© 2005 Oxford University Press
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Duration of Radiotherapy for Palliation of Bone MetastasesRadiation therapy is effective in palliating pain from bone metastases, but controversy remains whether shortcourse radiation therapy is equivalent to long-course radiation therapy in palliating pain. Hartsell et al. (p. 798) studied whether 8 Gy delivered in a single treatment provided equivalent pain and narcotic relief to that of the standard treatment of 30 Gy delivered in 10 treatments over 2 weeks. They found that the regimens were equivalent in terms of pain and narcotic relief at 3 months and were well tolerated. Patients in the 8-Gy arm had a higher rate of re-treatment but had less acute toxicity than those in the 30-Gy arm, and pathologic fracture rates were similar. The authors conclude that results from this trial should help determine whether a single treatment of 8 Gy becomes the standard treatment for palliating localized painful bone metastases.
In an editorial, Kachnic and Berk (p. 786) note that now three large randomized trials comparing single-fraction with multiple-fraction radiation therapy have demonstrated that single-fraction radiation therapy is sufficient to achieve palliation of painful bone metastases. They conclude by wondering whether this approach will finally become the standard of care in the United States. They note that this outcome may distinguish whether U.S. radiation oncologists practice evidence-based or remuneration-based medicine.
Cancer and Long-Term Cognitive Defects and Dementia
To determine if cancer survivors are more prone to long-term cognitive deficits than the general population, Heflin et al. (p. 854) compared the cognitive function of 702 cancer survivors aged 65 years and older and their cancer-free twins. The authors found that cancer survivors were more likely than their co-twins to have cognitive dysfunction and dementia, although only the differences in cognitive function were statistically significant. The authors conclude that cancer patients are at an increased risk for long-term cognitive dysfunction compared with individuals who have never had cancer.
In a related editorial, Wefel and Meyers (p. 788) describe the theory of diminished cognitive reserve and point out limitations of the Heflin et al. study. They stress that longitudinal, multidisciplinary studies need to be performed to identify neurotoxic cancer treatments, the course of cognitive dysfunction, the mechanisms involved, host risk factors, and the risk of developing late-emerging nononcologic neurologic diseases.
NSAIDS and Breast Cancer
Although an inverse association between non-steroidal anti-inflammatory drug (NSAID) use and colorectal cancer has been observed, its role in breast cancer is unclear. To investigate the relationship between use of NSAIDs, such as aspirin and ibuprofen, and breast cancer, Marshall et al. (p. 805) analyzed data on more than 114,000 female California teachers who provided information on NSAID use and other risk factors at baseline and were followed for 6 years. Regular use (i.e., more than once a week) of any NSAID or aspirin was not associated with breast cancer risk overall. However, long-term daily users of aspirin had an increased risk of estrogen receptor or progesterone receptor (ER/PR)- negative breast cancer but a non–statistically significant decreased risk of ER/PRpositive breast cancer. Long-term daily users of ibuprofen had an increased risk of breast cancer. The authors conclude that long-term daily use of ibuprofen may be associated with increased risk of breast cancer whereas the risks associated with aspirin use may depend on tumor subtypes.
Cancer Risks in Heterozygous ATM Mutation Carriers
Ataxia telangiectasia (A-T) is a rare neurologic disorder typically diagnosed in early childhood. Nearly all A-T cases are associated with compound heterozygous mutations in the ATM gene, which encodes a protein involved in DNA repair. To determine the cancer risks associated with heterozygous ATM mutations, Thompson et al. (p. 813) obtained cancer incidence and mortality data for 1160 relatives of A-T patients in the United Kingdom through the National Health Service Central Registry. The authors found that the relatives, especially those younger than age 50 years, had an increased risk of breast cancer compared with the general population and observed some excess risks of colorectal and stomach cancer. The authors conclude that heterozygous ATM mutation carriers have a moderately increased risk of breast cancer and possible excess risks of other cancers but no large mutation-specific increase in cancer risk.
Formylpeptide Receptor FPR and Malignant Human Gliomas
FPR is a G-protein–coupled receptor that mediates chemotaxis of phagocytic leukocytes induced by a bacterial peptide, N-formyl-methionyl-leucyl-phenylalanine (fMLF), and is expressed on some human glioma cells. Zhou et al. (p. 823) investigated the relationship between FPR and the biologic behavior of glioma cells. They found that highly malignant human glioblastoma cell lines, grade IV glioblastoma multiforme, and grade III anaplastic astrocytomas express FPR. Glioma cells respond to fMLF by chemotaxis, increased cell proliferation, and increased production of vascular endothelial growth factor. Inhibiting FPR with its short interfering RNA substantially reduced tumorigenicity of glioma cells injected into nude mice. The authors also found that necrotic glioblastoma cells released a factor(s) that activated FPR in glioma cells. They concluded that FPR may mediate motility, growth, and angiogenesis of malignant human gliomas by interaction with host-derived agonists.
Increased Pulmonary Metastasis in NM23-null Mice
The NM23 gene is thought to suppress the metastatic spread of solid tumors. Boissan et al. (p. 836) used transgenic mice that lacked the mouse NM23-M1 gene (NM23-M1–/– mice) in two mouse models of hepatocarcinogenesis to examine the role of NM23 in hepatic tumor development and metastatic dissemination. They found that in both models, the Nm23 protein was overexpressed in the primary liver tumors of NM23-M1+/+ mice compared with non-tumor liver tissue; however, the lack of the NM23-M1 gene had no effect on primary tumor formation in either model. In one mouse model, mice developed pulmonary metastases that expressed a hepatocyte-specific antigen, whereas the few pulmonary nodules that developed in the other mouse model did not. More mice that lacked the NM23-M1 gene developed lung metastases than mice that expressed the gene. The authors conclude that a lack of NM23-M1 expression promotes metastasis in one animal model of liver carcinogenesis.
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