Colon Adenocarcinoma 

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

Background

Invasive colorectal cancer is a preventable disease. Early detection through widely applied screening programs is the most important factor in the recent decline of colorectal cancer in developed countries (see Deterrence/Prevention). Full implementation of the screening guidelines[1] can cut mortality rate from colorectal cancer in the United States by an estimated additional 50%; even greater reductions are estimated for countries where screening tests may not be widely available at present. New and more comprehensive screening strategies are also needed.

Fundamental advances in understanding the biology and genetics of colorectal cancer are taking place. This knowledge is slowly making its way into the clinic and being employed to better stratify individual risks of developing colorectal cancer, discover better screening methodologies, allow for better prognostication, and improve one’s ability to predict benefit from new anticancer therapies.

In the past 10 years, an unprecedented advance in systemic therapy for colorectal cancer has dramatically improved outcome for patients with metastatic disease. Until the mid 1990s, the only approved agent for colorectal cancer was 5-fluorouracil. New agents that became available in the past 10 years include cytotoxic agents such as irinotecan and oxaliplatin,[2] oral fluoropyrimidines (capecitabine and tegafur), and biologic agents such as bevacizumab, cetuximab, and panitumumab.[3]

Though surgery remains the definitive treatment modality, these new agents will likely translate into improved cure rates for patients with early stage disease (stage II and III) and prolonged survival for those with stage IV disease. Further advances are likely to come from the development of new targeted agents and integration of those agents with other modalities such as surgery, radiation therapy, and liver-directed therapies.

An image depicting standard colectomies for adenocarcinoma of the colon can be seen below.

Standard colectomies for adenocarcinoma of the colStandard colectomies for adenocarcinoma of the colon.
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Pathophysiology

Genetically, colorectal cancer represents a complex disease, and genetic alterations are often associated with progression from premalignant lesion (adenoma) to invasive adenocarcinoma. Sequence of molecular and genetic events leading to transformation from adenomatous polyps to overt malignancy has been characterized by Vogelstein and Fearon.[4] The early event is a mutation of APC (adenomatous polyposis gene), which was first discovered in individuals with familial adenomatous polyposis (FAP). The protein encoded by APC is important in activation of oncogene c-myc and cyclin D1, which drives the progression to malignant phenotype. Although FAP is a rare hereditary syndrome accounting for only about 1% of cases of colon cancer, APC mutations are very frequent in sporadic colorectal cancers.

In addition to mutations, epigenetic events such as abnormal DNA methylation can also cause silencing of tumor suppressor genes or activation of oncogenes, compromising the genetic balance and ultimately leading to malignant transformation.

Other important genes in colon carcinogenesis include KRAS oncogene , chromosome 18 loss of heterozygosity (LOH) leading to inactivation of SMAD4 (DPC4), and DCC (deleted in colon cancer) tumor suppression genes. Chromosome arm 17p deletion and mutations affecting p53 tumor suppressor gene confer resistance to programmed cell death (apoptosis) and are thought to be late events in colon carcinogenesis.

A subset of colorectal cancers is characterized with deficient DNA mismatch repair. This phenotype has been linked to mutations of genes such as MSH2, MLH1, and PMS2. These mutations result in so-called high frequency microsatellite instability (H-MSI), which can be detected with an immunocytochemistry assay. H-MSI is a hallmark of hereditary nonpolyposis colon cancer syndrome (HNPCC, Lynch syndrome), which accounts for about 6% of all colon cancers. H-MSI is also found in about 20% of sporadic colon cancers.

About 15% of colorectal cancers initially develop because of defective function of the DNA mismatch repair system. A study by Sinicrope et al showed that patients with deficient mismatch repair colon cancers have less frequent tumor recurrence than patients with proficient mismatch repair colon cancers.[5] Additionally, patients with deficient mismatch repair typically have a delayed time to recurrence when compared to proficient mismatch repair patients, and their survival rates are also higher. Distant recurrences were decreased by 5-FU-based adjuvant treatment in deficient mismatch repair stage III tumors. Additionally, a subset analysis suggested that any treatment benefit was restricted to suspected germline compared with sporadic tumors.

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Epidemiology

Frequency

United States

The American Cancer Society estimated that 148,810 individuals would be diagnosed with colorectal cancer and 49,960 would die from this disease in the United States in 2008.[6]

International

In 2003, the World Health Organization estimated that approximately 940,000 individuals were be diagnosed with colorectal cancer worldwide and 492,000 died from it that year.

Mortality/Morbidity

Colorectal cancer is a major health burden worldwide. The incidence and mortality from colon cancer has been on a slow decline over the past 20 years in the United States; however, colon cancer remained the third most common cause of cancer-related mortality in 2008. A multitude of risk factors have been linked to colorectal cancer, including heredity, environmental exposures, and inflammatory syndromes affecting gastrointestinal tract.

A review of 8 trials by Rothwell et al found allocation to aspirin reduced death caused by cancer. Individual patient data were available from 7 of the 8 trials. Benefit was apparent after 5 years of follow-up. The 20-year risk of cancer death was also lower in the aspirin group for all solid cancers. A latent period of 5 years was observed before risk of death was decreased for esophageal, pancreatic, brain, and lung cancers. A more delayed latent period was observed for stomach, colorectal, and prostate cancer. Benefit was only seen for adenocarcinomas in lung and esophageal cancers. The overall effect on 20-year risk of cancer death was greatest for adenocarcinomas.[7]

A study by Burn et al found that 600 mg of aspirin per day for a mean of 25 months reduced cancer incidence after 55.7 months among known carriers of hereditary colorectal cancer; however, further studies are needed to determine the optimum dose and duration of treatment.[8]

Patients with preexisting mental disorders have an overall higher mortality rate than their counterparts. This higher mortality rate can be attributed to a lack of surgery, chemotherapy, and radiation therapy, especially in patients with psychotic disorders and dementia. Improved public health initiatives are needed to improve colon cancer detection and treatment in older adults with mental disorders.[9]

A study by Phipps et al found that smoking is also associated with increased mortality after colorectal cancer diagnosis, especially among patients with colorectal cancer with high microsatellite instability.[10]

A study by Dehal et al found that patients with colorectal cancer and type 2 diabetes mellitus have a higher risk of mortality than those without, most notably a higher risk due to cardiovascular disease.[11]

Race

Recent trends in the United States suggest a disproportionally higher incidence and death from colon cancer in African Americans than in whites. Hispanic persons have the lowest incidence and mortality from colorectal cancer.

A study by Yothers et al found that black patients with resected stage II and stage III colon cancer had worse overall and recurrence-free survival compared with white patients who underwent the same therapy.[12]

A study by Lasser et al found that patient navigation increased completion of colorectal cancer screening among ethnically diverse patients. In order to reduce disparities in colorectal cancer screening, targeting patient navigation to black and non-English-speaking patients may be useful.[13]

Sex

The incidence of colorectal cancer is about equal for males and females.

Age

Age is a well-known risk factor for colorectal cancer, as it is for many other solid tumors. The timeline for progression from early premalignant lesion to malignant cancer ranges from 10-20 years. The incidence of colorectal cancer peaks at about age 65 years.

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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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