Tag Info

New answers tagged

1

Two things... Rapidly proliferating tissues (esp tumours) rewire their energy metabolism anyway to aerobic glycolysis where you have energy being produced by lactic acid fermentation even if oxygen is present. This is called the Warburg effect.Here's the thing about "low yield" though - glycolysis chucks out less ATP per reaction at the end, but you can ...


0

Most cancers involve, in addition to genetic changes, a whole suite of epigenetic changes that orchestrate changes in transcriptional profiles. Additionally, multiple epigenetic modifiers (Eg - EZH2) are associated with worse prognoses. There is also the fact that chromatin modification machinery is very highly mutated in cancers; examples include EP300 - a ...


0

Bioluminescence could not be used but it is possible to 'tag' with fluorescence to better view pathways within the body. Tagging is often used in research, a simple google search should produce a plethora of results.


3

Not in human but you can use this technique with genetically modified model organisms as described here. The procedure is quite simple, you express the luciferase enzyme under the control of a specific promoter (specific for your cell type, like cancer) and provide luciferin via intravascular or intraperitoneal injection. The targeted cell type (for example ...


0

In vivo, none. Bioluminescence is cool, but it's not a powerful light source. Even if you could tag a cancer cell (all of them), unless it were on your skin or in your eye, you wouldn't be able to see it, even with some kind of scope.


1

Examining the literature it'd seem that the ROR pathways incl. ROR1 and ROR2 are critical for developing tissues in the majority of cases. We also see relevance in the expression of ROR1/2, more specifically ROR2, in cases where taxic cell types are required to migrate, branch, etc. Most of the literature determines much of this occurs through a noncanonical ...


1

I think you should start with immortalized cell lines and so in vitro division rates by perfect conditions. This is easier to measure than in vivo division rates. E.g. HeLa has a division time of 23 hours. MDA-MB-231 and A549 division times are around 28 hours. Growth of HeLa Cells Comparative Analysis of Dynamic Cell Viability, Migration and Invasion ...


3

With help of canadianer (thank you) I think I found the right article, so just want to share. This study not talking specifically about telomerase, but about the same approach of using promoters that are upregulated in tumors - exactly what I looked for. Published in 2014. http://symbiosisonlinepublishing.com/genetic-science/genetic-science03.pdf ...


4

I found a protocol by ATCC for NTERM2 cells, and it didn't mention any specific flask, so any cell culture flask would do. Since ATCC is basically a cell culture bank I trust that their protocol is valid.


1

Yes. The dbDEPC 2.0 database for example. If you want to extend your search to pathways the best database I know of is the KEGG. There are multiple databases out there. You might want to look at this wikipedia page. By the way what you are looking for is called a cancer proteomic signature.


0

So let's just quickly define what cadherins are, using general information from wikipedia, Source: Wikipedia Cells express E-cadherin (epithelial), N-cadherin (neuronal, or P-cadherin (placental). These generally interact with ß-catenins to modulate cell adhesion. There are pathways intrinsic to cancer which downregulate the expression of cadherins, ...


2

BioNumbers is a great site to answer this kind of question. This search produced a link to this paper , which has measurements for mitochondria per cell for multiple species and cell type.


6

This is a great question. Just to make it clear people with DS do have a reduced risk of solid cancers and an increased risk of blood cancers, (B-ALL and AML). You are correct in picking out DSRC1 because of its angiogenic implications. The current hypothesis centers around people with DS being less capable of driving angiogenesis, and therefore having an ...


2

I can't fault @WYSIWYG for mentioning the cited Vogelstein article in providing an answer. You point to what seems like a great explanation for why certain cancers arise in some tissues but not others. However, for those who look closely this paper has some serious errors in its derivation of the model, and for good reason it has come under strong fire in ...


1

There are a number of ways to screen for mutator genes. One straightforward approach in bacteria is to take an antibiotic sensitive non-mutator strain, grow it up, and expose to different antibiotics. Cells that survive in the presence of multiple antibiotics have acquired multiple de novo resistance mutations and thus are highly enriched for mutator ...


1

You should have a look at this interesting article published earlier this year in Science. There are two mechanisms by which cells can accumulate mutations in DNA: Replication errors External physicochemical agents such as UV, carcinogens etc In the abovementioned paper, the authors classify cancers into two types: That arise predominantly because of ...



Top 50 recent answers are included