TRIPLE POSITIVE GROUP

Kattis894

Thanks EleineTherese, I am getting Zoledronic Acid every 6 months that is suppose to also help the bones and prevent bone mets. They told me it is a fairly new drug. I have received it twice and lucky to not feel any complications such as a flew like symptom that some people seem to get a few days after the infusion. I guess Prolia might be similar but maybe given later on as the hormons slowly break down the bones? I am just glad to read there are so many different options of medication..:)

I am trying to understand the significant of having a total respons from Herceptin, something I did not have, however my tumor shrunk a lot and my Ki 65 went down as well, but not to 0%...my onc did say only about 20% of patients have a total respons and thought my cancer would be more sensitive to letrozole given it was 100% sensitive to oestrogen. Still a bit worried about this and trying to find out more.

ElaineTherese

Hmm, you're getting a biophosphonate, too. I think your drug is called Zometa or Reclast in the US. I would get Prolia if Fosamax doesn't work. Fosamax is cheaper so my insurance wants me to try that first.

PoseyGirl

Hi Kattis,

Wouldn't it be impossible to talk about response on Herceptin since it continues after surgery for awhile? Or are you meaning response to Herceptin up until surgery when they do the pathology?

I had complete response to chemo. My understanding with triple positive is that it's a favourable thing, but not as huge a prognosticator as with Her2 and triple negative subtypes. I've read a few articles where the possible explanation for this is that with our type, there is the Herceptin as well as hormonal therapy after chemo, surgery and radiation, and these things are big treatments in and of themselves. So, if someone doesn't get pcr, they still get continued Herceptin and the hormone therapy.

There is also the issue of crosstalk with our type, where being on two treatments can lead to escape pathways (don't ask me what this means), thereby leading to resistance to one of the treatments. Not sure how this plays into the pcr discussion, but apparently our subtype is still not understood as much as it will be. For instance, you can be fairly low ER positive and Her2 positive. Or strong ER and/or PR... how does this affect how each of our cancers are driven and corresponding treatment? It's all very complex. I hope much more is known soon

Others on this?

SpecialK

hapb - you may have no deleterious effect from anti-hormonals, but you should have a baseline DEXA so you know the position you are starting from. How recently was your last one done? I was osteopenic due to a total hysterectomy at 45, but stable and untreated, prior to chemo. I could not tolerate oral bisphosphonates due to reflux surgery in 1995 - tried both Boniva and Actonel. Reclast IV was not offered at that time by military hospitals, so I was out of options. I know what my baseline was because I had a DEXA the same day as the mammo and US that led to diagnosis. By the next DEXA slightly more than a year later - after chemo and Herceptin were done, and 6 months into letrozole, my density had declined. Prolia has brought me back to normal density and my oncologist has indicated that I will remain on it as long as I take an aromatase inhibitor.

Cowgirl13

I'm mainly a lurker here and remember when TonLee started this thread in 2011. I was 63 when diagnosed and my tumor was 2.6cm with 3.0cm of dcis. I had a lumpectomy, chemo was taxotere, carboplatin + herceptin, 19 rounds of radiation (Canadian protocol). Followed by 7-1/2 years of generic arimidex (Teva brand). I was so lucky that I had wonderful doctors..I found my oncologist when I went to him for a second opinion.

I had no idea how I was going to get through this when I started and I was terrified as my mother died of breast cancer when she was 56. But I did somehow and I live alone...brothers and sister just weren't in the picture, really, and they only lived 90 miles away. But what did come my way just before I was diagnosed was an older horse, Buck, who was about 25 years old. All I did was brush him and walk him and tell him he was wonderful...I just love older animals. He was with me through the whole year and then when I finished herceptin I found out that he had a very short time to live. Being that he was so old I knew it was better for him to cross the rainbow bridge. I knew I could go on without him now that I was out of the chemo/herceptin phase. It's like the universe brought him to me to go with me through all of this. And he is the horse that has meant the world to me.

My experience with arimidex was very difficult at first. I stuck with it and after 4 months things got better. It started to get better when I gave up sugar although that was probably coincidental. My advice is to try to stick with it for a while, change generic brands, and try different AI's. I do know that not everyone can tolerate it and that quality of life is everything.

So what am I rambling about...well I have wanted to share that I have been able to go off of arimidex (generic). During my last visit with my oncologist he suggested that we discuss my going off arimidex....he said that for me, there was no difference between 7.5 years and 10 years. I couldn't believe it...it was as if the barn door flew open. I feel like my old self again...the worry and anxiety have lessened tremendously and I am looking forward to the future. So whey did I wait to share this? Because I had great concern if I shared this it might scare those of you who are just starting.

My plan when I started was to throw the book at this because if I hadn't and a recurrence happened it would make me feel terrible.

So you will get through this and I think it is wonderful that you are able (on this thread) to honestly share when you are scared and frightened and have good times.

You are all in my thoughts and I give kudos to Special K.

Elizabeth

here's a pic of Buck (sorry it is so big)

kae_md99

SpecialK,

i was offered either prolia or reclast. i am leaning towards prolia because it is given every 6 months whereas reclast is once a year.i figured if i had side effects,then i could stop at the 6 month whereas with reclast i am afraid of side effects for the whole year. any thoughts? anyone here on reclast

kae_md99

cowgirl,

thanks for sharing your story!God bless you...also Specialk, thanks for sticking aroung for us..

SpecialK

cowgirl - hey! Good to "see" you here, and Buck's sweet face - yes, the universe brought him to you when you most needed him. Not only does your post bring hope to these ladies who are currently in the trenches, it also provides living testimony that we recover from treatment and go on to live our lives. I am with you on the sugar thing - it has made a difference in my level of joint pain, eliminating it has allowed me to stay on letrozole up to this point.

kae - I prefer Prolia because I like its mechanism better. Bisphosphonates coat the bone making it somewhat less elastic, while Prolia, a monoclonal antibody like Herceptin, slows down the old bone removal process and allows the new bone creation process to catch up. The side effects for both drugs only last for a few days after infusion or injection, if you even experience them.

kae_md99

thanks specialK!

moodyblues

Cowgirl.  Your post was so uplifting to me.  Thank you for sharing your story about your beloved Buck and for posting his picture as well.  What a smile it has brought to my face.  

Melanie

Kattis894

Such a lovely story and love the picture of you pal Buck..I love animals too and believe their intuition is something to listen too...Oh I guess perhaps the drug I am getting is called Zometa, I will change my profile. I find the profile very helpful as I move forward almost forgetting what has happened to me I can go back to it. There is so much I just do not understand but I guess science doesn´t either. I would think CpR would be an important factor but perhaps not. The status of the cancer can also change over time so this sneaky illness has the ability to change form to take you over as well. How I wish they knew and find a cure for all this. It seems like such a lottery, some make it some do not. No rime or reason why. Living in this limbo is just so difficult. Family just can not take the uncertainty and just want to sweep it all under the carpet so feeling alone with all of this. Thank you for being here ladys.

Cherry-sw

Cowgirl, thank you for sharing your story and posting the picture of Buck. You are such an inspiration, good luck to you.

Cherry-sw

Posey, I am also interested to know more about the crosstalk and how two treatments can lead to escape pathways.

SpecialK, I believe you mentioned it before or whether I was trying to ask you because I heard of it. Any information you have on this topic?

coachvicky

CowGirl13,

Thanks you for sharing your story. I have hope after reading your journey.

I have colleagues that have horses in their coaching businesses. They share that a horse always knows an authentic person. You had a gem in Buck

Vicky

SpecialK

Cross-talk has to do with eventual resistance to anti-hormonal therapies, predominantly Tamoxifen, caused by the interaction between Her2+ and ER+. Herceptin resistance can also occur, but this is usually a factor in more advanced and/or metastatic cases where Herceptin is used for a longer period (beyond the additional doses that make up the year of Herceptin) as a single agent, and can happen in a smaller number of cases of earlier stage cancer that goes on to become metastatic despite the use of available therapies. Why this happens, when this happens, and for whom this happens is very complex and I don't believe currently there is any way to predict this in the average early stage patient. Some studies have shown increased benefit in using aromatase inhibitors to treat the ER+ aspect, as this class of drugs seems to be more effective for Her2+ patients who are also ER+.

Cherry-sw

SpecialK, does it mean that usage of Herceptin weakens the effect of Tamoxifen during the first year? Does it mean that the cross-talk occurs only during the first year when Herceptin and Tamoxifen are given simultaneously? When they say that Herceptin finds the cell, binds the HER2 receptors and either signals for immune system to kill the cell or starves it to death on its own, what time frame are we talking about? And if I am 80% ER, 60% PR does it mean that I have 20% of ER negative cells and 40% of PR negative cells? What are they then? ER/PR-Her2+?

About whether the meds are working or not this is exactly the same answer I got from all four oncologists I met, one of them is holding educational lectures about Her2, I saw it after our appointment though. After the surgery there is no way to determine whether the meds are working or not it is just wait and see, which I had such a hard time to accept. I asked her whether it is possible to see if the excised tumor reacts for the treatment and she said that there was lots of attempts to test this way but however there are no conclusive results basically meaning that the tumor when excised do not behave the same way anymore. All four though claimed that the majority of early stagers are over-treated and receiving this aggressive treatment because the doctors aim to eliminate the bc. Then if it is coming back and why nobody knows.

PoseyGirl

Hi Cowgirl, thank you for jumping back into the forum and for offering your positive voice; you totally know from personal experience how it helps. Your story of Buck and yourself is so special; look at that lovely face. He was definitely your angel sent to you .

SpecialK, thanks for explaining this further. As my oncologist didn't seem to offer any confident kind of recommendation regarding hormonal therapy (and I was 47 when diagnosed, so heavily into perimenopause when all this happened), I read a bit and came to the conclusion that for me and my age and subtype, AI was the route to go (I too read that AI seemed to be more powerful). And, like you say, things are still so complex or not yet understood. I believe 100% that they WILL be understood. What we see as no rhyme nor reason probably does come down to reason. Just reason we don't yet understand.

Here are a couple links I alluded to before which I find interesting and somewhat inspiring in the sense that it makes me think that they (the research community) is working hard at drilling things down much further to understand more and therefore treat better, and ultimately - to cure.

First, Cowgirl, I just saw this and it's perfect timing with your post

http://www.express.co.uk/life-style/health/856461/...

So this is for triple negative women, but here is something they are working on:

http://www.dailymail.co.uk/health/article-4911682/...

This Boston Glob article speaks to the history, present and future of breast cancer research. It sort of touches on what I was talking about in an earlier post about how innovation will become exponential in BC research:

http://sponsored.bostonglobe.com/american-cancer-s...https://www.economist.com/news/leaders/21728893-science-will-win-technical-battle-against-cancer-only-half-fight-closing

SpecialK

No, it is not the Herceptin, it is the Her2+ itself. It is the communication between the ER+ and Her+ that makes the medications less effective not the medications themselves, but this is not universal - otherwise we would all eventually succumb to the cancer, which does not happen. Also, tumors are not homogenous - some parts of tumors may contain more ER/PR receptors, or Her2 overexpression, than other parts. Your percentages of receptors and amount of Her2 overexpression is listed based on the slide that was looked at under the microscope, and in your case there was enough to deem you "positive" for both ER and Her2. 10 different slides might contain differing numbers of receptors or levels of Her2, but you would still be considered positive based on enough slides that did. Determining degree of each is the only current way to know whether certain therapies are appropriate - in other words, are you Her2+ and are you ER+ and should we administer these known medications that are beneficial for the majority with these known attributes.

Cherry-sw

Thank you SpecialK, I understand that this is about Her2 and ER but this cross-talk does it mean that the meds will be less effective?

What I am still trying to understand is a time frame for the Herceptin and Tamoxifen working. The tumors are heterogeneous, some cells are ER+ some PR+, the same about Her2, some of them have over-expression and some of them do not. When they start the systemic treatment Herceptin is working on binding Her2 meanwhile chemo kills all dividing cells. Anything that is left is suppressed by Tamoxifen. Those cells that had no ER/PR+ or Her2, hopefully chemo kills them. If the tumor comes back soon it means Herceptin and chemo failed to do their job, if it comes back later it means the hormonal suppression did not work.

Herceptin is given during the first year and if it is successful it has to kill all the cells with Her2, hasn't it? Because if it does't then it is exactly as you said we all have to succumb to cancer. If any Her2 is left after Herceptin then it will come back or?

Sorry if I am asking stupid questions, I am just trying to understand.

SpecialK

cherry - yes, it can mean that but I believe it is more the case of the Her2+ aspect potentially making endocrine medicines less effective. Herceptin, usually if taken long term by more advanced cases of Her2+ breast cancer, becoming less effective due to resistance, but I am not sure this is as connected to the ER aspect. So this is actually two separate issues. Of course, there are also early stage patients for whom neither medicine works, or one or the other, for whatever reason progress. Your example, if I am understanding you correctly, is that Herceptin is working on some cells and anti-hormonals working on others. The problem is that Her2+ and ER+ exist on the same cells - it may not be an either/or problem. None of us knows which aspect, the Her2+ or the ER+, is driving the proliferation of our cancer - so we can't assume which treatment is controlling it, and controlling it in which timeframe. Also, chemo is thought to be less effective on highly ER+ cancers, so I am not sure there is any way to know which cells, or aspects of cells, the chemotherapeutic agents are killing. Generally Her2+ cancers, if they are going to recur, come back within the first couple of years, and a later recurrence is driven more by ER+, however there are those patients who recur later who are still Her2+, so there is a lot we don't yet know about this.

Kattis894

Thank you Special K for this explanation. My onc did tell me that even though I was not CpR most likely the letrozol will take care of the rest considering being 100% ER+. Interesting to know chemo might be less effective for me. The doctor seem to think the Ki65 percentage is a more valuable tool, not completely sure why, but understand it is a measurement how fast the cells are dividing. I wish it was 0% but understand 6% is considered very low, I was 30% before operation so it went down a lot.

T-Sue

Catching up after a few days offline; I'd like to jump in on the anxiety question Cherry posed.

First, Cherry, I'm so glad you sought help with your therapist. Your medical team is there to support you! The low dose antidepressant made a world of difference for me. I don't see it as a failure at all, it allows me to be calmer and more like myself.

During chemo I found relief from going on daily walks - the sunshine and movement have magical properties. Now that chemo is finished, I'm also back to cooking which I really enjoy. Great to hear how others manage their anxiety. Hope you find something that works for you!

Cherry-sw

Thank you SpecialK, you are right and even Her2 positive cancer still can recur years later. But why do highly ER positive cancers are not receptive to chemo? I thought that high cell proliferation and grade and high Ki67 is a given for chemo, because it is only effective on dividing cells. I even red in an scientific article about how Taxol works that it can get into a dormant cell and wait there for days meanwhile the rest of it is washed out of the system. When the cell starts dividing it damages its DNA and it can no longer replicate itself properly. I mean I am both ER+ and have high Ki67, the latter does actually bother me a lot.

Lita19901

SpecialK - from recent studies I've been reading, HER2+ BC is too heterogeneous to say that they normally recur in two years. That may be true when all HER2+ BC are grouped together but not true for some of the subtypes of HER2+ BC. Granted, as you say, it is impossible to know your subtype precisely, at least not at this moment in time, and that there are exceptions is a given.

It's frustrating to know that data is out there from major studies but is not being tapped into. For example, results from the HERA trial was published in 2005. It wasn't until 2016 - 11 years later - that data was pulled from the HERA trial that showed a difference in response to Herceptin based on HER2 ratio and ER positivity. Had this been considered at the time we might now be in a very different place in BC treatment. All that would have been involved was a re-sort of a spread sheet.

Cherry-sw

T-Sue, thank you for your concern, I really appreciate it. This is my fourth day on this medication and I am also taking an anti-anxiety drug with it. It is too soon to tell but I hope I will feel better compared to the mess I was last week. I really wanted to be able to handle it myself but I couldn't obviously. I am grateful for this forum, because it definitely did not fell as a failure when I know that I am not alone who ended up with anti-depressive.

I am also trying to go for a walk almost every day and I have always been into cooking. In case anyone is interested in sharing of their favorite recipe it will be a nice intermezzo. Not that we cannot find a topic to discuss, this group has most interesting discussions. I am also following So whats for dinner.

I never tried to make a real chili except for chili con carne variation where you basically add beans to a ragu bolognese, but a real spicy chili you in US eat in a cup like a thick soup. I would like to try one, vegetarian, with meat or chicken.

Cherry-sw

Lita 19901, HERA trial that showed a difference in response to Herceptin based on HER2 ratio and ER positivity? Is it what we discussed a couple of weeks ago that high over-expression of Her2 responds better to Herceptin meanwhile ER+ respond less?

Lita19901

Cherry, yes, the same study, but it is the *combination* of the ER+ and low HER 2 ratio factors that applies here rather than individual factors.

Here's the link:

http://www.breastcancer.org/research-news/her2-pos-bc-no-herceptin-response

I had an interesting conversation with a doctor who is doing HER2+ research about this. His take is that, based on this and some of their ongoing internal studies, it is possible that the reason this combo isn't responding to Herceptin is because it's not needed - because they're not really HER2 positive. It's a long shot at this point but still interesting.

Kattis894

Cherry, your K65 percentage might also go down a lot during treatment as mine did so perhaps not something you need to worry about at this stage just going threw treatment...

Cherry-sw

Kattis, I have adjuvant treatment, they have removed the tumor, so there is no way to know. My question to the oncologist was whether the cells when and if they break free and travel have the same Ki67 as they have in tumor? She asked me what I was working with, when I said procurement she looked a bit puzzled.

SpecialK

cherry - I think you are assuming in your question that high grade, high Ki67% is specifically linked to level of ER+, but I don't know if that analogy can be made. You can have a highly ER+ tumor that is still low grade and has a low Ki67%, and will respond well to anti-hormonal therapy but maybe not chemo, such as Luminal A breast cancers. It is certainly not universal that all highly ER+ tumors respond poorly to chemo, but in our cases as triple positives it is difficult to now which aspect of systemic treatment keeps us recurrence free. Most ER- tumors are high grade and have a high Ki67%, so they would not fit the analogy that these features follow ER positivity, as an absolute. As per the conversation above, it may be the Her2+ aspect of your cancer that was driving the grade and Ki67% - there is no way to know.

Here is a graphic that shows some study info on recurrence rates by arrangement of hormonal receptors and Her2 status:

http://www.medscape.com/viewarticle/859934?pa=vVpAV%2BBOaQiuVJ3R1aeqxcVPrJLciLH0eKhebhYg9MhFuz1TBEc9bkLaAcgp4wrgNFsYxDuz%2Fz2hge3aAwEFsw%3D%3D

lita - do you have the link for what you are seeing in studies on Her2+ recurrence? Also, I am curious about the HERA info you mentioned - my understanding of HERA was it was looking at length of time on Herceptin - 1 year or 2, was it further quantified beyond that to include information regarding other parameters?

Edited to add - lita, I now see the HERA link above, missed it! Thanks!