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NCI/PDQ® Health professionals: Colon Cancer Treatment (PDQ®)
National Cancer Institute
Last Modified: December 31, 2012
General Information About Colon Cancer
Back Up
Cancer of the colon is a highly treatable and often curable disease when localized to the bowel. Surgery is the primary form of treatment and results in cure in approximately 50% of the patients. Recurrence following surgery is a major problem and is often the ultimate cause of death.
Incidence and Mortality
Note: Estimated new cases and deaths from colon cancer in the United States in 2012: 1
- New cases: 103,170 (colon cancer only).
- Deaths: 51,690 (colon and rectal cancers combined).
Gastrointestinal stromal tumors can occur in the colon. (Refer to the PDQ® summary on Gastrointestinal Stromal Tumors Treatment for more information.)
Anatomy
Risk Factors
Groups that have a high incidence of colorectal cancer include those with hereditary conditions. Together, these groups account for 10% to 15% of colorectal cancers. These groups include the following:
- Familial polyposis.
- Hereditary nonpolyposis colon cancer (HNPCC) or Lynch syndrome variants I and II.
- A personal history of ulcerative colitis or Crohn colitis. 2 3
More common conditions with an increased risk include the following:
- A personal history of colorectal cancer or adenomas.
- First-degree family history of colorectal cancer or adenomas.
- A personal history of ovarian, endometrial, or breast cancer. 4 5
These high-risk groups account for only 23% of all colorectal cancers. Limiting screening or early cancer detection to only these high-risk groups would miss the majority of colorectal cancers. 6 (Refer to the PDQ® summaries on Colorectal Cancer Screening and Colorectal Cancer Prevention for more information.)
Screening
Because of the frequency of the disease, ability to identify high-risk groups, slow growth of primary lesions, better survival of patients with early-stage lesions, and relative simplicity and accuracy of screening tests, screening for colon cancer should be a part of routine care for all adults aged 50 years and older, especially for those with first-degree relatives with colorectal cancer. (Refer to the PDQ® summary on Colorectal Cancer Screening for more information.)
Prognostic Factors
The prognosis of patients with colon cancer is clearly related to the following:
- The degree of penetration of the tumor through the bowel wall.
- The presence or absence of nodal involvement.
- The presence or absence of distant metastases.
These three characteristics form the basis for all staging systems developed for this disease.
Other prognostic factors include the following:
- Bowel obstruction and bowel perforation are indicators of poor prognosis. 7
- Elevated pretreatment serum levels of carcinoembryonic antigen (CEA) have a negative prognostic significance. 8
Many other prognostic markers have been evaluated retrospectively for patients with colon cancer, though most, including allelic loss of chromosome 18q or thymidylate synthase expression, have not been prospectively validated. 9 10 11 12 13 14 15 16 17 18 Microsatellite instability, also associated with HNPCC, has been associated with improved survival independent of tumor stage in a population-based series of 607 patients younger than 50 years with colorectal cancer. 19 Patients with HNPCC reportedly have better prognoses in stage-stratified survival analysis than patients with sporadic colorectal cancer, but the retrospective nature of the studies and possibility of selection factors make this observation difficult to interpret. 20
Treatment decisions depend on factors such as physician and patient preferences and the stage of the disease, rather than the age of the patient. 21 22 23
Racial differences in overall survival after adjuvant therapy have been observed, without differences in disease-free survival, suggesting that comorbid conditions play a role in survival outcome in different patient populations. 24
Follow-up
Following treatment of colon cancer, periodic evaluations may lead to the earlier identification and management of recurrent disease. 25 26 27 28 The impact of such monitoring on overall mortality of patients with recurrent colon cancer, however, is limited by the relatively small proportion of patients in whom localized, potentially curable metastases are found. To date, no large-scale randomized trials have documented the efficacy of a standard, postoperative monitoring program. 29 30 31 32 33
CEA is a serum glycoprotein frequently used in the management of patients with colon cancer. A review of the use of this tumor marker suggests the following: 34
- A CEA level is not a valuable screening test for colorectal cancer because of the large numbers of false-positive and false-negative reports.
- Postoperative CEA testing should be restricted to patients who would be candidates for resection of liver or lung metastases.
- Routine use of CEA levels alone for monitoring response to treatment should not be recommended.
The optimal regimen and frequency of follow-up examinations are not well defined because the impact on patient survival is not clear and the quality of data is poor. 31 32 33 New surveillance methods, including CEA immunoscintigraphy 35 and positron emission tomography, 36 are under clinical evaluation.
Related Summaries
Other PDQ® summaries containing information related to colon cancer include the following:
References:
- American Cancer Society.: Cancer Facts and Figures 2012. Atlanta, Ga: American Cancer Society, 2012. Available online [PUBMED Abstract]
- Thorson AG, Knezetic JA, Lynch HT: A century of progress in hereditary nonpolyposis colorectal cancer (Lynch syndrome). Dis Colon Rectum 42 (1): 1-9, 1999. [PUBMED Abstract]
- Smith RA, von Eschenbach AC, Wender R, et al.: American Cancer Society guidelines for the early detection of cancer: update of early detection guidelines for prostate, colorectal, and endometrial cancers. Also: update 2001--testing for early lung cancer detection. CA Cancer J Clin 51 (1): 38-75; quiz 77-80, 2001 Jan-Feb. [PUBMED Abstract]
- Ransohoff DF, Lang CA: Screening for colorectal cancer. N Engl J Med 325 (1): 37-41, 1991. [PUBMED Abstract]
- Fuchs CS, Giovannucci EL, Colditz GA, et al.: A prospective study of family history and the risk of colorectal cancer. N Engl J Med 331 (25): 1669-74, 1994. [PUBMED Abstract]
- Winawer SJ: Screening for colorectal cancer. Cancer: Principles and Practice of Oncology Updates 2(1): 1-16, 1987. [PUBMED Abstract]
- Steinberg SM, Barkin JS, Kaplan RS, et al.: Prognostic indicators of colon tumors. The Gastrointestinal Tumor Study Group experience. Cancer 57 (9): 1866-70, 1986. [PUBMED Abstract]
- Filella X, Molina R, Grau JJ, et al.: Prognostic value of CA 19.9 levels in colorectal cancer. Ann Surg 216 (1): 55-9, 1992. [PUBMED Abstract]
- McLeod HL, Murray GI: Tumour markers of prognosis in colorectal cancer. Br J Cancer 79 (2): 191-203, 1999. [PUBMED Abstract]
- Jen J, Kim H, Piantadosi S, et al.: Allelic loss of chromosome 18q and prognosis in colorectal cancer. N Engl J Med 331 (4): 213-21, 1994. [PUBMED Abstract]
- Lanza G, Matteuzzi M, Gafá R, et al.: Chromosome 18q allelic loss and prognosis in stage II and III colon cancer. Int J Cancer 79 (4): 390-5, 1998. [PUBMED Abstract]
- Griffin MR, Bergstralh EJ, Coffey RJ, et al.: Predictors of survival after curative resection of carcinoma of the colon and rectum. Cancer 60 (9): 2318-24, 1987. [PUBMED Abstract]
- Johnston PG, Fisher ER, Rockette HE, et al.: The role of thymidylate synthase expression in prognosis and outcome of adjuvant chemotherapy in patients with rectal cancer. J Clin Oncol 12 (12): 2640-7, 1994. [PUBMED Abstract]
- Shibata D, Reale MA, Lavin P, et al.: The DCC protein and prognosis in colorectal cancer. N Engl J Med 335 (23): 1727-32, 1996. [PUBMED Abstract]
- Bauer KD, Lincoln ST, Vera-Roman JM, et al.: Prognostic implications of proliferative activity and DNA aneuploidy in colonic adenocarcinomas. Lab Invest 57 (3): 329-35, 1987. [PUBMED Abstract]
- Bauer KD, Bagwell CB, Giaretti W, et al.: Consensus review of the clinical utility of DNA flow cytometry in colorectal cancer. Cytometry 14 (5): 486-91, 1993. [PUBMED Abstract]
- Sun XF, Carstensen JM, Zhang H, et al.: Prognostic significance of cytoplasmic p53 oncoprotein in colorectal adenocarcinoma. Lancet 340 (8832): 1369-73, 1992. [PUBMED Abstract]
- Roth JA: p53 prognostication: paradigm or paradox? Clin Cancer Res 5 (11): 3345, 1999. [PUBMED Abstract]
- Gryfe R, Kim H, Hsieh ET, et al.: Tumor microsatellite instability and clinical outcome in young patients with colorectal cancer. N Engl J Med 342 (2): 69-77, 2000. [PUBMED Abstract]
- Watson P, Lin KM, Rodriguez-Bigas MA, et al.: Colorectal carcinoma survival among hereditary nonpolyposis colorectal carcinoma family members. Cancer 83 (2): 259-66, 1998. [PUBMED Abstract]
- Iwashyna TJ, Lamont EB: Effectiveness of adjuvant fluorouracil in clinical practice: a population-based cohort study of elderly patients with stage III colon cancer. J Clin Oncol 20 (19): 3992-8, 2002. [PUBMED Abstract]
- Chiara S, Nobile MT, Vincenti M, et al.: Advanced colorectal cancer in the elderly: results of consecutive trials with 5-fluorouracil-based chemotherapy. Cancer Chemother Pharmacol 42 (4): 336-40, 1998. [PUBMED Abstract]
- Popescu RA, Norman A, Ross PJ, et al.: Adjuvant or palliative chemotherapy for colorectal cancer in patients 70 years or older. J Clin Oncol 17 (8): 2412-8, 1999. [PUBMED Abstract]
- Dignam JJ, Colangelo L, Tian W, et al.: Outcomes among African-Americans and Caucasians in colon cancer adjuvant therapy trials: findings from the National Surgical Adjuvant Breast and Bowel Project. J Natl Cancer Inst 91 (22): 1933-40, 1999. [PUBMED Abstract]
- Martin EW Jr, Minton JP, Carey LC: CEA-directed second-look surgery in the asymptomatic patient after primary resection of colorectal carcinoma. Ann Surg 202 (3): 310-7, 1985. [PUBMED Abstract]
- Bruinvels DJ, Stiggelbout AM, Kievit J, et al.: Follow-up of patients with colorectal cancer. A meta-analysis. Ann Surg 219 (2): 174-82, 1994. [PUBMED Abstract]
- Lautenbach E, Forde KA, Neugut AI: Benefits of colonoscopic surveillance after curative resection of colorectal cancer. Ann Surg 220 (2): 206-11, 1994. [PUBMED Abstract]
- Khoury DA, Opelka FG, Beck DE, et al.: Colon surveillance after colorectal cancer surgery. Dis Colon Rectum 39 (3): 252-6, 1996. [PUBMED Abstract]
- Safi F, Link KH, Beger HG: Is follow-up of colorectal cancer patients worthwhile? Dis Colon Rectum 36 (7): 636-43; discussion 643-4, 1993. [PUBMED Abstract]
- Moertel CG, Fleming TR, Macdonald JS, et al.: An evaluation of the carcinoembryonic antigen (CEA) test for monitoring patients with resected colon cancer. JAMA 270 (8): 943-7, 1993. [PUBMED Abstract]
- Rosen M, Chan L, Beart RW Jr, et al.: Follow-up of colorectal cancer: a meta-analysis. Dis Colon Rectum 41 (9): 1116-26, 1998. [PUBMED Abstract]
- Desch CE, Benson AB 3rd, Smith TJ, et al.: Recommended colorectal cancer surveillance guidelines by the American Society of Clinical Oncology. J Clin Oncol 17 (4): 1312, 1999. [PUBMED Abstract]
- Benson AB 3rd, Desch CE, Flynn PJ, et al.: 2000 update of American Society of Clinical Oncology colorectal cancer surveillance guidelines. J Clin Oncol 18 (20): 3586-8, 2000. [PUBMED Abstract]
- Clinical practice guidelines for the use of tumor markers in breast and colorectal cancer. Adopted on May 17, 1996 by the American Society of Clinical Oncology. J Clin Oncol 14 (10): 2843-77, 1996. [PUBMED Abstract]
- Lechner P, Lind P, Goldenberg DM: Can postoperative surveillance with serial CEA immunoscintigraphy detect resectable rectal cancer recurrence and potentially improve tumor-free survival? J Am Coll Surg 191 (5): 511-8, 2000. [PUBMED Abstract]
- Lonneux M, Reffad AM, Detry R, et al.: FDG-PET improves the staging and selection of patients with recurrent colorectal cancer. Eur J Nucl Med Mol Imaging 29 (7): 915-21, 2002. [PUBMED Abstract]
Cellular Classification of Colon Cancer
Back Up
Histologic types of colon cancer include the following:
- Adenocarcinoma (most colon cancers).
- Mucinous (colloid) adenocarcinoma.
- Signet ring adenocarcinoma.
- Scirrhous tumors.
- Neuroendocrine. 1 Tumors with neuroendocrine differentiation typically have a poorer prognosis than pure adenocarcinoma variants.
References:
- Saclarides TJ, Szeluga D, Staren ED: Neuroendocrine cancers of the colon and rectum. Results of a ten-year experience. Dis Colon Rectum 37 (7): 635-42, 1994. [PUBMED Abstract]
Stage Information for Colon Cancer
Back Up
Treatment decisions should be made with reference to the TNM classification 1 rather than to the older Dukes or the Modified Astler-Coller classification schema.
The American Joint Committee on Cancer (AJCC) and a National Cancer Institutesponsored panel recommended that at least 12 lymph nodes be examined in patients with colon and rectal cancer to confirm the absence of nodal involvement by tumor. 2 3 4 This recommendation takes into consideration that the number of lymph nodes examined is a reflection of the aggressiveness of lymphovascular mesenteric dissection at the time of surgical resection and the pathologic identification of nodes in the specimen. Retrospective studies demonstrated that the number of lymph nodes examined in colon and rectal surgery may be associated with patient outcome. 5 6 7 8
AJCC Stage Groupings and TNM Definitions
The AJCC has designated staging by TNM classification to define colon cancer. 1 The same classification is used for both clinical and pathologic staging. 1
Table 1. Definitions of TNM Stage 0
| Stage |
TNMa,b |
Dukesc |
MACd |
Description |
Illustration |
Table 5.
| 0
|
Tis, N0, M0
|
|
|
Tis = Carcinoma in situ: intraepithelial or invasion of lamina propria.e
|
|
| N0 = No regional lymph node metastasis.
|
| M0 = No distant metastasis.
|
| T = primary tumor; N = regional lymph nodes; M = distant metastasis. |
| Reprinted with permission from AJCC: Colon and rectum. In: Edge SB, Byrd DR, Compton CC, et al., eds.: AJCC Cancer Staging Manual. 7th ed. New York, NY: Springer, 2010, pp 143-164. |
| The explanations for superscripts ag are at the end of |
Table 2. Definitions of TNM Stage I
| Stage |
TNMa,b |
Dukesc |
MACd |
Description |
Illustration |
Table 5.
| I
|
T1, N0, M0
|
A
|
A
|
T1 = Tumor invades submucosa.
|
|
| T2 = Tumor invades muscularis propria.
|
| N0 = No regional lymph node metastasis.
|
| T2, N0, M0
|
A
|
B1
|
M0 = No distant metastasis.
|
| T = primary tumor; N = regional lymph nodes; M = distant metastasis. |
| Reprinted with permission from AJCC: Colon and rectum. In: Edge SB, Byrd DR, Compton CC, et al., eds.: AJCC Cancer Staging Manual. 7th ed. New York, NY: Springer, 2010, pp 143-164. |
| The explanations for superscripts ag are at the end of |
Table 3. Definitions of TNM Stage II
| Stage |
TNMa,b |
Dukesc |
MACd |
Description |
Illustration |
Table 5.
| IIA
|
T3, N0, M0
|
B
|
B2
|
T3 = Tumor invades through the muscularis propria into pericolorectal tissues.
|
|
| N0 = No regional lymph node metastasis.
|
| M0 = No distant metastasis.
|
| IIB
|
T4a, N0, M0
|
B
|
B2
|
T4a = Tumor penetrates to the surface of the visceral peritoneum.f
|
| N0 = No regional lymph node metastasis.
|
| M0 = No distant metastasis.
|
| IIC
|
T4b, N0, M0
|
B
|
B3
|
T4b = Tumor directly invades or is adherent to other organs or structures.f,g
|
| N0 = No regional lymph node metastasis.
|
| M0 = No distant metastasis.
|
| T = primary tumor; N = regional lymph nodes; M = distant metastasis. |
| Reprinted with permission from AJCC: Colon and rectum. In: Edge SB, Byrd DR, Compton CC, et al., eds.: AJCC Cancer Staging Manual. 7th ed. New York, NY: Springer, 2010, pp 143-164. |
| The explanations for superscripts ag are at the end of |
Table 4. Definitions of TNM Stage III
| Stage |
TNMa,b |
Dukesc |
MACd |
Description |
Illustration |
Table 5.
| IIIA
|
T1T2, N1/N1c, M0
|
C
|
C1
|
T1 = Tumor invades submucosa.
|
|
| T2 = Tumor invades muscularis propria.
|
| N1 = Metastases in 13 regional lymph nodes.
|
| T1, N2a, M0
|
C
|
C1
|
N1c = Tumor deposit(s) in the subserosa, mesentery, or nonperitonealized pericolic or perirectal tissues without regional nodal metastasis.
|
| N2a = Metastases in 46 regional lymph nodes.
|
| M0 = No distant metastasis.
|
| IIIB
|
T3T4a, N1/N1c, M0
|
C
|
C2
|
T1 = Tumor invades submucosa.
|
|
| T2 = Tumor invades muscularis propria.
|
| T3 = Tumor invades through the muscularis propria into pericolorectal tissues.
|
| T4a = Tumor penetrates to the surface of the visceral peritoneum.f
|
| N1 = Metastases in 13 regional lymph nodes.
|
| N1c = Tumor deposit(s) in the subserosa, mesentery, or nonperitonealized pericolic or perirectal tissues without regional nodal metastasis.
|
| T2T3, N2a, M0
|
C
|
C1/C2
|
N2a = Metastases in 46 regional lymph nodes.
|
| N2b = Metastases in 7 regional lymph nodes.
|
| T1T2, N2b, M0
|
C
|
C1
|
M0 = No distant metastasis.
|
| IIIC
|
T4a, N2a, M0
|
C
|
C2
|
T3 = Tumor invades through the muscularis propria into pericolorectal tissues.
|
|
| T4a = Tumor penetrates to the surface of the visceral peritoneum.f
|
| T4b = Tumor directly invades or is adherent to other organs or structures.f,g
|
| T3T4a, N2b, M0
|
C
|
C2
|
N1 = Metastases in 13 regional lymph nodes.
|
| N2 = Metastases in 4 regional lymph nodes.
|
| N2a = Metastases in 46 regional lymph nodes.
|
| T4b, N1N2, M0
|
C
|
C3
|
N2b = Metastases in 7 regional lymph nodes.
|
| M0 = No distant metastasis.
|
| T = primary tumor; N = regional lymph nodes; M = distant metastasis. |
| Reprinted with permission from AJCC: Colon and rectum. In: Edge SB, Byrd DR, Compton CC, et al., eds.: AJCC Cancer Staging Manual. 7th ed. New York, NY: Springer, 2010, pp 143-164. |
| The explanations for superscripts ag are at the end of |
Table 5. Definitions of TNM Stage IV
| Stage |
TNMa,b |
Dukesc |
MACd |
Description |
Illustration |
acTNM is the clinical classification, and pTNM is the pathologic classification. The y prefix is used for those cancers that are classified after neoadjuvant pretreatment (e.g., ypTNM). Patients who have a complete pathologic response (ypT0, N0, cM0) may be similar to stage group 0 or I. The r prefix is to be used for those cancers that have recurred after a disease-free interval (rTNM).bA satellite peritumoral nodule in the pericolorectal adipose tissue of a primary carcinoma without histologic evidence of residual lymph node in the nodule may represent discontinuous spread, venous invasion with extravascular spread (V1/2), or a totally replaced lymph node (N1/2). Replaced nodes should be counted separately as positive nodes in the N category, whereas discontinuous spread or venous invasion should be classified and counted in the site-specific factor category Tumor Deposits.cDukes B is a composite of better (T3, N0, M0) and worse (T4, N0, M0) prognostic groups, as is Dukes C (any T, N1, M0 and any T, N2, M0).dMAC is the modified Astler-Coller classification.eTis includes cancer cells confined within the glandular basement membrane (intraepithelial) or mucosal lamina propria (intramucosal) with no extension through the muscularis mucosae into the submucosa.fDirect invasion in T4 includes invasion of other organs or other segments of the colorectum as a result of direct extension through the serosa, as confirmed on microscopic examination (e.g., invasion of the sigmoid colon by a carcinoma of the cecum) or, for cancers in a retroperitoneal or subperitoneal location, direct invasion of other organs or structures by virtue of extension beyond the muscularis propria (i.e., respectively, a tumor on the posterior wall of the descending colon invading the left kidney or lateral abdominal wall; or a mid or distal rectal cancer with invasion of prostate, seminal vesicles, cervix, or vagina).gTumor that is adherent to other organs or structures, grossly, is classified cT4b. However, if no tumor is present in the adhesion, microscopically, the classification should be pT14a depending on the anatomical depth of wall invasion. The V and L classifications should be used to identify the presence or absence of vascular or lymphatic invasion whereas the PN site-specific factor should be used for perineural invasion.
| IVA
|
Any T, Any N, M1a
|
|
|
TX = Primary tumor cannot be assessed.
|
|
| T0 = No evidence of primary tumor.
|
| Tis = Carcinoma in situ: intraepithelial or invasion of lamina propria.e
|
| T1 = Tumor invades submucosa.
|
| T2 = Tumor invades muscularis propria.
|
| T3 = Tumor invades through the muscularis propria into pericolorectal tissues.
|
| T4a = Tumor penetrates to the surface of the visceral peritoneum.f
|
| T4b = Tumor directly invades or is adherent to other organs or structures.f,g
|
| NX = Regional lymph nodes cannot be assessed.
|
| N0 = No regional lymph node metastasis.
|
| N1 = Metastases in 13 regional lymph nodes.
|
| N1a = Metastasis in 1 regional lymph node.
|
| N1b = Metastases in 23 regional lymph nodes.
|
| N1c = Tumor deposit(s) in the subserosa, mesentery, or nonperitonealized pericolic or perirectal tissues without regional nodal metastasis.
|
| N2 = Metastases in 4 regional lymph nodes.
|
| N2a = Metastases in 46 regional lymph nodes.
|
| N2b = Metastases in 7 regional lymph nodes.
|
| M1a = Metastasis confined to 1 organ or site (e.g., liver, lung, ovary, nonregional node).
|
| IVB
|
Any T, Any N, M1b
|
|
|
TX = Primary tumor cannot be assessed.
|
| T0 = No evidence of primary tumor.
|
| Tis = Carcinoma in situ: intraepithelial or invasion of lamina propria.e
|
| T1 = Tumor invades submucosa.
|
| T2 = Tumor invades muscularis propria.
|
| T3 = Tumor invades through the muscularis propria into pericolorectal tissues.
|
| T4a = Tumor penetrates to the surface of the visceral peritoneum.f
|
| T4b = Tumor directly invades or is adherent to other organs or structures.f,g
|
| NX = Regional lymph nodes cannot be assessed.
|
| N0 = No regional lymph node metastasis.
|
| N1 = Metastases in 13 regional lymph nodes.
|
| N1a = Metastasis in 1 regional lymph node.
|
| N1b = Metastases in 23 regional lymph nodes.
|
| N1c = Tumor deposit(s) in the subserosa, mesentery, or nonperitonealized pericolic or perirectal tissues without regional nodal metastasis.
|
| N2 = Metastases in 4 regional lymph nodes.
|
| N2a = Metastases in 46 regional lymph nodes.
|
| N2b = Metastases in 7 regional lymph nodes.
|
| M1b = Metastases in >1 organ/site or the peritoneum.
|
| T = primary tumor; N = regional lymph nodes; M = distant metastasis. |
| Reprinted with permission from AJCC: Colon and rectum. In: Edge SB, Byrd DR, Compton CC, et al., eds.: AJCC Cancer Staging Manual. 7th ed. New York, NY: Springer, 2010, pp 143-164. |
| |
| |
| |
| |
| |
| |
| |
References:
- Colon and rectum. In: Edge SB, Byrd DR, Compton CC, et al., eds.: AJCC Cancer Staging Manual. 7th ed. New York, NY: Springer, 2010, pp 143-64. [PUBMED Abstract]
- Colon and rectum. In: American Joint Committee on Cancer.: AJCC Cancer Staging Manual. 6th ed. New York, NY: Springer, 2002, pp 113-124. [PUBMED Abstract]
- Compton CC, Greene FL: The staging of colorectal cancer: 2004 and beyond. CA Cancer J Clin 54 (6): 295-308, 2004 Nov-Dec. [PUBMED Abstract]
- Nelson H, Petrelli N, Carlin A, et al.: Guidelines 2000 for colon and rectal cancer surgery. J Natl Cancer Inst 93 (8): 583-96, 2001. [PUBMED Abstract]
- Swanson RS, Compton CC, Stewart AK, et al.: The prognosis of T3N0 colon cancer is dependent on the number of lymph nodes examined. Ann Surg Oncol 10 (1): 65-71, 2003 Jan-Feb. [PUBMED Abstract]
- Le Voyer TE, Sigurdson ER, Hanlon AL, et al.: Colon cancer survival is associated with increasing number of lymph nodes analyzed: a secondary survey of intergroup trial INT-0089. J Clin Oncol 21 (15): 2912-9, 2003. [PUBMED Abstract]
- Prandi M, Lionetto R, Bini A, et al.: Prognostic evaluation of stage B colon cancer patients is improved by an adequate lymphadenectomy: results of a secondary analysis of a large scale adjuvant trial. Ann Surg 235 (4): 458-63, 2002. [PUBMED Abstract]
- Tepper JE, O'Connell MJ, Niedzwiecki D, et al.: Impact of number of nodes retrieved on outcome in patients with rectal cancer. J Clin Oncol 19 (1): 157-63, 2001. [PUBMED Abstract]
Treatment Option Overview for Colon Cancer
Back Up
Primary Surgical Therapy
Standard treatment for patients with colon cancer has been open surgical resection of the primary and regional lymph nodes for localized disease.
The role of laparoscopic techniques 1 2 3 4 in the treatment of colon cancer has been examined in two studies.
Evidence (laparoscopic techniques):
- A multicenter, prospective, randomized, noninferiority trial (NCCTG-934653) compared laparoscopic-assisted colectomy (LAC) with open colectomy in 872 patients.
- At a median follow-up of 4.4 years, 3-year recurrence rates (16% LAC vs. 18% open colectomy; hazard ratio [HR] for recurrence, 0.86; 95% confidence interval [CI], 0.631.17; P = .32) and 3-year overall survival (OS) rates (86% LAC vs. 85% open colectomy; HR for death in LAC, 0.91; 95% CI, 0.681.21; P = .51) were similar in both groups for all stages of disease evaluated. Tumor recurrence in surgical incisions was less than 1% for both groups. 5[Level of evidence: 1iiA]
- Decreased hospital stay (5 days LAC vs. 6 days open colectomy, P < .001) and decreased use of analgesics were reported in the LAC group. A 21% conversion rate from LAC to open procedure was shown.
- This study excluded patients with locally advanced disease, transverse colon and rectal tumor locations, and perforated lesions. Each of the 66 surgeons participating in the trial had performed at least 20 LACs and were accredited for study participation after independent videotape review assured appropriate oncologic and surgical principles were maintained. 5 The quality-of-life component of this trial was published separately and minimal short-term quality-of-life benefits with LAC were reported. 6[Level of evidence: 1iiC]
- One small, single-institution randomized study of 219 patients showed that the LAC procedure was independently associated with reduced tumor recurrence on multivariate analysis. 7[Level of evidence: 1iiB]
Surgery is curative in 25% to 40% of highly selected patients who develop resectable metastases in the liver and lung. Improved surgical techniques and advances in preoperative imaging have allowed for better patient selection for resection.
Adjuvant Chemotherapy
The potential value of adjuvant chemotherapy for patients with stage II colon cancer is controversial. Pooled analyses and meta-analyses have suggested a 2% to 4% improvement in OS for patients treated with adjuvant fluorouracil (5-FU)based therapy compared with observation. 8 9 10 (Refer to the Stage II Colon Cancer Treatment section of this summary for more information.)
Prior to 2000, 5-FU was the only useful cytotoxic chemotherapy in the adjuvant setting for patients with stage III colon cancer. Since 2000, capecitabine has been established as an equivalent alternative to 5-FU and leucovorin. The addition of oxaliplatin to 5-FU and leucovorin has been shown to improve OS compared with 5-FU and leucovorin alone. (Refer to the Stage III Colon Cancer Treatment section of this summary for more information.)
Adjuvant Radiation Therapy
While combined modality therapy with chemotherapy and radiation therapy has a significant role in the management of patients with rectal cancer (below the peritoneal reflection), the role of adjuvant radiation therapy for patients with colon cancer (above the peritoneal reflection) is not well defined. Patterns-of-care analyses and single-institution retrospective reviews suggest a role for radiation therapy in certain high-risk subsets of colon cancer patients (e.g., T4, tumor location in immobile sites, local perforation, obstruction, and residual disease postresection). 11 12 13 14 15 16
Evidence (adjuvant radiation therapy):
- Such observations led to the development of a phase III randomized intergroup study designed to test the benefit of adding radiation therapy to surgery and chemotherapy with 5-FU-levamisole for selected high-risk colon cancer patients (e.g., T4; or T3, N1N2 ascending and/or descending colon). 17
- This clinical trial closed early secondary to inadequate patient accrual, and analysis of 222 enrolled patients (the original goal was 700 patients) demonstrated no relapse or OS benefit for the group receiving radiation therapy, though the sample size and statistical power were inadequate to exclude benefit.
Adjuvant radiation therapy has no current standard role in the management of patients with colon cancer following curative resection, although it may have a role for patients with residual disease.
References:
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