I was initially diagnosed with non small cell lung cancer in April of 2005. My tumor was large (5 centimeters); a poor prognosticator. However, it had not spread beyond my lungs and I was staged at IB. One week after diagnosis I had the lower lobe of my left lung removed. As I was recovering from surgery my new oncologist introduced himself; Dr. Tom Lynch. I had no idea back then, but I was incredibly fortunate to have Tom select me as a patient. The reason behind his coming to me rather than the other way around? As a young (age 45) non smoking woman, I fit the profile of someone who might be EGFR+ and Tom was an early innovator in the investigation and treatment of EGFR+ patients.
I tested negative for an EGFR mutation but in the process acquired arguably one of the best oncologists in the world; someone who was always forward thinking and cutting edge in his approach to treatment. In fact, I was offered a chance to enroll in my first clinical trial soon after surgery. Because of the size of my tumor, adjuvant chemo was indicated and a trial that would include the addition of avastin was proposed. I was having a difficult time even being convinced to have chemotherapy (Tom was adamant) and I couldn’t wrap my head around the possibility of also being a medical research subject. As it turned out I would not have been a good candidate anyway–I am a bit of a bleeder and I was coughing up blood for weeks post lobectomy (there is a small but significant increased risk of serious pulmonary hemorrhage secondary to avastin).
Fast forward to September of 2008, two months after I’d been restaged to IV and advised that I likely only had three to four months to live. At my scan review after two months of tarceva–tried as a last ditch effort even though I was EGFR-, there was nothing but bad news from the radiologist. However Tom shared that a sample of my biopsy had been submitted for further genetic screening and had come back positive for an EML4-ALK translocation (another example of how ahead of the pack he was—the ALK mutation had been identified as a driver in NSCLC only months prior to that).
As we discussed the significance of this finding we also reviewed my options going forward. The way Tom saw it, there were four possible scenarios. I could stay on tarceva, return to traditional chemotherapy, do nothing (that option only underscored how serious my situation was) or attempt to enroll in a phase I clinical trial that targeted ALK mutations such as the one that was driving my cancer.
Would you believe me if I said I never hesitated but instead leapt at the opportunity to be in a clinical trial? Why now but not back in 2005?
This image of my scan says it all. The upper lobe of my left lung was now almost completely clouded with consolidated ground glass tumors which had spread to my right upper lobe. And I had been told that I might have three to four months to live two months ago. The math was easy—I had almost run out of time and out of the four options I’d been provided with, only one seemed to offer a glimmer of hope.
And glimmer is the operative word. There was no precedent for me back then—no reason to believe that this trial might actually prove effective. All Tom could offer me was the fact that I had been preceded by one other participant at MGH. ALK+ like me but so debilitated by disease that they were confined to a wheelchair. Their initial response had been extremely encouraging, to the point where the wheelchair was temporarily abandoned. But then they had died, in part due to the toxic effects of the trial drug on their liver.
So this is what I knew. One before me with a promising response who had succumbed both to disease and to the toxic effects of therapy. That the experimental therapy could in fact prove fatal to me as well. But that my cancer would certainly kill me if I did nothing. An easy choice, after all.
And so, on October 1 of 2008 I had my lead in dose of the drug that would eventually be known as Xalkori.
life and breath: outliving lung cancer 