Issues
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Cover Image
The survivin circuitries. Survivin is a universal tumor-associated molecule that intersects multiple signaling circuits of tumor cell maintenance. These include mitotic progression via microtubule-kinetochore attachment and bipolar spindle formation, preservation of endothelial cell viability during angiogenesis, and suppression of tumor cell apoptosis. Survivin is also intercalated in p53-dependent signaling as one of the genes repressed by wild type p53, and promotes tumor cell adaptation via its association with the stress response molecular chaperone, Hsp90. Because of its crossroads functions, survivin provides a hotly pursued target for multiple approaches of rational cancer therapy. For details, see the article by Altieri in this issue.
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Editorial
Review
ARTICLE
Combined inhibition of the phosphatidylinositol 3-kinase/Akt and Ras/mitogen-activated protein kinase pathways results in synergistic effects in glioblastoma cells
Combination therapy of androgen-independent prostate cancer using a prostate restricted replicative adenovirus and a replication-defective adenovirus encoding human endostatin-angiostatin fusion gene
The antitumor effect of LJ-529, a novel agonist to A3 adenosine receptor, in both estrogen receptor–positive and estrogen receptor–negative human breast cancers
NIK-333 inhibits growth of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells in association with blockade of nuclear factor-κB signal pathway
Semisynthetic homoharringtonine induces apoptosis via inhibition of protein synthesis and triggers rapid myeloid cell leukemia-1 down-regulation in myeloid leukemia cells
Modulation of chemotherapy resistance in regional therapy: a novel therapeutic approach to advanced extremity melanoma using intra-arterial temozolomide in combination with systemic O6-benzylguanine
Prediction of individual response to platinum/paclitaxel combination using novel marker genes in ovarian cancers
Low doses of cisplatin or gemcitabine plus Photofrin/photodynamic therapy: Disjointed cell cycle phase-related activity accounts for synergistic outcome in metastatic non–small cell lung cancer cells (H1299)
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