(Guest Lecture) October 2022 - Becoming a Partner with Your Healthcare Team

Music Check, check. Good. All right. Where's Greg? Can you step out? All right. So, Jenny, Greg, Health Tree, thank you. Thank you for hosting this roundtable here at our home, the Huntsman Cancer Institute. I welcome all of you who are here, both in person and online. It's a pleasure to have you. Hopefully today is both educational as well as fun. So I was given the job today to talk about what it is to become a partner with your health care team. And my instructions were as follows. One, no Kaplan-Meier survival curves. Those are out. Two, what's the essential knowledge that you need as a patient and family member? Three, what's risk in myeloma? And four, what are the, what's the importance of treatment strategies as we move from diagnosis all the way through relapse and refractory disease? And lastly, I was instructed to talk to you guys like you are coming into my clinic. Okay. So that's what I did. All right. There we go. So I'm inviting you through the front door into my clinical space. That first step that you take, that's our first opportunity to become partners. Walk through the front door, walk down the long hall, walk into my clinic room. You're scared, anxious, nervous, nervous and scared to hear that C word cancer. Even more nervous to hear those two words, multiple myeloma. You walk in, you have medical assistance, you have pharmacists, you have nurses. You're supposed to see this strange doctor with a strange last name like Hoffmeister. And then you notice that everybody's smiling. You're like, why is everybody smiling? They deal with cancer all day. They're not supposed to be smiling. They're smiling because they're waiting for you. Our job is to put our arm around you, bring you into our family, grow our trust and to become partners along your journey with multiple myeloma. In my humble opinion, that trust is gained through communication and education. So a lot of people give me a hard time because when you come into my clinic for the first time, I have this patient exam table. And you think you're supposed to get up on the table. That's not what it's for. It's my tapestry. That's where I do my art. It's where I tell the story. I am no artist. In fact, I'm a horrible artist, but I do my job to be my best Bob Ross. So we sit down, we talk about some small talk, get to know one another, go through the history and physical. And then I start talking about what you need to know about multiple myeloma. I was thinking, OK, well, I could probably try to get fancy with my PowerPoint and put together some kind of animation or whatever else. And then I decided, why not just show you what it looks like? So I went into the clinic work room or clinic room and I put this together. So this is how I describe myeloma to my patients. And there is poetic license that goes along with this. OK, and so I try to conceptualize for the patients and give them some ideas and introduce them to some vocabulary. So I start out by saying your bones are the factory. Your bones are the factory for all the cells that float around the blood. You have white blood cells, red blood cells and platelets. If you cut yourself, platelets bind together. They form a clot and they stop bleeding. Red blood cells carry oxygen around the body. You don't have enough red blood cells. You get tired. You don't have enough oxygen. Then you have white blood cells and white blood cells make up our immune system. The clear junk viruses, bacteria, other junk out of the system. There's two components of the immune system. You have the innate immune system and the adaptive immune system. So what does that mean? Well, the innate immune system is the first responders, the ambulance drivers, if you will. The adaptive immune system is your memory immune system, more specialized, maybe like your doctor. The way I try to introduce this concept is through the idea of a vaccine. Most, if not all of us, in fact all of us in this room should have the flu vaccine. So the flu vaccine is just us injecting some dead flu virus into your system. These first responders, looking around, they see dead flu virus. They say dead flu virus doesn't belong here. Let's get rid of it. So they do. Those cells get rid of the dead flu virus. But they also tell these guys, hey listen, we just saw the dead flu virus. We want you to remember it. Because if you get infected with a live flu in the middle of the winter, you want your immune system to recognize it. The way the immune system recognizes it is through this thing called an antibody. An antibody is a protein. It has another name. It's called an immunoglobulin or an Ig. There's a bunch of different types of antibodies or immunoglobulins. You have IgG, IgM, IgA, IgD, IgE. Ricky, Bobby, Tommy, Joey, Steve. Just different names for different types of antibodies. Now this antibody is made up of two components. You have this bigger part that's the heavy chain. And then you have this other part that's called the light chain. That can be the kappa or lambda. What does this look like? It looks like this. These antibodies float around your system. The fingers recognize flu. So these guys float around your system looking for things, surveillance. Hopefully that makes sense. Now a very important concept is that these antibodies, these immunoglobulins, this protein, is made by this cell called the plasma cell. And the plasma cell is a type of white blood cell, part of the adaptive immune system. This plasma cell normally lives here in the bones. When you become infected with something or you have some kind of inflammation, these cells wake up and they start throwing out these antibodies into your system. If you have myeloma, MGUS, smoldering, at some time one of these normal cells got a mutation. And that mutation causes that cell to act abnormally. So what do they do? They're always on. They always make that protein. Now the bone marrow is this beautiful place. It's like a tropical forest. And the bone marrow loves these cells. And these cells love the bone marrow. So they talk back and forth. I like you. I like you. Things happen. They start making more of each other. All of these cells, good, I like the snicker, that's the idea. All of these cells are the same. And they're all making the same type of protein or the same type of immunoglybulin. In doctor talk we call that monoclonal. Monoclonal stands for one clone. So these are monoclonal plasma cells that make the same type of protein, a monoclonal protein. We also call that the M-spike. Following so far? Very good. If you have a few of these cells in your bones not causing any problems, you have this entity called MGUS. Monoclonal gemopathy of undetermined significance. If you have some more of those cells still not causing any problems, that's smoldering myeloma. At some point those cells may cause problems. And at that point we call that multiple myeloma. Now, every patient who has multiple myeloma started here, then went here, then went here. But not every patient with MGUS or smoldering myeloma develops multiple myeloma. So what do these cells do? These cells sit in the bones and they secrete a substance. The substance eats away at bones like termites eat away at wood. When that happens, what do we see on it? We see bone lytic lesions. And that makes our patients more susceptible to fractures. Because the bones are a factory, they have limited resources. So if you have so many of these bad plasma cells in your bones, you can't, you don't have enough resources to make red blood cells and platelets. So what can happen? Well, you can have anemia. You can have a reduced number of red blood cells. And what happens? Patients are tired because they don't have enough oxygen. What else can happen? Well, if, sorry, Bob Ross. If your bones are being chewed up by termites, well, bones are made up of calcium. So that calcium can get spit out into the peripheral blood and you can have high calcium. The proteins that I was telling you about, they can be sticky and those proteins can glob up in the kidney. The kidney is essentially a pipe with filters on it. So if you have this sticky glob of goo, it can block up that pipe and you can have renal failure. That's the end organ damage associated with multiple myeloma. So risk. So we now understand what multiple myeloma is. When you see your doctor, we're trying to understand how your myeloma is going to behave. All right. So we look at the RISS, or revised international staging system, to try to get an idea as to how your myeloma will behave. This staging system is based upon a bunch of labs. It's also based upon what we call fish cytogenetics, which is an analysis of your mutations that are associated with those bad cells in the bones. Going back to my drawings, this is what I put on a piece of paper. Stage one, sensitive disease. It's less aggressive. So we need to give less aggressive long-term therapy. Three, resistant, higher risk disease. Because the cells are more resistant to our current therapeutics, we have to give more aggressive long-term therapy. That's risk. The most important time, in my opinion, to assess risk is at diagnosis. That's when we get an idea of what your treatment plan is going to be. How do we need to approach your myeloma in order to keep your disease under control for the longest period of time possible? So this is what happens when you first come in. This is how our brains think. So we diagnose you, we look at risk, and then we assess your fitness. We try to understand if you would be eligible for a high dose of chemotherapy in the form of an autologous transplant. And then once we make that determination, we move forward. Start some drugs. Either we continue those drugs or start those drugs, consolidate your response with this high dose of chemotherapy and a transplant, and then move on to maintenance therapy. All with the goal of controlling your disease. If we are able to kill those cancer cells, those cancer cells can't keep eating away at your bones. If we can kill those cancer cells, they're not making the protein that can cause kidney damage. And then as you would expect, we want to maximize disease control. We want to keep tabs on those bad cells. We want them to be quiet for as long as possible. So this is our myeloma toolbox. I won't go through it in deep detail because we have a couple of speakers that will do so. But I point out that we have a lot of drugs. And our job as your provider is to try to figure out which drugs to use at which time to make sure that you can live as long as possible with the best possible quality of life. And as you can see here, this is not a Kaplan-Meier curve, if Greg is watching. This is just to point out that we're improving. As you guys know, because you're savvy, we have a lot of new drugs. A lot of technology, a lot of growth in myeloma. And what's that leading to? That's leading to better survival in our patients. That's my introduction to the day. I'm really, really happy to introduce my colleagues that will be joining me over the course of the day. We have Dr. Craig Hoffmeister, who taught me everything I know about multiple myeloma. Happy to have him from Emory University. Dr. Natalie Callender, who's the director of the myeloma program at the University of Wisconsin-Madison. Christina Gowin will be joining us from a campsite, I believe, somewhere in Arizona this afternoon. And then Moni, Dr. Moni Mouyadine is our newest partner here at the Huntsman. And he's currently on service. So when he's done rounding, he'll be down here. So please join me in welcoming our esteemed colleagues. Music