lpas wrote:Do you know the specific variant of KRAS? From what I've read, not all KRAS types have the same prognosis. Keep in mind that most people don't have their tumor tested for specific mutations until and unless they're stage 4, so those who were KRAS mutants at a lower stage and survived are generally omitted from the sample. I am one of the exceptions to this rule and had my tumor tested as a stage III. Have been NED (so far) since my diagnosis in November 2014.
Nohogirl wrote:lpas wrote:Do you know the specific variant of KRAS? From what I've read, not all KRAS types have the same prognosis. Keep in mind that most people don't have their tumor tested for specific mutations until and unless they're stage 4, so those who were KRAS mutants at a lower stage and survived are generally omitted from the sample. I am one of the exceptions to this rule and had my tumor tested as a stage III. Have been NED (so far) since my diagnosis in November 2014.
Thank you lpas for the quick response. Was your tumor also KRAS, MSS?
My husband's KRAS mutation characteristics are protein alteration -p.Q61Ha, exon-5, and variant frequency 15%. Although i have no idea what each of these means. I also did not know there were different KRAS.
lpas wrote:Nohogirl wrote:lpas wrote:Do you know the specific variant of KRAS? From what I've read, not all KRAS types have the same prognosis. Keep in mind that most people don't have their tumor tested for specific mutations until and unless they're stage 4, so those who were KRAS mutants at a lower stage and survived are generally omitted from the sample. I am one of the exceptions to this rule and had my tumor tested as a stage III. Have been NED (so far) since my diagnosis in November 2014.
Thank you lpas for the quick response. Was your tumor also KRAS, MSS?
My husband's KRAS mutation characteristics are protein alteration -p.Q61Ha, exon-5, and variant frequency 15%. Although i have no idea what each of these means. I also did not know there were different KRAS.
Yes! My tumor tested MSS and I have the KRAS A146T mutation (see my signature below) which is one of the rarer variants. Your husband's Q61H is also somewhat less frequent. Codons 12 and 13 seem to be the most common. I've linked a few articles below that talk about different KRAS types and their association with prognosis. You'll see that neither one identifies Q61H as a particular variant that confers inferior outcomes.
Of course, the biggest drawback to having a KRAS mutation is the decreased number of chemo options (i.e. no erbitux or vectibix) if you reach the stage where that becomes important.
https://medicalresearch.com/genetic-research/only-some-kras-gene-mutations-linked-to-worse-prognosis-in-colon-cancer/14635/
https://molecular-cancer.biomedcentral.com/articles/10.1186/1476-4598-13-135
Brearmstrong wrote:I too am KRAS and MSS. Have had folfiri and folfox so future lines of chemo or treatments are unlikely. BUTT, here's to hoping I stay NED forever.
-Brenda
rp1954 wrote:Take a deep breath. I would look very hard now at CEA, LDH and CA199 (you probably need to order these your self for speed and convenience, at least a first time).
It may be that a choice could be made between normal Xeloda treatment, Xeloda+mild, generic adjuncts, and Folfox. The results from some papers suggest circumstances that oral 5FU + mild adjuncts might be superior to Folfox for recurrence, and a lot less debilitating. Also, to avoid chemos' worst side effects is a plus.
GrouseMan wrote:There is evidence accumulating I believe that the KRAS G13D mutant is actually sensitive to treatment with EGFr Inhibitors like Erbitux. See the following two links, they are both pretty new:
https://www.omicsonline.org/open-access ... ?aid=88407
https://www.biorxiv.org/content/biorxiv ... 6.full.pdf
Most Kras mutations turn the Kras pathway on. It cannot be inhibited by its natural substrate so it remains activated and this often results in downstream activation of other growth factors of which EGF is one.
Here are some other publications that are older but talk about Kras Mutations. Most of these are in Lung Cancer but the idea still applies to Colon Cancer as well.
The following talks about Mutations and testing:
https://biochemmack.ru/upload/iblock/42 ... 9ab5ba.pdf
This one is about he new third generation EGFr Inhibitors and why they may work with KRAS mutant Lung Cancers. Again This is lung Cancer but I suspect this will also be true for colon cancer as well. The drug they discuss in this paper is neratinib which is similar to a drug I worked on recently approved as Vizimpro (dacomitinib). Take note of a statement made in the third paragraph of the introduction!
http://stm.sciencemag.org/content/10/44 ... citransmed
I suspect that when all is said and done and proper clinical trials are run some of the new Pan Erbb inhibitors will start to make their way into colon cancer treatment regardless of KAS status.
Good luck
GrouseMan
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