Hello,
I had the Hai pump installed in February. Still tumor is growing. I wasd told nasty cancer was Kras+T54 mutation. They want to try oxy and 5FU systemically and myocin and in the pump
I am thinking this is a shot in the dark. Any info??
sdino wrote:Here is my take on the TP53's: So... Healthy P53’s fight cancerous DNA. But when they get sick or mutated they stop fighting the bad cells. So there is efforts to boost the healthy P53’s to fight harder but years of testing, nothing has made it to the Market. Researchers are trying to restore the P53’s back to their normal state to carry-on the fight. They are finding drugs that bind to and prop up copies of mutated p53, restoring its shape and ability to carry out its job. One such drug has already passed an early stage safety trial in humans, and a more advanced clinical trial is now underway in Europe. The payoff could be big, however. Not only could the strategy treat many kinds of cancer, but just a handful of drugs might be enough,
particularly when coupled with chemotherapy drugs that induce the tumor cell damage to which p53 responds. P53 mutations tend to be clustered in the core of the protein, where it binds to DNA.
Another protein, MDM2, latches onto P53 molecules and destroys them, keeping their numbers in check. But this control mechanism can fail in multiple ways. For starters, when p53 itself is mutated, MDM2 cannot attack it. As a result, the malfunctioning protein builds up in cells unchecked and keeps the remaining healthy p53 from doing its job. Without the genome’s guardian on patrol, precancerous cells survive and reproduce. This gives them the opportunity to build up the additional mutations they need to become fully malignant.
At this point, it’s slightly unclear which if any P53 stabilization strategy will pan out. They are trying like hell... with some promising results.
SIDE NOTES
- ovarian cancer, almost always has p53 mutations.
- Healthy P53’s = Good to fight Cancer
- Mutated P53’s = Not good, they are essentially working on restoring them back to healthy P53’s. Hope I explained this OK, hopefully Im not to far off base with my understanding ? I will post another question regarding trials of P53's vs. also worrying about other mutations (Kras, Braf, ect.. ) as the waters get
LPL wrote:Dear GrouseMan,
Do you know if I should care that my husband has another kind of Kras? See my signature, ”Kras G13D”. We do not know about any other mutations, like T53 etc. No test done for that as far as I know.
NHMike wrote:
KRAS G13D would be similar to G12D, it's just in the 13th Codon instead of the 12th.
LPL wrote:NHMike wrote:
KRAS G13D would be similar to G12D, it's just in the 13th Codon instead of the 12th.
Well.. thank you for replying Mike.
I do understand it is in a different codon. Not sure it is “similar to G12D” though.. I have seen research where they say there are differences between Kras codon 12 and 13 - in respons to treatments for example. Also some trials have specific Kras xxxx mentioned so why do they have that if it is ‘the same’?
Maybe all KRAS are not the same?
That is why I asked GrouseMan since he is a researcher.
LPL wrote:NHMike wrote:
KRAS G13D would be similar to G12D, it's just in the 13th Codon instead of the 12th.
Well.. thank you for replying Mike.
I do understand it is in a different codon. Not sure it is “similar to G12D” though.. I have seen research where they say there are differences between Kras codon 12 and 13 - in respons to treatments for example. Also some trials have specific Kras xxxx mentioned so why do they have that if it is ‘the same’?
Maybe all KRAS are not the same?
That is why I asked GrouseMan since he is a researcher.
GrouseMan wrote:The Letters represent the amino acid substitution in the protein or in this case the Kras Gene. So for Kras G12D that is - in position 12 of the Kras Gene the normal wild type has a Glycine (Abbreviated G) that has been changed to an Aspartic Acid (abbreviated D) in the mutation. These two amino acids are very different in shape and as a result greatly effects the binding of inhibitors of KRAS. Kras G12D is the most common mutation of Kras but there are others. I believe about 30% of colon cancers have mutations in Kras.
Regards,
GrouseMan
Jackar0e wrote:GrouseMan wrote:The Letters represent the amino acid substitution in the protein or in this case the Kras Gene. So for Kras G12D that is - in position 12 of the Kras Gene the normal wild type has a Glycine (Abbreviated G) that has been changed to an Aspartic Acid (abbreviated D) in the mutation. These two amino acids are very different in shape and as a result greatly effects the binding of inhibitors of KRAS. Kras G12D is the most common mutation of Kras but there are others. I believe about 30% of colon cancers have mutations in Kras.
Regards,
GrouseMan
Thank you so much that is very well put, My oncologist dose not seem hopeful. I looked at the letters and mine are G12S stupid ? but why the S and not the D?? they are trying one last chemo of oxy and 5FU then I guess clinical Trial I appreciate all the help I can get. We are the best advocates for ourselves
boxhill wrote:The report on my tumor from Dana Farber/Brigham Women's says:
KRAS c.35G>A (p.G12D), exon 2 - in 18% of 321 reads*
TP53 c.993+2T>C () - **TP53 is a tumor suppressor gene. TP53 mutations are
frequently seen in colorectal adenocarcinoma (PMID: 22810696).
Thanks to this thread I now have a better idea of what those mean.
But I seem to have missed something: what is TIL?
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