cancer found on initial biopsy. Urology 2002 Nov; 60(5): 851-4[Medline].
23. Iczkowski KA, Bassler TJ, Schwob VS, et al: Diagnosis of “suspicious for malignancy” in prostate biopsies: predictive value for cancer. Urology 1998 May; 51(5): 749-57; discussion 757-8[Medline].
24. Jemal A, Murray T, Samuels A, et al: Cancer statistics, 2003. CA Cancer J Clin 2003 Jan-Feb; 53(1): 5-26[Medline].
25. Johansson JE, Andrén O, Andersson SO, et al: Natural history of early, localized prostate cancer. JAMA 2004 Jun 9; 291(22): 2713-9[Medline].
26. Klein EA, Thompson IM, Lippman SM, et al: SELECT: the Selenium and Vitamin E Cancer Prevention Trial: rationale and design. Prostate Cancer Prostatic Dis 2000 Nov; 3(3): 145-151[Medline].
27. Kolonel LN, Nomura AM, Cooney RV: Dietary fat and prostate cancer: current status. J Natl Cancer Inst 1999 Mar 3; 91(5): 414-28[Medline].
28. Labrie F, Candas B, Dupont A, et al: Screening decreases prostate cancer death: first analysis of the 1988 Quebec prospective randomized controlled trial. Prostate 1999 Feb 1; 38(2): 83-91[Medline].
29. Langer JE, Rovner ES, Coleman BG, et al: Strategy for repeat biopsy of patients with prostatic intraepithelial neoplasia detected by prostate needle biopsy. J Urol 1996 Jan; 155(1): 228-31[Medline].
30. Lee F, Siders DB, Torp-Pedersen ST, et al: Prostate cancer: transrectal ultrasound and pathology comparison. A preliminary study of outer gland (peripheral and central zones) and inner gland (transition zone) cancer. Cancer 1991 Feb 15; 67(4 Suppl): 1132-42[Medline].
31. McCahy PJ, Harris CA, Neal DE: Breast and prostate cancer in the relatives of men with prostate cancer. Br J Urol 1996 Oct; 78(4): 552-6[Medline].
32. Morgan TO, Jacobsen SJ, McCarthy WF, et al: Age-specific reference ranges for prostate-specific antigen in black men. N Engl J Med 1996 Aug 1; 335(5): 304-10[Medline].
33. Moyad MA: Soy, disease prevention, and prostate cancer. Semin Urol Oncol 1999 May; 17(2): 97-102[Medline].
34. Ndubuisi SC, Kofie VY, Andoh JY, Schwartz FM: Black-white differences in the stage at presentation of prostate cancer in the District of Columbia. Urology 1995 Jul; 46(1): 71-7[Medline].
35. Punglia RS, D’Amico AV, Catalona WJ, et al: Effect of verification bias on screening for prostate cancer by measurement of prostate-specific antigen. N Engl J Med 2003 Jul 24; 349(4): 335-42[Medline].
36. Rodríguez C, Calle EE, Tatham LM, et al: Family history of breast cancer as a predictor for fatal prostate cancer. Epidemiology 1998 Sep; 9(5): 525-9[Medline].
37. Ruijter ET, Miller GJ, van de Kaa CA, et al: Molecular analysis of multifocal prostate cancer lesions. J Pathol 1999 Jul; 188(3): 271-7[Medline].
38. Sellers TA, Potter JD, Rich SS, et al: Familial clustering of breast and prostate cancers and risk of postmenopausal breast cancer. J Natl Cancer Inst 1994 Dec 21; 86(24): 1860-5[Medline].
39. Smith JR, Freije D, Carpten JD, et al: Major susceptibility locus for prostate cancer on chromosome 1 suggested by a genome-wide search. Science 1996 Nov 22; 274(5291): 1371-4[Medline].
40. Stemmermann GN, Nomura AM, Chyou PH, Yatani R: A prospective comparison of prostate cancer at autopsy and as a clinical event: the Hawaii Japanese experience. Cancer Epidemiol Biomarkers Prev 1992 Mar-Apr; 1(3): 189-93[Medline].
41. Theodorescu D, Broder SR, Boyd JC, et al: p53, bcl-2 and retinoblastoma proteins as long-term prognostic markers in localized carcinoma of the prostate. J Urol 1997 Jul; 158(1): 131-7[Medline].
42. Theodorescu D, Frierson HF, Sikes RA: Molecular determination of surgical margins using fossa biopsies at radical prostatectomy. J Urol 1999 May; 161(5): 1442-8[Medline].
43. Thompson IM, Goodman PJ, Tangen CM, et al: The influence of finasteride on the development of prostate cancer. N Engl J Med 2003 Jul 17; 349(3): 215-24[Medline].
44. Walsh PC, Vaughan ED, Retik AB, Wein A, eds: Campbell’s Urology. Vol 3. 7th ed. Philadelphia, Pa: WB Saunders; 1998: 2487-656.
45. Weinrich MC, Jacobsen SJ, Weinrich SP, et al: Reference ranges for serum prostate-specific antigen in black and white men without cancer. Urology 1998 Dec; 52(6): 967-73[Medline].
46. Whitmore WF Jr: Expectant management of clinically localized prostatic cancer. Semin Oncol 1994 Oct; 21(5): 560-8[Medline].
47. Xu J, Meyers D, Freije D, et al: Evidence for a prostate cancer susceptibility locus on the X chromosome. Nat Genet 1998 Oct; 20(2): 175-9[Medline].
48. Yatani R, Shiraishi T, Nakakuki K, et al: Trends in frequency of latent prostate carcinoma in Japan from 1965-1979 to 1982-1986. J Natl Cancer Inst 1988 Jul 6; 80(9): 683-7[Medline].
49. Zimmerman SM: Factors influencing Hispanic participation in prostate cancer screening. Oncol Nurs Forum 1997 Apr; 24(3): 499-504[Medline].

Prostate Cancer Resource Books

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Pancreatic Cancer Symptoms:

The main symptoms of pancreatic cancer include the following:

• Pain in the abdomen, the back, or both
• Weight loss, often associated with the following:
• Loss of appetite (anorexia)
• Bloating
• Diarrhea or fatty bowel movements that float in water (steatorrhea)
• Rarely may present with new diabetes in a person with weight loss and nausea
• Jaundice (yellowing of the skin)

The symptoms of pancreatic cancer are generally vague and can easily be attributed to other less serious and more common conditions. This lack of specific symptoms explains the high number of people who have a more advanced stage of disease when pancreatic cancer is discovered.

Pancreatic Cancer Symptoms

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The pancreas is a comma-shaped organ about six inches long that is situated horizontally behind the stomach. The pancreatic duct joins the lower end of the bile duct and both ducts drain into the small intestine. The pancreas secretes enzymes that aid digestion and the production of insulin. Insulin regulates sugar metabolism. The pancreas connects through the bile ducts to the small intestine.
Surgery

Surgeons typically recommend surgery for tumors contained in the pancreas. The specific operation depends upon whether the tumor is located in the head, neck, body or tail of the pancreas. In general, tumors located in the head and neck area of the pancreas are managed with the Whipple resection, whereas those in the body and tail are managed with the distal pancreatectomy. Occasionally, a total pancreatectomy is required, though it is used less commonly. Occasionally, portal vein removal may be possible.
Radiation Therapy

Radiation therapy is usually recommended for patients who have localized pancreatic cancers that cannot be removed. It is also generally recommended either following surgical removal of the pancreatic tumor or before an attempt at removal. High-dose radiation can be directed toward the pancreas to destroy cancer cells and reduce a tumor’s size. Most commonly, radiation is delivered from a source outside of the body, usually with high-energy linear accelerators. Sometimes radiation therapy may be delivered with electrons during surgery. Radiation oncologists have developed 3-dimensional conformal techniques that deliver radiation to the area of the pancreas cancer and lymph node sites at risk while protecting important organs such as the kidneys, spinal cord and liver.

Sometimes radiation therapy may be delivered with electrons during surgery in a process called intraoperative radiation therapy (IORT). IORT may be an option for patients in whom the cancer appears to be borderline resectable or unresectable based on images of the tumor. In such instances, the physician team may determine that the external radiation plus chemotherapy component of treatment should be given before surgery to remove the cancer. At the time of subsequent surgery (usually 4-6 weeks after completion of combined chemoradiation), IORT can be delivered to a site of narrow resection margins or to unresectable cancer, as needed.

Specialists typically use radiation in combination with other therapies such as chemotherapy. Clinical trials investigating the best combinations of drugs with radiation therapy are available. Clinical trials may offer the best treatment options for some patients.
Chemotherapy

Chemotherapy can be administered orally or through a vein into the blood stream. Oncologists usually recommend chemotherapy to treat pancreatic cancer that has spread to other parts of the body. It can be combined with other therapies, and physicians usually recommend it for patients who receive radiation therapy. Chemotherapy is given during radiation to enhance the local effects of radiation, and additional cycles of chemotherapy are given after the combined chemoradiation in an attempt to prevent spread of the cancer elsewhere in the body.

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Pancreatic Cancer Info:

Pancreatic cancer is one of the most serious of cancers. It develops when cancerous cells form in the tissues of your pancreas — a large organ that lies horizontally behind the lower part of your stomach. Your pancreas secretes enzymes that aid digestion and hormones that help regulate the metabolism of carbohydrates.

Pancreatic cancer spreads rapidly and is seldom detected in its early stages, which is a major reason why it’s a leading cause of cancer death. Signs and symptoms may not appear until the disease is quite advanced. By that time, the cancer is likely to have spread to other parts of the body and surgical removal is no longer possible.

For years, little was known about pancreatic cancer. But researchers are beginning to understand the genetic basis of the disease — knowledge that may eventually lead to new and better treatments. Just as important, you may be able to reduce your risk of pancreatic cancer with some lifestyle changes.

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Info on Pancreatic Cancer:

Cancer of the pancreas is a disease in which cancer (malignant) cells are found in the tissues of the pancreas. The pancreas is about 6 inches long and is shaped something like a thin pear, wider at one end and narrowing at the other. The pancreas lies behind the stomach, inside a loop formed by part of the small intestine. The broader right end of the pancreas is called the head, the middle section is called the body, and the narrow left end is the tail.

The pancreas has two basic jobs in your body. It produces juices that help you break down (digest) your food, and hormones (such as insulin) that regulate how your body stores and uses food. The area of the pancreas that produces digestive juices is called the exocrine pancreas. About 95% of pancreatic cancers begin in the exocrine pancreas. The hormone-producing area of the pancreas is called the endocrine pancreas. Only about 5% of pancreatic cancers start here. This statement has information on cancer of the exocrine pancreas. For more information on cancer of the endocrine pancreas (also called islet cell cancer) see the PDQ Patient Information Statement on Islet Cell Carcinoma.

Cancer of the pancreas is hard to find (diagnose) because the organ is hidden behind other organs. Organs around the pancreas include the stomach, small intestine, bile ducts (tubes through which bile, a digestive juice made by the liver, flows from the liver to the small intestine), gallbladder (the small sac below the liver that stores bile), the liver, and the spleen (the organ that stores red blood cells and filters blood to remove excess blood cells). The signs of pancreatic cancer are like many other illnesses, and there may be no signs in the first stages. You should see your doctor if you have any of the following: nausea, loss of appetite, weight loss without trying to lose weight, pain in the upper or middle of your abdomen, or yellowing of your skin (jaundice).

If you have symptoms, your doctor will examine you and order tests to see if you have cancer and what your treatment should be. You may have an ultrasound, a test that uses sound waves to find tumors. A CT scan, a special type of x-ray that uses a computer to make a picture of the inside of your abdomen, may also be done. Another special scan called magnetic resonance imaging (MRI), which uses magnetic waves to make a picture of the inside of your abdomen, may be done as well.

A test called an ERCP (endoscopic retrograde cholangiopancreatography) may also be done. During this test, a flexible tube is put down the throat, through the stomach, and into the small intestine. Your doctor can see through the tube and inject dye into the drainage tube (duct) of the pancreas so that the area can be seen more clearly on an x-ray. During ERCP, your doctor may also put a fine needle into the pancreas to take out some cells. This is called a biopsy. The cells can then be looked at under a microscope to see if they contain cancer.

PTC (percutaneous transhepatic cholangiography) is another test that can help find cancer of the pancreas. During this test, a thin needle is put into the liver through your right side. Dye is injected into the bile ducts in the liver so that blockages can be seen on x-rays.

In some cases, a needle can be inserted into the pancreas during an x-ray or ultrasound so that cells can be taken out to see if they contain cancer. You may need surgery to see if you have cancer of the pancreas. If this is the case, your doctor will cut into the abdomen and look at the pancreas and the tissues around it for cancer. If you have cancer and it looks like it has not spread to other tissues, your doctor may remove the cancer or relieve blockages caused by the tumor.

Stages Of Cancer Of The Pancreas
Once cancer of the pancreas is found, more tests will be done to find out if the cancer has spread from the pancreas to the tissues around it or to other parts of the body. This is called staging. The following stages are used for cancer of the pancreas:

Stage I Cancer is found only in the pancreas itself, or has started to spread just to the tissues next to the pancreas, such as the small intestine, the stomach, or the bile duct.

Stage II Cancer has spread to nearby organs such as the stomach, spleen, or colon, but has not entered the lymph nodes. (Lymph nodes are small, bean-shaped structures that are found throughout the body; they produce and store infection-fighting cells).

Stage III Cancer has spread to lymph nodes near the pancreas. The cancer may or may not have spread to nearby organs.

Stage IV Cancer has spread to places far away from the pancreas, such as the liver or lungs.

Recurrent Recurrent disease means that the cancer has come back (recurred) after it has been treated. It may come back in the pancreas or in another part of the body.

How Cancer Of The Pancreas Is Treated
There are treatments for all patients with cancer of the pancreas. Three kinds of treatment are used: surgery (taking out the cancer or relieving symptoms caused by the cancer) radiation therapy (using high-dose x-rays or other high-energy rays to kill cancer cells) chemotherapy (using drugs to kill cancer cells).

The use of biological therapy (using the body’s immune system to fight cancer) is being tested for pancreatic cancer.

Surgery may be used to take out the tumor. Your doctor may take out the cancer using one of the following operations:

A Whipple procedure removes the head of the pancreas, part of the small intestine, and some of the tissues around it. Enough of the pancreas is left to continue making digestive juices and insulin.

Total pancreatectomy takes out the whole pancreas, part of the small intestine, part of the stomach, the bile duct, the gallbladder, spleen, and most of the lymph nodes in the area.

Distal pancreatectomy takes out only the tail of the pancreas.

If your cancer has spread and it cannot be removed, your doctor may do surgery to relieve symptoms. If the cancer is blocking the small intestine and bile builds up in the gallbladder, your doctor may do surgery to go around (bypass) all or part of the small intestine. During this operation, your doctor will cut the gallbladder or bile duct and sew it to the small intestine. This is called biliary bypass. Surgery or x-ray procedures may also be done to put in a tube (catheter) to drain bile that has built up in the area. During these procedures, your doctor may make the catheter drain through a tube to the outside of the body or the catheter may go around the blocked area and drain the bile to the small intestine. In addition, if the cancer is blocking the flow of food from the stomach, the stomach may be sewn directly to the small intestine so you can continue to eat normally.

Radiation therapy uses high-energy x-rays to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external radiation therapy) or from putting materials that produce radiation (radioisotopes) through thin plastic tubes in the area where the cancer cells are found (internal radiation therapy).

Chemotherapy uses drugs to kill cancer cells. Chemotherapy may be taken by pill, or it may be put into the body by a needle in the vein or muscle. Chemotherapy is called a systemic treatment because the drug enters the bloodstream, travels through the body, and can kill cancer cells outside the pancreas.

Biological therapy tries to get your own body to fight cancer. It uses materials made by your own body or made in a laboratory to boost, direct, or restore your body’s natural defenses against disease. Biological therapy is sometimes called biological response modifier (BRM) therapy or immunotherapy. Biological therapy is being tested in clinical trials.

Treatment By Stage

Treatment for cancer of the pancreas depends on the stage of your disease, your age, and your overall condition.

You may receive treatment that is considered standard based on its effectiveness in a number of patients in past studies, or you may choose to go into a clinical trial. Most patients with cancer of the pancreas are not cured with standard therapy and some standard treatments may have more side effects than are desired. For these reasons, clinical trials are designed to find better ways to treat cancer patients and are based on the most up-to-date information. Clinical trials are going on in most parts of the country for all stages of cancer of the pancreas. If you wish to know more about clinical trials, call the Cancer Information Service at 1-800-4-CANCER (1-800-422-6237); TTY at 1-800-332-8615.

STAGE I PANCREATIC CANCER
Your treatment may be one of the following: 1. Surgery to remove the head of the pancreas, part of the small intestine, and some of the surrounding tissues (Whipple procedure). 2. Surgery to remove the entire pancreas and the organs around it (total pancreatectomy). 3. Surgery to remove the tail of the pancreas (distal pancreatectomy) for tumors in the tail of the pancreas. 4. Surgery followed by chemotherapy and radiation therapy. 5. Clinical trials of radiation therapy with or without chemotherapy given before, during, or after surgery.

STAGE II PANCREATIC CANCER
Your treatment may be one of the following: 1. Surgery or other treatments to reduce symptoms. 2. External radiation therapy with or without chemotherapy. 3. Surgery to remove all or part of the pancreas with or without chemotherapy and radiation therapy. 4. Clinical trials of radiation therapy and chemotherapy given before surgery. 5. Clinical trials of radiation therapy plus drugs to make cancer cells more sensitive to radiation (radiosensitizers). 6. Clinical trials of chemotherapy. 7. Clinical trials of radiation therapy given during surgery with or without internal radiation therapy.

STAGE III PANCREATIC CANCER
Your treatment may be one of the following: 1. Surgery or other treatments to reduce symptoms. 2. External radiation therapy with or without chemotherapy. 3. Surgery to remove all or part of the pancreas with or without chemotherapy and radiation therapy. 4. Clinical trials of radiation therapy given before surgery. 5. Clinical trials of surgery plus radiation therapy plus drugs to make cancer cells more sensitive to radiation (radiosensitizers). 6. Clinical trials of chemotherapy. 7. Clinical trials of radiation therapy given during surgery, with or without internal radiation therapy.

STAGE IV PANCREATIC CANCER
Your treatment may be one of the following: 1. Surgery or other treatments to reduce symptoms. 2. Treatments for pain. 3. Clinical trials of chemotherapy or biological therapy.

RECURRENT PANCREATIC CANCER
Your treatment may be one of the following: 1. Chemotherapy. 2. Surgery or other treatments to reduce symptoms. 3. External radiation therapy to reduce symptoms. 4. Treatments for pain. 5. Other medical care to reduce symptoms. 6. Clinical trials of chemotherapy or biological therapy

Pancreatic Cancer © by cancer-info.com

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The 2002 TNM staging system is used to stage prostate cancer, as follows:

T - Primary tumor
TX - Primary tumor cannot be assessed
T0 - No evidence of primary tumor
T1 - Clinically inapparent tumor not palpable or visible by imaging
T1a - Tumor incidental histologic finding in less than or equal to 5% of tissue resected
T1b - Tumor incidental histologic finding in greater than 5% of tissue resected
T1c - Tumor identified by needle biopsy (because of elevated PSA level); tumors found in 1 or both lobes by needle biopsy but not palpable or reliably visible by imaging
T2 - Tumor confined within prostate
T2a - Tumor involving less than half a lobe
T2b - Tumor involving less than or equal to 1 lobe
T2c - Tumor involving both lobes
T3 - Tumor extending through the prostatic capsule; no invasion into the prostatic apex or into, but not beyond, the prostatic capsule
T3a - Extracapsular extension (unilateral or bilateral)
T3b - Tumor invading seminal vesicle(s)
T4 - Tumor fixed or invading adjacent structures other than seminal vesicles (eg, bladder neck, external sphincter, rectum, levator muscles, pelvic wall)
NX - Regional lymph nodes (cannot be assessed)
N0 - No regional lymph node metastasis
N1 - Metastasis in regional lymph node or nodes

Regional lymph nodes are assessed by surgical removal or biopsy of the pelvic lymph nodes, including the obturator chain. The surgical boundaries are the bifurcation of the common iliac, the obturator nerve, and the node of Cloquet.

Distant metastasis:
PM1c - More than 1 site of metastasis present
MX - Distant metastasis cannot be assessed
M0 - No distant metastasis
M1 - Distant metastasis
M1a - Nonregional lymph node(s)
M1b - Bone(s)
M1c - Other site(s)

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DRE and PSA are the 2 components necessary for a modern screening program. Transrectal ultrasound (TRUS) has been associated with a high false-positive rate, making it unsuitable as a screening tool, although it is very useful for directing prostatic biopsies.

The indications for screening are controversial. The American Cancer Society recommendations are as follows:
Both prostate specific antigen (PSA) and digital rectal examination (DRE) should be offered annually, beginning at age 50 years, to men who have at least a 10-year life expectancy and to younger men who are at high risk. Information should be provided to patients regarding potential risks and benefits of intervention.

Advocates of screening believe that early detection is crucial in order to find organ-confined disease and, thereby, impact mortality. If patients wait for symptoms or even positive DRE results, less than half have organ-confined disease. Those who do not advocate screening worry that screening will detect some cancers that are not organ confined or that it may find cancers that are not biologically significant. Currently, age-specific PSA cutoffs are used to guide screening. The trend is toward lowering the threshold level to 2.5 ng/dL, but this has not been widely accepted as yet.

Men who choose to undergo screening should begin at age 50 years. Men in high-risk groups, such as those with a strong familial predisposition (2 or more first-degree relatives are affected) and those of African American race, should begin screening at a younger age (40-45 y). These men are less likely to have the latent form of the disease and benefit from treatment. More data on the precise age to start prostate cancer screening are needed for men at high risk.

Recent data from Canadian and Austrian studies suggest that mortality rates are lower as a result of PSA screening. Canadian data have shown that from 1989-1996, the mortality rate was lower in the PSA-screened cohort than the control group. Recent studies from Tyrol, Austria also show a beneficial result for screening in reducing disease-specific mortality. These beneficial effects are likely due to the fact that treatment rather than observation may enhance disease-specific survival. This was recently shown in a 2002 Scandinavian study that reported significantly reduced disease-specific mortality for radical prostatectomy patients when compared with watchful waiting. No difference in overall survival was noted. Currently, US data have shown a decrease in mortality of 1% per year since 1990, which coincides with the advent of PSA screening. Other theories have been proposed to account for the decrease, and these include changing treatment practices and artifacts in mortality rates secondary to the changing incidence.

Abnormal rectal examination findings
Findings from the DRE are crucial. An irregular, firm prostate or nodule is typical, but many cancers are found in prostates that feel normal. Pay careful attention to the prostate consistency, along with the seminal vesicles and adjacent organs, to detect spread of the disease to these structures.

Overdistended bladder due to outlet obstruction

• Neurologic findings secondary to cord compression: Other subtle findings, such as paresthesias or wasting, are uncommon.
• Lower extremity lymphedema
• Supraclavicular adenopathy
• Lower extremity deep venous thrombosis
• Cancer cachexia

Transrectal ultrasound
TRUS is used to examine the prostate for hypoechoic areas, which are commonly associated with cancers but are not specific enough for diagnostic purposes. At least 6 or, more recently, 10 or more systematic biopsy specimens of peripheral and, occasionally, transitional zones are taken under ultrasound guidance. Samples should include most areas of the gland, irrespective of ultrasonographic abnormalities.

Differential diagnosis
Benign prostatic hypertrophy
Calculi
Prostatic cysts
Prostatic tuberculosis
Prostatitis

© Dan Theodorescu
© Tracey L Krupski

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Pathophysiology
Prostate cancer develops when the rates of cell division and cell death are no longer equal, leading to uncontrolled tumor growth. Following the initial transformation event, further mutations of a multitude of genes, including the genes for p53 and retinoblastoma, can lead to tumor progression and metastasis. Most prostate cancers are adenocarcinomas (95%).

Approximately 4% of cases of prostate cancer have transitional cell morphology and are thought to arise from the urothelial lining of the prostatic urethra. Few cases have neuroendocrine morphology. When present, they are believed to arise from the neuroendocrine stem cells normally present in the prostate or from aberrant differentiation programs during cell transformation.

Of cases of prostate cancer, 70% arise in the peripheral zone, 15-20% arise in the central zone, and 10-15% arise in the transitional zone. Most prostate cancers are multifocal, with synchronous involvement of multiple zones of the prostate, which may be due to clonal and nonclonal tumors.

Natural history
The natural history is still relatively unknown, and many aspects of progression are poorly understood. Symptoms or abnormal DRE findings in the pre-PSA era only brought 40-50% of patients with prostate cancer to medical attention, and these patients usually had locally advanced disease. The advent of PSA testing has helped identify patients with less-advanced, organ-confined disease.

Evidence suggests that most prostate cancers are multifocal and heterogeneous. Cancers can start in the transitional zone or, more commonly, the peripheral zo