Therapeutic Options in the Management of Colon Cancer: 2005 Update

Abstract

Recently, major developments in the treatment of colon cancer have emerged. These developments include improvements in surgical technique and staging and the introduction of new molecularly targeted pharmacologic agents. Improvements in surgical management involve enhanced staging techniques, allowing more accurate determination of risk of recurrence. Newer agents, such as oxaliplatin, cetuximab, and bevacizumab, now are approved for the treatment of colon cancer. The data associated with use of oxaliplatin in adjuvant and metastatic settings continue to mature; survival benefits are expected to become more fully apparent in the next two years. Bevacizumab, a monoclonal antibody that neutralizes vascular endothelial growth factor, when combined with irinotecan, 5-fluorouracil, and leucovorin (IFL), was superior to IFL alone in achieving median and progression-free survival. Cetuximab, a monoclonal antibody directed against the epidermal growth factor receptor, when given in combination with irinotecan, achieved an increased objective response and increased time to progression, compared with cetuximab alone, in patients refractory to irinotecan-containing regimens. In addition to surgical and pharmacologic developments, the recognition that genetics and molecular markers play an important role in carcinogenesis has heightened research to integrate this knowledge into practice. Nurses play a pivotal role in the care of patients with colon cancer and must be conversant in the new advances in treatment.

Hand-Foot Syndrome (Hand-Foot Skin Reaction, Palmar-Plantar Erythrodysesthesia): Focus on Sorafenib and Sunitinib

“…In sorafenib trials, HFS generally appeared within the first 6 weeks of therapy [11]. It tends to get progressively worse with continued chemotherapy [70], and can result in notably decreased quality of life for many patients because of pain and disfigurement, required care and expense, and increased infection risk from loss of skin integrity [71,72]. …”

“…Other anatomic or physiologic factors that are unique to the acral surfaces and that may explain the location of HFS include a rapidly dividing epidermis, the absence of hair follicles or sebaceous glands, wide dermal papillae [6], and the high degree of pressure routinely localized to the palms and soles, which may result in capillary rupture and escape of drug from the vasculature into the acral skin [71,96]. The latter observation is intriguing in that it could explain a report of hand-foot-and-stump syndrome in a lower extremity amputee on sorafenib who regularly wore a prosthesis [93].…”

“…Anecdotal evidence suggests benefit in lifestyle modification, such as avoiding high temperatures, excessive exercise, or ill-fitting clothes and shoes [71,116,117]. Emollients seem to provide symptomatic relief to some patients, and two have been singled out as particularly helpful in individual case series: Mortimer et al [80] found improved benefit in combining pyridoxine with Udderly Smooth® udder cream, but not with any other emollients, and Chin et al [118] observed that petroleum-/lanolin-based ointment containing the antiseptic hydroxyquinolone (Bag Balm®) provides symptomatic relief to HFS patients.…”

Hypertension and targeted therapy

“…Blood pressure should be monitored every 2 to 3 weeks and more frequently if hypertension develops [22]. It has been recommended that blood pressure should be monitored before each chemotherapy treatment, between physician visits and for as long as 3 months after completion of bevacizumab therapy [23]. Hypertension has to be monitored and antihypertensive drugs have to be slowly discontinued after bevacizumab is stopped.…”

Hypertension Associated With Bevacizumab

“…Without the formation of new vascular growth, tumors are unable to increase in size by more than 1-2 mm from their blood supply (Berlin, 2002;Fernando & Hurwitz, 2004). Bevacizumab is theorized to prevent cancer from spreading by blocking the attachment of VEGF to endothelial cells, thereby stopping the signal to stimulate growth of new vessels necessary for cell proliferation and spread of the tumor (Fernando & Hurwitz;Wilkes, 2005). Rather than directly destroying cells to reduce tumor burden as conventional chemotherapy does, this drug prevents the growth and spread of cancer cells (Fernando & Hurwitz; Hurwitz et al).…”