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  • 0 posts edited
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  • 26 votes cast
Sep
1
awarded  Custodian
Aug
18
answered How can a chromosome translocation in somatic cells lead to disease?
Jul
28
answered Bernoulli’s Principle in the Cardiovascular System
Jul
28
answered How to validate the use of an anti-virus monoclonal antibody in IHC by spiking a fresh organ with infected cultured cells?
Jul
20
comment What specific mutations can cause an apoptosis mechanism to malfunction?
Yes, it's just not a magic bullet. There's been lots of research on this-- try reading the review I linked above. Also, try looking into the concept of "immune checkpoint inhibitors" that shut down genes like CTLA4 and PD1. Those are showing some promise in certain settings.
Jul
16
comment What specific mutations can cause an apoptosis mechanism to malfunction?
That's part of it. They also downregulate their MHC complexes and secrete their own inhibitory cytokines. It's a big and complicated problem that's had a lot of research done on it. Here's a review: ncbi.nlm.nih.gov/pmc/articles/PMC1857231
Jul
16
comment What specific mutations can cause an apoptosis mechanism to malfunction?
Tumor immunosurveillance is a whole new topic worth its own question, but there are two basic reasons: (1) Mutated KRAS is not immunologically very different from wild-type KRAS-- it just doesn't change the overall surface shape of the protein that much, and (2) even when the immune system does recognize mutated cell products, the tumor cells react by upregulating anti-inflammatory pathways, such as recruiting regulatory T cells.
Jul
15
answered What specific mutations can cause an apoptosis mechanism to malfunction?
Jul
10
awarded  Nice Answer
Jun
29
awarded  Commentator
Jun
29
comment Deciding a reasonable threshold for copy number variation in a CNV (SNP array) TCGA dataset
Hmm, okay, I think I see. No, you don't want to compare the intensity of the tumor at any one position against the 5-95% distribution of the normal across the whole array. You want to compare the intensity of the tumor at one position against the normal at that position. This will normalize for sequence-specific binding differences.
Jun
26
awarded  Informed
Jun
26
answered Deciding a reasonable threshold for copy number variation in a CNV (SNP array) TCGA dataset
Jun
22
awarded  Editor
Jun
22
revised What does it mean to “map the human genome”
added 47 characters in body
Jun
22
comment What does it mean to “map the human genome”
Good point, I'll edit. I was thinking of the Celera DNA, which I thought was Venter's, but it turns out that they were using a pool, too. (Venter was just in the pool.)
Jun
22
awarded  Yearling
Jun
22
answered What does it mean to “map the human genome”
May
13
comment Downstream analysis after in vivo pathogen RNAseq
Right. The main thing is that you want your groups in an RNA-Seq experiment to focus as cleanly as possible on the difference you want to investigate. If you're interested in antibiotic resistance, use a resistant and a non-resistant strain. If you're interested in immune evasion, use samples in the presence and absence of an immune response. You expect many differences between cultured and in vivo samples-- you've already mentioned metabolism, antibiotic resistance, and immune evasion, and I'm sure there are lots more. So it's hard to relate any given gene expression change to a phenotype.
May
12
comment Downstream analysis after in vivo pathogen RNAseq
The reason I say it's not the clearest model, especially for antibiotic design, is that you're investigating the difference between bacteria in the host and bacteria on the plate. An antibiotic in particular probably isn't going to care about that-- it should kill in both situations, right? And for a vaccine, there are so many differences between culture and in vivo that I'm not sure that you can attribute differences you see to immune evasion. Are there immune-compromised pig models? In vivo samples from those would be a much cleaner control for immune evasion.