Topic: Abemaciclib Verzenio for Stage IV

Forum: Stage IV/Metastatic Breast Cancer — Please respect that this forum is for members with stage IV/metastatic breast cancer ONLY. There is a separate forum for caregivers and friends: Caring for Someone with Stage IV or Mets.

Posted on: Jan 1, 2018 05:03AM - edited Jun 18, 2018 12:19AM by zarovka

Posted on: Jan 1, 2018 05:03AM - edited Jun 18, 2018 12:19AM by zarovka

zarovka wrote:

Luckylegs and friends on Abemaciclib - I am bumping the Verzenio discussion in the hopes that more people have started abemaciclib. We need to get a community going. I have not started abemaciclib but it is on my short list. Like many I am very interested in how people do on this treatment do, both as a monotherapy and in combination with hormone suppression and other treatment. I am hoping that this thread can capture the experience of everyone on Abemaciclib in whatever combination. This is a very important treatment option that we all need to be evaluating.

I would expect more people on the drug given the significant advantages of abemaciclib over the first generation CDK 4/6 inhibitors. However, the FDA has approved abemaciclib for only limited indications. We have not established its use as a first line treatment nor as something to switch to from Ibrance. At the same time, they haven't made it clear that the drug can and should be used after Ibrance. As a result, the setting for using abemaciclib is supremely unclear.

I believe abemaciclib can be used either instead of or after palbo/ribo depending on whether you view abemiciclib as another class of drug or the same class of drug with significant improvement. One can make arguments for either strategy. If you've already done palbo/ribo, it is certainly worth trying abemaciclib. If you haven't done palbo/ribo, the current guideline that you start with the first generation CDK 4/6 is reasonable, but not necessary IMO. A lot depends on the side effect profile you can tolerate the best as the drugs have significant differences in side effects and also whether you are at risk of brain mets. Abemaciclib is better at crossing the blood brain barrier.

The following summary of abemaciclib data taken from a thread started by Constantine on Inspire. I moved his entire discussion from three posts because it's that good. Thank you Constantine.

ABEMACICLIB (VERZENIO)
Preliminary data from a phase I study of abemaciclib [SABCS 2014] in patients with five different tumor types including HR-positive metastatic breast cancer, with I note a median of seven prior systemic therapies (outliers out to 11 lines) found an objective response rate of 19% and a disease control rate (including stable disease (SD) under RECIST definition of >24 weeks of ) of 81% for HR-positive MBC patients. This Phase I study was expanded to evaluate abemaciclib plus fulvestrant in HR-positive MBC [ASCO 2014.] with patients having a median of four prior systemic therapies (and outliers out to the eight line), finding an objective response rate of 62% confirmed PRs.

A subsequent Phase I study [Tolaney et al, J Clin Oncol 2015;33(Suppl 1).] of abemaciclib in combination with different endocrine therapies for HR-positive MBC (median lines of treatment = 3, with outliers out to 8) demonstrated a disease control rate (CR + PR + SD) was 67% for those on abemaciclib + AI therapy, and 75% for those on abemaciclib + tamoxifen.

The phase II MONARCH-1 trial evaluated abemaciclib MONOTHERAPY in HR-positive, HER2-negative MBC patients with a median of 3 lines of prior therapy for advanced disease, including a median of 2 lines of chemotherapy (as opposed to endocrine or biological therapy) for advanced disease, yielding an objective response rate (ORR) of 17.4% and a clinical benefit rate (CBR) of 42.4%.

What's important to remember about MONARCH-1 is that many women in the study had already received multiple lines of endocrine treatment (median 3 - 5 previous lines in the metastatic setting, with outliers beyond that), developed resistance and were refractory to all of these treatments, AND progressed, many of whom also received chemotherapy, and these results were for MONOTHERAPY in a heavily pretreated population, which as I determined through examination of historical controls with any other agent achieves at best only 10 to 20% clinical benefit rates - half of that achieved by single-agent abemaciclib, and with responses of short duration.

Hence, the collective results of these trial, including MONARCH 1 (MONARCH-2 (with letrozole) and MONARCH-3 (with fulvestrant) are exceptionally exciting breakthrough in breast cancer therapeutics.

BREAKTHROUGH SURVIVAL
In addition, for me, the overall survival (OS) of these heavily pretreated MBC patients was 17 months, and that compares to historical control I review from all clinical trials to date, as significantly better than other survival results, which are usually are at best 13 months. Thus, consider that for the current champ, eribulin chemotherapy in this setting, the EMBRACE trial achieved a median overall survival (OS) was 13 months, we clearly have here a major advance and improvement in overall survival in the highly challenging later-line settings (past at least 3 lines of therapy).

HIGH TOLERABILITY
The major limiting constraint with all CDK4/6 inhibitors to date, like palbociclib (Ibrance), is their most common adverse effect, that of myelotoxicity via neutropenia (low WBC neutrophils), with palbociclib (Ibrance inducing some degree of neutropenia in over half of women on it, with associated dose interruptions and sometimes dose reductions, a toxicity that so fat from the available data seems to also afflict ribociclib.
But abemaciclib (Verzenio) evades a good deal of this because although strictly a CDK4/6 inhibitor, it is more specific in inhibiting CDK4, that is it is CDK4-selective, and myelotoxicity including neutropenia is primarily associated with CDK6, making the incidence of neutropenia on abemaciclib significantly lower and more manageable.

CLINICAL LESSONS ON ABEMACICLIB (VERZENIO)
And unlike palbociclib (Ibrance):

1. abemaciclib has strong single-agent activity in HR–positive MBC,
2. has durable response in later line settings,
3. a good tolerability profile with reduced neutropenia, and
4. to date the highest OS in these challenging heavily pretreated settings of any oncotherapeutic agent, whether endocrine therapy, chemotherapy, or biological therapy.

SOME NUANCES
1. The ESMO-reported MONARCH 3 Trial found an response rate of 48.2% for all patients, BUT for the subgroup of patients with measurable disease, a response rate (ORR) of 59.2%, these being the highest ever response rates achieved to date for ANY endocrine therapy in breast cancer.
2. And although data needs to mature further for survival outcomes, it is anticipated based on exploratory analyses that PFS will weigh in at an improvement of close to 12 months, again an extraordinary gain.
3. In addition, Verzenio was most effective in challenging populations like those with visceral metastases (especially liver) and those with rapidly recurrent (short disease-free-interval (DFS)) patients.
4. Finally, 16 patients across two of the three MONARCH trials were NED (complete response (CR)), likely to increase once the MONARCH-3 data matures, more still I anticipate when results are reported from the MONARCH PLUS and other trials.

DIARRHEA AND ITS MANAGEMENT
To put the adverse events into a bit of perspective, although it is true that with Verzenio, all-grade diarrhea was between 86 - 90%, yet serious (Grade 3+) incidence was 13 - 20% but this is aggregated across the trials, and note further that diarrhea incidence is concentrated during the first month, and more narrowly the MTO (median time to onset) of the first diarrhea event was 6 days, lasting a median duration of just 6 days for Grade 3. Furthermore, for the most recent MONARCH-3 RCT, grade 4 diarrhea was zero, and grade 3 diarrhea was just 9.5%.

An aggressive proactive regimen of:

- high-dose loperamide/Imodium (4 mg but NOT ever de-escalated down to 2mg (and up to 16 -32 mg daily);
- "Big Pink" (Petpto Bismol Extra Strength) used in "priming" mode (started on day 4 and also used for immediate relief during loperamide dosing;
- budesonide (Symbicort) for recalcitrant cases;
PLUS "adjunct interventions:
- high-dose probiotic (28 billion microorganism count in two divided doses), and
- electrolyte powder (most of the refractory diarrhea was analyzed to be secondary to disturbed microflora and electrolyte imbalances)
- at least 12 8 oz glasses of fluid daily, 8 of which should be electrolyte-enhanced

brought the rate of diarrhea-related drug omission or dose reduction down from 22% (MONARCH 1 and 2) to under 1 - 2% in the cohorts run by my research teams in India and the Middle East.
NOTE: We found that the adjunct interventions of Big Pink, high-dose probiotic, electrolyte rebalancing, and assured fluid intake were at least important as the conventional agents, and in cases that seem intractable, converted to success, given that therapy-driven diarrhea inevitably causes GI tract flora, and electrolyte, imbalances, aggravated by inadequate hydration. Also critical was "through-and-through" loperamide dosing: 4 mg at each episode, but NOT de-escalating - as current protocols do - down to 2 mg after first (that de-escalation regimen we found indifferently effective, with large numbers of failures.

And although not reported to date, I note that in the MONARCH 3 trials the incidence of ANY grade diarrhea dropped to just 2% (courtesy of data provided by Levi Garraway at Lilly).

ACTIVITY IN LOBULAR CARCINOMA
The trials largely fail to report to date differential invasive-type stats, but the impression from conversations with some principals is that lobular breast cancer subjects are unlikely to experience significant decrement, and I also extrapolate from some hints surrounding the PELOPS (Palbociclib and Endocrine Therapy for LObular Breast Cancer Preoperative Study) Trial another CDK4/6 inhibitor palbociclib (Ibrance), as well as from some molecular considerations (the p27 gene is a key regulator of certain types of progression (G1 to S-phase) and it appears that lobular carcinomas tend to have higher p27 which in a complex way under contextual effects can have either positive or negative effects on phase progression), but we have to await sub-group analysis to report on this issue explicitly. I am cautiously confidant of little differential outcome, which I think may be confirmed across the general class of CDK inhibitors. In addition, both the lobular and the ductal groups appear to have benefited from the addition of palbociclib (Ibrance) in the PALOMA-/TRIO-18 Trial, but I note that the difference observed in PFS in that trial is likely to be an artificial artifact of the small patient in the subgroup with lobular carcinoma arm (n = 18/19) compared to n = 117 in the ductal subgroup, so this is a small sample size effect not a robust finding, an impression in agreement with that of the principal investigators (Richard Finn and UCLA and colleagues). As we learn more about lobular BC and abemaciclib in particular, I will offer further clarifications.

DEGREE OF DIFFERENCE - IBRANCE v VERZENIO
Given the dramatic 14-fold (!) greater CDK4 activity in abemaciclib (Verzenio) compared to palbociclib (Ibrance) and ribociclib (Kisqali), as MONARCH 3 lead author Angelo Di Leo has established and noted in interview, and other consequent fundamental molecular pathway differences, I view these as only shared-class (CDK), but therapeutically distinct, agents, more like the difference between third-generation capecitabine (Xeloda) versus first-generation 5-FU although these are both fluoropyrimidines.

So: More different than same as witness also the high degree of relative invariance of efficacy and durable response in later-line treatments for Verzenio compared to that of Ibrance (see my original posting, above). These differences are sufficient warrant for me to classify palbociclib (Ibrance) as a first-generation CDK inhibitor, and abemaciclib (Verzenio) as a second-generation CDK inhibitor. The devil - as always - is in the details.

CNS (BRAIN) ACTIVITY
We have preclinical data [Raub et al. Drug Metab Dispos. 2015] of the cross-BBB (blood-brain barrier) capability of Verzenio, as witness the remarkable benefit in GBM (glioblastoma, being even non-inferior to temozolomide (TMZ), the standard of care in cross-BBB activity, and this although not a human clinical, was an in vivo, not just in vitro, study. And the Dana-Farber JPBO human clinical trial (I3Y-MC-JPBO) under Sara Tolaney is investigating single-agent abemaciclib in patients with ER+/HER2+ brain metastases, where I fully expect clinically relevant CNS benefit to be confirmed, with first phase interim results reported in June at ASCO 2017 showing 2 patients (8.7%) out of 23 having confirmed partial response (PR).

I should point out that there has been some provisional data on palbociclib (Ibrance) having potential cross-BBB activity in brain metastasis, but I hasten to note that strong in vivo data show a 10-fold greater cross-BBB activity for abemaciclib than palbociclib, with abemaciclib brain levels being more efficient at substantially lower doses than palbociclib and also active for longer duration, and finally abemaciclib was active as monotherapy, palbociclib was not.

Finally, as to leptomeningeal metastases, no explicit data bears on this question directly, but as to date all agents active in brain metastases have also been active in leptomeningeal metastases, activity would be expected.

THE ISSUE OF SWITCHING
It remains an open question whether patients who have progressed on or after another CDK inhibitor like palbociclib (Ibrance) may derive significant benefit from continuance of CDK4/6 inhibition by using a following CDK inhibitor like abemaciclib (Verzenio), with many in-progress trials like TRINITI-120 (and NCT0185719319 and NCT0263204521, among others) exploring the issue. But there is some plausible extrapolation from some preclinical data which has suggested non–cross-resistance among CDK4/6 inhibitors. A Barts Cancer Institute study reported at SABCS 2016 found that some palbociclib(Ibrance)- and ribociclib(Kisqali)-resistant cell clones were sensitive to abemaciclib (Verzenio).

For patients now on Ibrance (or Kisqali) but who have NOT PROGRESSED , is it motivated to switch to abemaciclib (Verzenio)? This is an issue that needs to be thrashed about candidly with your oncology team and is a highly individual decision, but my own sense at this time is that it may be more optimal in the long run to stay the course, and consider abemaciclib (Verzenio) for recourse upon progression either off-label until the FDA expands its approval, or on one of the many abemaciclib (Verzenio) clinical trials available.

I would however entertain some specialized exceptions in which a switch now, off of Ibrance or Kisqali, onto abemaciclib (Verzenio), might be motivated; for example:

1. If a patient is experiencing repeated difficult-to-manage neutropenia, occasioning multiple drug interruptions or reductions (neutropenia being dramatically less with abemaciclib (Verzenio)), but the patient must weigh the associated countervailing issue of higher incidence - but still manageable I would argue - diarrhea on abemaciclib (Verzenio).
2. If a patient is in advanced later-line setting (say, more than 5 to 7 lines or so of treatment in the metastatic setting already completed), where it is suspected that abemaciclib (Verzenio) may be somewhat more consistent and durable in response and benefit in such challenging contexts. This is a difficult one to judgment-call, and I would tend to want to weigh each patient's circumstance and their complex treatment history and individual pathology to assist in the decision, since we have no hard data to be dispositive on this decision.

Yes, these are arguable and have to be intensively debated (as in a tumor board setting), but they are not wholly unreasonable. Outside of these exceptions, however, I do not see sufficient motivation to prematurely abandon Ibrance or Kisqali, as these have strong track records of efficacy and should be push to progression.

FDA APPROVAL

Abemaciclib is currently approved ...
1. as combination therapy with fulvestrant (Faslodex) for the treatment of women with HR+/HER2- advanced or metastatic breast cancer who experience disease progression AFTER ENDOCRINE therapy.

2. as monotherapy for the treatment of women with HR+/HER2- advanced or metastatic breast cancer who experience disease progression AFTER ENDOCRINE therapy AND prior CHEMOTHERAPY in the metastatic setting.

(Z) MO's have latitude to prescribe outside of these indications and there are strong arguments for doing so. My MO appears to have wide latitude to prescribe Abemaciclib and get insurance approval in other settings.

EXPANDED ACCESS:
Abemaciclib continues to be available through Lilly's attractive Expanded Access Program (EAP):
https://clinicaltrials.gov/ct2/show/NCT02792725?term=abemaciclib&rank=24
which is active and recruiting currently in several US locations (California, Florida, Minnesota, Missouri, Texas, and West Virginia), more being added. However that is for patients who have not as yet progressed on a previous CDK inhibitor like palbociclib (Ibrance), that is, for "switchers" who may want to explore the improved benefits of abemaciclib (Verzenio) over Ibrance (assuming the patient meet the other trial criteria); but not for patients who have already progressed on Ibrance.

RECHALLENGE

In several cases I have known, I counseled that although someone progressed on Ibrance, to reintroduce it after a hiatus of 3 - 6 months, and in many cases this washout appeared to resensitize the tumor cells to Ibrance, which upon re-introduction was newly effective. It is a variant of a trick I have counseled and seen working not infrequently with other agents like capecitabine (Xeloda) where after progression on it, I advised a trial on a new metronomic schedule (low-dose, continuous, daily, capecitabine) and seen again it newly effective despite previous progression, just by this shift I schedule (there is some provisional data for this, but not decisive). But these are beyond convention and reserved for highly special circumstances.

MARKERS THAT PREDICT RESPONSE TO CDK 4/6 INHIBITION
I am not convinced that there is any biomarker - protein or otherwise - that reliably identifies responsivity to CDK inhibitors, and Fabrice Andre of the Institut Gustave Roussy and colleagues, as reported in their presentation at ASCO 2017, were unable to identify any such biomarkers of response: neither Rb levels, p16 protein levels, Ki-67 cell proliferation, CDKN2A, CCND1, nor even ESR1 gene expression, all the usual suspects, and others, had any response-predictive value whatsoever. To date the only established biomarker for response to CDK4/6 inhibitors, remain hormone receptor positivity (HR+). Of course not everyone responds, but response rates remain historical high - and higher than any other treatment to date - and as long as one is HR+, one has the potential to benefit from a CDK inhibitor.

Constantine Kaniklidis
Director, Medical Research, No Surrender Breast Cancer Foundation (NSBCF)
Oncology Reviewer, Current Oncology [journal]
Society for Integrative Oncology (SIO)
Member, European Association for Cancer Research (EACR)

Ibrance/Letrozol Feb '16 -Sep '17. Adoptive Cell Therapy Oct 2017. Jan 2018 SBRT to sternum met and liver mets. Jan 2018 start Faslodex. Dx 12/28/2015, IDC, Left, 4cm, Stage IV, metastasized to bone/liver, Grade 3, ER+/PR-, HER2- Hormonal Therapy 1/17/2016 Femara (letrozole) Targeted Therapy 2/2/2016 Ibrance (palbociclib)
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Jan 3, 2019 03:11PM chatsworthgirl wrote:

Hello all,

Well, it looks like I am done with Verzenio. My markers went from 783 down to 325 then to 330 then to 417. I was told to take a break for my vaca because of the incessant diarrhea. I stopped for nine days but then asked the onc if I should continue since he wanted to see one more month of blood work to see if the numbers continued to rise and I thought it would be a much more valid test if I was still on the drug. He was less than helpful. As I have mentioned previously, if I tell him that I am experiencing pain or diarrhea or anything, he comments that I "complained" about the drug so perhaps I shouldn't be on it.

I can't figure out what he wants me to do. I would think that he would want to know what side effects I was experiencing so that we could make an informed decision as to what I should do. He has absolutely no empathy, compassion or even a tiny bit of sympathy. I sure hope he never has to go through this. He wouldn't be able to handle it I'm sure.

Anyway, I decided to go back on the V but two weeks into it I woke up with severe pain from the base of my scull to my knees. All I had was Excedrin but that worked somewhat. I had also been having severe shortness of breath - a side effect that is listed on the Verzenio site as something to take very seriously. So I decided to quit again so that I could at least have a vaca of some pleasure. The first few days of my vaca I was still in some pain, had a massage, pain worse for a day then got better.

I told him of my experiences. A mistake. Once again he acts like I am such a pain the arse because I tell him this stuff. I have now been off everything since December 22 and I feel really good.

I just had a blood draw on Wednesday, Won't know what the markers are until Monday. My white blood cell count is extremely low. He is suggesting Xeloda next but wants all drugs cleared from my body and my white count up before proceeding. He said there is no point in my doing the Faslodex by itself since I progressed very quickly on it when it was flying solo.

I told him I wanted the Foundation 1 test which is now done with blood rather than a biopsy. He said usually that's done after all other drugs have failed. !!!!!????? Am I the only person who finds this reasoning completely wrong? Surely rather than putting me through 5 or 6 drugs with varying side effects, it would be better to do the Foundation 1 test and find out (hopefully) that there are certain drugs that are more likely to help with my particular cancer biology. I said since my insurance paid for it why not. He said he would do it. A struggle but I won.

I am so grateful for these forums because there is a wealth of real time information from others who are going through this. The clinical trials that get drugs to market are extremely small and limited. We are the real clinical trials. We are the ones on the front line letting the doctors and researches really know what works and for how long.

I would like to advise doctors to read our discussions. It would be enlightening for them. They might actually learn some important things.

Chats

Dx 6/6/2011, IDC, Left, 2cm, Stage IIA, Grade 2, 1/1 nodes, ER+/PR+, HER2- Surgery 7/15/2011 Lumpectomy: Left; Lymph node removal: Left, Sentinel; Mastectomy: Left, Right Chemotherapy 10/5/2011 Cytoxan (cyclophosphamide), Taxotere (docetaxel) Radiation Therapy 4/15/2012 Breast, Lymph nodes Dx 2/20/2017, ILC/IDC, 2cm, Stage IV, metastasized to bone, Grade 2, 1/1 nodes, ER+/PR+, HER2- Hormonal Therapy 2/21/2017 Femara (letrozole) Hormonal Therapy Faslodex (fulvestrant)
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Jan 3, 2019 04:07PM - edited Jan 3, 2019 04:15PM by Frisky

Chats, It's stressful to change MOs BUT yours sounds like a real @#$('ole(* ......

I am on xeloda and have been for the past 6 months....

of all the TXs I've been on this one is the best...I only wish that like some of the lucky women on this board I can be on it for the next five years....it's sooooo easy.....and tolerable....I'm lucky also because I'm not suffering from hand and foot diseases....just fatigue which can be fixed by adjusting the number of pills taken.

And During the off week, I get to feel completely normal....I just hope it keeps on working....

Foundation 1 results could be helpful, but I read recently somewhere that the results between Caris and Foundation differ wildly using the same blood....so it's really all phantasy land...

Two of my three MO's smiled when I asked them to do those tests...the first one did...but than she placed the results, the size of a yellow pages phone book in my lap, and said: here...you read this...see if you can make any sense out of it, and she was a leading MO at MSK in NYC.....my current one however said that he would use a blood sample when the time comes....so maybe things are improving

“Things are not always what they seem; the first appearance deceives many; the intelligence of a few perceives what has been carefully hidden.” Phaedrus Dx 3/9/2015, ILC, Left, Stage IV, metastasized to bone/liver, ER+/PR+, HER2- Hormonal Therapy 3/15/2015 Femara (letrozole) Hormonal Therapy 3/10/2017 Faslodex (fulvestrant) Targeted Therapy 3/10/2017 Ibrance (palbociclib) Surgery 4/5/2017 Radiation Therapy 4/10/2017 External: Bone Hormonal Therapy 1/5/2018 Tamoxifen pills (Nolvadex, Apo-Tamox, Tamofen, Tamone) Targeted Therapy 2/10/2018 Afinitor (everolimus) Chemotherapy 6/2/2018 Xeloda (capecitabine) Chemotherapy 7/20/2019 Doxil (doxorubicin) Chemotherapy 12/15/2019 Navelbine (vinorelbine)
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Jan 3, 2019 08:03PM sandilee wrote:

Chats and Miomix- I am astonished at the attitude of your oncologists when it comes to Foundation One tests. I had one at my request a few years ago- when they first came out. That one didn't help that much because they hadn't developed any drugs that matched my mutations. In 2018 my onc suggested that I get another one with a new biopsy ( he wanted a BX of the liver anyway) because they had improved a lot. My results this time were extremely helpful, and put me on the Verzenio track that I've been on for the last 6 months.

I guess I am lucky in that my doctor listens to me and respects my ideas and concerns. He has been with me from the get-go- since 2007- and without the trust I have in him, I'm sure I wouldn't be doing as well psychologically. It's really worth a lot to find someone you can connect with on a personal level as well as someone knowledgeable with all the new treatment. Both are equally important.

Dx 11/2007, IDC, 1cm, Stage IA, Grade 2, 0/6 nodes, ER+/PR-, HER2- Hormonal Therapy 1/10/2008 Aromasin (exemestane) Dx 6/2011, IDC, mets Radiation Therapy 6/30/2011 Bone Hormonal Therapy 7/15/2011 Faslodex (fulvestrant) Hormonal Therapy 4/10/2015 Femara (letrozole) Targeted Therapy 4/20/2015 Ibrance (palbociclib) Chemotherapy 8/4/2015 Xeloda (capecitabine) Hormonal Therapy 3/11/2016 Tamoxifen pills (Nolvadex, Apo-Tamox, Tamofen, Tamone) Chemotherapy 10/13/2016 Doxil (doxorubicin) Chemotherapy 4/4/2018 Navelbine (vinorelbine) Hormonal Therapy 6/6/2018 Faslodex (fulvestrant) Targeted Therapy 6/6/2018 Verzenio Chemotherapy 4/23/2019 Carboplatin (Paraplatin), Gemzar (gemcitabine)
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Jan 3, 2019 09:38PM - edited Jan 3, 2019 09:48PM by Frisky

hi Sandilee, the reason why I'm so skeptic about the state of the arts is because the genetic test that was done revealed a few actionable mutations, one of which was the AKT marker, but when I was placed on Afinitor, the medication that should have matched that mutation, my cancer markers tripled and the pet scan indicated progression three months later. I didn’t get much benefit from Faslodex either, that matched my ESR mutation. Thus in my view the current “science" is no more than throwing darts on the wall and hope that they stick....therefore the roll of the eyes by my MOs that are aware of these ridiculous results.

I do have and always have had a great relationship with my doctors...as I am a very accomplished artist and they tend to respect that....but the truth is that when I read these posts, except for Zarovka's enterprising attitude regarding her treatments, everyone is prescribed the exact same medications in the exact same order. The variance is only based on ER, PR and HER2 status. Which leads me to believe that the results of these tests don't affect yet the treatments and worse yet, the end results....

Hopefully some real progress will be made soon with these tests and the corresponding TX....who knows maybe in our lifetime....

“Things are not always what they seem; the first appearance deceives many; the intelligence of a few perceives what has been carefully hidden.” Phaedrus Dx 3/9/2015, ILC, Left, Stage IV, metastasized to bone/liver, ER+/PR+, HER2- Hormonal Therapy 3/15/2015 Femara (letrozole) Hormonal Therapy 3/10/2017 Faslodex (fulvestrant) Targeted Therapy 3/10/2017 Ibrance (palbociclib) Surgery 4/5/2017 Radiation Therapy 4/10/2017 External: Bone Hormonal Therapy 1/5/2018 Tamoxifen pills (Nolvadex, Apo-Tamox, Tamofen, Tamone) Targeted Therapy 2/10/2018 Afinitor (everolimus) Chemotherapy 6/2/2018 Xeloda (capecitabine) Chemotherapy 7/20/2019 Doxil (doxorubicin) Chemotherapy 12/15/2019 Navelbine (vinorelbine)
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Jan 4, 2019 09:21AM blainejennifer wrote:

Genomic testing is in its infancy. We can get a snap shot of any individual's genetic array, and we have some data on that relationship with treatment outcomes. But, we've got little bloody clue yet on what turns those genes on or off in response to treatment. There's epigenetic factors that continue to boggle.

So, as it stands now, the testing is for information compilation. I would never turn down a therapy based on genomic assay. NEVER. I might lean in one direction or another, but I've heard too many stories that begin like this, "Well, Foundation One said it wasn't supposed to work, but i've been NED for . . . ." I'd also take a shot at something that wasn't meant to do well, especially if I were in a position to need experimentation.

I'll tell you this - if money will provide the answers, we are in good shape. Institutions are throwing money at this research. Just dumping truckloads of the stuff. The researchers leading these initiatives are . . . sometimes dizzy with options. Just think about the institution that cracks it first. My golly.

ER/PR+, HER2-, Grade 3. Stage 4, July 2012. Currently on Gemzar/Carboplatin Dx 5/2006, IDC, 4cm, Stage IIB, Grade 3, 4/12 nodes, ER+/PR+, HER2- Dx 3/2012, IDC, Stage IV, 4/12 nodes, ER+/PR+, HER2- Chemotherapy 6/28/2012 Taxol (paclitaxel) Hormonal Therapy 6/5/2013 Faslodex (fulvestrant) Chemotherapy 7/1/2014 Xeloda (capecitabine) Hormonal Therapy 8/14/2015 Femara (letrozole) Chemotherapy 1/31/2016 Halaven (eribulin) Chemotherapy 8/31/2016 CMF Chemotherapy 11/1/2016 Halaven (eribulin) Chemotherapy Carboplatin (Paraplatin), Gemzar (gemcitabine)
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Jan 4, 2019 01:49PM chatsworthgirl wrote:

Maiomix, you mentioned that your current doctor would do the blood test when the time came. I am curious as to what that time would be? For myself, I figure I can find out something that might be useful now rather than waiting until everything I try has failed. I am no scientist but I can't see that there would be a difference in my genetic profile between now and then.

And yes. My doctor is an arse. I think he is one of those that has a God complex and doesn't want you telling him what to do. I am supposed to sit quietly like a good little girl and take whatever medicine he decides to give me. Please... I am so not like that and It seems to really piss him off. I believe that we have to listen to our guts and speak up. Who knows your body better than you? Intuition is a valuable tool.

Sandilee seems to have benefited from the Foundation 1 test and appears to have a doctor who is much more interested than mine in exploring whatever tool is available.

I am going forward with the test. What the hell. It will be interesting if nothing else. I intend to go on to Xeloda anyway regardless. But if that fails then I will see if there is anything in that test that I can try that might work. At this point we are just throwing spaghetti at the wall to see if something sticks. Maybe the test will show that linguine sticks better? LOL

Chats

Dx 6/6/2011, IDC, Left, 2cm, Stage IIA, Grade 2, 1/1 nodes, ER+/PR+, HER2- Surgery 7/15/2011 Lumpectomy: Left; Lymph node removal: Left, Sentinel; Mastectomy: Left, Right Chemotherapy 10/5/2011 Cytoxan (cyclophosphamide), Taxotere (docetaxel) Radiation Therapy 4/15/2012 Breast, Lymph nodes Dx 2/20/2017, ILC/IDC, 2cm, Stage IV, metastasized to bone, Grade 2, 1/1 nodes, ER+/PR+, HER2- Hormonal Therapy 2/21/2017 Femara (letrozole) Hormonal Therapy Faslodex (fulvestrant)
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Jan 4, 2019 03:34PM - edited Jan 4, 2019 03:57PM by Frisky

chats you made me laugh...your MO's attitude points to a strong sense of inferiority. Poor thing...and what if his you know what is small on top of not being loved as a child? That would explain it all....

as far as my updated genetic profile testing is concerned, it will take place when xeloda fails me, to see if I can go on herceptin, which I consider the only TX that works for years instead of months for 50% of the patients. When I proposed that I would be willing to be experimented upon, my mo didn't say no....just listened.

I'm also interested in Immunotherapy that unfortunately doesn't seem to work on breast cancer YET! But who knows maybe the researchers luck will change and they will actually come up with something that does soon. Kattysmith is currently participating in a clinical trial with an Immunotherapy drug at Md.Anderson that we all need to pay attention to. It might end up being a really fabulous T!

Meanwhile, if you have to, give X a chance...as far as I'm concerned I would stay on it for ever if I could. It's been very easy so far....I am more active now than I have been since the days of letrazole that turned me into a zombie. At times I feel like my old self again....




“Things are not always what they seem; the first appearance deceives many; the intelligence of a few perceives what has been carefully hidden.” Phaedrus Dx 3/9/2015, ILC, Left, Stage IV, metastasized to bone/liver, ER+/PR+, HER2- Hormonal Therapy 3/15/2015 Femara (letrozole) Hormonal Therapy 3/10/2017 Faslodex (fulvestrant) Targeted Therapy 3/10/2017 Ibrance (palbociclib) Surgery 4/5/2017 Radiation Therapy 4/10/2017 External: Bone Hormonal Therapy 1/5/2018 Tamoxifen pills (Nolvadex, Apo-Tamox, Tamofen, Tamone) Targeted Therapy 2/10/2018 Afinitor (everolimus) Chemotherapy 6/2/2018 Xeloda (capecitabine) Chemotherapy 7/20/2019 Doxil (doxorubicin) Chemotherapy 12/15/2019 Navelbine (vinorelbine)
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Jan 4, 2019 03:57PM chatsworthgirl wrote:

Miaomix,

I am actually looking forward to Xeloda! From what I have read the SE's are not so terrible and I might get lucky and not get too many. He is starting me out on a lower dose since I react so harshly to drugs.

Faslodex alone did nothing but make me hurt and cause my TM's to rise. Verzenio actually did something for a while. However, it was a really hard drug on me. The 150 mg was so bad I couldn't take it and had to lower to 100 mg. But I never really felt very good. I wondered if I should continue on V because we have only had two months of rising markers. My scan showed no change from previous meaning stable? But the arse wants to move me to Xeloda.

I thought you had to be HER2 positive for Herceptin to work. I would gladly do Herceptin if I can being ER/PR positive since I also have read how long it works.

I hope Xeloda is as good for me as it has been for you. I am a high energy person and the Fas and V just beat me up severely. Since I have been off everything except Xgeva, I feel like myself again. So good to eat food that tastes like it should and to not feel like I am 150 years old!

Chats

Dx 6/6/2011, IDC, Left, 2cm, Stage IIA, Grade 2, 1/1 nodes, ER+/PR+, HER2- Surgery 7/15/2011 Lumpectomy: Left; Lymph node removal: Left, Sentinel; Mastectomy: Left, Right Chemotherapy 10/5/2011 Cytoxan (cyclophosphamide), Taxotere (docetaxel) Radiation Therapy 4/15/2012 Breast, Lymph nodes Dx 2/20/2017, ILC/IDC, 2cm, Stage IV, metastasized to bone, Grade 2, 1/1 nodes, ER+/PR+, HER2- Hormonal Therapy 2/21/2017 Femara (letrozole) Hormonal Therapy Faslodex (fulvestrant)
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Jan 4, 2019 08:12PM chatsworthgirl wrote:

I have read that scans are what tells the real story. But then I read that scans lag behind TM's.

I would love to know which it is. Chicken or egg. LOL

Chats

Dx 6/6/2011, IDC, Left, 2cm, Stage IIA, Grade 2, 1/1 nodes, ER+/PR+, HER2- Surgery 7/15/2011 Lumpectomy: Left; Lymph node removal: Left, Sentinel; Mastectomy: Left, Right Chemotherapy 10/5/2011 Cytoxan (cyclophosphamide), Taxotere (docetaxel) Radiation Therapy 4/15/2012 Breast, Lymph nodes Dx 2/20/2017, ILC/IDC, 2cm, Stage IV, metastasized to bone, Grade 2, 1/1 nodes, ER+/PR+, HER2- Hormonal Therapy 2/21/2017 Femara (letrozole) Hormonal Therapy Faslodex (fulvestrant)
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Jan 5, 2019 11:40AM pajim wrote:

Chiming in here to agree that all the genomic testing is in it's infancy. Chemo sensitivity testing might or might not work, but there are very very few actionable mutations.

I've been wondering why my MO doesn't want to do a liver biopsy (I brought it up) and will ask him again but I think it's because the only actionable things they could find are PD-1 or whatever it is that apelisib works on. So it's not worth the risk to the liver.

Chat, you need a new doctor. If his reaction to you're telling him what is going on is to roll his eyes, that's not acceptable. He should be ASKING you what's going on.

Dx 4/20/2008, IDC, Right, 4cm, Stage IIIA, Grade 2, 1/15 nodes, ER+/PR+, HER2- Dx 2/1/2013, IDC, Stage IV, metastasized to bone, mets, ER+/PR+, HER2- Hormonal Therapy 2/27/2013 Femara (letrozole) Hormonal Therapy 4/22/2013 Faslodex (fulvestrant) Targeted Therapy 2/25/2016 Ibrance (palbociclib) Chemotherapy 6/19/2017 Xeloda (capecitabine) Targeted Therapy 8/15/2018 Verzenio Chemotherapy 1/2/2019 Halaven (eribulin) Chemotherapy 12/30/2019 CMF

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