Spouse is a 54 y/o asian non-smoker with Stage 4 nsclc, exon 19 deletion present (Roche). She has an 8 cm mass in her RUL, local rib invasion with mediastinal nodes and liver metastases diagnosed in November 2014. She underwent radiotherapy to her upper right lung and mediastinum having 20 Gy over 5 fractions, and then started gefitinib. However, after 3 months her repeat CT scan showed new lesions in her RLL, and liver, though lesions inside the DXT field have shrunk.
She was deemed a non-responder ( though has remained feeling quite well ), and changed to carboplat/gemcitabine. She had day 1, but was admitted a week later with a large pleural effusion which has since been drained, and pleurodesis attempted. Day 8 is being delayed until she recovers from this.
Since she is a non-responder, is it worthwhile trying a different TKI? Or is her best bet platinum doublet therapy?
Reply # - April 3, 2015, 08:31 AM
Hi zhaosr,
Hi zhaosr,
I'm very sorry your wife is having such bad luck with therapies. There is the possibility she has a T790 mutation that kept her from responding to gefitinib. There's a 3rd generation drug that is showing good much promise for those with the t790 mutation.
I'm afraid there's a glitch in the forums that's not allowing me to paste links here so I've written the titles to a video. You can search with our search feature, "co1686 - 3rd Generation Drug for Acquired Resistance in EGFR Lung Cancer"
This is a group of video on acquired resistance, "The Acquired Resistance Patient Forum 2014 Videos" specifically the presentation presented by Lecia Sequest (video #3).
Immunotherapies are also promising in a portion of people with nsclc however it still isn't know what subset that is so trials are testing squamous and non squamous subtypes.
While all these options are still in clinical trials it may be worth looking into them. If your wife isn't being seen a an academic research center and 2nd opinion at one may be in order to get access to these options.
Let us know if you have further questions,
Janine
Reply # - April 3, 2015, 03:30 PM
Thanks. I mentioned the
Thanks. I mentioned the possibility of a T790M mutation but the oncologists said it would have been detected by the Roche Cobas assay.
So, she is a primary non-responder rather than secondary failure, and most of the links I've read refer to secondary failure which I don't know applies or not.
Reply # - April 4, 2015, 09:09 AM
Without other options a re
Without other options a re testing may not be out of the question.
Reply # - April 4, 2015, 02:23 PM
Yes, more data is useful but
Yes, more data is useful but she's in no shape for another biopsy. I gather common resistance is either by t790m mutation, and MET amplification.
I've read of a cfDNA test Guardant360.I have no idea of the cost, and whether it's even feasible to get that done when you live in Australasia.
Without that information, I guess best treatment is to resume the platinum doublet therapy.
Reply # - April 5, 2015, 10:42 AM
Dear Zaosr,
Dear Zaosr,
From what I know you could get specimens from her pleural fluids for mutation testings.
Regarding Guartdanthealth I had access their website and their panel of 60 odd testings fro genomic abnormalities does not include T 790M.
Regards and all the best.
Peter
Reply # - April 5, 2015, 11:49 AM
Fortunately (or not ) her
Fortunately (or not ) her pleural fluid only has a few red cells so they couldn't test for mutations. Pity about the liquid biopsy test from Guardant.
I just read this paper which came out a few days ago suggesting that innate resistance might be mediated through NF-κB signaling, and that an experimental melanoma drug PBS-1086 might restore TKI effectiveness.
http://www.cell.com/cell-reports/abstract/S2211-1247%2815%2900265-X#/ce…
Is this clinically relevant now, and is this PBS-1086 drug available?
Reply # - April 6, 2015, 09:22 AM
PBS-1086 doesn't appear to be
PBS-1086 doesn't appear to be tested in humans, at least not yet.
Reply # - April 6, 2015, 11:31 AM
But it does raise the
But it does raise the possibility that another drug that inhibits nf-kb might work as well.
Nf-kb inhibitors include aspirin, statins, and quercertin, all of which are readily available. It would be great if that was all one needed to enhance tki activity.
Reply # - April 6, 2015, 04:27 PM
It's also possible that this
It's also possible that this is a separate type of cancer. IMHO, I'd get a biopsy of at least one of the new areas. Take care, Judy