Interestingness: 3
By Alicia Hurtado, Jen-Chieh Tseng, and Daniel Meruelo. Rejuvenation Research.
Spring 2006,
9(1): 36-44.
doi:10.1089/rej.2006.9.36.
I've heard about these cancer-killing viruses many times but I've never read one of the papers.
In this one, they injected cells from human ovarian cancer into mice, and after five days they started injecting them with a non-replicating version of the Sindbis virus. They modified the virus to also express green fluorescent protein (GFP) so they could also check that the bits that were green inside the mouse were the bits where in the tumours and not in the healthy tissue or in control mice that weren't injected with cancers. They also tried two other variants adding genes for interleukin-15 and -17 to the infected virus.
They claim that tumour sizes reduced in the places where the virus infected, and lifespan of the mice was extended, especially for the IL-15 and IL-17 versions. They don't show survival curves which is a pity. They also say that they weren't able to clear the tumours.
Their theory for specificity is that the cancer expresses higher amounts of laminin receptor (LAMR) and that the virus binds to it. LAMR is upregulated in many cancers. They tested the theory by blocking LAMR production through siRNA and saw the amount of virus infection drop in those cancers.
Showing posts with label cancer. Show all posts
Showing posts with label cancer. Show all posts
Sunday, March 31, 2013
Thursday, February 2, 2012
Telomerase, Telomerase Inhibition, and Cancer
Interestingness: 3
By Ali Ahmed and Trygve O. Tollefsbol, in the Journal of Anti-Aging Medicine, December 2003, 6(4): 315-325. doi:10.1089/109454503323028911.
It didn't turn up to be as interesting as I first thought, but definitely new information regarding telomerase, mostly of the type that I'll forget by tomorrow (ie these genes upregulate this, these downregulate it). In factoid form: telomerase is present in normal human liver cells in an inactive form, c-Myc upregulates telomerase, Mad1 suppresses it.
Telomerase is probably a good thing to test for when looking for cancer since it's very commonly present, ranging from 50-90% of the tests, with the lower numbers mostly seeming from fluids from tests. It is quite rare for it to be expressed in non-cancer cells, outside of the immune system, and even when it is, the numbers are much higher in cancer cells.
Some numbers from the paper: 90% of bladder cancers, 80% of prostate cancers, 69% of renal cancers, 82% of thyroid cancers, 95% of breast cancers. Some studies seem to show a correlation between cancer stage and quantity of telomerase. They also mention correlation between telomerase levels in the tumour and mortality and/or recurrence.
It then talks about methods of downregulating telomerase: transfecting with a dominant negative hTERT gene, antisense on the RNA component of telomerase, and immune hammering of telomerase-positive cells. I didn't know dominant negative genes would be easy to make. They express the usual concerns about what turning off telomerase would do to stem cells and germ cells, but say that both those types are likely to have much longer telomeres than cancer cells.
By Ali Ahmed and Trygve O. Tollefsbol, in the Journal of Anti-Aging Medicine, December 2003, 6(4): 315-325. doi:10.1089/109454503323028911.
It didn't turn up to be as interesting as I first thought, but definitely new information regarding telomerase, mostly of the type that I'll forget by tomorrow (ie these genes upregulate this, these downregulate it). In factoid form: telomerase is present in normal human liver cells in an inactive form, c-Myc upregulates telomerase, Mad1 suppresses it.
Telomerase is probably a good thing to test for when looking for cancer since it's very commonly present, ranging from 50-90% of the tests, with the lower numbers mostly seeming from fluids from tests. It is quite rare for it to be expressed in non-cancer cells, outside of the immune system, and even when it is, the numbers are much higher in cancer cells.
Some numbers from the paper: 90% of bladder cancers, 80% of prostate cancers, 69% of renal cancers, 82% of thyroid cancers, 95% of breast cancers. Some studies seem to show a correlation between cancer stage and quantity of telomerase. They also mention correlation between telomerase levels in the tumour and mortality and/or recurrence.
It then talks about methods of downregulating telomerase: transfecting with a dominant negative hTERT gene, antisense on the RNA component of telomerase, and immune hammering of telomerase-positive cells. I didn't know dominant negative genes would be easy to make. They express the usual concerns about what turning off telomerase would do to stem cells and germ cells, but say that both those types are likely to have much longer telomeres than cancer cells.
Subscribe to:
Posts (Atom)
Posts
