KRAS question

Options
TLG320
TLG320 Member Posts: 167
edited March 2014 in Colorectal Cancer #1
Hi all,

A quick question - apologies for my ignorance. I've been reading about some patients having KRAS mutations which makes types certain types of chemo ineffective. I'm trying to do some research but can't find anything that explains this to me in laymens terms. My husband is Stage 2A. We've not met with his oncologist yet (appointment next week). Is this something that patients are autmoatically tested for before the type of treatment is determined?

Thanks for your help!
Tashina

Comments

  • dianetavegia
    dianetavegia Member Posts: 1,942 Member
    Options
    Not usually but....
    the type chemo hubby will be given/ offered is effective on KRAS and non KRAS types. It's two drugs used for Stage IV that will not work on the KRAS mutant. Not to worry! :o)
  • lisa42
    lisa42 Member Posts: 3,625 Member
    Options
    Erbitux
    Hi Tashina,

    I believe it's standard for patients to now be tested right after surgery. Samples from the removed tumor are sent in for the testing. They usually keep tumor tissue samples preserved in some kind of parrafin wax or something like that. I was tested several months after having liver surgery. I didn't even know they kept samples of my removed tumors, but they did & that's what they were able to do the testing from.
    Diane said they do it for stage IV, but I think they also will for lesser stages too, if requested. It really isn't probably something to worry about now- Folfox and/or Folfiri are the types of chemos they normally use first and they are not affected by kras status.
    It's a drug called Erbitux and another called Vectibux that are the drugs that are not effective if you've got the kras mutation, but do work if you're kras wild type (no mutation).

    Hope this info helps-
    Lisa
  • cyndi2324
    cyndi2324 Member Posts: 72
    Options
    Kras mutated
    I am sorry about your husband. I may not be the norm. for mutated kras but here is my experience. I was diagnosed April, 2008 after colon surgery as PT3 with PN1. I was not tested for kras mutation at that time. I was put on FolFox4 I could only tolerate 3 courses (lots of health problems with it) then I was put on Xeloda to finish my therapy. My CEA (blood test) started to go up from .5 to 7.6. Had a CTPET test it showed my cancer was back in 4 more places
    6-3-09. I had to have a colostomy at this surgery. Had one of my tumors sent out for Kras test. The test came back that I was Kras mutated (not wild type) My Dr. told me that is why my
    first year with chemo didn't work. When my kras test was done they tested to see what might work on my cancer. We were told to try CPT-11 (Irinotecan). I took 5 courses of that then CEA started to go up again 5.6. Had another CTPET it showed my cancer has come back. I am now considered a stage 4 and there are no approved drugs left for me to take that will work and I can not have any more surgery (I have a MET AT S2). I am not sending this to scare you as your husbands stage is a lot less than where I started. I'm sending this because not all Drs. test automatically test for kras as it is a pretty new suggested standard. But is it very important. I am now in a Clinical trial phase 1 to find a drug that might work.
    I WISH YOU AND YOUR HUSBAND THE VERY BEST.
    Cyndi
  • TLG320
    TLG320 Member Posts: 167
    Options
    Thank you all!
    Thanks ladies! I appreciate your responses. I'll ask the oncologist about it at our appointment on Monday.
  • tom88
    tom88 Member Posts: 17
    Options
    TLG320 said:

    Thank you all!
    Thanks ladies! I appreciate your responses. I'll ask the oncologist about it at our appointment on Monday.

    I can try to clarify the
    I can try to clarify the Kras status question from a scientific point of view.

    K-ras is a molecule in the cell that signals the cell to divide and grow. In cancer cells, K-ras is turned on excessively causing uncontrolled cell multiplication. There is another molecule on the cell surface that usually controls whether k-ras is on or off. Certain types of anticancer drugs will target that k-ras controller to shut that off, which in turn will shut off any signal to k-ras, therefore the cell won't multiply anymore. The reason they test your k-ras status is that if your k-ras is normal, then you can use the drug to block the k-ras controller and expect k-ras to be subsequently shut off. However, if your k-ras is mutated to be always ON, then no matter what you do to the controller it won't stop the cell division. In short, it's to predict whether the cancer will respond to a particular type of drug.