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There are many methods for the analysis of CNV. If you are an R user I would recommend you to take a look at the Bioconductor package list, in particular the section for copy number variation. Currently it contains 50 packages!


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Your suggested approach of comparing to the baseline distribution on a point-by-point basis isn't bad, although it's going to be susceptible to small false positives from noise. You'd probably want to only use events that span a certain minimum number of consecutive observations. You might also want to look into circular binary segmentation, as described ...


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Any apparently "magical" powers of cisplatin in testicular cancer have more to do with the disease than the drug. Unlike the similarly male-specific prostate cancer, testicular cancer is generally seen in young men in their 20s or 30s (click on "number of new cases and deaths"). This paper suggests, as is generally thought to be the case for earlier-onset ...


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Aflatoxin causes liver, kidney, and colon cancers in rats. The TD50 is the chronic dose-rate in mg/kg/day, which causes tumors in half of the population and is a measure of carcinogenic potency. The aflatoxin TD50 in rats is 0.0032 mg/kg/day. Assuming the daily food consumption of rats to be about 10g / 100g, this translates to aflatoxin levels of 32 ppb in ...


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Cancer is successful at killing it's victims because it is genetically still very similar to the host. The immune system does not respond to it sufficiently to eradicate the mutated cells and this allows it to grow out of control. When dealing with any kind of transmittal this would be close to an organ donation. Without a very close match, and ...


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Although transmissible cancer has been found in some species, such as Tasmanian Devils and clams, it is quite rare in most species. Certain viral and bacterial agents that cause cancer, however, can be transmitted. One example is HPV, which can cause cervical cancer


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It seems you are confused with some other gene instead of caspase 9, but if KO of some gene causes development of breast cancer, and you want to compare something between none-cancerous and cancerous states, you could take several ways: See if you could have littermates carrying and not carrying cancer. You could compare them. Sometimes, phenotype do not ...


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The short answer is that it is likely a bad experiment; being that it would be expensive and is not likely to provide useful new information. The long answer (i.e. why) is identifying an interesting target gene (e.g. caspase-9 in breast cancer) is only the first step, and considerable study of what is already known is required before planning an experiment ...


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This post goes over what MuTec requires as input. mark duplicates and indel realignment will probably have to be done on bam file to use it as input. BQSR is optional and does not change the quality too much. HaplotypeCaller is used for germline not somatic variant calling. If you have followup bioinformatics questions, you might be able to find answers ...


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From the dedicated cisplatin website and Drugbank it appears its use is quite diverse and not confined to testicular cancers. Further, your linked (Siddick, 2003) paper mentions on the first line of its abstract that cisplatin has clinical activity against a wide variety of solid tumors. Cisplatin.org mentions that cisplatin finds use as chemotherapy ...


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Yes, one sample can contain different alterations. For each patient there is typically one tumour specimen that is removed. That specimen may be divided up into several samples (e.g. one for DNA sequencing, one for RNA sequencing, one for methylation microarray, and one for copy-number variation microarray), however each sample contains thousands of ...


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In a PNAS paper by Palti's group (2007) they explain the hypothesis behind the technique: They reason alternating currents of 100 kHz to 1 MHz specifically affects dividing cells and thereby targets cancer cells. Note that this is the same basic idea as chemotherapy and radiotherapy, which also target dividing cells mostly. The mechanism of action of ...


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This is more of a comment Mutation in tumour suppressor is a recessive trait and there is no active "silencing" of the mutation. If a tumour suppressor is a TF then a mutation in the DNA binding domain can have no effect if there is a complementary mutation in its binding site. This is just a theoretical possibility and I have not heard of any examples as ...


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TGF-beta would be a good candidate. To cite: "TGF-β inhibits G1/S progression in a variety of eukaryotic cell types. Among these, untransformed epithelial cells are particularly sensitive to the growth inhibition by TGF-β." http://genesdev.cshlp.org/content/14/24/3093.full Fetal bovine serum (FBS) contains a high level of latent TGF-β. Human serum as well ...



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