Latest Developments
Recent descriptions of the pathobiology of oral mucositis (OM) have greatly
expanded scientific knowledge of how OM develops.1 While OM is a
much more complex disease than was thought previously, this complexity offers
many new opportunities for preventing and treating it by targeting some of
the many biological pathways in its development process.2
Stephen T. Sonis has provided several excellent descriptions of these agents:
- L-glutamine is being developed to help prevent OM by counteracting metabolic
deficiencies that result from cancer treatment.
- Amifostine is a free-radical scavenger that reduces pro-inflammatory cytokines.
- Keratinocyte growth factor activates NRF2 to reduce ROS and stimulates
epithelial growth.
- N-acetylcysteine inhibits NF-kB activation.
- Manganese superoxide dismutase detoxifies ROS.3
The challenge for all therapies will be to achieve the protection
or targeting of healthy tissue without compromising tumorcidal power.3
Future treatment strategies will most likely involve combining these new therapies
with each other and with other known agents. For instance, combining anti-inflammatory
therapies with those that inhibit OM development may prove viable.2
One of the problems facing oncologists today is that it is difficult to predict
how a patient will react to a therapy.2 Consequently, studies of
genetic factors are underway that may someday improve outcomes by providing
pretreatment genetic polymorphism analyses and risk factor analysis.3
References
- Sonis ST, Elting LS, Keefe D, Peterson DE, et al. Perspectives on cancer
therapy-induced mucosal injury: pathogenesis, measurement, epidemiology,
and consequences for patients. Cancer 2004; 100:1995-2025.
- Epstein JB, Schubert MM. Oropharyngeal mucositis in cancer therapy.
Review of pathogenesis, diagnosis, and management. Oncology (Huntingt) 2003;
17:1767-79.
- Sonis ST. The pathobiology of mucositis. Nat Rev Cancer 2004;
4:277-84.
