Thomas Secher, Olivier Gaillot, Bernhard Ryffel and Mathias Chamaillard
Cancer Res March 1 2010 70 (5) 1749-1752; DOI:10.1158/0008-5472.CAN-09-3401
Findings suggest that inhibiting a type of cell-cell communication in antigen-presenting cells can promote antitumor immune responses.
A novel epigenetic mechanism for activation of NF-κB might be offer prognostic information and a therapeutic target for colorectal cancer treatment.
Mathematical simulations infer that the signaling circuitry in cancer cells can be rewired by changing expression of all members of a multiprotein signaling complex, not just cell surface receptors.
Circadian rhythm genes that control glucose and fatty acid metabolism act to reinforce the survival of breast cancer cells.
microRNAs that serve as modifiers of apoptosis signaling at the level of the mitochondria are defined.
A mechanistically unique approach to target VEGF-mediated angiogenesis via gene therapy approach is presented.
Findings suggest that blocking lymphangiogenesis by antagonizing VEGF-C expressed by breast cancer cells may retard the growth of pulmonary metastases after the removal of the primary tumor.
One of the therapeutic benefits of proteosome inhibition may be to improve the effectiveness of antitumor T cell responses.
Findings encourage the concept that vitamin D deficiencies in breast cancer patients may encourage bone metastasis.
Findings identify a simple, low cost therapeutic strategy to blunt cancer-associated inflammation and immune escape for cancer treatment.
Findings elucidate mechanisms of an important tumor suppressor gene in childhood kidney and brain tumors.
ING proteins found in chromatin modifying complexes appear to control expression of a core regulator of microRNA biogenesis, perhaps providing a novel mechanism for deregulation of microRNAs in cancer cells.
Defects in DNA damage control in cancer not only affect the tumor cell itself, but also the local tumor microenviroment by increasing chronic inflammation that may support cancer development.
An adapter protein found in focal adhesion complexes stimulates survival and invasion of prostate cancer cells by limiting anoikis.
Mechanistic findings suggest a novel therapeutic approach to prevent metastasis in aggressive renal cancers.
Tumor suppressor microRNAs such as miR-31 offer opportunities for multi-pronged attack on important signaling pathways in cancer.
A single microRNA may be able to independently segregate pleural mesotheliomas by time to progression as well as by survival.
An edible melon extract with breast cancer chemopreventive properties is characterized.
A volatile sulfur ingredient of garlic has chemopreventive effects on mouse skin tumor promotion mediated by a pathway of COX-2 suppression.
The natural spice compound cucurmin can selectively radiosensitize carcinoma cells, but the underlying mechanism has yet to be fully understood.
Small and affordable inhibitors of the mammalian target of rapamycin pathway represent a promising therapeutic strategy to disrupt fundamental tumor growth angiogenesis, which occurs by the activated crosstalk between endothelial cells and tumor cells.
Findings suggest applications of a BH3 mimetic that triggers Bax-mediated apoptosis for treatment of cholangiocarcinoma.
A second generation proteasome inhibitor with a shorter halflife of proteasome dissociation offers improved pharmacokinetics, pharmacodynamics and antitumor activity, compared to bortezomib.
Arsenic is a major worldwide health hazard in ground water, but the mechanistic basis for its risk as a carcinogen has not been understood.
Complexities in the application of EGF receptor inhibitors emerge as a result of rapid shifts in receptor reliance made by tumor cells after inhibitor exposure.
Findings suggest strategies to increase tumor susceptibility to mTOR inhibitors and to reverse emergent resistance to this class of drugs.
Negative regulation of cyclin D1 may underlie the resistance to chemotherapy that is conferred by overexpression of hypoxia inducible factor HIF-1, which occurs widely in human cancers.
Two pathways downstream of the Jak2 kinase are revealed that have opposing effects on EMT, with possible implications for understanding EMT as well as the clinical application of Jak2 inhibitors.
Based on their gene expression profiles, glioblastoma cancer stem cells can resemble either fetal or adult neural stem cells, suggesting distinct molecular subclasses of this disease.
Findings reveal a functional linkage between a telomere-binding protein and the mitotic failure induced by oncogene.
A novel member of the FOX family of transcription factors is implicated in colon tumorigenesis through its ability to restrict expression of the pivotal cell cycle regulator p21WAF1.
An atypical member of the PKC family of kinases may be vital to pancreatic cancers and other K-Ras-driven cancers, suggesting it as a novel therapeutic target to attack these cancers.
A new candidate driver oncogene in melanoma is identified based on chromosomal copy number analysis.
Findings focus interest on the receptor tyrosine kinase FGFR1 as a target to thwart resistance to in breast endocrine therapy.
A tumor suppressive kinase, Protein Kinase D1, with homology to calcium/calmodulin-dependent kinases is found to increase secretion of MMPs in prostate cancer that may retard cancer in this setting.
Cyclin D1 is well described as a cell cycle regulator but it also exerts a function in cell invasion in cancer that is mechanistically less understood.
FoxA transcription factors suppress the epithelial-mesenchymal transition, preventing the acquisition of invasive and metastatic properties.
Ovarian cancers exhibit elevated choline kinase and phosphatidylcholine-specific phospholipase C resulting in increased phosphocholine, providing novel targets for imaging-based diagnosis and treatment.