Breaking Advances
Cancer Res June 1 2011 71 (11) 3733-3734;
Metabolic changes in the tumor and brain tissue during anti-VEGF therapy can serve as imaging biomarkers for predicting treatment response in patients with recurrent malignant glioblastomas.
Enhancing drug uptake through the use of a novel electrode technology can achieve high rates of complete response in a rat model of brain cancer.
Findings highlight the central role of interferon-γ in determining cancer-promoting versus cancer-suppressing inflammation.
This study addresses paradoxes concerning the role of STAT3 and NF-κB as pro-oncogenic yet also immunostimulatory to T-cell responses against cancer.
Findings reveal a previously unrecognized activity of placental growth factor, a proangiogenic factor that contributes to tumor angiogenesis and progression in many types of cancer.
Preparation of the metastatic niche in lymph nodes relies in part on the ability of a primary tumor to secrete nanovesicles that can remodel the nodal microenvironment and permit its colonization by tumor cells.
Findings offer preclinical proof-of-concept for antibody targeting of a marker of metastatic progression as a potential new adjuvant therapy for clinical investigation.
Cells undergoing injury turn on EGF ligand production, which induces the developmental transcription factor SOX9 and supports emergence of a migratory, invasive phenotype.
This study finds that epithelial cell organization does not pose a barrier to Myc oncogenicity, pointing to roles for tumor suppression mechanisms other than three-dimensional structure in antagonizing Myc during carcinogenesis.
Myeloproliferative neoplasms rely on support from stromal cells in the bone marrow microenvironment that release IL-6, FGF, and CXCL10.
N-Myc activation is associated with direct repression of a microRNA program that is not generally suppressive to neuroblastoma cells, with possible implications for how to better attack this aggressive pediatric cancer.
Long noncoding RNAs (lncRNAs) are a rapidly emerging area of cancer research because of their suspected roles in interacting with messenger RNAs, regulatory microRNAs, and proteins and modulating their functions.
Studies of thyroid cancer, the most common endocrine cancer, will benefit from the development of a high-penetrance, genetically- engineered mouse model, which recapitulates key features of the genetics and pathophysiology of the human disease.
Preclinical findings show how mild systemic hyperthermia in mice bearing tumors can increase tumor blood flow and improve the efficacy radiation therapy, prompting immediate attention for clinical evaluation.
A large genetic association study of growth factor signaling and estrogen metabolism defines a variant in an estrogen receptor-binding transcriptional co-activator that may confer a reduced risk of breast cancer.
Brisk walking after diagnosis may inhibit or delay prostate cancer progression among men diagnosed with clinically localized prostate cancer.
Common inherited variants in miRNA biogenesis genes may be useful to identify high-risk populations and to develop novel cancer diagnostic, prognostic, and therapeutic strategies.
An important cytoprotective factor is found to sensitize the bladder to a major tobacco carcinogen, but a chemopreventive strategy is suggested to limit this pitfall.
Proof-of-concept and mechanistic findings prompt clinical evaluation for a novel drug combination that could improve cancer treatment.
Results address the longstanding question of how an aggressive childhood cancer might be prompted to undergo terminal differentiation, suggesting new strategies to improve therapy.
Findings suggest that the cytotoxicity of EGFR kinase inhibitors in cancer cells may be based in large part on induction of oxidative stress via hydrogen peroxide produced by NOX4 signaling.
Findings offer preclinical proof-of-concept that ErbB3 disruption may be therapeutically effective in PI3K/Akt-driven breast cancers.
Compared to taxanes and epothilones, the two major classes of antimitotic drugs used in cancer treatment, a new FDA approved antitubulin drug may cause far less debilitating nerve damage in cancer survivors.
The findings of this study suggest that chemotherapy may prime later recurrence by decreasing recruitment of normal glial progenitor cells into a brain tumor microenvironment.
Inhibitors of the JAK/STAT3 signaling pathway represent a very appealing therapeutic direction because of the central importance of this pathway in tumor cells and the tumor microenvironment in sustaining malignant growth and progression.
Ras-activated MAP kinases promote invasion and metastasis by stabililizing a master regulator of epithelial-mesenchymal transition.
This report identifies a pair of ovarian cancer stem cell markers that may be functionally critical for stem cell differentiation in cancers.
This study identifies an important prognostic role of Hedgehog pathway in breast cancer and highlights its potential as a novel therapeutic target in metastatic carcinoma.
This study shows how tumor cells exposed to more intense periods of hypoxia in the microenvironment will respond to improve their likelihood of survival and progression, with implications for therapeutic targeting.
Mechanistic results reveal how the prometastatic transcription repressor EZH2 coordinately blocks Wnt antagonists, thereby promoting Wnt/β-catenin signaling in cancer.
Altering the sequence of mutations in a mouse model of sarcomagenesis shows that mutation order dictates tumor phenotype.