Year: 2007
Type: article
Abstract: BaCkgrOund: Every 3.5 minutes, someone is diagnosed with colorectal cancer (CrC); every 9 minutes, someone dies from CrC; and every 5 seconds, someone who should be screened for CrC is not. The 5-year mortality for people diagnosed with CrC is approximately 40%; however, survival improves substantially if the cancer is diagnosed while still localized. OBjECTIvE: To track and review the rapid progress researchers have made in CrC. SuMMary: among patients who have CrC, approximately 50% will eventually develop liver metastases. The oncology field’s significant advances in the last few years, especially in CrC, challenge clinicians and patients. Multiple facets of care intersect in CrC: medical management, pharmacy management, symptom management, case management, and patient advocacy. CrC develops over many years as environmental and genetic factors interact. The american Cancer Society recommends screening all men and women older than 50 years and those at high risk at an earlier age. In the past, patients presenting with the same stage of CrC were considered similar. The staging criteria of the american joint Committee on Cancer recognizes that subsets of patients with varying survival statistics can be identified and that each patient requires a strategic approach. The u.S. Food and drug administration approval of irinotecan in 1996 and oxaliplatin in 2002 changed the landscape, and ultimately, the oral agent capecitabine and the biologics bevacizumab and cetuximab also significantly expanded treatment options. COnCLuSIOn: Clinicians must consider all available treatment options and regimen sequences across multiple lines of therapy, creating an early plan for each patient to extend survival while minimizing side effects. kEywOrdS: Bevacizumab, Capecitabine, Cetuximab, Colorectal cancer, FOLFOX, Irinotecan, Oxaliplatin, Panitumumab J Manag Care Pharm. 2007;13(6)(suppl S-c):S5-S18 Copyright© 2007, Academy of Managed Care Pharmacy. All rights reserved. AL B. BENSoN III, MD, FACP, is a professor of medicine, Division of Hematology/oncology, Feinberg School of Medicine, Northwestern university, Chicago, Illinois. AuTHoR CoRRESPoNDENCE: Al B. Benson III, MD, FACP, Professor of Medicine, Northwestern Medical Faculty Foundation, Division of Hematology/oncology, 676 N. St. Clair St., Suite 850, Chicago, IL 60611. Tel: (312) 695-6180; Fax: (312) 695-6189; E-mail:[email protected] Author Epidemiology, Disease Progression, and Economic Burden of Colorectal Cancer CRC is very common worldwide, with 850,000 people developing it annually and 500,000 dying of the disease.4 Its prevalence and preventable nature makes CRC a primary focus in the oncology community. In fact, estimates indicate that gastrointestinal cancers represent about 20% of all cancers. The broad diversity in the types of patients and stages at which the disease is diagnosed creates multidisciplinary challenges. Among patients who have CRC, a majority will eventually develop liver metastases. In 30% to 40% of CRC patients, metastases are confined to the liver when they are initially found. One quarter to one third of patients who are able to undergo resection of liver metastases will live 5 years or longer; median survival after resection is between 24 and 40 months. This high rate of liver metastases has transformed treatment and evaluation in an effort to improve cure rates.5 More recent data indicate that survival rates may be increasing.6-8 The risk factors for CRC for people who live in the United States are presented in Table 1. CRC does not discriminate by gender or ethnicity in terms of incidence or mortality. Socioeconomic groups in the lower income ranges tend to present with more advanced disease. Men tend to develop CRC slightly more often than women.2 The disease affects all ethnic groups, and epidemiologic studies confirm that environmental exposure is probably a factor. For example, people who immigrated to the United States from Japan—where CRC was once a low-incidence disease—eventually developed CRC at a rate similar to native-born Americans. Today, Japan’s incidence of CRC is rising dramatically, probably due to Western influence, particularly in diet; dietary intake of milk, meat, eggs, and fat/oil increased remarkably in Japan from 1950 to 1970, and it remains at this elevated level today.9 Globally, some differences in incidence remain related to location and low socioeconomic status. Japan’s experience supports what we know: diet is a leading risk factor for CRC. CRC is considered a completely preventable disease by most experts, and the fact that many of its risk factors are related to lifestyle reflect that belief. High-fat diets with few fruits and vegetables, inactivity, obesity, smoking, and alcohol use increase risk. Interest in chemoprevention is high, and trials suggest that nonsteroidal anti-inflammatory drugs (NSAIDs, such as ibuprofen) and cyclooxygenase-2 (COX-2) inhibitors (such as rofecoxib or celecoxib) may reduce the risk of CRC. The CRC-related mortality has been reduced 40% to 50% in individuals who regularly take aspirin and other NSAIDs. Additionally, COX-2 is elevated in 85% to 95% of CRCs; overexpression has been shown to decrease cancer cell death.10,11 One study of a COX-2 inhibitor (celecoxib) showed a significant reduction in polyps.12-14 Approximately 70% of CRCs are nonhereditary, or sporadic, and about 20% are familial. Two key hereditary syndromes are familial adenomatous polyposis (FAP) and hereditary nonpolyposis colon cancer (HNPCC). The FAP syndrome develops from inherited mutations of the adenomatous polyposis coli (APC) gene, and accounts for approximately 1% to 2% of all CRC cases. Patients with FAP develop hundreds to thousands of polyps before age 30, and inevitably develop CRC. Usually, CRC develops at an early age (average, 39 years) in FAP patients, but it can be prevented by surgically removing the colon.15 Lynch syndrome, or HNPCC, is caused by inherited mutation in any 1 of 5 mismatch repair (MMR) genes, and accounts for 3% to 5% of all CRC cases. The term nonpolyposis does not mean that the cancer does not emanate from polyps; it is used to distinguish HNPCC from FAP. Polyps do not develop earlier in people with HNPCC, but once they do, their tendency to become malignant more rapidly leads to a 70% to 80% lifetime risk of CRC. In these patients, CRC occurs at early age (average 44 years). Some patients with HNPCC also elect to have a complete colectomy because of their increased risk of rapid development of colon cancer. Experts stress the need for detailed family history to identify individuals who are at risk to provide appropriate screening, genetic counseling, and treatment. It has been recommended that people who have a first-degree relative who has had CRC should be screened annually beginning at age 40, rather than at age 50. Family members of patients who developed CRC very early (i.e., before age 50) should be screened 10 years before the age at which the relative developed CRC. For example, if a patient’s brother, or other first-degree relative, developed CRC at age 45, the patient should begin screening at age 35.16-18
Source: Journal of Managed Care Pharmacy
Authors: Al Benson, Kathleen Kaa, Neil Minkoff
Language: English
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2330876067