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View the Table of Contents for the January 1 issue of Clinical Cancer Research.
Tang et al. Page 169
In treatment of advanced prostate cancer, chemotherapy is commonly used after the failure of androgen ablation. Tang et al. treated SCID mice bearing human LNCaP prostate tumors with chemotherapy (docetaxel) and/or hormone therapy (surgical castration) applied singly, concurrently, or in different sequences. The best outcome in terms of antitumor activity in this model was docetaxel followed by castration. Next to castration alone, the least effective treatment was castration followed by docetaxel. This study suggests that giving chemotherapy before hormone ablation may provide a better outcome than the current practice of using chemotherapy in patients who fail hormone therapy.
Pöttgen et al. Page 97
Multimodality protocols, including induction chemoradiotherapy and surgery, represent the most aggressive treatment approach for patients with locally advanced non–small cell lung cancer. Pöttgen et al. have evaluated the role of PET/CT scans during neoadjuvant chemoradiotherapy. In primary tumors, a decrease of 18F-FDG-accumulation measured by standard uptake values (SUV) of 0.45-0.55 was found to separate histopathologic responders from nonresponders. SUV response was associated with higher extracerebral relapse-free survival. In the mediastinal lymph nodes, preoperative SUV predicted an ypN0 status with high sensitivity and specificity. For the clinician, serial PET/CT scans represent a valuable tool in patient care during neoadjuvant therapy.
Kröger et al. Page 159
The role of high-dose chemotherapy in high-risk breast cancer is still uncertain. To investigate immunohistochemistry as prognostic and predictive factor for high-risk breast cancer, Kröger et al. investigated the effect of p53, Her2/neu, Bcl2, Ki67, and other histochemical factors in tumor specimens of patients treated within a randomized study comparing high-dose chemotherapy with standard-dose chemotherapy. For the entire study, Her2/neu-positivity and p53- and Bcl2-negativity were significant negative prognostic factors for event-free survival. A predictive effect of immunohistochemical factors on different treatment could be only shown for p53, meaning p53-negative patients did better with standard-dose chemotherapy in comparison with high-dose chemotherapy and p53-positive patients did better with high-dose chemotherapy in comparison with standard-dose chemotherapy. Therefore, the study highlights the importance of including biological factors within randomized study trials to select patients who might benefit from different treatment approaches.
Asano et al. Page 43
EGFR mutations are found in non–small cell lung cancer (NSCLC) and are related to tumor responsiveness to gefitinib or erlotinib, suggesting the usefulness of EGFR as a biomarker. Because clinical samples may consist of a small fraction of tumor and a large amount of nonmalignant cells, a sensitive assay for detecting mutation is critical for clinical applications. Asano et al. developed the mutant-enriched PCR assay targeting EGFR and successfully detected mutations in CT-guided needle lung biopsies and pleural fluid. The newly developed assay provides a valuable method for potentially detecting and monitoring recurrences of NSCLC and establishing the therapeutic strategy for EGFR-related NSCLC.
Febbo et al. Page 152
Unbiased genomic approaches to determine biological effects of targeted therapy may prove critical to understand determinants of response and to rationally combine therapies. Febbo et al. performed laser capture microdissection, RNA amplification, and microarray analysis to glean biological insight from prostate cancer samples before and following treatment with imatinib mesylate. Results from sample replicates and immunohisto-chemistry validated the technical feasibility and the expression pattern of the gene with greatest differential expression, respectively; gene set enrichment analysis suggests that imatinib mesylate may have a greater effect on the microvasculature than the malignant epithelial cells.