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| Registros recuperados: 382 | |
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| Vladimir Trifonov; Laura Pasqualucci; Riccardo Dalla-Favera; Raul Rabadan. |
| Recent developments in extracting and processing biological and clinical data are allowing quantitative approaches to studying living systems. High-throughput sequencing, expression profiles, proteomics, and electronic health records are some examples of such technologies. Extracting meaningful information from those technologies requires careful analysis of the large volumes of data they produce. In this note, we present a set of distributions that commonly appear in the analysis of such data. These distributions present some interesting features: they are discontinuous in the rational numbers, but continuous in the irrational numbers, and possess a certain self-similar (fractal-like) structure. The first set of examples which we present here are drawn... |
| Tipo: Manuscript |
Palavras-chave: Biotechnology; Cancer; Genetics & Genomics; Bioinformatics. |
| Ano: 2010 |
URL: http://precedings.nature.com/documents/5037/version/1 |
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| Michael Dean; Latoya Silverton; Julie Sawitzke. |
| Breast cancer is the most common cancer among American women. Any woman can be affected by breast cancer, with risk for the disease increasing with age. Risk for breast cancer is also exacerbated in women who have certain genetic alterations. Mutations in the BRCA1 and BRCA2 genes predispose women to breast and ovarian cancer, and are increasingly recognized in prostate and pancreatic cancers (1-3). In Caucasian and Asian ethnicities BRCA mutations are associated with basal-type/triple-negative disease. However this association between BRCA gene mutations and basal/triple-negative disease has been understudied in other ethnicities (4-6). The incidence and mortality of breast cancer of Hispanics and Native Americans are lower than other ethnicities;... |
| Tipo: Marker Paper / Data Plan |
Palavras-chave: Cancer; Genetics & Genomics; Bioinformatics; Data Standards. |
| Ano: 2011 |
URL: http://precedings.nature.com/documents/5691/version/2 |
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| Kanipakam Hema; Sadnala Giribabu; Sandeep Swargam; Amineni Umamaheswari. |
| Human pancreatic ribonuclease (RNase1) is a small digestive and pyramidine specific enzyme secreted by the pancreas. RNase1 contributes in the regulation of extracellular RNA by hydrolyzing RNA phosphodiester bonds. High levels of RNase1 in cardiovascular disease patients project the enzyme as an attractive drug target. The known RNase1 inhibitors, citric acid and U1S were searched for structural analogs from Ligand.info database to compile 783 ligands. The ligands' 3D structures and their tautomeric states were generated using LigPrep. The 3424 prepared conformations were subjected to QikProp analysis and filtered based on Lipinski rule of five and zero reactive functional group. The 3376 conformations with good ADME (absorption, desorption,... |
| Tipo: Poster |
Palavras-chave: Cancer; Bioinformatics. |
| Ano: 2011 |
URL: http://precedings.nature.com/documents/6527/version/1 |
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| Kenji Ohe; Toshiaki Utsumi; Akila Mayeda. |
| Estrogen receptor (ER)-[alpha]46 is known as an important isoform for ER[alpha]. It inhibits the function of full length ER[alpha] in MCF-7 mammary carcinoma cells and associated with cell cycle arrest. On the other hand, the oncogene _HMGA1_ (formally _HMG I/Y_) is known to have increased expression in mammary carcinoma correlating with the degree of malignancy. We present here that HMGA1a (HMG I) induces the exon skipped product, ER[alpha]46 mRNA, by tethering U1 snRNP to an upstream pseudo 5' splice site, which is quite analogous to the PSI-mediated splicing regulation of _Drosophila_ P-element.
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| Tipo: Poster |
Palavras-chave: Cancer; Molecular Cell Biology. |
| Ano: 2009 |
URL: http://precedings.nature.com/documents/4104/version/1 |
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| Katsuyuki Hamada; Ting Zhang; Junzo Desaki; Koh-ichi Nakashiro; Hiroshi Ito; Kenzaburo Tani; Yoshiyuki Koyama; Hiroyuki Hamakawa. |
| The squamous cell carcinoma antigen (SCCA) serves as a serological marker for squamous cell carcinomas. Molecular cloning of the SCCA genomic region has revealed the presence of two tandemly arrayed genes, SCCA1 and SCCA2. We examined the promoter activity of the 5'-flanking proximal region of the SCCA1 gene. Deletion analysis of SCCA1 promoter identified a 175-bp core promoter region and an enhancer region at -525 to -475 bp upstream of the transcription start site. The transcriptional activity of the SCCA1 promoter was up-regulated in squamous cell carcinoma cells, compared with normal keratinocyte, normal non-keratinocyte and adenocarcinoma cells. Five tandem repeats of enhancer increased SCCA1 promoter activity by 4-fold. Oncolytic adenovirus... |
| Tipo: Manuscript |
Palavras-chave: Cancer. |
| Ano: 2009 |
URL: http://precedings.nature.com/documents/3213/version/1 |
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| Edwin Wang. |
| What is cancer systems biology? Why should we conduct systems biology research in cancer? What is the relationships between systems biology and personalized medicine? How do we conduct cancer systems biology research? This paper illustrates strategies, procedures and computational techniques for the study of cancer systems biology by focusing on network reconstruction, network analysis and modeling. Finally, certain challenges and hurdles in cancer systems biology will also be discussed. |
| Tipo: Manuscript |
Palavras-chave: Cancer; Genetics & Genomics; Bioinformatics. |
| Ano: 2010 |
URL: http://precedings.nature.com/documents/4322/version/2 |
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| Rodrick Wallace. |
| For a broad spectrum of low level cognitive regulatory and other biological phenomena, isolation from signal crosstalk between them requires more metabolic free energy than permitting correlation. This allows an evolutionary exaptation leading to dynamic global broadcasts of interacting physiological processes at multiple scales. The argument is similar to the well-studied exaptation of noise to trigger stochastic resonance amplification in physiological subsystems. Not only is the living state characterized by cognition at every scale and level of organization, but by multiple, shifting, tunable, cooperative larger scale broadcasts that link selected subsets of functional modules to address problems. This multilevel dynamical viewpoint has implications... |
| Tipo: Manuscript |
Palavras-chave: Biotechnology; Cancer; Developmental Biology; Immunology; Molecular Cell Biology; Pharmacology. |
| Ano: 2012 |
URL: http://precedings.nature.com/documents/6973/version/1 |
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| Lakshmanane Boominathan. |
| The tumor suppressor p53 homologues, TA-p73, and p63 have been shown to function as tumor suppressors. However, how they function as tumor suppressors remains elusive. Here I present a number of models that illustrates how the TA-p73/p63 could function as tumor suppressors. Remarkably, the guardians—p53, p63, and p73—of the genome are in control of most of the known tumor suppressor miRNAs. 
TA-p73/p63 and p53, by suppressing the expression of c-Myc through TRIM32 and miR-145, they could up regulate the expression of tumor suppressor microRNAs, such as miR-15/16a, miR-29, miR-34, miR-26, let-7a/d/g, miR-30b/c/d/e, miR-146a, and a number of tumor suppressor genes. It appears that p53/TA-p73/p63-mediated repression... |
| Tipo: Poster |
Palavras-chave: Cancer; Genetics & Genomics; Molecular Cell Biology; Bioinformatics. |
| Ano: 2009 |
URL: http://precedings.nature.com/documents/4112/version/1 |
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| Trevor Marshall. |
| The US FDA currently accepts carcinogenicity studies of pharmaceutical drugs based on murine models. In addition to 6 month studies with p53(+/-) and ras.H2 transgenic mice, lifetime studies (typically 2 years) in WT mice or rats are also considered as evidence that a drug lacks carcinogenic activity. This model is not always exhaustive. For example, during the acceptance testing of the ARB Olmesartan[1], possible carcinogenicity observed in hamsters was not able to be duplicated in rats, or in transgenic mice. We have previously used the static molecular modeling of AutoDock to demonstrate that Olmesartan has agonostic activity in the PDB:1DB1 model of the human VDR Nuclear Receptor[2], while it has antagonistic activity in the PDB:1RK3 model of the rat... |
| Tipo: Poster |
Palavras-chave: Biotechnology; Cancer; Immunology; Pharmacology; Bioinformatics. |
| Ano: 2007 |
URL: http://precedings.nature.com/documents/52/version/1 |
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| Reza sheikhnejad. |
| Synthetic "microDNAs (MIDs)"is a new class of ~ 20-25 nucleotide-long DNAs capable of repressing the activity of the target gene at the level of transcription by mechanisms that have not been clarified yet. However they are designed to target non-coding regions of the cancer causing genes, thus interfering with transcription. The inhibition might be possible through the direct binding of MIDs to cis-regulatory sites and/or to some Transcription Factors (TF) that normally activate transcription. Synthetic MIDs in some ways are similar to the newly discovered microRNAs a mechanism by which cell regulates its genetic activities at post-transcriptional level. Synthetic MIDs can provide a powerful tool to prevent massive production of mRNA by... |
| Tipo: Manuscript |
Palavras-chave: Cancer; Genetics & Genomics; Molecular Cell Biology. |
| Ano: 2009 |
URL: http://precedings.nature.com/documents/3931/version/1 |
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| Petr Lokhov; Balashova Elena. |
| Antigens expressed on the surface of cancer cells are accessible targets for both humoral and cell-mediated immune responses, and are therefore potential candidates for vaccine development. Treating surface of live human breast adenocarcinoma cells (MCF-7) with trypsin yields a digest that contains 0.7% of total cell protein. Despite this difference, the trypsin digest stimulates in cytotoxicity assays anti-tumor response which kills 10-40% more cancer cells than those stimulated with cells themselves. From these results, we concluded that trypsin digest obtained from live cancer cells contains the essential antigens to induce an immune-mediated anti-tumor effect, and therefore, is candidate for anti-tumor vaccine development. |
| Tipo: Manuscript |
Palavras-chave: Biotechnology; Cancer; Immunology. |
| Ano: 2010 |
URL: http://precedings.nature.com/documents/4895/version/1 |
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| Takuma Hayashi; Akiko Horiuchi; Hiroyuki Aburatani; Nobuo Yaegashi; Susumu Tonegawa; Ikuo Konishi. |
| Uterine leiomyosarcoma (ULMS) develops more often in the muscle tissue layer of the uterine body than in the uterine cervix. The development of gynecologic tumors is often correlated with female hormone secretion; however, the development of uterine ULMS is not substantially correlated with hormonal conditions, and the risk factors are not yet known. Importantly, a diagnostic-biomarker which distinguishes malignant ULMS from benign tumor leiomyoma (LMA) is yet to be established. Accordingly, it is necessary to analyze risk factors associated with uterine ULMS, to establish a treatment method. Proteasome low-molecular mass polypeptide 2(LMP2)/b1i-deficient mice spontaneously develop uterine LMS, with a disease prevalence of ~40% by 14 months of age. We... |
| Tipo: Manuscript |
Palavras-chave: Cancer. |
| Ano: 2012 |
URL: http://precedings.nature.com/documents/7082/version/1 |
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| Salvatore Oliviero; Alessio Zippo; Alessandra De Robertis; Riccardo Serafini. |
| The serine/threonine kinase PIM1, cooperates with MYC in cell cycle progression and tumorigenesis. However, the nature of this cooperation remains elusive. Here we show that PIM1 contributes to the transcriptional activation of MYC-target genes by phosphorylating the histone H3 nucleosome at Serine 10 (H3S10). Recombinant PIM1 directly phosphorylates H3S10 on the nucleosome _in vitro_. Following growth factor stimulation, PIM1 accumulates in the nucleus where it forms a complex with the MYC/MAX dimer via the MYC BoxII domain (MBII). Immunofluorescence analysis coupled with _in vivo_ run-on shows a high degree of PIM1 and MYC co-localization in the nucleus at sites of active transcription. Expression profile analysis revealed that PIM1 contributes to the... |
| Tipo: Manuscript |
Palavras-chave: Cancer; Molecular Cell Biology. |
| Ano: 2007 |
URL: http://precedings.nature.com/documents/100/version/1 |
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| Li-Ling Lin; Hsuan-Cheng Huang; Satoshi Ogihara; Jin-Town Wang; Chiung-Nien Chen; Hsueh-Fen Juan. |
| Membrane repair is a universal response against physical and biological insults and enables cell survival. Helicobacter pylori is one of the most common human pathogens and the first formally recognized bacterial carcinogen associated with gastric cancer. However, little is known about host membrane repair in the context of H. pylori infection. Here we show that H. pylori disrupts the host plasma membrane and induces Ca2+ influx, which triggers the translocation of annexin family members A1 and A4 to the plasma membrane. This in turn activates a membrane repair response through the recruitment of lysosomal membranes and the induction of downstream signaling transduction pathways that promote cell survival and proliferation. Based on our data, we propose a... |
| Tipo: Manuscript |
Palavras-chave: Cancer; Microbiology; Molecular Cell Biology. |
| Ano: 2010 |
URL: http://precedings.nature.com/documents/4887/version/1 |
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| Registros recuperados: 382 | |
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