Limph nodes positive to PET-CT after response to IRESSA - 1245268

watu
Posts:45

Hello,

I would like to share with you all the case of my father and possibly get your views on the current situation.

My father is now 70 years old, never smoker.

This is the timeline of his lung cancer:

04/2009 - found a suspicious nodule in his upper left lobe
07/2009 - after lobectomy of his upper left lobe, confirmed 2cm adeno with no positive lymph nodes (T1N0M0). No adjuvant chemo.
01/2010 - found another nodule in his lower left lobe (possibly unnoticed in 2009)
04/2010 - after completion pneumonectomy, confirmed 2cm adeno with only a couple of regional limph nodes found positive (T2N1M0). No adjuvant chemo.
09/2010 - PET-CT fully negative
04/2011 - PET-CT shows a number of positive limph nodes in the mediastinal and sovraclavear regions.
05/2011 - biopsy of 1 sovraclavear lymph node confirms it is adeno met, also found EGFR mutation.
06/2011 - started therapy with IRESSA
09/2011 - PET-CT fully negative. Great response to IRESSA
02/2012 - PET-CT fully negative
07/2012 - PET-CT shows 4 regions with positive lymph nodes (right sovraclavear SUV 2.2, right axillary SUV 5.2, right paratracheal SUV 3.9, mediastinal SUV 2.2).

With these positive lymph nodes, his cancer is probably T2N2M0 now and, although the primary tumor was fully removed with the pnumonectomy, these are mets and we need to deal with them.

Not sure what the best approach would be here. We are still waiting for his oncologist to define some actions. I've been reading a lot on GRACE and there a number of different options.

Should we first understand the degree of progression before changing the therapy?
Is it really helpful in this specific case to biopsy the sovraclavear lymph node and check whether we have a T790M mutation or MET amplification? (this may add valuable information, but I still don't see a target drug)

Maybe the combination of IRESSA and chemo would be enough at this stage to keep the progression under control.

What do you think?

Thanks for your help and best regards.

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Reply # - July 17, 2012, 08:58 AM

catdander
Posts:

Hello watu,
I'm sorry to read about your father's experience. He is in a situation that has much promising research being done. However there are no definite answers yet. You probably have already read these but I'll point these links out just in case you haven't and also for others who may read this. http://cancergrace.org/lung/tag/acquired-resistance/

Thank you for your GRACE question. Your question has been assigned to one of our GRACE Faculty. You will receive a response as soon as possible. Please keep in mind that our faculty doctors also have active practices, which can sometimes delay their response. Some answers may also require additional research time, but you can usually expect a response within 1-3 days.
We recommend you subscribe to this topic (see the Subscribe link in the green bar above your post in the forum). Doing so will ensure that you will receive an email notice when a response has been posted. Your post will be moved to the appropriate GRACE forum category when a response is received, but the direct URL link to your original topic will not change. You can also locate the thread by going to your forum Profile (green link on most forum pages) and checking your Forum Topics Created list.
Much luck moving forward,
Janine
forum moderator

Reply # - July 17, 2012, 07:19 PM

drsequist
Posts: 15

Hi Watu -

While it is very hard to tell you exactly what the next step should be without having seen the CT scans or examined your dad, it does sound like he had a really good response to iressa and now may be showing some early signs of resistance. Patient with EGFR mutations can have a variety of types of progression on iressa/tarceva- sometimes it is a sudden and rapid growth, but more often it is a slow process that evolves over months or even a year or more. Practice has shifted toward trying to keep patients on iressa/tarceva as long as possible before switching therapies, or adding a new therapy to iressa/tarceva in such as chemotherapy. Often, trying to get a repeat biopsy of a growing area can be helpful, especially if clinical trial participation is an option. Where is your dad located (I am guessing it's not in the US since he's on Iressa)? If his oncologist does not see a lot of EGFR mutation-positive patients, it may be worth thinking about traveling to a regional center that sees EGFR patients frequently and/or has clinical trials available. There are a lot of exciting advances in this field so I do hope that a) he doesn't need to switch therapies quite yet and b) he may be able to go on a clinical trial of some sort. But he would need to be evaluated in person for both of these questions.

Thanks -

Reply # - July 17, 2012, 09:15 PM

Dr West
Posts: 4735

I entirely agree with Dr. Sequist's very thoughtful response (thanks!). She happens to be among the world experts in this area of "acquired resistance", an area where good studies lag behind clinical experience as teaching us, so people who work with many patients in this situation are coming to develop their own sense of best practices that often go beyond where there is lots of solid data from clinical trials to guide us. Now we're starting to see clinical trials beginning to try to address these questions, but these tend to be available primarily at centers where they have a lot of experience specializing in managing lung cancer.

-Dr. West

Reply # - July 18, 2012, 03:30 PM

watu
Posts: 45

Dr Sequist, Dr West,
Thanks for your prompt and encouraging replies.
My dad is based in Italy. if you are aware of any centre in Italy where specific "post-Iressa" clinical trials are being carried out, please let me know.

Can you suggest any specific drug or trearment that is expected to offer promising outcomes in my dad's specific situation? Based on the information available today, shall I be looking for something concretely?

Thank you and best regards,
Michelangelo

Reply # - July 18, 2012, 04:16 PM

certain spring
Posts: 762

Michelangelo, I am sorry about your father.
This is just a thought, but if you look on www.clinicaltrials.gov, there are some trials in Italy that might be worth considering. There is a Phase III Astra Zeneca trial, called Impress, specifically for people who have progressed on Iressa. It aims to compare what happens if these patients are treated with chemotherapy alone (Alimta/pemetrexed and cisplatin) vs continuing the Iressa and adding chemotherapy. It has sites in Rome, Genoa, Pisa, Parma, Rozzano and Orbassano (and across Europe, Russia and Japan):
http://www.clinicaltrials.gov/ct2/show/NCT01544179
Could I also say how wonderful it is to hear from Dr Sequist, who has done so much work on acquired resistance to Iressa and Tarceva?

Reply # - July 18, 2012, 04:29 PM

catdander
Posts:

Hi watu, I want to make sure that you make use of the link I pasted in my prior post. The first 3 blog/posts are the most up to date information about acquired resistance to tarceva/iressa, they were written in the past month.

This one is a webinar by Dr. Sequist. You have an option to listen to it and there is also a transcript and visuals. http://cancergrace.org/lung/2011/03/29/dr-sequist-on-acquired-resistanc…

I did a search on clinicaltrials.gov and did not come across any trials for "acquired resistance nsclc Italy". However I took out acquired resistance and came up with this. It will at least give you an idea of where studies on nsclc are taking place in Italy. One of the good things about the new understandings has to do with treatment that is available thus not needing a trial to access, but you do want to access an oncologist who is up to date on the subject (the links discuss this). I'm sure Dr. West will return to this post and if he has input about specific centers will reply.

The doctors won't be able to make a suggestion for your dad's next step not just because they don't have all his information but also it would be illegal for them to do so.

I hope your father will not need to make any changes soon,
Janine

Reply # - July 18, 2012, 07:30 PM

Dr West
Posts: 4735

There is quite a bit written here about "acquired resistance" if you want to search for the term, but there is nothing really so clearly ahead of other choices that I could really make a recommendation. I was thinking about the IMPRESS trial that certain spring mentioned as a leading international effort, but there may well be other promising trials that are only available at a particular regional center, and there are too many trials to track all of the possibilities.

Good luck.

-Dr. West

Reply # - July 23, 2012, 02:44 PM

watu
Posts: 45

Thank you all. I'm so impressed by how active GRACE is and how helpful your contributions might be to people struggling and fighting against their illness. Thank you again.

My dad has got just one kidney and with a mild insufficiency, so we need to be careful with a potential chemotherapy. A good option could be to start a treatment with Gemcitabine (GEMZAR), which should be less nephrotoxic than other chemotherapic drugs. (we would see whether in combination with IRESSA or with IRESSA temporarily suspended).

Are you aware of any trial or study with Gemcitbine used after resistance to EGFR TKI?

Reply # - July 24, 2012, 04:06 PM

watu
Posts: 45

Thanks Dr West.

I found this interesting study: http://onlinelibrary.wiley.com/doi/10.1002/ijc.24657/pdf

and, if I understand well, results are not really encouraging for our specific case.

1. Patients with a previously favorable response to gefitinib had a lower response rate to second-line treatment than those without treatment response to gefitinib (9.3% vs. 19.4%).

2. Patients bearing tumors with EGFR mutations tended to have a lower second-line response rate than those with wild-type EGFR.

3. Specifically, response rates for Gemcitabine as a Single-Agent (no platinum) were very poor and absolutely 0% among responders to gefitinib or with EGFR mutation.

I cannot really see the second-line treatment with Gemcitabine as a single agent for a EGFR mutation potitive patient with good response to IRESSA being supported by positive clinical findings.

Is this really the right way to go?

Thank you.

Reply # - July 24, 2012, 09:40 PM

Dr West
Posts: 4735

I don't know that it is, but I don't think there's any evidence-based choice to point to here, especially if limited by kidney function. All of these options are limited by being just a few patients to draw any real conclusions from. The implication of the paper is that a platinum-based doublet is associated with greater activity, but that also entails more risk to kidney function.

-Dr. West

Reply # - July 25, 2012, 02:54 AM

certain spring
Posts: 762

watu, is the gemzar recommended by your father's oncologist? You mentioned earlier that you were waiting for him/her to come up with a plan. And is the Impress trial out the question because of your father's kidney problems?
I thought the suggestion from Dr Sequist and Dr West of seeking an opinion at a big teaching hospital was a good one - is that possible? Very best.

Reply # - July 25, 2012, 10:07 AM

watu
Posts: 45

Our oncologist is still away, but I've been able to exchange a couple of emails with him. He proposes gemzar, but next Monday we will have to discuss it a bit further to make sure that really is the best option.
I believe this is the only tratment they can offer because they don't have any trial in progress ay their hospital.

IMPRESS sounds interesting, but the chemotherapy is based on cisplatin and I'm afraid my father would be excluded because of his renal condition. I'm trying to contact an oncologist at one Centre in Italy running IMPRESS to get his opinion.

I've also been in contact with an oncologist in another hospital in Italy running a trial with Afatinib, but I'm still unsure of the benefits we can get from this drug as a second-line treatment. If I remember well, afatinib has shown interesting results in terms of PFS, but not in OS. Anyway, it is another option available.

Still gathering information and valuable opinions. I will keep you tuned.
Thank you all for your contributions and support.

Reply # - July 25, 2012, 07:53 PM

Dr West
Posts: 4735

Thanks, and watu, you're remembering correctly. Afatinib was compared in the LUX-Lung 1 trial to placebo in patients who had already received Iressa (gefitinib) or Tarceva (erlotinib). Afatinib was associated with a prolongation of progression-free survival (PFS) but not overall survival (OS) vs. placebo; in fact, the arm that received placebo had a numically longer median survival (the different was not statistically significant).

We'll be interested to learn what the best option ultimate is felt to be, and especially to learn how things go. Good luck.

-Dr. West

Reply # - July 26, 2012, 01:39 AM

certain spring
Posts: 762

Could I just return to the question in watu's first post, about whether it is worth a biopsy to see if the T790M mutation is present? Would that help in any way with the afatinib decision? My understanding was that patients with T790M did better on the afatinib/cetuximab trial than those without, but does that apply only to the trial combination - not to afatinib on its own?

Reply # - July 26, 2012, 07:33 AM

watu
Posts: 45

Just got the confirmation that dad cannot be included in the IMPRESS trial because of his kidney conditions.

So, two options left:

1. Suspend IRESSA, start Gemcitabine and possibly restart IRESSA (it seems that technically they are not authorized to mantain IRESSA during the chemo treatment, at least outside an official trial)

2. Switch to Afatinib as a single-agent (the association with cetuximab is not available in our country).

The second option is interesting, also because is the least toxic and possibly with fewer side effects.
Although Afatinib is still a EGFR TKI, I wonder whether it really makes sense to stop IRESSA at this early stage of a possible resistance and with an undefined progression (slow or quick?).

Would it be a good choice to consider Afatinib as a third-line therapy, after IRESSA and the Gemcitabine (as it was done during the LUX-Lung 1 trial) or is this the right time to get the most benefit from it?

I believe this is hard to answer.

Reply # - July 26, 2012, 08:59 AM

certain spring
Posts: 762

watu, on your point about whether it is too early to stop the Iressa, I thought you might be interested in a recent post by Dr West (if you have not already seen it):
http://cancergrace.org/lung/2012/06/19/chemo-with-or-without-ongoing-eg…
plus one on re-treatment with a targeted therapy:
http://cancergrace.org/lung/2012/06/30/re-treatment-with-targeted-rx/
As to afatinib, we do have some GRACE members who are taking afatinib on its own after several lines of treatment. They may want to come in on this. I would just caution, however, that they have reported the side-effects, especially in relation to the skin and nails, as being quite tough - in some cases very tough.

Reply # - July 26, 2012, 09:58 AM

graceabchen
Posts: 52

I would like to add Dr. West’s report on 2012 ASCO at http://cancergrace.org/lung/2012/06/09/ar-local-rx/#more-11228 to the above discussion. The main point is that continuing TKI (tarceva or Irresa) upon progression and applying stereotactic radiation or surgery on the local tumors can extend the TKI therapy before switching to other treatments. AB

Reply # - July 26, 2012, 07:33 PM

Dr West
Posts: 4735

I really can't provide an answer between the two alternatives suggested here. They're both so untested that I just think it would be complete speculation, and I just don't think that I or likely anyone has enough information for this situation to suggest that one approach would be clearly preferable to the other.

I wish I could be more helpful.

-Dr. West

Reply # - July 27, 2012, 01:14 AM

watu
Posts: 45

I think we will give Gemcitabine a try (hopefully without comporomising his current extremely good physical conditions) and leave Afatinib as an option for later. In this way, we would also have the chance to test a possible re-challange with IRESSA. As Dr. West described in one of his recent posts, there is some initial evidence that there might be a possible resensitization to the EGFR TKI. This is also being tested in the interesting ICARUS Italian trial:

http://clinicaltrials.gov/ct2/show/NCT01530334

Reply # - July 31, 2012, 05:12 PM

watu
Posts: 45

I spoke to our oncologist today. We decided to repeat the PET-CT in 4 weeks (it would be 8 weeks from the previous scan) and try to understand the degree of progression before proceeding with the second-line therapy (gemcitabine). As Dr. Sequist mentioned in her first post, if the progression is slow, it may make sense just to keep the first-line therapy with IRESSA.
I only hope that during this period the cancer doesn't go out of control.

Reply # - August 1, 2012, 07:14 AM

catdander
Posts:

Good luck to your father. I wish I could say don't worry with any kind of reassurance that the message would fall on open ears; but I know the feeling of worry. So I'll say take it moment by moment and know that an increase in the speed of progression in this situation is very low.

Reply # - September 7, 2012, 05:03 PM

watu
Posts: 45

Hello,

Hope to find you all well. Just a brief update on the topic.
This week, my father has had another PET-CT (9 weeks after the previous one). The main objective was to try to understand the speed of progression and, based on that, decide whether to stay on IRESSA or start a second-line treatment with Gemcitabine.

The same positive lymph nodes are still there, with slightly higher SUVs:

- right supraclavicular SUV 4.7 (it was 2.2)
- right axilllary SUV 5.5 (it was 5.2)
- right paratracheal SUV 4.7 (it was 3.9)
- mediastinal SUV 2.5 (it was 2.2)

In addition to these, they have seen a couple of new ones: right subclavicular SUV 2 and pretracheal SUV 2.6.

The question now is: can this be interpreted as a slow progression?

We'll see the oncologist next week and start discussions again.

If you can share any experience with PET-based monitoring of adenopathies, I would really appreciate.

Take care

Reply # - September 7, 2012, 06:33 PM

Dr West
Posts: 4735

I'm personally not that inclined to use SUV numbers on PET to determine whether to change therapies. I really favor the changing size of existing lesions or appearance of new ones to lead me to change therapies or not.

The SUV numbers you've given aren't that substantial. It sounds like his is a case where there's still a good role for individual judgment, ideally by someone who can directly assess both the scans and how your father is doing.

Good luck.

-Dr. West

Reply # - September 8, 2012, 02:17 AM

certain spring
Posts: 762

I'd like to say that as a patient I have been struck by the consensus on this: virtually every doctor who comments regularly on GRACE has said they don't use SUV numbers as a fail-safe marker for what is going on with a patient - only in conjunction with CT scans and symptoms.
I hope your father is feeling OK and managing well with the Iressa. Best wishes.

Reply # - December 6, 2012, 04:19 PM

watu
Posts: 45

Dear all,

Just following up on my father's case about 3 months after my last post.
In September, we finally decided to stay a bit more on IRESSA. On November 30th, my father had a new PET-CT, which confirmed all previous adenopathies, again with slightly higher SUV numbers, and identified a couple of new ones, together with 3 minor spots in the following areas:

- Segment VI of the liver (SUV 3.9)
- Rib IX (SUV 4.6)
- Vertebra L3 (SUV 8.2)

We are trying now to take arrangements for a CT scan with contrast, just to make sure that these new findings are real and not false positive.

It seems that this time it does make sense to stop IRESSA and start a second-line treatment with a chemo drug (we'd leave afatinib for a later stage).

As I mentioned in July, we were thinking of Gemzar as a good option, considering the mild renal insifficiency suffered by my father. However, our oncologist has now informed us that Taxotere would be feasible too. Docetaxel is mainly metabolised in the liver, so it should not affect the kidney function.

Has any of you had experience with Taxotere vs. Gemzar as a second line treatment after acquired resistance to an EGFR-TKI?
In this specific case, I wonder whether it really makes sense to suffer the much higher level of toxicity Taxotere has for an illness apparently mainly limited to the lymph nodes and that might respond relatively well to a milder drug like Gemzar.

Many thanks

Reply # - December 6, 2012, 09:54 PM

Dr West
Posts: 4735

There isn't any information out there in terms of actual studies to answer this question. I don't know if someone in the GRACE community has experience to share here on the subject. I suspect this may be a situation that is specific enough that neither the faculty nor fellow patients or caregivers here can offer real insight into your particular question.

Good luck.

-Dr. West

Reply # - December 6, 2012, 10:07 PM

catdander
Posts:

watu, I'm sorry your father has suspicious findings on his PET. It doesn't look like we've mentioned the blog posts written about acquired resistance. There are other options other than afatinib. Here is what Dr. West has written in his most recent blog on the subject. Note that tarceva can be substituted for iressa and vis vers in the post.
http://cancergrace.org/lung/2012/08/05/acquired-resistance-faq/

Taxotere is a standard tx option for 2nd line treatment, it has been tested and shown beneficial though gemzar is often used with success but it hasn't been tested as a single agent 2nd line. From what I understand taxotere's toxicity profile isn't too bad as long as peripheral neuropathy (numbness and pain in the feet and hands) doesn't become a problem.

This is a thread asking the very question of gemzar v taxotere. http://cancergrace.org/forums/index.php?topic=3208.0

I hope this is helpful,
Janine

Reply # - December 9, 2012, 09:36 AM

watu
Posts: 45

Thank you all for your inputs.

Yes, Dr. West's blog on this topic is extremely interesting and reports really "state-of-the-art" information.

Another good question now is: Do we keep IRESSA while on the 2nd-line chemo-based treatment or shall we take some time off from it hoping in a re-sensitization to the EGFR-TKI?

I found this interesting article, which claims: [...] Conventional chemotherapy given during the TKI-free interval could also have resulted in reduction of TKI-resistant clones, leaving TKI-sensitive ones susceptible to subsequent rechallenge with the same drug.

On the other hand, I also agree with Dr. West when he says that concurrent chemo and EGFR-TKI therapy might be effective, especially in patients with a driver mutation (the acquired resistance might be only partial). This approach will also keep us safe from a potential risk of disease flare following the discontinuation of the EGFR-TKI, as reported here http://clincancerres.aacrjournals.org/content/17/19/6298.full.pdf

Are you aware of any specific trial/study on this?

Thank you.

Reply # - December 9, 2012, 10:07 AM

certain spring
Posts: 762

Actually Dr West just answered a question about this ("disease flare"/"rebound progression") on another thread:
http://cancergrace.org/topic/question-about-tarceva
It sounds as if that MSK study is the main evidence so far. I have seen suggestions that it might have overestimated the prevalence and severity of disease flare.
I'm sure you've also see Dr West's interesting post dealing with the scenario of continuing the TKI but adding chemotherapy, which sounds relevant to your father's situation:
http://cancergrace.org/lung/2012/06/19/chemo-with-or-without-ongoing-eg…
Best of luck to your dad, and I hope he continues to do well.

Reply # - December 9, 2012, 10:58 AM

watu
Posts: 45

Thanks certain spring.

That post from Dr. West is exactly what I was looking for. I remember I read it a few months ago, but it has been useful to go through it again. Thank you.

I understand there's still no clinical evidence to clarify the doubts I have on this subject.

I wonder whether the "just-in-case" approach could make sense. In other words, if so far we haven't seen any detrimental effect from the combination of chemo with the EGFR-TKI therapy (ref. Sarah Goldberg's study at Dana Farber Cancer Institute), shall we keep IRESSA anyway while adding a 2nd-line chemo drug?

Reply # - December 9, 2012, 12:53 PM

catdander
Posts:

Exactly. That's what's going on with tarceva in the US. As the discussion suggests, many doctors have their patients stay on tarceva and add chemo. It seems like a lot of drug to me but I've not been confronted with the situation in my home either. For many it has been what they do.

Reply # - December 9, 2012, 08:34 PM

Dr West
Posts: 4735

I would say that there's still plenty of variability in the recommendations to patients, including in the US, and including by lung cancer specialists. There's certainly a very reasonable alternative in taking a break from it and potentially restarting it later, when we can sometimes see responses or at least some degree of improvement in responsiveness. And there are also many patients who are progressing so much on EGFR inhibitor therapy that continuing it adds nothing more than side effects.

Although I think that continuing the EGFR inhibitor is appropriate for many patients, I don't consider it to be the ideal approach for every patient with an EGFR mutation who develops acquired resistance to EGFR tyrosine kinase inhibitor therapy.

-Dr. West

Reply # - December 10, 2012, 01:16 AM

watu
Posts: 45

Understood.

I've actually just spoken to our oncologist and he said that unfortunately in Italy they are not allowed to combine IRESSA with chemo outside of a clinical trial. The IMPRESS trial is active here, but it does not use Taxotere, so my father cannot be included.

We have no option other than taking a break from IRESSA and trying a re-challenge at a later stage.
We will discuss with the oncologist how we can monitor the risk of disease flare.

By the way, can any of you comment on the which regimen for Taxotere is advisable? I mean weekly vs. 3-week. As far as I've read, the weekly regimen should be less toxic and not significantly less effective.

Our oncologists are suggesting the 3-week regimen anyway, which is expected to affect less the kidney function, although Texotere should be mainly metabolised in the liver.

Just a bit concerned about QoL, which is pretty good so far, but we are talking about a 71 year old patient, with one lung, etc..

Thank you.

Reply # - December 10, 2012, 06:38 AM

Dr West
Posts: 4735

The evidence is that weekly Taxotere (docetaxel) is perhaps marginally less challenging, but not as much of a difference as you might think, and the efficacy is at least a shade or two less. For these reasons, it isn't my general recommendation, though it's certainly not so much less effective that it isn't reasonable. There's just little to no reason to prefer it.

-Dr. West

Reply # - December 11, 2012, 10:50 AM

watu
Posts: 45

Thanks Dr. West. Let's hope the side effects are not too heavy on his case.

We have been prescribed Prednisone to be taken for 3 days starting about 12 hours before the treatment. Is that equivalent to the dexamethasone I've been reading so much about with Taxotere?

Reply # - December 12, 2012, 02:15 PM

watu
Posts: 45

Hello,

This morning my father had the CT scan with contrast, just to confirm the findings of the last PET-CT and set a more reliable baseline before starting the treatment with Taxotere tomorrow.

Unfortunately, it seems that the situation is much worse than what we expected. Positive lymph nodes more or less all confirmed, but in addition to them they have detected a 7.5mm parietal nodule (hyperdense, brain met?), several 3-4mm nodules in the right lung, a 10mm nodular lesion in the VI segment of the liver (hypodense, liver met?) and osteolytic areas in the XI rib and L3 vertebra (bone mets?).

This doesn't change the current plan to start Taxotere tomorrow, but it certainly shows a much tougher situation with, I believe, a poorer prognosis.

Who knows how long these mets have been there. During the treatment with IRESSA (18 months), we have been monitoring the situation only by PET-CT and so far they had not been detected. I'd like to think that their metabolism is probably slow, but I don't know if that necessarily means slow growth. Anyway, now we have no option other than attacking them with the chemo.

We really thought we would be able to manage much better a disease that was classified T1N0M0 after the left lobectomy in 2009 and T2N1M0 after the completion pneumonectomy in 2010. Although the area of the primary tumor was fully resected, apparently, at an early stage, that was probably already too late.

We'll try to be strong and move forward.

Mike

Reply # - December 12, 2012, 02:35 PM

Dr West
Posts: 4735

Mike,

I'm sorry to hear about those new findings, but you're right that this doesn't change the plan now. In general, being minimally detectable or undetectable on PET scan is associated with a slower growing process. I certainly hope that's the case.

-Dr. West

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