The Longest Run

Cancer was not new to me. I first confronted it when I was 26 and it was melanoma. In February 1983 I had no idea what the word melanoma meant other than anything ending with “oma” was not good. Well, I managed to survive that encounter. It led to leaving the Navy and starting a second career. Speed ahead to 2010 and I have a 2nd melanoma found. Was I a bit complacent after 26 years? Sure, but I charged ahead and thought that my surgeon had gotten ahead of things. Well, this time, cancer decided to take a different path, just like going on a run. And once again like 1984, I had to find that path to get ahead and defeat the melanoma cancer cells.

It was just prior to the 2014 Boston Marathon and I felt a hard marble-like ball in my left upper shoulder. It was just above the surgical site of my 2010 melanoma excision. My mind raced. Could the cancer have spread to an unknown or unforeseen lymph node? In 2010, I had surgery to excise the area around the site of the melanoma lesion. It was not pretty. In fact later that summer, my then-5year old nephew saw me and asked what happened to my arm? I said shark bite. It made him step back in awe. Not me. I knew that the surgery was the best step at the time to get ahead. One aspect of that surgery was to inject nuclear dye at the original cancer site and see where it would go inside my lymphatic system. This procedure is called the “sentinel node”. In my case, the melanoma cells followed a less traveled path. On that day, I was both anxious and pissed. I had not been vigilant checking all areas around my left shoulder, yet I was told that I was free and clear. I had no scheduled visits to see the surgical oncologist or an oncologist. That was a medical mistake and that’s what angered me that day in 2014. All I was thinking is could we stay ahead. [Just like running a race, you want to stay ahead of your competitors to win; in cancer’s case the race to win is critical to beating cancer]. I went in for surgery and had my entire left armpit lymph nodes removed. All the nodes were negative, good news. The one piece of news that jarred me came from the radiology oncologist. He said that while the other nodes were negative, the primary node that was positive (cancer) had broken through its wall lining. Now I was fighting the odds of staying ahead of cancer cells’ moves.

I was on the way to the PENN RELAYS in late April 2015, one week after the Boston Marathon weekend. I got a call from the radiology lab where I had gone for a CT. Something was small yet visible on my liver. Now my heart was racing. I call my oncologist and we talked about possibilities. It could be a non-lesion or it could be a metastasized melanoma lesion. It was the latter. My path ahead was not full of roses. I did not hear many great outcomes. This is when I called out for help. My friend Bill and wife Debbie went to work and started researching the advancements that were occurring in fighting advanced melanoma [I did not like using the term Stage for where I was clinically with cancer]. All I was hearing from my then-oncologist was a shot to see if I was genetically pre-disposed for a type of mutated gene – the BRAF gene. It turns out that about half of melanoma patients are BRAF positive, meaning they have the mutated BRAF gene. A new immunotherapy drug was available for those patients who were BRAF Positive. In my case, I was in the other half – BRAF Negative or what I would hear later BRAF WILD.



Quick layman’s talk on immunotherapy drugs and their remarkable effect:
These drugs can halt a T-cell inhibitor and unleash the ability of your immune system to go beyond the T-1 inhibitor and find the melanoma cells and lesions. [Pardon me if I have screwed up the medical terminology and description].

It is now early May and I feel directionless. Yet my team let me emphasize the point of “team”; yes my team had come up with options that sounded futuristic and potentially a miracle cure. No oncologist likes to use that “C” word when it comes to defeating cancer. Bill had uncovered through his research on Pubmed.org that there were highly successful clinical trials involving other immunotherapy drugs. The good news was that these drugs were working on patients who were “BRAF WILD” (remember I talked about a test for a mutated BRAF gene). We all met, Debbie my wife and Bill. Looking over things it appeared there were options that my oncologist was not offering nor even mentioned to me in our meetings. Time was ripe for a summit meeting. In fact the doctors had their own meeting ahead of meeting with us. It was their “tumor board”. They said to us that it was their opinion that I start taking the immunotherapy drug that was not a great match for me --- Pembrolimab. The three of us were a bit perplexed. Fortunately another new to the team oncologist agreed to talk to us privately. He had come to this new team from Georgetown University Hospital’s LOMBARDI CANCER CLINIC. Bill brought up the clinical trial that involved two immunotherapy drugs, nivolumab and ipilumumab. This oncologist had just come from the Melanoma team at Georgetown. I asked him the one question that few others would answer: “What would you do if in my position?”

Three days later I had an appointment at the Lombardi Clinic at Georgetown University Hospital. The three of us went to the appointment with the Clinical Trial team. The very first thing I felt was a sense of calm. These people were here to help me. They were upbeat and talked about how the Trial would work. Downsides were discussed along with side effects. What remained was the upbeat and positive nature of this team. I know it’s whoey, but I felt like I belonged. That day the #2 oncologist for the Melanoma team told me I was accepted. In a matter of a week after some blood tests and a follow up scan, I could start treatment.



Onto the phase of infusion
. Not Chemo! What the dual immunotherapy drugs were hoped to do: I came up with my own suspense imagery. The drugs were the magic potion that allowed the “wild wolves”, aka the Super Cancer Fighters to go bounding throughout my body and seek, encompass and destroy all melanoma lesions and cells. Sounds like a video game, right? That is what I hoped would happen. Based on the initial results in the first two phases of the clinical trial, the duo of NIVO and IPILU were out there unlocking the wild wolves in over 60% of cases; plus that percentage was rising. Now it was my time. Infusion is done in similar way to Chemo. The main difference is Immunotherapy is not poison. Also as a patient, I did not get a “port”. My first infusion was in mid June. The plan was to have 4 infusion dates of the dual immunotherapy drugs. The protocol involved coming in every week for blood work. Everything went fine. A week later, all was normal. I was still running and felt good.

It was now August and I had had my third infusion. One thing had happened on my neck. An obvious lymph node that had been enlarged as considered cancerous had disappeared – gonzo. I was a couple weeks out from my 4th and final infusion. We had planned a vacation to Cape Cod with a rental home. So on the way to the house I started feeling exhausted, a plain case of no energy. On Day 2 of vacation it was worse. I felt like a big sloth just sitting there. We call the on-call oncologist fellow and I was advised to go to the local ER. It turns out in Falmouth MA; this was their biggest event of the year, the Falmouth Road Race. The hospital was semi-deserted when I arrived. Most of the ER staff had worked the event and the basic crew was there. Next thing I know after a chest x-ray and CT, I am being admitted. It was a Sunday night and I am miserable. It turns out I had had the first major side effect of the dual immunotherapy drugs. My endocrine system had been overwhelmed. The wild wolves can attack things at-will that are not cancerous. So it went with my pituitary gland, thyroid gland and adrenal gland. Now came the powerful steroids to right my system.

It’s September and I had started the dual infusion treatments in early to mid June. It was time for scans. I also found out that the oncology team felt the 4th dual infusion would be overkill. In addition, the Clinical Trial director at Bristol-Myers-Squibb removed me from the Trial due to my side effects. I wanted back “in”. Through this period of misery in the hospital and good results visually of my neck lymph node, my lead oncologist and the team felt that they’d see a stable or shrinking scene on my liver. The CT scans confirmed it: my cancer was stagnated and the lesions appeared to be shrinking or surrounded. [Previous biopsies on similar patients earlier in the Trial showed dead tissue surrounded by immune cells and material]. Good, actually really great news! It appeared that the immune system had found the cancer lesions and cells and was attacking or had attacked and defeated the cancer. Could this be a cure?

It is now February 2017. I am coming up on the two year mark. This is the time that a couple of melanoma oncologists initially felt was a good marker for survival. Nothing is guaranteed. Yet the most experienced of the oncologists who have worked on defeating melanoma for decades are now smiling. Dr Atkins, the lead oncologist on melanoma at Lombardi, sent out invitations in March 2016 to come attend a “Melanoma Survivors Luncheon”. Anytime a cancer patient receives an invitation that says you are a “Survivor”, please do attend. Since that day, I keep battling side effects that have been tough yet somewhat tolerable. I am not back to running….yet. I may never be able to play golf again due to the shoulder deterioration caused by the “wild wolves”. Still, it’s a miracle. I am convinced that the success in beating cancers like melanoma with immunotherapy drugs will have success in other cancers. You are seeing transferable use in treatment against lung cancer. I knew it as named NIVOLUMAB or NIVO. On TV it is Opdivo.

This story does not define me. It has opened a door to a second chance at life. For all of you who have had to endure cancer and continue to battle it today, I offer you hope.

With sincerity,

Dave Watt
ARA and AMAA Executive Director

Seen and Heard…while coaching

Ron Hill. This guy was a stud distance runner unlike no other. As he reached his 70s, the running streak became more than a news item only known to the “Streakers Association”. Ron Hill was not your ordinary jogger or long distance runner. He was one of the best of the early running boom. He won the Boston Marathon in a then-record time of 2:10 and change. The previous record was 2:13. He was a 3 time United Kingdom (UK) Olympian who really likes to run. You do not run every day for at least one mile each day unless you love to run. On January 29, 2017 Ron Hill decided it was time to quit the streak. The day prior he ran a mile where his heart rate and general feeling were just not good. Some would say it was a strong sign. His streak record of 52 years 39 days may never be broken. But don’t say that to our own Mark Courtney. Mark and I have grown to be good friends since I met him in my first year on the job at our AMAA Boston meeting in 2002. Little did I know when I ran an easy 2 mile run in and around Back Bay in Boston the day after Mark ran a 2:40 something Boston Marathon that I was just a witness to the daily routine of running for Mark. His own streak continues since it began in 1979. See Mark and I are the same age and I sometimes wonder what I would have had to do to keep a streak alive like Mark. I believe he told me that he did take out a catheter in the hospital once for a kidney stone to go run a mile. This is the mindset the streak runner must have to keep going. I am sure Ron Hill has it too, except when he saw that he might die on one more mile run, he better call it quits. If Mark does break Ron’s record, I think it will happen just as it began: not a lot of fanfare and just will be that day when a few of us will be waiting with freshly tapped beer at the end to celebrate.

High School aged runners up to the Pro’s are running the mid-Distance faster than ever (and history gives us some foreshadowing of why runners today are setting American and World records). Just this past month, the indoor 800m records for women was broken on the same track by two different women in the same race. The winner of the race, Ajee Wilson, broke the World Indoor record in the 800m to run 1:58+. Back in 6th place was a high school runner from New York, Sammy Watson. She ran 2:01+ and broke the National High School record in the 800m. How could this happen in one day and in the same race? For one, female athletes are moving into events in the mid-distances like the 600m, 800m and 1000m. Many of these young girls and women in the past were inclined to stick to the sprint events where their natural speed was first noticed. Coaches simply put these athletes where their first time trials showed them to be dominant. Then along come the men in the 800m several years ago. Guys like Jeremy Wariner were natural 400m guys. Then a coach or two would realize that you could harness that 400m speed and give it some longer distance training and end up with an athlete who could be dominant.

---Dave Watt

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