Showing papers in "Cancer Cell in 2007"

TL;DR: Recent progress in understanding mTOR signaling is discussed, paying particular attention to its relevance in cancer and the use of rapamycin in oncology.

TL;DR: This work shows that endothelial cells interact closely with self-renewing brain tumor cells and secrete factors that maintain these cells in a stem cell-like state, and proposes that brain CSCs are maintained within vascular niches that are important targets for therapeutic approaches.

TL;DR: This study provides insight into different mechanisms of action of this class of drugs in recurrent glioblastoma patients and suggests that the timing of combination therapy may be critical for optimizing activity against this tumor.

TL;DR: The unique metabolic profile of cancer (aerobic glycolysis) might confer apoptosis resistance and be therapeutically targeted and the orally available DCA is a promising selective anticancer agent.

TL;DR: Assessment of PI3K pathway activation may provide a biomarker to identify patients unlikely to respond to trastuzumab-based therapy, and the combined analysis of PTEN and PIK3CA identified twice as many patients at increased risk for progression compared to PTEN alone.

TL;DR: In this paper, gene expression and genetic profiles of cells purified from cancerous and normal breast tissue using markers previously associated with stem-cell-like properties were determined using markers from the TGF-β pathway, where its inhibition induced a more epithelial phenotype.

TL;DR: It is reported that selective expression of an endogenous K-Ras(G12V) oncogene in embryonic cells of acinar/centroacinar lineage results in pancreatic intraepithelial neoplasias (PanINs) and invasive PDA, suggesting that PDA originates by differentiation of acINs or their precursors into ductal-like cells.

TL;DR: In this paper, an integrated analysis of high-density oligonucleotide array CGH and gene expression profiling data from 155 multiple myeloma samples identified a promiscuous array of abnormalities contributing to the dysregulation of NF-kappaB in approximately 20% of patients.

TL;DR: It is demonstrated that addiction to the NF-kappaB pathway is frequent in myeloma and suggest that IKKbeta inhibitors hold promise for the treatment of this disease.

TL;DR: It is found that the mutations activate the EGFR kinase by disrupting autoinhibitory interactions, and that they accelerate catalysis as much as 50-fold in vitro.

TL;DR: It is shown that hypoxia-inducible factor 1 negatively regulates mitochondrial biogenesis and O(2) consumption in renal carcinoma cells lacking the von Hippel-Lindau tumor suppressor (VHL), and that transcription of the gene encoding the coactivator PGC-1beta is C-MYC dependent.

TL;DR: It is proved that the inhibition of an overexpressed UCR induces apoptosis in colon cancer cells, and the findings argue that ncRNAs and interaction between noncoding genes are involved in tumorigenesis to a greater extent than previously thought.

TL;DR: It is demonstrated here that HIF-2alpha promotes cell-cycle progression in hypoxic RCCs and multiple other cell lines and correlates with enhanced c-Myc promoter binding, transcriptional effects on both activated and repressed target genes, and interactions with Sp1, Miz1, and Max.

TL;DR: Cells and mice with reduced levels of the mitosis-specific, centromere-linked motor protein CENP-E are shown to develop aneuploidy and chromosomal instability in vitro and in vivo, and a role is revealed in preventing tumorigenesis.

TL;DR: O(2) deprivation (hypoxia) and cellular proliferation engage opposite cellular pathways, yet often coexist during tumor growth, so acting in concert these transcription factors reprogram metabolism, protein synthesis, and cell cycle progression, to "fine tune" adaptive responses to hypoxic environments.

TL;DR: It is shown that overexpression of Mad2 in transgenic mice leads to a wide variety of neoplasias, appearance of broken chromosomes, anaphase bridges, and whole-chromosome losses, as well as acceleration of myc-induced lymphomagenesis.

TL;DR: It is shown that the Chk1 inhibitor UCN-01 also potently inhibits MK2, suggesting that its clinical efficacy results from the simultaneous disruption of two critical checkpoint pathways in p53-defective cells.

TL;DR: A small molecule mimetic of Smac/Diablo that specifically counters the apoptosis-inhibiting activity of IAP proteins has been shown to enhance apoptosis induced by cell surface death receptors as well as chemotherapeutic drugs.

TL;DR: It is proposed that blocking NRP1 function inhibits vascular remodeling, rendering vessels more susceptible to anti-VEGF therapy, and generated two monoclonal antibodies that bind to the Sema- and VEGF-binding domains of N RP1.

TL;DR: It is shown that beta-catenin-deficient mice can form HSCs, but that these cells are deficient in long-term growth and maintenance, and Wnt signaling is required for the self-renewal of normal and neoplastic stem cells in the hematopoietic system.

TL;DR: NEMO-mediated NF-κB activation in hepatocytes has an essential physiological function to prevent the spontaneous development of steatohepatitis and hepatocellular carcinoma, identifying NEMO as a tumor suppressor in the liver.

TL;DR: Using a panel of 18 lymphoma cell lines, a strategy is developed that can identify apoptotic defects in cancer cells and separate them into three main classes based on position in the apoptotic pathway, and predict sensitivity to conventional chemotherapeutic agents.

TL;DR: Computational modeling revealed that transcellular gradients of CCR7 ligand were created under flow to drive this response, illustrating how tumor cells may be guided to lymphatics during metastasis.

TL;DR: Findings add a new, challenging layer of complexity to the p53 network as the initial evidence suggesting that miR-34 genes are central mediators of p53 function is summarized here.

TL;DR: Gen expression analysis comparing ETs with a variety of normal tissues shows that the profiles of different EWS-FLI1-silenced Ewing cell lines converge toward that of mesenchymal stem cells (MSC).

TL;DR: The convergence of these genes in a shared role reveals underlying biology of these illnesses and suggests still other breast cancer genes.

TL;DR: It is reported that antioxidants inhibited three tumorigenic models in vivo and challenge the paradigm that antioxidants diminish tumorigenesis primarily through decreasing DNA damage and mutations and provide significant support for a key antitumorigenic effect of diminishing HIF levels.

TL;DR: It is demonstrated that high TGFbeta-Smad activity is present in aggressive, highly proliferative gliomas and confers poor prognosis in patients with glioma.

TL;DR: A MGUS/MM phenotype in transgenic mice with Eμ-directed expression of the XBP-1 spliced isoform (XBP- 1s), a factor governing unfolded protein/ER stress response and plasma-cell development is reported, which serves to implicate X BP-1s dysregulation in MM pathogenesis.

TL;DR: It is shown that miR-223 is a direct transcriptional target of AML1/ETO, and an additional action for a leukemia fusion protein linking the epigenetic silencing of a microRNA locus to the differentiation block of leukemia is identified.