Lung laser surgery + ADAPT and still NED

[Sophy]

Hi folks, i wanted to share that I am now over 40 months since rectal cancer was found in my lungs, 30 months since my third lung laser thoracotomy in Europe August 2014, taking the ADAPT protocol of capecitabine and celecoxib since surgery, and scan last week shows I am still NED.

'Its amazing, you're unique' my surgeon commented when he gave me the good news. But I knew that this good result was thanks to the people here at the Colon Club - the place where I learnt that a recurrence could be treated and that knowledge of the best treatments available in the world might lead to a cure in the future.

Thanks especially to Maia and CB75 for their help.

[KElizabeth]

May I ask what the cost of treatment was, where you had treatment and does insurance help with the cost. Maybe these questions are stupid, but I really don't know and would very much like to.
How painful was treatment and how much scar tissue is left after treatment?

[stu]

Excellent news.
Enjoy,
Stu

[plastikos]

I have always been intrigued by ADAPT but confess that I have never done the research. Who or what center is best to consult about it? How does one know if he is a good candidate for ADAPT? Any tests?

[Sophy]

Kelizabeth and Plastikos - if you do a search on here for Lung Laser or for ADAPT there are many helpful threads from people who have followed this path.

[Maia]

So so so HAPPY for you, Sophy!! It warms my heart each time I see your posts

KElizabeth, some of the answers you're looking for can be found in this previous dialogue: viewtopic.php?f=1&t=56506&start=15#p447004 and also maybe in this viewtopic.php?f=1&t=52487#p411935

I have always been intrigued by ADAPT but confess that I have never done the research. Who or what center is best to consult about it? How does one know if he is a good candidate for ADAPT? Any tests?

Plastikos: ADAPT did intrigue me since I heard about it so years ago I put together all what I could find in this thread:

(ongoing) XCEL-ADAPT trial Phase II -OPEN

It's several pages, but all the pertinent papers are posted in them. By reading in order, you can see how the therapy changed its names, other similar clinical trials, etc.
Because of what I've read, a good candidate for ADAPT is one that is NED but in high chances of recurrence: for example, someone who got NED with chemo and not resection; or someone who got a resection/ablation of many nodules (in any area: lung, liver, peritoneum). (This last one could be the case of Sophy; I remember her onc told her that she could try capecitabine + celecoxib first, since she had Folfiri to revisit, anyway; meaning, he thought it was going to recur quite soon). Years ago, the idea was that ADAPT might work for those with low tumour burden to keep things going as a chronic condition; I do know someone (user jimc) who tried that years ago (December 2012) for his wife, when the doctors were offering her only Stivarga. They went for ADAPT instead and that gave them time, until it was progression later. I posted about that in that same ADAPT long thread, here: viewtopic.php?f=1&t=39924&start=45#p341341
(BTW, so you all have hope: jimc's wife is still here in 2017, facing challenges and looking for the right immunotherapy trial to show up, but working and living. Had the pleasure to finally exchange some greeting with her like one month ago) .
Still, it's difficult to say in which cases ADAPT would work to prevent recurrence, or to keep things stable during a while. Regarding molecular profiles/ mutations, I do know that KRAS status seems indifferent for ADAPT and that there is evidence that there are higher chances to work in those with an alteration in PI3K.

Abstract presentation from the 2014 ASCO Annual Meeting (June 2014) http://meetinglibrary.asco.org/content/132787-144

Journal of Clinical Oncology, 2014 ASCO Annual Meeting Abstracts.
Vol 32, No 15_suppl, 2014: 3610

Perturbations in PI3K pathway and cyclin dependent kinase (CDK) pathway to predict complete responders in CRC patients treated with ADAPT therapy

Edward H. Lin, Xiaowei Yan, John Dallas Scarborough, David Wu, Jing Tang, Lingheng Li, Douglas E. Wood, Shilpen A. Patel, Edward Y. Kim, Raymond Sze Yeung, Jonathan F. Tait, Colin C. Pritchard and Qiang Tian

Seattle Cancer Care Alliance, Seattle, WA; Institute for Systems Biology, Seattle, WA; University of Washington, Seattle, WA; Stowers Institute for Medical Research, Kansas City, MO; The Institute for Systems Biology, Seattle, WA

Abstract 3610

Background:
Aspirin or selective COX-2 inhibitor may improve overall survival (OS) in colorectal cancer (CRC) patients with PIK3CA mutations. However, routine use of anti-inflammatory agents in metastatic CRC patients remains controversial. We showed that 3-year maintenance celecoxib, also a stemness inhibitor coupled with capecitabine in a two-step ADAPT (activating dormant tumor cells and potentiate targeting) therapy led to 40% complete responders (CR) whose median survival reached 92.7 months in patients with unresectable stage IV CRC (Lin et al. AACR LBA254). We sought to determine genetic aberrations and related pathways as predictor of CR to ADAPT therapy.

Methods:
We retrospectively reviewed 50 consecutive stage IV CRC patients who had achieved CR [complete response] with ADAPT therapy alone or in conjunction with metastectomy between 2006-2012 at University of Washington. All patients were tested for a panel of 199 cancer-related genes (UW Oncoplex) with Illumina deep sequencing platform.

Results:
We select first 25 patients as training set to derive classifier for CR versus none CR that were at first blind to biostaticians. We found that genes involved in the PI3K pathway were significantly mutated in the CR [complete response] group whereas CDK pathways were altered in the none CR group (p< 0.0001, sensitivity 91.7%, specificity 76.9%). CR [complete response] events were independent of other worst prognostic factors including K-ras, B-raf, and p53. In vitrotreatment of CRC cell lines with ADAPT drugs confirms strongest PI3K pathway inhibition effects (p = 0) and cell cycle pathway (p < 0.05). Validation set analysis will be reported at the meeting.

Conclusions:
Altered PI3K and CDK pathways predict CR from ADAPT therapy in advanced unresectable CRC patients. Ongoing retrospective and prospective phase II ADAPT studies intend to validate these above findings.

(that was posted in that ADAPT thread by my friend Kenny: viewtopic.php?f=1&t=39924&start=60#p349203)

Other good thread about ADAPT was started by dear Cb75 (Carmen), who visited Dr Lin but never got her Canadians doctor on board to help her with that (she also had laser assisted lung surgery with Dr Rolle, and was not NED after it but with low tumour burden) . viewtopic.php?f=1&t=48774 (BTW, that was the case also for my friend Faith, from Canada, for whom I joined the forum. She visited Dr Lin in Seattle, she even had a PI3K mutation. Her Princess Margaret Hospital doctor walked out of the room on her, after reading Dr Lin's letter to him, saying that that was not proved yet. He was right, of course; it's not even proven now).
Because of what I know, Dr Lin is no longer taking new patients or seeing patients, and he's focused on laboratory research. I don't know the reasons. Not other centers; it is basically a protocol he designed and he applied with his patients at SCCA in Seattle, but he was very willing to share with any oncologist from around the world who contacted him.

I'll update that old thread about ADAPT with more recent data I have, soon.

And this was the first thread with all about LAPM: Laser Assisted Pulmonary Metastasectomy (8 to 100 mets)

[stevieb]

absolutely awesome!!!

[plastikos]

So so so HAPPY for you, Sophy!! It warms my heart each time I see your posts

KElizabeth, some of the answers you're looking for can be found in this previous dialogue: viewtopic.php?f=1&t=56506&start=15#p447004 and also maybe in this viewtopic.php?f=1&t=52487#p411935

I have always been intrigued by ADAPT but confess that I have never done the research. Who or what center is best to consult about it? How does one know if he is a good candidate for ADAPT? Any tests?

Plastikos: ADAPT did intrigue me since I heard about it so years ago I put together all what I could find in this thread:

(ongoing) XCEL-ADAPT trial Phase II -OPEN

It's several pages, but all the pertinent papers are posted in them. By reading in order, you can see how the therapy changed its names, other similar clinical trials, etc.
Because of what I've read, a good candidate for ADAPT is one that is NED but in high chances of recurrence: for example, someone who got NED with chemo and not resection; or someone who got a resection/ablation of many nodules (in any area: lung, liver, peritoneum). (This last one could be the case of Sophy; I remember her onc told her that she could try capecitabine + celecoxib first, since she had Folfiri to revisit, anyway; meaning, he thought it was going to recur quite soon). Years ago, the idea was that ADAPT might work for those with low tumour burden to keep things going as a chronic condition; I do know someone (user jimc) who tried that years ago (December 2012) for his wife, when the doctors were offering her only Stivarga. They went for ADAPT instead and that gave them time, until it was progression later. I posted about that in that same ADAPT long thread, here: viewtopic.php?f=1&t=39924&start=45#p341341
(BTW, so you all have hope: jimc's wife is still here in 2017, facing challenges and looking for the right immunotherapy trial to show up, but working and living. Had the pleasure to finally exchange some greeting with her like one month ago) .
Still, it's difficult to say in which cases ADAPT would work to prevent recurrence, or to keep things stable during a while. Regarding molecular profiles/ mutations, I do know that KRAS status seems indifferent for ADAPT and that there is evidence that there are higher chances to work in those with an alteration in PI3K.

Abstract presentation from the 2014 ASCO Annual Meeting (June 2014) http://meetinglibrary.asco.org/content/132787-144

Journal of Clinical Oncology, 2014 ASCO Annual Meeting Abstracts.
Vol 32, No 15_suppl, 2014: 3610

Perturbations in PI3K pathway and cyclin dependent kinase (CDK) pathway to predict complete responders in CRC patients treated with ADAPT therapy

Edward H. Lin, Xiaowei Yan, John Dallas Scarborough, David Wu, Jing Tang, Lingheng Li, Douglas E. Wood, Shilpen A. Patel, Edward Y. Kim, Raymond Sze Yeung, Jonathan F. Tait, Colin C. Pritchard and Qiang Tian

Seattle Cancer Care Alliance, Seattle, WA; Institute for Systems Biology, Seattle, WA; University of Washington, Seattle, WA; Stowers Institute for Medical Research, Kansas City, MO; The Institute for Systems Biology, Seattle, WA

Abstract 3610

Background:
Aspirin or selective COX-2 inhibitor may improve overall survival (OS) in colorectal cancer (CRC) patients with PIK3CA mutations. However, routine use of anti-inflammatory agents in metastatic CRC patients remains controversial. We showed that 3-year maintenance celecoxib, also a stemness inhibitor coupled with capecitabine in a two-step ADAPT (activating dormant tumor cells and potentiate targeting) therapy led to 40% complete responders (CR) whose median survival reached 92.7 months in patients with unresectable stage IV CRC (Lin et al. AACR LBA254). We sought to determine genetic aberrations and related pathways as predictor of CR to ADAPT therapy.

Methods:
We retrospectively reviewed 50 consecutive stage IV CRC patients who had achieved CR [complete response] with ADAPT therapy alone or in conjunction with metastectomy between 2006-2012 at University of Washington. All patients were tested for a panel of 199 cancer-related genes (UW Oncoplex) with Illumina deep sequencing platform.

Results:
We select first 25 patients as training set to derive classifier for CR versus none CR that were at first blind to biostaticians. We found that genes involved in the PI3K pathway were significantly mutated in the CR [complete response] group whereas CDK pathways were altered in the none CR group (p< 0.0001, sensitivity 91.7%, specificity 76.9%). CR [complete response] events were independent of other worst prognostic factors including K-ras, B-raf, and p53. In vitrotreatment of CRC cell lines with ADAPT drugs confirms strongest PI3K pathway inhibition effects (p = 0) and cell cycle pathway (p < 0.05). Validation set analysis will be reported at the meeting.

Conclusions:
Altered PI3K and CDK pathways predict CR from ADAPT therapy in advanced unresectable CRC patients. Ongoing retrospective and prospective phase II ADAPT studies intend to validate these above findings.

(that was posted in that ADAPT thread by my friend Kenny: viewtopic.php?f=1&t=39924&start=60#p349203)

Other good thread about ADAPT was started by dear Cb75 (Carmen), who visited Dr Lin but never got her Canadians doctor on board to help her with that (she also had laser assisted lung surgery with Dr Rolle, and was not NED after it but with low tumour burden) . viewtopic.php?f=1&t=48774 (BTW, that was the case also for my friend Faith, from Canada, for whom I joined the forum. She visited Dr Lin in Seattle, she even had a PI3K mutation. Her Princess Margaret Hospital doctor walked out of the room on her, after reading Dr Lin's letter to him, saying that that was not proved yet. He was right, of course; it's not even proven now).
Because of what I know, Dr Lin is no longer taking new patients or seeing patients, and he's focused on laboratory research. I don't know the reasons. Not other centers; it is basically a protocol he designed and he applied with his patients at SCCA in Seattle, but he was very willing to share with any oncologist from around the world who contacted him.

I'll update that old thread about ADAPT with more recent data I have, soon.

And this was the first thread with all about LAPM: Laser Assisted Pulmonary Metastasectomy (8 to 100 mets)

As always Maia, thanks. Will consider this when I get to NED.