Breaking Advances
Cancer Res April 15 2011 71 (8) 2807-2808;
This study offers important insights into the function of the PTEN phosphatase in the nucleus, where this important tumor suppressor appears to act to suppress cancer in addition to its well-described roles in the cytoplasm.
This study uses multiscale mathematical modeling to study how hypoxic tumor cells can be attacked most effectively, using a proposed cell-based therapy that takes advantage of several targeting principles.
A comprehensive mechanistic mathematical model gives evidence that the main driving mechanism for CML blast crisis origination is interaction between leukemic and normal cells.
Endothelial cell specific knockout illustrates a critical role for a stress chaperone in the tumor microenvironment, extending its known role in tumor cells and deepening its significance to therapeutic and imaging applications.
This study offers a clear rationale for the development of a powerful new vaccine adjuvant for dendritic cell-based immunotherapies, an emerging area of cancer therapy with the first FDA-approved product appearing in 2010.
Successful application of adoptive therapy of cancer using autologous T cells genetically targeted to tumor associated antigens is dependent upon prior depletion of tumor infiltrating regulatory T cells.
Findings define how a critical tumor suppressor gene becomes attenuated in chronic myeloid leukemia, and how this attenuation leads to apoptotic resistance and disease progression.
Findings offer preclinical proof-of-concept for therapeutic targeting of a important cell surface-based driver of immune escape in cancer, perhaps involved in many types of human cancer.
Findings advance understanding of the pathophysiology of primary myelofibrosis, a bone marrow–derived disease, and suggest applications for drugs that target a key megakaryocytic signaling pathway as a new strategy to evaluate for treating this disease.
Findings reveal a mechanism through which plasminogen activator-dependent conversion of plasminogen to plasmin is attenuated, reducing tumor cell capacity for invasion and metastasis in the tumor microenvironment.
This study establishes a novel nodal oncomiR in breast cancer that acts through several pathways to promote metastatic tumor progression.
Findings establish the critical role of a neuronal differentiation factor in neuroblastoma and its functional relationship with a neuronal repellent factor.
A gene implicated in cancer progression proves to directly support metastasis by activating a PAK kinase implicated in invasive cell motility.
A novel tumor suppressor collaborates with p53 in tumor formation and epithelial-mesenchymal transition.
This study identifies a potential p53 activating E3 ligase located in the cytoplasm that functions as a tumor suppressor.
A class of mutations that lead to mitochondrial DNA depletion and apoptotic resistance may be important drivers of tumorigenesis in most microsatellite-unstable colorectal cancers.
A genome-wide study of DNA methylation patterns suggests clinically useful theranostic markers in breast cancer, as well as new candidate pathways in etiology, progression, and therapy.
Findings support the notion that RAD51L1 and other DNA repair genes play a role in the etilogy and development of nasopharyngeal carcinoma.
This study reports a simple proteomic signature in bronchial specimens as a quantitative tool for the diagnostic assessment of lung cancer beyond qualitative histology methods.
An oral nanocarrier of docetaxel favors lymphatic uptake in preclinical studies, potentially stimulating clinical studies that could allow docetaxel chemotherapy to be switched from intravenous to oral delivery in patients.
A drug used widely to treat erectile dysfunction in men is found to abrogate two common mechanisms of chemotherapeutic drug resistance, with immediate potential applications to improve the treatment of many advanced cancers.
DNA re-replication elicited in cancer cells by a small molecule inhibitor currently in Phase I trials creates an unrecoverable cellular insult, with implications for gaining deeper understanding of a unique therapeutic mechanism of cytotoxicity in cancer treatment.
This study employed a novel RNAi approach useful for context-dependent target validation in vivo, applying it to demonstrate that the protein kinase PDK1 is not a rate limiting factor for PI3K-pathway activation or tumor formation in PTEN-deficient mouse models.
Findings define an important role in glioma recurrence and poor prognosis for a G-protein coupled receptor that is part of the Wnt signaling family governing stemness and invasiveness of glioma stem cells.
Findings identify a member of the FOXO family of transcription factors as a critical regulator of EMT, stem cell properties, and chemotherapeutic resistance in cancer cells.
This study extends present concepts of how EMT contributes to cancer progression by showing that it can also contribute to cancer initiation, by promoting clonal expansion and stem-like properties in premalignant lung epithelial cells.
Using immunocompetent mouse models and methodologies to better preserve cell surface epitopes allowed the identification of a melanoma stem cell marker associated with metastatic disease.
Results offer experimental proof of the expected powerful effects of hypoxia on the progression of early stage pancreatic cancer, with potential to target these effects therapeutically.
Findings suggest how an important metastasis susceptibility gene may predispose tumor cells to convert to more de-differentiated or primitive states that are metastatically aggressive.
An uncharacterized member of the human kinome is revealed to be a pseudokinase that acts downstream of the MET oncoprotein, the activation of which mediates powerful effects on the progression of many types of human cancer.
Findings define properties of a gene involved in neuronal differentiation that support its assignment as a 1p36 tumor suppressor gene in neuroblastoma.
There has been a recent flood of cancer kinome sequence data, but the functional consequences of the reported protein kinase mutations have been inferred largely through statistical approaches, and our studies represent a critical first step in assessing the functional relevance of putative driver mutations experimentally.
Findings of this extensive study define a functionally important extracellular theranostic marker of metastasis in nasopharengeal carcinoma, a common deadly cancer in Asia.