© 2004 by Oxford University Press
© 2004 Oxford University Press
IN THIS ISSUE |
Colon Cancer Survival Rates in Different Staging Systems
The recently revised American Joint Committee on Cancer (AJCC) sixth edition staging system increased the stratification within colon cancer stages II and III. O'Connell et al. (p. 1420) used data from the Surveillance, Epidemiology, and End Results Program (SEER) to compare survival rates associated with colon cancer stages defined according to both the new (sixth edition) and the old (fifth edition) system. They found that the new AJCC system stratifies survival more distinctly than the old AJCC system by providing more substages. However, they point out, under the new system, stage IIIa colon cancer is associated with statistically significantly better survival than stage IIb. In current clinical practice, stage III patients receive chemotherapy but stage II patients generally do not; this practice, they conclude, may be the reason for the differences in survival.
In an editorial, Burke (p. 1408) points out that the TNM staging system does not include new molecular biomarkers or therapies other than surgery. These and other limitations reduce its clinical utility. He concludes that a new, computer-based system may become necessary for accurate outcome prediction.
Arylamines and Bladder Cancer Risk
Some arylamine family members are established human bladder carcinogens. Arylamine compounds coming from environmental sources other than cigarette smoke and permanent hair dye may also be human bladder carcinogens. Gan et al. (p. 1425) conducted a population-based case–control study to assess the relationship between nine different arylamine–hemoglobin adducts and bladder cancer risk. The authors found that levels of all arylamine–hemoglobin adducts, with the exception of 2,6-dimethylaniline (2,6-DMA), were higher in smokers than in nonsmokers and that levels of all adducts were higher in case subjects than in control subjects. The authors also found that higher levels of three adducts, including 2,6-DMA, were all independently associated with bladder cancer risk after adjusting for cigarette smoking at the time of blood collection, lifetime smoking history, and other potential risk factors. Because the same three adducts were associated with bladder cancer risk in nonsmokers, the authors conclude that it will be important to identify the environmental sources of these compounds.
Explaining Mammographic Sensitivity in Younger Women
Women aged 40–49 years have lower mammographic sensitivity than older women—that is, younger women have a higher rate of interval cancers (breast cancers detected clinically after a negative mammogram) than older women. Several factors, including breast density, mammographic quality variables, tumor growth rates, and distributions of other breast cancer risk factors have been found to contribute individually to the difference in mammographic sensitivity. In this issue, Buist et al. (p. 1432) evaluated the relative contributions of all of these factors in explaining the lower mammographic sensitivity in younger women 12 and 24 months after a negative screen. They found that greater breast density explained 68% of the decreased sensitivity in younger women at 12 months, whereas rapid tumor growth explained 31% and greater breast density 38% of the decreased sensitivity at 24 months. The authors conclude that a 12-month versus a 24-month screening interval in younger women may reduce the adverse impact of faster-growing tumors on mammographic sensitivity.
A Combined Approach for Diagnosing Dual-Site Cancers
Cancer patients often have concurrent tumors. However, the prognosis and clinical management of patients with synchronous, independently derived, nonmetastatic tumors and those with related metastatic tumors are different. To develop a method that would allow clinicians to better distinguish independently derived tumors from related tumors, Brinkmann et al. (p. 1441) designed a genetic and statistical algorithm to establish the clonality of synchronous endometrial and ovarian, bilateral ovarian, or endometrial and bilateral ovarian tumors using genetic data gathered from paraffin-embedded concurrent tumors. They then compared the resulting genetic diagnoses with those previously made from histopathology reports. For a majority of the patients, genetic and histopathologic diagnoses were in agreement and diagnostic confidence was improved. The authors conclude that the genetic analysis of paraffin-embedded tissues can be used as a rapid diagnostic test for the clinical management of cancer patients with concurrent tumors.
Depsipeptide and EBV-Positive Lymphoproliferative Disorder
Epstein-Barr virus (EBV) is frequently associated with Burkitt lymphoma and lymphoproliferative disorders in immunedeficient patients. To determine whether depsipeptide, a histone deacetylase inhibitor, would be an effective treatment for EBV-positive lymphoproliferative disorders, Roychowdhury et al. (p. 1447) evaluated its effect in EBV-positive lymphoblastoid cell lines (LCLs) and on Burkitt lymphoma cell lines. They used a mouse model to investigate survival and cell culture to explore the action of depsipeptide. They found that treatment with depsipeptide was associated with increased survival of mice carrying LCL tumors but was not associated with survival of mice carrying Burkitt lymphoma tumors. They also found that depsipeptide acted by inducing apoptosis via caspase-dependent and -independent pathways in LCLs. They conclude that the use of depsipeptide as a treatment for lymphoproliferative disorders should be explored further in clinical trials.
Monitoring Chemotherapy Response of Neuroblastoma
Proton magnetic resonance (1H-MRS) has been used previously to estimate neuroblastoma tumor viability. In this issue (p. 1457), Lindskog et al. used this technique to measure responses of neuroblastoma cell lines to various chemotherapy drugs. They observed that death of drug-sensitive cells treated with cytotoxic drugs was associated with changes in the methylene-to-choline ratio. When rats carrying drug-sensitive and drug-resistant human neuroblastoma xenograft tumors were treated with chemotherapy drugs, the methylene-to-choline ratio of drug-sensitive tumors changed before the tumors regressed. However, the methylene-to-choline ratio in drug-resistant tumors, which did not regress after treatment, did not change. The authors conclude that response or resistance to chemotherapy is accurately predicted by 1H-MRS in experimental neuroblastoma models in vivo.
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