Hi all, after a scan last week I was disappointed to see that 3 months of Piqray has had mixed results (3 spots grew, 1 shrank, 4 stayed the same). I want to stay on oral medications as long as possible before having to go the IV route, so my doctor is giving me a short-term extension on Piqray and we’ll scan again in 8 weeks. We’re testing to see if I’m qualified to take Orserdu, and if so that will be my last oral option. So the IV’s are coming sooner or later. I’m burning through all these treatment options way faster than I’d like :-(.
It makes me feel like my life expectancy may end up being shorter than I’d hoped. Maybe 3-5 more years? Does anyone else have these thoughts? It’s so impossible to predict, given potential new treatments and the uniqueness of each case. But I’m moving down the road faster than I had hoped.
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Mixed results isn’t bad. I’ve had similar results with Piqray. First scan showed good progress, next one had some new Mets which we zapped with cyberknife, next one after that showed many brighter, rest stable but no new ones. My oncologist wants to keep me on it as long as possible. Ibrance didn’t work for me; I was bummed because so many people are on it for years, I also felt like I lost several years.
But we must not think about life expectancy numbers. I totally ignore that. There are new drugs all the time!
A big development is that Enhertu seems to be good for Estrogen +, not just Her2. Enhertu is an Antibody Drug Conjugate. It carries chemo to targeted cells.
To me it sounds like you are stable so try not to worry and enjoy the present.
They used cyberknife on three mets on my spine. The process is to locate the exact position of the lesion using ctscan and using that info to direct zillions of rays from different directions at the lesion. The radiation from each ray is very small but they all meet at the lesion and after a while destroy the cancer cells. It’s used when you have a relatively small number of mets.
Yes, I have those thoughts. I am lucky in that my cancer is indolent and the first two treatments worked wonders, from a huge tumor and many mets (in pleura and bones) to NEAD. I am asymptomatic -- wouldn't know I have cancer except for scans. That is on the plus side.
What worries me, really, is that I am moving through treatments so fast. Onc has no idea why I keep developing resistance after a great response. -- Although the last one didn't work that well and failed before 1 year on it.
So--- I am thinking about how far I will want to go with the harsher treatments, and annoyed (maybe I mean scared) that, despite my general good health and lack of symptoms, my life span is going to be shortened by my tendency or my cancer's tendency to override any effective treatment.
Has your oncologist offered any explanation? Mine just says, "mutation." Like the cancer keeps mutating. Another doctor said mutations happen all the time, they are random, just some of them take off.
I don't have any mutations, though. At least, none that dictate a particular treatment.
Dana Farber and others say that resistance can come from other sources, not mutation. That is why a treatment can stop working, then, after a "vacation," start working again. My oncologist doesn't buy that.
Obviously, for us, resistance is the problem. There was a paper on that at ASOC in the past few years. I need to look it up again. One of the articles I found on causes of resistance was really technical and over my head.
Just looked again. Astra Zeneca is promoting one cause (AKT) and solution (I think it is for PIQ3, though). Another focuses on nanotherapies and delivery systems of chemotherapies...The discouraging summary is below. Apparently, the development of resistance is attributable to the treatments themselves (like CDK4/6 inhibitors). I will probably keep looking, now that you have sent me down this path, and will pm you if I find anything.
"Mechanisms of drug resistance in cancer are very complex. Molecular amendments, tumor microenvironment (hypoxic conditions leading to vascularization), and genetic rewriting are chief architects to cellular repair mechanisms, such as activation of DNA repair, mutant p53, impaired apoptosis, and so on. From pharmaceutical stand points, drug bioavailability at therapeutic concentrations in the target cancer cells is the major impediment of chemotherapy. Despite many recent discoveries on therapeutic interventions, cancer chemotherapy represents the most common treatment modalities for the disease. Successful treatment modalities impose three to four drugs at once. Patients in early stage of cancer respond, but due to MDR, cancer cells adapt treatment resistance and cause a relapse by overpowering therapy [319,320,321,322]. As a result of high and complex dosing regimens with multiple drugs, high toxicity is caused and many treatments fail. Hopefully, current trends on targeted nano-therapeutics may overcome some of these inadequacies and advent successful breast cancer therapy."
Man, I am so sorry to hear this. I wish you the beat of luck. Im early diagnosed and am already matastisis with Ibrance. So I'm waiting to get to Mayo Clinic. 3 weeks right now without anything. Freefalling. I feel you, My friend. 53. 10 year old special needs child who really needs me around
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:-(. 
Piqray 
Nervous about Fulvestrant and Piqray treatment
Anyone heard of Piqray?
Scan results mixed 😢
Scan results after 11 months of Fulvestrant and Ibrance-75
