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Oropharyngeal Mucositis in Cancer Therapy

Oropharyngeal mucositis is a common and treatment-limiting sideeffect of cancer therapy. Severe oral mucositis can lead to the need tointerrupt or discontinue cancer therapy and thus may have an impacton cure of the primary disease. Mucositis may also increase the risk oflocal and systemic infection and significantly affects quality of life andcost of care. Current care of patients with mucositis is essentially palliativeand includes appropriate oral hygiene, nonirritating diet andoral care products, topical palliative mouth rinses, topical anesthetics,and opioid analgesics. Systemic analgesics are the mainstay of painmanagement. Topical approaches to pain management are under investigation.The literature supports use of benzydamine for prophylaxisof mucositis caused by conventional fractionationated head andneck radiotherapy, and cryotherapy for short–half-life stomatoxic chemotherapy,such as bolus fluorouracil. Continuing studies are investigatingthe potential use of biologic response modifiers and growth factors,including topical and systemic delivery of epithelial growth factorsand agents. Progress in the prevention and management of mucositiswill improve quality of life, reduce cost of care, and facilitate completionof more intensive cancer chemotherapy and radiotherapy protocols. Inaddition, improved management of mucositis may allow implementationof cancer treatment protocols that are currently excessively mucotoxicbut may produce higher cure rates. Continuing research related to thepathogenesis and management of mucositis will undoubtedly lead to thedevelopment of potential interventions and improved patient care.

Latest Article

Monitoring Changes in the Microenvironment During Targeted Therapies

This review covers progress to date in the identification of molecular targets on blood vessels in cancers, as well as agents that act on those targets, with emphasis on those currently in clinical trials. Current vascular-targeting therapies comprise two general types—antiangiogenic therapy and antivascular therapy. Advances in antiangiogenic therapies, particularly inhibitors of vascular endothelial growth factors and their receptors, have clarified the capacity of these inhibitors to change tumor-associated vessel structure to a more normal state, thereby improving the ability of chemotherapeutics to access the tumors. The responses of other antiangiogenesis target molecules in humans are more complicated; for example, αvβ3 integrins are known to stimulate as well as inhibit angiogenesis, and cleavage of various extracellular proteins/proteoglycans by matrix metalloproteinases produces potent regulators of the angiogenic process. Antivascular therapies disrupt established blood vessels in solid tumors and often involve the use of ligand-based or small-molecule agents. Ligand-based agents, irrespective of the antiangiogenic capacity of the ligand, target antivascular effectors to molecules expressed specifically on blood vessels, such as aminopeptidase N, fibronectin extra-domain B, and prostate-specific membrane antigen. Small-molecule antivascular agents, which are not targeted to molecules on blood vessels, rely on physical differences between the vasculatures in tumors and those in normal tissues.