Topic: Abemaciclib Verzenio for Stage IV

Forum: Stage IV/Metastatic Breast Cancer ONLY — 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 03:03AM - edited Jun 17, 2018 09:19PM by zarovka

Posted on: Jan 1, 2018 03:03AM - edited Jun 17, 2018 09:19PM 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.

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.

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).

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.

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.

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.

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).

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.

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.

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.

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.


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.

Abemaciclib continues to be available through Lilly's attractive Expanded Access Program (EAP):
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.


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.

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 1/16/2016 Femara (letrozole) Targeted Therapy 2/2/2016 Ibrance (palbociclib)
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Jan 5, 2019 08:37PM Chemokaze wrote:

Saw med/onc yesterday. Going to try lower dose Verzenio (100mg twice a day). She suggested to try Ibrance since it does not have GI side effects, but I was reluctant, mostly because I just didn’t want to change meds and I am concerned about neutopenia and thrombocytopenia. I appreciate that Verzenio crosses the blood brain barrier. I asked if a lower dose of Verzenio is less effective and she said it was not. PET scan next week, so fingers crossed for no surprises.

Good luck Chats...sounds like it’s time for a change

Pajim - Did your treatment plan change

10/2018: NEAD; 7/2018: Onward to Verzenio, Zometa, Faslodex, & CyberKnife to single met to L4 spine. Dx 9/1996, IDC, Left, Stage IB, Grade 3, 0/21 nodes, ER+/PR+ Dx 5/2016, IDC, Right, Stage IIIC, Grade 2, 14/21 nodes, ER+/PR+, HER2- Dx 6/2018, Stage IV, metastasized to bone
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Jan 7, 2019 03:42PM chatsworthgirl wrote:

Well, I got my TM's today. Not good. CA 27 right back up to 740. Alk Phos at 91. Ast at 63, well above the high normal but Alt is still low at 19.9 but higher than last test.

I did read that Verzenio can cause liver damage. I am so disappointed. I was hoping for at least stable or small increase but this is a big jump from 417 to 740. Pretty bummed right now.

My WBC is 2.7 I know that the granules were low at 1.7 and the onc wants to recheck this Wednesday to see if my WBC has come up so that I can start Xeloda.

As a side issue I have had some really weird and very bad muscle and joint pain all over my body. I have no idea what this all means. So scared that the beast is spreading.


Dx 6/6/2011, IDC, Left, 2cm, Stage IIA, Grade 2, 1/1 nodes, ER+/PR+, HER2- Surgery 7/14/2011 Lumpectomy: Left; Lymph node removal: Left, Sentinel; Mastectomy: Left, Right Chemotherapy 10/4/2011 Cytoxan (cyclophosphamide), Taxotere (docetaxel) Radiation Therapy 4/14/2012 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 7, 2019 04:09PM - edited Jan 7, 2019 04:23PM by Frisky

chats, if you recall....cancer markers do not offer a very reliable view of what could be happening...of course we all rather see low numbers. Hopefully xeloda will smack them right down.

In my case the markers have stayed the same after 6 months on X, BUT I feel better than ever, I can accomplish a lot more every day and that makes me very happy....

After x initially brought my normal liver markers all the way up, I disobeyed my MO and started taking NAC and other antioxidants and anti inflammatories that brought them back to normal and so far so good...according to my last pet scan...I treat random aches and pains with magnesium oil massaged into the affected areas.

The x is fast acting, it goes around killing fast dividing cells, good and bad, for only two hours after you take I figured for myself that by lunch time it's safe to start repairing the damage that it wreaks on my precious organs...I figured I don't have much to lose since sooner or later it will stop working, and much to gain by protecting what's still working, but it's a gamble

“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 3/14/2015 Femara (letrozole) Hormonal Therapy 3/9/2017 Faslodex (fulvestrant) Targeted Therapy 3/9/2017 Ibrance (palbociclib) Surgery 4/4/2017 Radiation Therapy 4/9/2017 External: Bone Hormonal Therapy 1/4/2018 Tamoxifen pills (Nolvadex, Apo-Tamox, Tamofen, Tamone) Targeted Therapy 2/9/2018 Afinitor (everolimus) Chemotherapy 6/1/2018 Xeloda (capecitabine) Chemotherapy 7/19/2019 Doxil (liposomal doxorubicin) Chemotherapy 12/14/2019 Navelbine (vinorelbine)
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Jan 7, 2019 05:31PM - edited Jan 7, 2019 05:32PM by luce

i would strongly advise against pausing verzenio due to side effects. reduce dose instead. verzenio causes false senesense in cancer cells (true senescence is permanent), meaning cells rapidly cyle again once the drug is withdrawn. and its half life is no more than 14 hours (it may be as short as 7; used to know exactly how long but can't be bothered to look it up now). this has been shown in studies and in my personal experience when pausing it for three days when i was fasting. after those three days, my cancer markers went up, and they have been merely stable, never dropping again since. i think pausing verzenio is risky. i also think continuous dosing is what gives verzenio the edge over other cdk4/6 inhibitors. i think pausing helps cancer cells rebound and adapt.

Dx 12/12/2016, ILC/IDC, Left, Stage IV, metastasized to bone/lungs/other, Grade 2, 0/3 nodes, ER+/PR+, HER2-
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Jan 7, 2019 06:05PM chatsworthgirl wrote:


Well my liver markers have been pretty good except now I am seeing a rise in the AST. I read that one of the side effects of V is liver damage. So who knows. I do have a spot on a part of my liver that according to the last scan is mets. I have read that X does kill the liver buggers so here's hoping.


My numbers were rising prior to the break . It was my incessant diarrhea that the onc thought I should break for. According to the V website, it is sometimes necessary to break when the toxicity is too much and to resume at a lower dose.

Faslodex by itself did nothing but make the TMs rise fast. When V was added I got a good response for 5 months and then the numbers started to creep up. So the combo did work for a while but starting in October the numbers rose and I didn't break until December.

At this point I think moving on to X is the best option. I have asked and am getting the Foundation 1 test. It will be interesting to see what it has to report.

I still can't get a definitive answer regarding TM's v. scans. I have searched. My last scan on November 21 showed no change but the TMs on December 5 showed a rise from the previous TM from 330 to 417.

My Pollyanna self would like to believe that the scans tell the true story and the TMs do not. But when my TMs rose before the scan showed progression. The scary thing is that if this is progression it has happened very quickly. Do I have an aggressive cancer now? as opposed to the "indolent" one I had when I was first diagnosed in 2011?

Not a happy camper right now.


Dx 6/6/2011, IDC, Left, 2cm, Stage IIA, Grade 2, 1/1 nodes, ER+/PR+, HER2- Surgery 7/14/2011 Lumpectomy: Left; Lymph node removal: Left, Sentinel; Mastectomy: Left, Right Chemotherapy 10/4/2011 Cytoxan (cyclophosphamide), Taxotere (docetaxel) Radiation Therapy 4/14/2012 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 8, 2019 01:50PM luce wrote:

yes, my advice to not pause is not in the insert. i am reporting my gut feeling, experience, and further research about that.also, early on (when side effects seem to be strongest) rebound and adaptation and resistance may still be lesser dangers, so pausing may be less risky.

Dx 12/12/2016, ILC/IDC, Left, Stage IV, metastasized to bone/lungs/other, Grade 2, 0/3 nodes, ER+/PR+, HER2-
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Jan 8, 2019 06:47PM Chemokaze wrote:

I’m thrilled to report NEAD after my PET scan today

10/2018: NEAD; 7/2018: Onward to Verzenio, Zometa, Faslodex, & CyberKnife to single met to L4 spine. Dx 9/1996, IDC, Left, Stage IB, Grade 3, 0/21 nodes, ER+/PR+ Dx 5/2016, IDC, Right, Stage IIIC, Grade 2, 14/21 nodes, ER+/PR+, HER2- Dx 6/2018, Stage IV, metastasized to bone
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Jan 8, 2019 09:25PM - edited Jan 8, 2019 09:27PM by vlnrph

Yay for chemokaze's no evidence of active disease! I'm a few months behind you on a similar regimen (with Verzenio at 100mg twice a day due to GI effects). With the dose decrease and an additional pause in therapy while having radiation, I'm thinking my first follow-up PET scan might not be until early March.

I started with the 27.29 tumor marker which was at 120 upon diagnosis then 125 a couple weeks later. The lab now reports CA 15-3 which is apparently another way of measuring the same thing. It's been stable...

My RO, a research oriented MD PhD but also very caring, called colleagues at other institutions when deciding whether or not to have me hold the abemaciclib while she zapped me over Thanksgiving. With a delayed start to the 5 treatments, my break stretched into 10 days. There is a study going on with Ibrance to try and resolve the question but they get a prescribed week off anyway. Luce has an interesting perspective on the issue.

original diagnosis included a 2nd tumor - IDC in a different quadrant; bone mets 8/2018: Zometa (stopped after 3 years due to tooth extraction), Faslodex, Verzenio; numerous liver mets 11/2022 Dx 3/7/2011, ILC, 2cm, Stage IIA, Grade 2, 1/25 nodes, ER+/PR+, HER2-
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Jan 10, 2019 10:45AM NouzayO wrote:

hello ladies!

Hope you all had a wonderful Christmas and a happy New Years! I wanted to update you on the most recent news. Unfortunately I will be leaving Verzenio and moving on .. I don’t have a ton of treatment options I think and ready wished Verzenio would last longer and be effective for some double digits months but it is what it is.

After my Y90 my scans showed bone cancer more active but the report never stated exactly how much. Against a couple of MO’s advice I decided to stick with Verzenio a little longer on the basis that I haven’t been taking it regularly during the month of recovery from Y90.

I did take it religiously for two months 150 at night and 100 in the am. The first month the tumor markers stayed stable and I took it as a good sign. I had my scans right before Christmas and it came back showing again « more bone activity » but also a few new liver mets!!!! In just one short month and my tumor markers rose by 30 points. I’m so bummed right now because that means that all the Y90 suffering was for nothing and may have to go through all this again if my next treatment didn’t work.

I’m trying Lynparza next even thiugh I only have a somatic mutation not a genetic one. I was also offered Afinitor but the comments on that thread have been very discouraging. I also have Halaven as an option but aside from trying to avoid IV chemos at the moment I’m trying to save it when liver mets are a lot more because then I’ll need something that can act fast.

Hopefully I made the right choice and can live with the new side effects.

Good luck to you all .. hopefully you are luckier than I am

Dx 9/15/2016, DCIS/IDC, Right, 1cm, Stage IV, metastasized to bone/liver, ER+/PR+, HER2-, Hormonal Therapy 10/1/2016 Femara (letrozole) Targeted Therapy 10/14/2016 Ibrance (palbociclib) Chemotherapy 3/31/2017 Abraxane (albumin-bound or nab-paclitaxel) Chemotherapy 12/8/2017 Xeloda (capecitabine) Chemotherapy 2/13/2018 Doxil (liposomal doxorubicin) Targeted Therapy 5/13/2018 Verzenio Hormonal Therapy 5/15/2018 Faslodex (fulvestrant) Targeted Therapy 1/11/2019 Lynparza
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Jan 12, 2019 02:51PM SchnauzerMom wrote:

I would be interested to hear from anyone taking 200 mg Verzenio as mono therapy. How has that been for you? Side effects? How are you feeling?

I started with 200 mg in July, but after 2 weeks was dropped to 150 because of neutropenia. I remember having an infection and being very tired (lots of diarrhea) on the higher dose. My tumor markers have been dropping, and blood work has been good, so my oncologist "promoted" me back to 200 mg last week. I've had a UTI this week, and just feel weak and crummy. PET scan next Wednesday. Just hoping to get some energy back.

mets to liver, bones Dx 11/21/1987, ILC, <1cm, Stage I, ER+/PR+, HER2- Dx 12/11/1989, ILC, Stage IIIA, mets, ER+/PR+, HER2- Chemotherapy 1/9/1990 CMF Hormonal Therapy 7/30/2012 Faslodex (fulvestrant) Hormonal Therapy 7/30/2012 Femara (letrozole) Dx 7/31/2012, ILC, Stage IV, mets, ER+/PR+ Targeted Therapy 1/14/2013 Avastin (bevacizumab) Chemotherapy 1/14/2013 Taxol (paclitaxel) Chemotherapy 11/9/2013 Abraxane (albumin-bound or nab-paclitaxel) Chemotherapy 4/1/2014 Navelbine (vinorelbine) Hormonal Therapy 7/21/2014 Aromasin (exemestane) Targeted Therapy 7/22/2014 Afinitor (everolimus) Chemotherapy 11/12/2014 Doxil (liposomal doxorubicin) Chemotherapy 7/12/2016 Xeloda (capecitabine) Chemotherapy 12/2/2016 Halaven (eribulin) Hormonal Therapy 5/31/2017 Tamoxifen pills (Nolvadex, Apo-Tamox, Tamofen, Tamone) Targeted Therapy 7/17/2018 Verzenio

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