 Good morning. Hi, my name is Sandy Srinivas. I'm a medical oncologist here at Stanford. I'm the lead medical oncology. I lead our clinical program here at Stanford in urology oncology. And I want to welcome all of you and thank you all for choosing to spend your Saturday with us here today. I'd like to thank the Kidney Cancer Association for allowing us to host this event here at Stanford. I've been here at Stanford for about 19 years now. And this Kidney Cancer Association has been hosting this event for much longer than that. They used to do it up in San Francisco with Dr. Miner leading this at CPMC. And then many years ago, Dr. Miner asked me to take over this. And we've been doing that up in the city. And I think in the last three years, because we have such a nice place here at Stanford, we decided to host it here at Stanford campus itself. Again, this is a day just totally dedicated for you. We have put together a good group of people to help educate and tell you what's the best and what's upcoming in kidney cancer. So my job is to do a brief introduction just to set the stage right. But I have a good group of people here talking. So all I'm going to do is just do an introduction and then I love the rest of the day to go on. So here I'm gonna start off by saying that this is the picture of the kidney. And not every cancer that starts in the kidney is kidney cancer. So the kidney is made up of the cortex. Let me see if I can make this pointer work. So this is the cortex, all this white part. And then this part is all called the renal pelvis. This is where urine is made and urine then is transported to this tube called the ureter. And that's a different type of cancer. That's called renal pelvis or urinary type of cancer, which is not what we are going to be talking about today. All of the cancers that we are talking about are those that arise in the cortex. That's what kidney cancer is. And this is an estimate of what the total number of kidney cancers per year are. This is the incidence of cancer in men and women and the estimated deaths that happen from cancer. Fortunately, kidney cancer is not very common. It affects only about 40,000 people, but it does come under the top 10 cancers that affect people. There's good and bad to it when a cancer is not very common. We don't get enough resources. We don't get enough attention paid to a cancer like this. But it does feature in the top 10 in both men and women. And there are still even today significant deaths that happen from this disease. So clearly it's a disease where we need to pay more attention and have our resources and energy in figuring out better treatment options. So here is what happens to patients. Curability depends on the stage of cancer. So we think about kidney cancer as being localized when the disease is just contained in the kidney. There's a second group of patients where we think about it as being locally advanced where it goes beyond the kidney to affect the major blood vessels or sometimes even the draining lymph nodes. And then finally, metastatic disease is when it escapes the kidney and gets to other organs such as lung, liver, bone. A large, I mean, 45% of patients present with early stage disease and for them removal is all that's needed and they achieve a very high cure rate. Unfortunately, 30% of patients today present with metastatic disease as their first sight so it's not uncommon for patients to go to the emergency room for a cough or back pain and they get a scan done and there is spread outside of the kidney. The kidney is an organ, it's located in such a place that it can grow and not have any symptoms at all. So people are lucky if they notice blood in their urine. Certainly we don't tend to ignore that. When you have blood in your urine, it brings you to medical attention and they can detect the disease but not all patients present with blood in the urine. So again, 30% of patients present with disease that's quite advanced even at the time of diagnosis. So here is a scheme of what the staging system looks like. So stage one are small tumors that are less than seven centimeters. Those are considered to be stage one. Seven seems like a big size but so long as it's contained within the kidney that's stage one and there is a cure rate with kidney removal of close to about 85 to 90% if you can remove it then. Stage two are tumors that are greater than seven centimeters but still contained in the kidney and even for that group of patients so long as we're able to remove it there is still a very high cure rate. Stage three again is what we call as locally advanced disease. These are tumors that have escaped the kidney gone into the blood vessel, either the renal vein or the big blood vessel called the inferior vena cava or the surrounding fat. And then finally, stage four is if we have disease that spread outside of the draining lymph nodes for the kidney so if someone were to have a neck lymph or obviously disease that gets to lung, bone and other organs would be considered stage four. So kidney cancer we know is not one disease. This is the majority of patients have a histologic subtype called clear cell and then we group everything else as non clear cell. I'm not gonna spend too much time on this because subsequent speakers are going to dedicate a talk just on pathology but I just wanted to set the stage to say that it's not one disease. There are many subtypes and hopefully in the years to come we'll have a drug for every one of these subtypes. So here is a little bit of background on the treatment. So prior to, so 10 years ago all we had for kidney cancer was immunotherapy with a drug called interferon which was very, very ineffective and tough for people to take. And then subsequently there was another drug called intraleukin two that came about. Unfortunately, intraleukin two was not a drug, a treatment that could be delivered to every patient. You really required it to have completely normal organ systems because it was a remarkably toxic treatment. So the treatment that we had 10 years ago was applicable to a very small number of patients. And then the last 10 years have just seen I'm going to show you but I think we have close to 10 drugs today for patients with kidney cancer and I think it's really the effort of all of the efforts that have been put into understanding the biology and behavior of this disease that's led to this. So to show that here is my slide that shows the progress that we have made in kidney cancer. So 1992 was the first approved drug with high dose intraleukin two and then there was really a lull there was not much that happened between 1992 and 2005. And the first targeted drug was approved in 2005 with a drug called Saurafinib. And then you can see almost every year there was a new drug that was FDA approved. In 2006, we had a drug called Sunitinib. In 2007, there was a new class of drug called mTOR inhibitors with a drug called Temsirolimus. 2008, there was a drug called Bevacissimab. 2009, we had both Everolimus approved which is an oral drug that's in the same class as Temsirolimus. In 2010, there was a drug called Pazopinib. 2012, Axitinib. So it's just been a remark of it's that we call it the embarrassment of riches where we really had a pretty large number of drugs that we could pick from. And I think the excitement with a new class of drugs that became available was in 2015 with another immunotherapy drug called Nivolimab. And I think this is really going to change the way we take care of patients with kidney cancer that now we have come to a point where we are asking our own immune system to do what it takes to go fight the cancer. And then in 2016, again, we have two other drugs, CaboXantinib and a combination of Lenvatinib and Everolimus. So here is my summary slide for what is the current treatment in 2016. We have immunotherapy with the old drugs like Interferon, Interleukin2, and Nivolimab. And then you can see that this class of drugs called VEGF inhibitors have really, that list is long but is only getting longer. And then we have MTOR inhibitors. So in some of the talks today, we are going to talk about how can we pick from this list? What is best for a given individual? How do we juggle these drugs around so that all our patients can benefit from each of these drugs in a logical way? So this is a little confusing slide, but these are the cells. These are the players that are engaged in these various drugs, and these are the different drugs. So you're looking at this is the tumor cell. This whole thing and beyond is the tumor cell. This is the lymphocyte, which are immune fighting cells. And then these are the blood cells called the endothelial cells. So what we know so far, at least in terms of the biology, and you'll hear more about it during the rest of the talks today, is that when you have an inactivated VHL, that causes some downstream effects that results in increase in an activation of certain genes, which are the VEGF genes, vascular endothelial growth factor genes. And all of our drugs that we have in that list of VEGF inhibitors work at this endothelial cell. Then working in the T cell are our immunotherapy drugs. And you'll hear about a few today, but there's definitely that list is getting long. And our hope for the future is that we'll be able to combine several of these things to give us the best outcome. So what are the important clinical questions that we have today? We used what we think are clinically relevant and what our strengths here are at Stanford to be able to give you a day to day that's going to be educational for you. So to address is kidney cancer one disease, you're going to hear from our GU pathologist, Sunny, about that in the next talk. What improvements can be done in local therapy? Should the kidney be removed in patients with stage four disease? How best can we take care of localized kidney cancer without causing a lot of morbidity? We're going to have Dr. Ben Chung, who's one of our urologists talk about that today. There's so much information out there from big data. How can we use technology being in the Silicon Valley? How can we use information like that to leverage what we can do for our patients? One of our urologists, John Leppert, is going to talk about how can we learn from existing information and learn to do things in a smarter way. I showed you that long list with various therapies. How do we pick therapy? And I'm going to have one of our junior fellows, Sumit Shah. He's going to talk about picking medical therapy. And then finally, with all of this list, one of the disappointing things in kidney cancer has been, how do we pick the best drug for a given patient? Is there a biomarker that can help us choose among these 10 drugs for a given individual? We're really delighted to have Alice Fan, one of our medical oncologists here at Stanford, address that today. And then I'm really excited about this last talk, which is the whole field of oncology is moving towards precision medicine and individualized medicine. How can molecular information and genomics help us pick a therapy? So Alex's election, who's one of our fellows, is going to address that today. And finally, we'll end up with my favorite part of the day, which is really engaging all of you in a patient forum with Jordan Chavez. So I think I'll stop with that. And here is the agenda. All of you have that in front of you. And with that, I'd like to welcome Kari Konoski from the Kidney Cancer Association to speak briefly.