Breaking Advances
Cancer Res August 15 2011 71 (16) 5363-5364;
Preclinical studies validate a novel class of small molecule inhibitors of the enzyme GSK-3, which exert potent antitumor properties by blocking both tumor invasion and angiogenesis.
The lack of a complete cytogenetic response in chronic phase CML patients treated with the ABL kinase inhibitor imatinib can be explained by loss of the remaining normal ABL1 allele in CML cells.
This study identifies an important mechanism of ERG regulation in human prostate cancers, with implications for understanding prostate tumor progression.
IL-18 suppresses the crucial role of natural killer cells (NK cells) in supporting tumor immunosurveillance, with implications for clinical strategies to reverse this mechanism of tumoral immune escape.
Findings illustrate a novel approach to creating cell-specific computational models of signaling networks based on biochemical data, applying it in this study to define deregulated pathways in hepatocellular carcinoma.
The tissue microenvironment in human lung carcinomas suppresses the tumoricidal activity of natural killer cells, thereby contributing to immune escape and progression.
Findings define a critical cellular mechanism of immune escape in human ovarian cancers, offering new insights into the pathophysiology of this often fatal cancer.
Study findings suggest that useful peptide antigens for cancer vaccination might be derived from proteins commonly expressed in normal cells but abnormally proteolyzed in cancer.
Findings elucidate how anti-tumor responses are elicited by CTLA-4 antibody ipilimumab, recently approved by the FDA for treatment of melanoma.
A chemokine receptor that is critical to organize leukocyte trafficking responses to infection is also found to be critical for T cell-mediated responses against tumors, suggesting mechanistic similarities in the way that the immune system interprets cancer cells and infectious pathogens.
Findings suggest that the anti-tumor properties of a potent immune stimulatory Toll receptor ligand with therapeutic potential may be reduced or negated if the Toll receptor TLR4 is also activated, with implications for the design of immunotherapy trials.
Findings show that increased aromatase levels may play an even larger role in breast cancer progression than overexpression of estrogen receptor-alpha.
This study illustrates the importance of ‘immunogenic’ cell death signaling for blocking lung cancer, the progression of which relies upon the activation of pro-inflammatory mechanisms that not only block cancer cell apoptosis but also promote their immune escape.
Understanding the functional impact of specific mutations in the VHL tumor suppressor pathway in deadly kidney cancers may be critical for selecting appropriate individualized therapies in patients.
Results show an association between VEGFR-2 copy number gains and reduced overall survival in patients with non-small cell lung cancer.
A druggable target implicated in promoting metastasis is found to coordinately promote immune escape, illustrating the important linkage between these two processes in ovarian cancer progression.
Combined inhibition of Raf and MEK may offer a clinical strategy to bypass or overcome acquired resistance to MEK inhibitors that can arise as the result of a powerful activating mutation in MEK1.
This study suggests novel strategies to re-sensitize p53-deficient breast cancer cells to genotoxic chemotherapy by restoring nuclear shuttling which is dysfunctional in such cells.
Findings identify a novel G protein-coupled receptor that regulates VEGF production, offering a new therapeutic target for angiogenesis inhibition.
A transcription factor required for embryonic brain development also contributes in later life to brain tumor development, due to its roles in normal and malignant neural stem cells.
This article reports a new regulatory node in cancer in which a protein methyltransferase works in conjunction with the tumor suppressor PDCD4 to cause accelerated tumor growth.
This study defines an important new link in the control of mitochondrial function by oncogenes that influence cellular metabolism.