© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 10, 815,
May 19, 1999
© 1999 Oxford University Press
IN THIS ISSUE |
To determine whether there is an association between the long-term clinical outcome of patients with metastatic germ cell cancer, particularly those with a poor prognosis, and the experience of the treating institution, Collette et al. (p. 839) analyzed data on 380 patients at 49 institutions in Europe who were enrolled in a randomized clinical trial of chemotherapy for this disease. The authors report that patients treated in institutions that entered fewer than five patients into the trial had statistically significant worse survival than patients treated in institutions that entered five patients or more.
In an editorial, Feuer et al. (p. 816) discuss how the findings of Collette et al. further substantiate and extend past observations that centers need to treat a certain number, a "critical mass," of patients with a rare cancer, such as testicular cancer, to achieve optimal patient outcome.
Costs of Patients in Clinical Trials
Because of the dearth of information about how entry into clinical trials affects the cost of care for the cancer patient, Wagner et al. (p. 847) conducted a matched case-control comparison of the incremental costs of participation in cancer treatment trials. They found that enrollees incurred modestly (no more than 10%) higher costs than patients not enrolled in trials. They conclude that cancer chemotherapy trials may not imply budget-breaking costs.
". . . [O]ver the full 5-year follow-up period, the Kaplan-Meier sample average monthly cost across the entire sample of case subjects was only $38 higher than the monthly cost for the control subjects."—Wagner et al.
In an editorial, Brown (p. 818) discusses the timeliness of the study by Wagner et al. and its limitations. He points to several ongoing larger studies that may be able to establish more definitively whether the costs of patient care in clinical trials are substantially greater than those for standard care.
Trichloroethylene and Kidney Cancer
A specific gene mutation may be the link between exposure to the industrial solvent trichloroethylene and renal cell cancer (RCC). This cancer frequently results from mutations in the von Hippel-Lindau (VHL) tumor suppressor gene and has been associated with environmental exposure to trichloroethylene. Brauch et al. (p. 854), in a study of 44 patients with RCC who were exposed to the solvent at work, 107 patients with RCC but without known exposure, and 97 healthy control subjects, report that a specific mutation at VHL nucleotide 454 was found only in patients with RCC who had occupational exposure to trichloroethylene. This mutation was not found in DNA from tumors obtained from unexposed patients, nor was it observed in lymphocyte DNA from the healthy control subjects, according to the researchers.
Chronic Lymphocytic Leukemia Trials
Randomized trials to evaluate the timing and intensity of the initial chemotherapy for chronic lymphocytic leukemia (CLL) have in general been too small to provide separately reliable results. Richards and collaborators (p. 861) conducted a meta-analysis and compared the effects on patient survival of (a) immediate versus deferred chemotherapy for early stage CLL and (b) combination chemotherapy (e.g., cyclophosphamide and vincristine, plus prednisone/prednisolone [COP] or COP plus doxorubicin) versus single-agent chlorambucil as first-line treatment for more advanced disease. In terms of survival, the findings suggest an advantage for a conservative treatment strategy: no chemotherapy for most patients with early stage disease and single-agent chlorambucil as the first line of treatment for most patients with advanced disease. The authors say that this strategy will need to be reconsidered as mature results become available from trials of other agents.
Tangled Web of Factors Affecting Screening Mammography
In a commentary in this issue, Baines and Dayan (p. 833) discuss biologic and life style factors that may reduce the accuracy of screening mammography—and thus reduce its effectiveness. They maintain that everything possible should be done to identify the optimal biologic conditions for enhancing the effectiveness of screening mammography.
A Prognostic Marker in Colorectal Cancer
Urokinase plasminogen activator receptor (uPAR) is thought to play a role in tumor cell invasion and metastasis because of its involvement in cell-surface activation (i.e., cleavage) of plasminogen (to form plasmin, a proteolytic enzyme). Normally, the soluble form of this receptor (suPAR) is present at low levels in the blood, but it is found at increased levels in the blood of patients with several types of cancer. Stephens et al. (p. 869) have investigated the relationship between plasma levels of suPAR and survival in 591 patients with colorectal cancer. They found that there was an increasing risk of mortality with increasing levels of plasma suPAR.
Possible Bladder Cancer Suppressor Gene
In the search for organ-specific tumor suppressors, transcription factor E2F-1, whose activity is regulated in part by interaction with the retinoblastoma protein (pRB), has been implicated in bladder cancer in a report by Rabbani et al. (p. 874). In this study, the researchers analyzed E2F-1 gene sequences and expression of E2F-1 protein in tumors and normal bladder tissue from 133 patients with bladder cancer. Although they discovered a genetic polymorphism in the protein coding region of the gene, they did not identify any mutations. However, patients whose tumors exhibited decreased expression of E2F-1 protein had statistically significant increases in their risks of progression to metastases and death, suggesting that E2F-1 may function as a tumor suppressor in bladder cancer.
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