Colon Adenocarcinoma Clinical Presentation

  • Author: Tomislav Dragovich, MD, PhD; Chief Editor: Jules E Harris, MD   more...
 
Updated: Feb 13, 2012
 

History

Due to increased emphasis on screening practices, colon cancer is now often detected during screening procedures. Other common clinical presentations include iron-deficiency anemia, rectal bleeding, abdominal pain, change in bowel habits, and intestinal obstruction or perforation. Right-sided lesions are more likely to bleed and cause diarrhea, while left-sided tumors are usually detected later and could present with bowel obstruction.

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Physical

Physical findings could be very nonspecific (fatigue, weight loss) or absent early in the disease course. In more advanced cases, abdominal tenderness, macroscopic rectal bleeding, palpable abdominal mass, hepatomegaly, and ascites could be present on physical examination.

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Causes

Colorectal cancer is a multifactorial disease process, with etiology transcending genetic factors, environmental exposures (including diet), and inflammatory conditions of digestive tract.

Though much about colorectal cancer genetics remains unknown, current research indicates that genetic factors have the greatest correlation to colorectal cancer. Hereditary mutation of the APC gene is the cause of familial adenomatous polyposis (FAP), where affected individuals carry an almost 100% risk of developing colon cancer by age 40 years.

Hereditary nonpolyposis colon cancer syndrome (HNPCC, Lynch syndrome) carries about 40% lifetime risk of developing colorectal cancer; individuals with this syndrome are also at increased risk for urothelial cancer, endometrial cancer, and other less common cancers. Lynch syndrome is characterized by deficient mismatch repair (dMMR) due to inherited mutation in one of the mismatch repair genes, such as hMLH1, hMSH2, hMSH6, hPMS1, hPMS2, and possibly other undiscovered genes. HNPCC is a cause of about 6% of all colon cancers. Although the use of aspirin may reduce the risk of colorectal neoplasia in some populations, a study by Burn et al found no effect on the incidence of colorectal cancer among carriers of Lynch syndrome with use of aspirin, resistant starch, or both.[14]

Dietary factors are the subject of intense and ongoing investigations.[15] Epidemiological studies have linked increased risk of colorectal cancer with a diet high in red meat and animal fat, low-fiber diet, and low overall intake of fruits and vegetables. A study by Aune et al found that a high intake of fiber was associated with a reduced risk of colorectal cancer. In particular, cereal fiber and whole grains were found to be effective.[16] A study by Pala et al found that high yogurt intake was also associated with a decreased risk for colorectal cancer.[17]

Factors associated with lower risk include folate intake, calcium intake, and estrogen replacement therapy. However, most of these studies were retrospective epidemiological studies and have yet to be validated in prospective, placebo-controlled, interventional trials.

Lifestyle choices such as alcohol and tobacco consumption, obesity, and sedentary habits have also been associated with increased risk for colorectal cancer. Current screening guidelines recommend that clinicians be aware of an increased CRC risk in patients with smoking and obesity, but do not highlight the increase in CRC risk in patients with diabetes. A meta-analysis of case-control and cohort studies identified diabetes as an independent risk factor for colon and rectal cancer. Subgroup analyses confirmed the consistency of the findings across study type and population. This information may have an impact on screening guidelines and on building risk models of CRC.[18]

Association between body mass index (BMI) and risk of colorectal adenomas and cancer has been reported, but few studies have had adequate sample size for conducting stratified analyses. Jacobs et al pooled data from 8,213 participants in 7 prospective studies of metachronous colorectal adenomas to assess whether the association between BMI and metachronous neoplasia varied by sex, family history, colorectal subsite, or features of metachronous lesions. Exploratory analyses indicated that BMI was significantly related to most histologic characteristics of metachronous adenomas among men but not among women. The researchers concluded that body size may affect colorectal carcinogenesis at comparatively early stages, particularly among men.[19]

A study by Morikawa et al found that among obese patients, activation of the cadherin-associated protein beta-1 (CTNNB1) was associated with better colorectal cancer-specific survival and overall survival, suggesting that alterations in the WNT-CTNNB1 pathway on outcome are modified by BMI and physical activity.[20]

Inflammatory bowel diseases such as ulcerative colitis and Crohn’s disease also carry an increased risk of developing colorectal adenocarcinoma. The risk for developing colorectal malignancy increases with the duration of inflammatory bowel disease and the greater extent of colon involvement.

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Contributor Information and Disclosures
Author

Tomislav Dragovich, MD, PhD  Chief, Section of Hematology and Oncology, Banner M D Anderson Cancer Center

Tomislav Dragovich, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Society of Clinical Oncology, and Southwest Oncology Group

Disclosure: Nothing to disclose.

Coauthor(s)

Vassiliki L Tsikitis, MD  Assistant Professor of Surgery, Department of Surgery, Division of General and Gastrointestinal Surgery, Oregon Health and Science University School of Medicine

Vassiliki L Tsikitis, MD is a member of the following medical societies: American College of Surgeons, American Society of Colon and Rectal Surgeons, and Association of Women Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

from Memorial Sloan-Kettering - Philip Schulman, MD  Chief, Medical Oncology, Department of Medicine, Memorial Sloan-Kettering Cancer Center

from Memorial Sloan-Kettering - Philip Schulman, MD is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, American Society of Hematology, and Medical Society of the State of New York

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Rajalaxmi McKenna, MD, FACP  Southwest Medical Consultants, SC, Department of Medicine, Good Samaritan Hospital, Advocate Health Systems

Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis

Disclosure: Nothing to disclose.

Chief Editor

Jules E Harris, MD  Clinical Professor of Medicine, Section of Hematology/Oncology, University of Arizona College of Medicine, Arizona Cancer Center

Jules E Harris, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Association of Immunologists, American Society of Hematology, and Central Society for Clinical Research

Disclosure: GlobeImmune Salary Consulting

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Standard colectomies for adenocarcinoma of the colon.
Table 1. TNM Staging System for Colon Cancer
StagePrimary Tumor (T)Regional Lymph Node (N)Remote Metastasis (M)
Stage 0Carcinoma in situ (Tis)N0M0
Stage ITumor may invade submucosa (T1) or muscularis propria (T2)N0M0
Stage IITumor invades muscularis (T3) or adjacent organs or structures (T4)N0M0
Stage IIAT3N0M0
Stage IIBT4aN0M0
Stage IICT4bN0M0
Stage IIIAT1-4N1-2M0
Stage IIIBT1-4N1-2M0
Stage IIICT3-4N1-2M0
Stage IVAT1-4N1-3M1a
Stage IVBT1-4N1-3M1b
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