http://precedings.nature.com/tags/cancer Recently posted documents tagged with 'cancer' Nature Publishing Group en Nature Precedings http://precedings.nature.com/images/header_logo.gif http://precedings.nature.com http://dx.doi.org/10.1038/npre.2009.3485.1 Clinical MRI and MRS have promise in molecular imaging. Microimaging techniques offer a promising research tool to get noninvasive data in monitoring the effect of drugs. http://dx.doi.org/10.1038/npre.2009.3485.1 Mon, 03 Aug 2009 18:59:28 UTC Quantitative MRI and MR Spectroscopy of Multiple Sclerosis, Alzheimer’s Disease, Epilepsy and Cancer Microimaging Techniques doi:10.1038/npre.2009.3485.1 2009-08-03 Rakesh Sharma Nature Precedings 2009-08-03T18:59:28Z Presentation Biotechnology Cancer Neuroscience http://creativecommons.org/licenses/by/3.0/ http://dx.doi.org/10.1038/npre.2009.3515.1 We present the design and development of NanoParticle Ontology (NPO). The ontology is implemented in the Ontology Web Language (OWL). The domain terms in NPO currently represent entities, which describe knowledge about physical, chemical, and functional properties of nanoparticles characterized in cancer nanotechnology research. The upper-level of NPO is formed using terms from the Basic Formal Ontology (BFO). http://dx.doi.org/10.1038/npre.2009.3515.1 Wed, 29 Jul 2009 19:57:25 UTC NPO: Ontology for Cancer Nanotechnology Research doi:10.1038/npre.2009.3515.1 2009-07-29 Dennis Thomas Nature Precedings 2009-07-29T19:57:25Z Poster Cancer Bioinformatics http://creativecommons.org/licenses/by/3.0/ http://dx.doi.org/10.1038/npre.2009.3514.1 We present the design and development of NanoParticle Ontology (NPO). The ontology is implemented in the Ontology Web Language (OWL). The domain terms in NPO currently represent entities, which describe knowledge about physical, chemical, and functional properties of nanoparticles characterized in cancer nanotechnology research. The upper-level of NPO is formed using terms from the Basic Formal Ontology (BFO). http://dx.doi.org/10.1038/npre.2009.3514.1 Wed, 29 Jul 2009 19:55:50 UTC NPO: Ontology for Cancer Nanotechnology Research doi:10.1038/npre.2009.3514.1 2009-07-29 Dennis Thomas Nature Precedings 2009-07-29T19:55:50Z Manuscript Cancer Bioinformatics http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/1980/version/2 We introduce a new effective method to control hormone refractory prostate cancer cells by using an activated rubber/resin form (RB), far-infrared ray emitter, with or without sodium butyrate (SB). The growth of three human prostate cancer cell lines (Du145, PC-3 and LNCaP) was suppressed in vitro and in vivo by using RB, and the cells were eradicated with RB + 3 mM SB. G1 arrest and apoptotic pathway proteins were induced by RB with intensified expressions of apoptosis – related mRNA on cDNA microarray. RB radiates far-infrared rays of the 4 to 25 μm wavelengths to an object which exert a favorable influence on a cancer control. These results may render us a new therapeutic modality in hormone refractory prostate cancer. http://precedings.nature.com/documents/1980/version/2 Fri, 20 Mar 2009 12:43:46 UTC Far-infrared rays control prostate cancer cells in vitro and in vivo hdl:10101/npre.2009.1980.2 2009-03-20 Hiroki Shima Nature Precedings 2009-03-20T12:43:46Z Manuscript Cancer http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/2880/version/1 There are numerous mathematical or statistical models have been given out for radiation cell killing mechanism. Unfortunately, none of the model could explain the mechanism perfectly. The more advanced model for it is still necessary to be researched. Following common assumption, a new theoretical model named “target cumulating” model is induced from the molecular and particle physics level. The result of theoretical calculation gives the equation of cell survival rate corresponding to delivered dose and other sensitivity parameters. In addition to fit the cell survival curve well, the new model showed advantages with comparing to previous models. Also, the new model predicts or explains some phenomenon that had been observed in laboratory (e.g. dose rate effect and low dose hypersensitivity). http://precedings.nature.com/documents/2880/version/1 Wed, 18 Feb 2009 17:15:14 UTC A new mathematical model for radiation cell killing mechanism: Target cumulating model hdl:10101/npre.2009.2880.1 2009-02-18 Zhao Liang Nature Precedings 2009-02-18T17:15:14Z Manuscript Cancer http://creativecommons.org/licenses/by/3.0/ http://dx.doi.org/10.1038/npre.2009.2769.1 Inhibition of Aurora kinase, a member of serine/threonine kinase involved in the regulation of cell division is emerging as a new molecular targeted cancer treatment option. Three isoforms of Aurora kinase, A, B and C are known. Both Aurora A and B are over expressed in many human cancers and are linked to chromosome instability, oncogenic transformation, tumour progression and development of chemoresistance. Inhibitors of Aurora kinase, regardless of their kinase specificity spectrum have shown to promote cancer cell death by induction of apoptosis and mitotic catastrophe. Based on the current success of Aurora kinase inhibitors in the development of kinase-based cancer therapy, we have initiated a structure-based virtual screening for the identification of Aurora kinase inhibitors by using published aurora protein structure (PDB code:1MQ4). Small molecule and natural product compound libraries were docked into the active site/ATP binding site using the programs Gold 3.0 and Glide 4.5. A total of six compounds were identified with high priority scores through this method to possess Aurora A inhibition. One of the virtual screen (VS) hit, BPR1K0025S0 was synthesised in 3 steps and found to have Aurora A IC50~15 M and x-ray co-crystal structure in complex with the aurora protein was solved for this compound. Based on the binding mode of this compound to Aurora A protein, further modification in the ester part was envisaged and a total of around 40 compounds were synthesised. Many of them possessed enhanced activity level compared to the original hit. Of particular interest is the aniline series of compounds, which showed submicromolar activity in the enzyme based Aurora inhibition assay. Thus a forty-fold improvement in activity for BPR1K0269S0 was achieved from the initial virtual screen hit BPR1K0025S0. http://dx.doi.org/10.1038/npre.2009.2769.1 Mon, 12 Jan 2009 21:01:45 UTC Structure-based design of novel pyrazoles as aurora kinase A inhibitors. doi:10.1038/npre.2009.2769.1 2009-01-12 Mohane Coumar Nature Precedings 2009-01-12T21:01:45Z Poster Biotechnology Cancer Chemistry http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/2737/version/1 In the past few years, many high-throughput techniques have been developed and applied to biological studies. These techniques such as “next generation” genome sequencing, chip-on-chip, microarray and so on can be used to measure gene expression and gene regulatory elements in a genome-wide scale. Moreover, as these technologies become more affordable and accessible, they have become a driving force in modern biology. As a result, huge amount biological data have been produced, with the expectation of increasing number of such datasets to be generated in the future. High-throughput data are more comprehensive and unbiased, but ‘real signals’ or biological insights, molecular mechanisms and biological principles are buried in the flood of data. In current biological studies, the bottleneck is no longer a lack of data, but the lack of ingenuity and computational means to extract biological insights and principles by integrating knowledge and high-throughput data. Here I am reviewing the concepts and principles of network biology and the computational methods which can be applied to cancer research. Furthermore, I am providing a practical guide for computational analysis of cancer gene networks. http://precedings.nature.com/documents/2737/version/1 Tue, 06 Jan 2009 17:02:32 UTC Computational methods in cancer gene networking hdl:10101/npre.2008.2737.1 2009-01-06 Edwin Wang Nature Precedings 2009-01-06T17:02:32Z Manuscript Cancer Genetics & Genomics Bioinformatics http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/2374/version/1 CD138 (Syndecan1) is highly expressed on multiple myeloma (MM) cells. In this study, we examined the anti-MM effect of murine/human chimeric CD138-specific monoclonal antibody (mAb) nBT062 conjugated with highly cytotoxic maytansinoid derivatives in vitro and in vivo. These agents significantly inhibited growth of CD138-positive MM cell lines and primary tumor cells from MM patients, without cytotoxicity against peripheral blood mononuclear cells from healthy volunteers. In MM cells, they induced G2/M cell cycle arrest followed by apoptosis associated with cleavage of PARP and caspase-3, -8 and -9. Non-conjugated nBT062 completely blocked cytotoxicity induced by nBT062-maytansinoid conjugate, confirming that binding is required for inducing cytotoxicity. Moreover, nBT062-maytansinoid conjugates blocked adhesion of MM cells to bone marrow stromal cells (BMSCs). Co-culture of MM cells with BMSCs, which protects against dexamethasone-induced death, had no impact on the cytotoxicity of the immunoconjugates. Importantly, nBT062-SPDB-DM4 and nBT062-SPP-DM1 significantly inhibited MM tumor growth in vivo in both human multiple myeloma xenograft mouse models and in SCID-human bone grafts (SCID-hu mouse model). These studies provide the preclinical framework supporting evaluation of nBT062-maytansinoid derivatives in clinical trials to improve patient outcome in MM. http://precedings.nature.com/documents/2374/version/1 Wed, 08 Oct 2008 21:05:05 UTC The monoclonal antibody nBT062 conjugated to maytansinoids has potent and selective cytotoxicity against CD138 positive multiple myeloma cells in vitro and in vivo hdl:10101/npre.2008.2374.1 2008-10-08 Hiroshi Ikeda Nature Precedings 2008-10-08T21:05:05Z Manuscript Cancer Molecular Cell Biology http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/2281/version/1 Background: The transcription factor PAX2 regulates key developmental processes, including mediation of resistance to apoptosis. Inappropriate PAX2 expression has been implicated in facilitating tumour survival, and we have previously shown that siRNA-mediated blockade of PAX2 signalling at the transcript level in EJ bladder carcinoma cells promotes cell death. In this study, we attempted to disrupt PAX2 transcriptional activity in EJ cells by using a decoy oligodeoxynucleotide (ODN). Results: We could not show an interaction between PAX2 and our PAX2 decoy ODN, and in both PAX2-positive EJ and PAX2-negative HEK293 control cells, decoy and control ODN transfection resulted in a marked retardation of cell growth, irrespective of sequence, but not in COS7 and NZM4 melanoma cells. Conclusions: Our data indicate that decoy ODN transfection had off-target effects that inhibited cell growth in a cell line-dependent manner, and we suggest caution is required to determine the specificity of decoy ODN sequences before considering their application as a potential therapeutic agent. http://precedings.nature.com/documents/2281/version/1 Wed, 10 Sep 2008 10:25:34 UTC Off-target response to decoy oligodeoxynucleotide treatment hdl:10101/npre.2008.2281.1 2008-09-10 Aaron R. Jeffs Nature Precedings 2008-09-10T10:25:34Z Manuscript Cancer Developmental Biology Molecular Cell Biology http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/2190/version/1 We describe multifunctional magnetic nanoparticles (MNPs) encapsulated in thermosensitive, drug-bearing shells and delivered to the tumor site by genetically modified and non-pathogenic strains of bacteria with known affinity to tumors for an effective and minimally invasive protocol for tumor management. The magnetic nanoparticles also serve as a non-invasive imaging contrast agent, heating agent as well as thermometry monitoring agents. We have shown an efficient tumor management on a mouse model utilizing the MNPs. Our studies showed that these novel MNPs significantly reduce the progress of tumor and prolong the animal life and function as an imaging contrast to visually monitor the tumor treatment and evolution. http://precedings.nature.com/documents/2190/version/1 Thu, 21 Aug 2008 01:34:53 UTC Multifunctional Nanoparticles for Imaging Guided Interventions hdl:10101/npre.2008.2190.1 2008-08-21 Yousef Haik Nature Precedings 2008-08-21T01:34:53Z Manuscript Biotechnology Cancer http://creativecommons.org/licenses/by/3.0/