Picture shows my surgeon Dr Chetty with me at a recent doctor-patient symposium
For those of you who are wondering what’s happening, I’m still waiting for a clear way forward.
I was disqualified from joining the trabectedin trial on account of having had too much prior chemotherapy. The conditions specified no more than 2 prior lines of treatment, but I’ve already had chemo 3 times.
When I first heard of trabectedin, I was told it is derived from a sea sponge and I was very excited because of my own contribution to this work years’ ago. One of my best jobs ever was diving on the reef collecting sponges to send to the National Cancer Institute in the US. My samples were screened for potential use as cancer medicines. It turns out trabectedin comes from a Caribbean tunicate, not a sponge, and now it is synthesised from fermented bacteria, to spare the natural populations.
This little story is so you can imagine how keen I was to be included in the clinical trial, and how disappointed I am to be ruled out. Boo hoo! I wanted to try that sea squirt medicine!
By lucky timing, my specialist heard last week that a trial for a different new drug is just now opening up to recruit women like me, veterans having had 3 or more chemotherapy treatments. This one is called rucaparib, it’s taken as tablets, and I think there’s about a 25% chance it might be helpful in my case.
There are many different types of ovarian cancer resulting from a variety of mutations – that’s why it is so difficult to treat. Cancer research is slowly sifting through the genetics of different types with a goal of finding a specific effective treatment for each individual.
One way to understand cancer is that damaged cells accumulate to form a tumour – cells with mutated DNA that should never have been repaired. Therefore scientists have been searching for ways to stop cancer cell repair. PARP is a repair enzyme, and recuparib is a PARP inhibitor, that stops the repair process, so those cells with horrible mutations will break down and be cleared away naturally.
Two of the ways known for repairing damaged cells are homologous recombination (HR) and PARP. There’s no point taking a PARP inhibitor if HR is functional. Fifty percent of patients are HR deficient and then a PARP inhibitor may be helpful. So I will have a tumour biopsy for genetic testing, hoping to find out that the mutations evident in my cancer tissue are of the HR deficit type.
The recuparib trial is being conducted at a different hospital (RBWH) so I will be going there for a while. I have met the doctor who will be looking after me because one of his patients is my friend and last year I went with her to an appointment when she needed a support person and note-taker. He seems to be another of these dedicated and highly respected oncologists working hard to save us.
Although it is not a huge chance for recuparib to work for me, it is worth a try because it could give me months or years with the disease under control and give my body a rest from toxic chemotherapy. Rucaparib is a targeted therapy, as also is trabectedin and farletuzumab (the trial drug I was on a couple of years’ ago). This means they directly control cancer cells, so it is a relatively mild treatment. In comparison, chemo is the “sledge hammer” approach, killing all fast-growing cells, healthy ones as well as cancer.
I don’t have dates or a timetable yet and there will be a waiting period for the biopsy results to come back from the US. I am hoping and hoping that I qualify this time! If not, then I will have chemotherapy with caelyx.
I have been very preoccupied with all this – reading, learning, hoping, grieving, coming to terms with each new possibility. I’m ok though. Thanks to you all for thinking of me and sending kind wishes! 🙂