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View the Table of Contents for the April 15 issue of Cancer Research.
Page 3030
At present, the cancer pathological stage obtained from prostatectomy is the only way to evaluate the appropriateness and effectiveness of the surgery for the patient and to direct adjuvant therapies. To explore the utility of tumor metabolism, Cheng et al. analyzed prostatectomy samples with tissue MR spectroscopy. Tissue metabolite profiles were found to be extremely sensitive in differentiate cancer versus histologically benign samples obtained from the same patients. Furthermore, metabolite profiles measured from histologically benign samples differentiate tumor pathological stages. Tissue metabolite profiles show promise as a clinically relevant tool in screening biopsy of cancer patients and directing effective treatments.
Page 3035
Human adult stem cells are being evaluated widely for various therapeutic approaches and are thought to be highly resistant to transformation. It was, nonetheless, recently proposed that altered stem cells can give rise to cancer stem cells. Rubio et al. show that human mesenchymal stem cells (MSC) can undergo spontaneous transformation following long-term in vitro culture. This is the first report of spontaneous transformation of human adult stem cells, supporting the hypothesis of cancer stem cell origin. These findings indicate the importance of biosafety studies of MSC biology to efficiently exploit their full clinical therapeutic potential.
Page 3081
Prostate cancer is initially responsive to androgen-ablation therapy and progresses to androgen-unresponsive states that are refractory to treatment. The mechanism of this transition is unknown. Lin et al. employed two high-throughput technologies, massively parallel signature sequencing (MPSS) and isotope-coded affinity tag (ICAT), to gain a system-wide understanding of this transition in LNCaP and CL1 cell line models. They found that 37 BioCarta and 14 KEGG pathways are up-regulated and 23 BioCarta and 22 KEGG pathways down-regulated during this transition. Their efforts represent a significant step towards a systems approach to understanding prostate cancer progression.
Page 3347
Virotherapy of cancer is based on the selective replication of modified viruses in malignant cells. Jeeninga et al. tested whether the human immunodeficiency virus (HIV-1) can be transformed such that it replicates exclusively in leukemic T cells. When the HIV-1 genome was stripped from all accessory functions, the resulting mini-HIV variant was totally replication-impaired in normal T cells. Interestingly, this mini-HIV can still replicate in leukemic T cells and is able to selectively kill these cells in a mixed culture with untransformed control cells.
Page 3374
Inflammatory C-C chemokines are thought to facilitate cancer progression by binding to chemokine receptors on leukocytes or tumor cells. van Deventer et al. show that absence of one of these receptors, chemokine receptor 5 (CCR5), decreases tumor metastases. However, experiments with CCR5-/- and wild type bone marrow chimeric mice imply this effect is not mediated by CCR5 on white blood cells. The importance of CCR5+ stromal cells was confirmed by the transfer of these cells into CCR5-/- mice. This data provide an understanding of how CCR5 inhibitors that have been developed for HIV patients can benefit patients with cancer.