Colorectal cancer: Difference between revisions

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===Vaccine===
===Vaccine===
In November 2006, it was announced that a [[vaccine]] had been developed and tested with very promising results.<ref>[http://www.dailymail.co.uk/pages/live/articles/news/news.html?in_article_id=416006&in_page_id=1770 Wheldon, Julie. Vaccine for kidney and bowel cancers 'within three years' ''The Daily Mail'' [[2006-11-13]]]]</ref> The new vaccine, called [[TroVax]], works in a totally different way to existing treatments by harnessing the patient's own immune system to fight the disease. Experts say this suggests that [[gene therapy]] vaccines could prove an effective treatment for a whole range of cancers. [http://www.oxfordbiomedica.co.uk/ Oxford BioMedica] is a British spin-out from Oxford University specializing in the development of gene-based treatments. Phase III trials are underway for renal cancers and planned for colon cancers.<ref>[http://www.medscape.com/viewarticle/561321?src=mp Vaccine Works With Chemotherapy in Colorectal Cancer (Reuters) [[2007-08-13]]]</ref>
In November 2006, it was announced that a [[vaccine]] had been developed and tested with very promising results.<ref>[http://www.dailymail.co.uk/pages/live/articles/news/news.html?in_article_id=416006&in_page_id=1770 Wheldon, Julie. Vaccine for kidney and bowel cancers 'within three years' ''The Daily Mail'' [[2006-11-13]]]]</ref> The new vaccine, called [[TroVax]], works in a totally different way to existing treatments by harnessing the patient's own immune system to fight the disease. Experts say this suggests that [[gene therapy]] vaccines could prove an effective treatment for a whole range of cancers. [http://www.oxfordbiomedica.co.uk/ Oxford BioMedica] is a British spin-out from Oxford University specializing in the development of gene-based treatments. Phase III trials are underway for renal cancers and planned for colon cancers.<ref>[http://www.medscape.com/viewarticle/561321?src=mp Vaccine Works With Chemotherapy in Colorectal Cancer (Reuters) [[2007-08-13]]]</ref>
===Treatment of colorectal cancer metastasis to the liver===
According to the American Cancer Society statistics in 2006 [http://www.cancer.org/docroot/PRO/content/PRO_1_1_Cancer_Statistics_2006_Presentation.asp]greater than 20% of patients present with metastatic (stage IV) colorectal cancer at the time of diagnosis, and up to 25% of this group will have isolated liver metastasis that is potentially resectable. Lesions which undergo curative resection have demonstrated 5-year survival outcomes now exceeding 50%.<ref> Simmonds PC, et al. Surgical Resection of hepatic metastasis from colorectal cancer: A systemic review of published studies. Br J Surg. 2006;94:982-999. PMID 16538219 </ref>
Resectability of a liver met is determined using preoperative imaging studies (Ct or MRI), intraoperative ultrasound, and by direct palpation and visualization during resection. Lesions confined to the right lobe are amenable to en bloc removal with a right hepatectomy (liver resection) surgery. Smaller lesions of the central or left liver lobe may sometimes be resected in anatomic "segments", while large lesions of left hepatic lobe are resected by a procedure called hepatic trisegmentectomy. Treatment of lesions by smaller,non-anatomic "wedge" resections is associated with higher recurrence rates. Some lesions which are not initially amenable to surgical resection may become candidates if they have significant responses to preoperative chemotherapy or immunotherapy regimines. Lesions which are not amenable to surgical resection for cure can be treated with modalities including radio-frequency ablation (RFA), cryoablation, and chemoembolization.
Patients with colon cancer and metastatic disease to the liver may be treated in either a single surgery or in staged surgeries (with the colon tumor traditionally removed first) depending upon the fitness of the patient for prolonged surgery, the difficulty expected with the procedure with either the colon or liver resection, and the comfort of the surgery performing potentially complex hepatic surgery.
Poor pronostic factors of patients with liver metastasis include
* Synchronous (diagnosed simultaneously) liver and primary colorectal tumors
* A short time between detecting the primary cancer and subsequent development of liver mets
* Multiple metastatic lesions
* High blood levels of the tumor marker, carcino-embryonic antigen ('''CEA'''), in the patient prior to resection
* Larger size metastatic lesions


==Prognosis==
==Prognosis==

Revision as of 20:24, 9 December 2011

For patient information click here

Template:DiseaseDisorder infobox

Colorectal cancer Microchapters

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Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Differentiating Colorectal cancer from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

X Ray

CT

MRI

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Treatment

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Editor(s)-in-Chief: C. Michael Gibson, M.S.,M.D. [1] Phone:617-632-7753; Elliot B. Tapper, M.D., Beth Israel Deaconess Medical Center

Overview

History & Symptoms

Risk factors

Screening

Diagnosis

History and Symptoms | Physical Examination | Staging | Lab Studies | Electrocardiogram | X Ray | MRI | CT | Echocardiography | Other imaging findings

Pathophysiology

Treatment

The treatment depends on the staging of the cancer. When colorectal cancer is caught at early stages (with little spread) it can be curable. However when it is detected at later stages (when distant metastases are present) it is less likely to be curable.

Medical therapy | Surgical options | Primary prevention | Secondary prevention | Financial costs | Future therapies

Vaccine

In November 2006, it was announced that a vaccine had been developed and tested with very promising results.[1] The new vaccine, called TroVax, works in a totally different way to existing treatments by harnessing the patient's own immune system to fight the disease. Experts say this suggests that gene therapy vaccines could prove an effective treatment for a whole range of cancers. Oxford BioMedica is a British spin-out from Oxford University specializing in the development of gene-based treatments. Phase III trials are underway for renal cancers and planned for colon cancers.[2]

Prognosis

Survival is directly related to detection and the type of cancer involved. Survival rates for early stage detection is about 5 times that of late stage cancers. CEA level is also directly related to the prognosis of disease, since its level correlates with the bulk of tumor tissue.

Follow-up

The aims of follow-up are to diagnose in the earliest possible stage any metastasis or tumors that develop later but did not originate from the original cancer (metachronous lesions).

The U.S. National Comprehensive Cancer Network and American Society of Clinical Oncology provide guidelines for the follow-up of colon cancer.[3][4] A medical history and physical examination are recommended every 3 to 6 months for 2 years, then every 6 months for 5 years. Carcinoembryonic antigen blood level measurements follow the same timing, but are only advised for patients with T2 or greater lesions who are candidates for intervention. A CT-scan of the chest, abdomen and pelvis can be considered annually for the first 3 years for patients who are at high risk of recurrence (for example, patients who had poorly differentiated tumors or venous or lymphatic invasion) and are candidates for curative surgery (with the aim to cure). A colonoscopy can be done after 1 year, except if it could not be done during the initial staging because of an obstructing mass, in which case it should be performed after 3 to 6 months. If a villous polyp, polyp >1 centimeter or high grade dysplasia is found, it can be repeated after 3 years, then every 5 years. For other abnormalities, the colonoscopy can be repeated after 1 year.

Routine PET or ultrasound scanning, chest X-rays, complete blood count or liver function tests are not recommended.[3][4] These guidelines are based on recent meta-analyses showing that intensive surveillance and close follow-up can reduce the 5-year mortality rate from 37% to 30%.[5][6][7]

Prevention

Most colorectal cancers should be preventable, through increased surveillance, improved lifestyle, and, probably, the use of dietary chemopreventative agents.

Surveillance

Most colorectal cancer arise from adenomatous polyps. These lesions can be detected and removed during colonoscopy. Studies show this procedure would decrease by > 80% the risk of cancer death, provided it is started by the age of 50, and repeated every 5 or 10 years.[8]

As per current guidelines under National Comprehensive Cancer Network, in average risk individuals with negative family history of colon cancer and personal history negative for adenomas or Inflammatory Bowel diseases, flexible sigmoidoscopy every 5 years with fecal occult blood testing annually or double contrast barium enema are other options acceptable for screening rather than colonoscopy every 10 years (which is currently the Gold-Standard of care).

Lifestyle & Nutrition

The comparison of colorectal cancer incidence in various countries strongly suggests that sedentarity, overeating (i.e., high caloric intake), and perhaps a diet high in meat (red or processed) could increase the risk of colorectal cancer. In contrast, a healthy body weight, physical fitness, and good nutrition decreases cancer risk in general. Accordingly, lifestyle changes could decrease the risk of colorectal cancer as much as 60-80%.[9]

A high intake of dietary fiber (from eating fruits, vegetables, cereals, and other high fiber food products) has, until recently, been thought to reduce the risk of colorectal cancer and adenoma. In the largest study ever to examine this theory (88,757 subjects tracked over 16 years), it has been found that a fiber rich diet does not reduce the risk of colon cancer. [10] A 2005 meta-analysis study further supports these findings.[11]

The Harvard School of Public Health states: "Health Effects of Eating Fiber: Long heralded as part of a healthy diet, fiber appears to reduce the risk of developing various conditions, including heart disease, diabetes, diverticular disease, and constipation. Despite what many people may think, however, fiber probably has little, if any effect on colon cancer risk." [12]

Chemoprevention

More than 200 agents, including the above cited phytochemicals, and other food components like calcium or folic acid (a B vitamin), and NSAIDs like aspirin, are able to decrease carcinogenesis in preclinical models: Some studies show full inhibition of carcinogen-induced tumours in the colon of rats. Other studies show strong inhibition of spontaneous intestinal polyps in mutated mice (Min mice). Chemoprevention clinical trials in human volunteers have shown smaller prevention, but few intervention studies have been completed today. Calcium, aspirin and celecoxib supplements, given for 3 to 5 years after the removal of a polyp, decreased the recurrence of polyps in volunteers (by 15-40%). The "chemoprevention database" shows the results of all published scientific studies of chemopreventive agents, in people and in animals.[13]

Aspirin chemoprophylaxis

Aspirin should not be taken routinely to prevent colorectal cancer, even in people with a family history of the disease, because the risk of bleeding and kidney failure from high dose aspirin (300mg or more) outweigh the possible benefits.[14]

A clinical practice guideline by the U.S. Preventive Services Task Force (USPSTF) recommended against taking aspirin (grade D recommendation).[15] The Task Force acknowledged that aspirin may reduce the incidence of colorectal cancer, but "concluded that harms outweigh the benefits of aspirin and NSAID use for the prevention of colorectal cancer". A subsequent meta-analysis concluded "300 mg or more of aspirin a day for about 5 years is effective in primary prevention of colorectal cancer in randomised controlled trials, with a latency of about 10 years".[16] However, long-term doses over 81 mg per day may increase bleeding events.[17]

Calcium

A meta-analysis by the Cochrane Collaboration of randomized controlled trials published through 2002 concluded "Although the evidence from two RCTs suggests that calcium supplementation might contribute to a moderate degree to the prevention of colorectal adenomatous polyps, this does not constitute sufficient evidence to recommend the general use of calcium supplements to prevent colorectal cancer.".[18] Subsequently, one randomized controlled trial by the Women's Health Initiative (WHI) reported negative results.[19] A second randomized controlled trial reported reduction in all cancers, but had insufficient colorectal cancers for analysis.[20]

Mathematical modeling

Colorectal cancer has been for years subject of mathematical modeling.[21] For a comprehensive overview of current computational approaches on colorectal cancer see the Integrative Biology web page.

References

  1. Wheldon, Julie. Vaccine for kidney and bowel cancers 'within three years' The Daily Mail 2006-11-13]
  2. Vaccine Works With Chemotherapy in Colorectal Cancer (Reuters) 2007-08-13
  3. 3.0 3.1 NCCN Clinical Practice Guidelines in Oncology - Colon Cancer (version 1, 2008: September 19, 2007).
  4. 4.0 4.1 Desch CE, Benson AB 3rd, Somerfield MR, et al; American Society of Clinical Oncology (2005). "Colorectal cancer surveillance: 2005 update of an American Society of Clinical Oncology practice guideline" (PDF). J Clin Oncol. 23 (33): 8512–9.
  5. Jeffery M, Hickey BE, Hider PN (2002). "Follow-up strategies for patients treated for non-metastatic colorectal cancer". Cochrane Database Syst Rev. CD002200.
  6. Renehan AG, Egger M, Saunders MP, O'Dwyer ST (2002). "Impact on survival of intensive follow up after curative resection for colorectal cancer: systematic review and meta-analysis of randomised trials". BMJ. 324 (7341): 831–8.
  7. Figueredo A, Rumble RB, Maroun J, et al; Gastrointestinal Cancer Disease Site Group of Cancer Care Ontario's Program in Evidence-based Care. (2003). "Follow-up of patients with curatively resected colorectal cancer: a practice guideline". BMC Cancer. 3: 26.
  8. Winawer SJ, Zauber AG, Ho MN, O'Brien MJ, Gottlieb LS, Sternberg SS, Waye JD, Schapiro M, Bond JH, Panish JF, Ackroyd F, Shike M, Kurtz RC, Hornsby-Lewis L, Gerdes H, Stewart ET, The National Polyp Study Workgroup. Prevention of colorectal cancer by colonoscopic polypectomy. N Engl J Med 1993;329:1977-81. PMID 8247072.
  9. Cummings, JH (1998). "Diet and the prevention of cancer". BMJ: 1636–40. PMID 9848907. Text "issue317" ignored (help); Unknown parameter |coauthors= ignored (help)
  10. "Dietary Fiber and the Risk of Colorectal Cancer and Adenoma in Women". New England Journal of Medicine (340): 169–76. 1999.
  11. "Dietary Fiber and Colorectal Cancer: An Ongoing Saga". Journal of the American Medical Association (294(22)): 2904–2906. 2005. PMID 16352792.
  12. "Health Effects of Eating Fiber".
  13. "Colorectal Cancer Prevention: Chemoprevention Database". Retrieved 2007-08-23.
  14. Agency for Healthcare Research and Quality (2007-03-05). "Task Force Recommends Against Use of Aspirin and Non-Steroidal Anti-Inflammatory Drugs to Prevent Colorectal Cancer". United States Department of Health & Human Services. Retrieved 2007-05-07.
  15. "Routine aspirin or nonsteroidal anti-inflammatory drugs for the primary prevention of colorectal cancer: U.S. Preventive Services Task Force recommendation statement". Ann. Intern. Med. 146 (5): 361–4. 2007. pmid=17339621. PMID 17339621
  16. Flossmann E, Rothwell PM (2007). "Effect of aspirin on long-term risk of colorectal cancer: consistent evidence from randomised and observational studies". Lancet. 369 (9573): 1603–13. doi:10.1016/S0140-6736(07)60747-8. PMID 17499602. PMID 17499602
  17. Campbell CL, Smyth S, Montalescot G, Steinhubl SR (2007). "Aspirin dose for the prevention of cardiovascular disease: a systematic review". JAMA. 297 (18): 2018–24. doi:10.1001/jama.297.18.2018. PMID 17488967. PMID 17488967
  18. Weingarten MA, Zalmanovici A, Yaphe J (2005). "Dietary calcium supplementation for preventing colorectal cancer and adenomatous polyps". Cochrane database of systematic reviews (Online) (3): CD003548. doi:10.1002/14651858.CD003548.pub3. PMID 16034903.
  19. Wactawski-Wende J, Kotchen JM, Anderson GL; et al. (2006). "Calcium plus vitamin D supplementation and the risk of colorectal cancer". N. Engl. J. Med. 354 (7): 684–96. doi:10.1056/NEJMoa055222. PMID 16481636.
  20. Lappe JM, Travers-Gustafson D, Davies KM, Recker RR, Heaney RP (2007). "Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial". Am. J. Clin. Nutr. 85 (6): 1586–91. PMID 17556697.
  21. van Leeuwen I, Byrne H, Jensen O, King J (2006). "Crypt dynamics and colorectal cancer: advances in mathematical modelling". Cell Prolif. 39 (3): 157–81. PMID 16671995.Full text

See also

External links

Template:Gastroenterology Template:Tumors ar:سرطان القولون bs:Rak debelog crijeva bg:Рак на дебелото черво da:Kolorektal cancer de:Kolorektales Karzinom hr:Rak debelog crijeva id:Kanker usus besar it:Tumore del retto he:סרטן המעי הגס la:Cancer colorectalis lt:Storosios žarnos vėžys nl:Darmkanker no:Tarmkreft fi:Paksusuolen syöpä sv:Koloncancer yi:קישקע קענסער


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