 Thanks for the opportunity to speak today. I'm going to step back and look at what you should expect from the pathologist in terms of surgical pathology reporting. What are the essentials you should see in reports? This is important not only for primary but for metastatic lesions in terms of prognosis. So the essential features are of course subtype, grade, presence of tumor necrosis, sarcomatoid-rabdoid differentiation, and stage. I want to go back a little bit historically. When I first started training 20 years ago, we were still using the term hypernefroma. So we come a long way in a relatively short time. The first classifications really took off in the 1996, 1997 Heidelberg and Rochester conferences where really the current format for classification was established. I do want to highlight 2012 in Vancouver. There was a consensus conference of urologic pathologist on staging prognostic features grade that appears in this month's American Journal of Surgical Pathology. It was an excellent meeting. A lot of recommendations for changes were made, including grade. Historically, I have two figures there. One is Professor Grawitz. He's a lower photo, not a very pleasant man, not very socially. He went to one meeting his entire career. And for some reason, a urologic pathologist at our social event, we call it the Grawitz Dinner at our national meeting. And I have no idea why. He actually hypothesized that these tumors were adrenal origin, hence the term hypernefroma, and that lasted for decades. Dr. Bell is a pathologist at Minnesota. The three centimeter rule, anything smaller than three centimeters was benign, greater than three centimeters was malignant. And of course, both those individuals were incorrect. So since hypernefroma, our classification system has changed dramatically. We've added a number of new entities. Some are increasing in frequency as we're recognizing them more often. Clear cell papilla and chromophobic clearly make up the majority of tumors we'll see. But it's important that we recognize these other variants. Here's a clear cell advanced stage, gross photo with involvement of the renal vein, high grade lesion. If you look in these tumors enough, you'll see low grade areas that you see in the right microscopically, a lot of lipid classic features. Papillary friable tumors, papillary cores with histiophomy histiocytes, fairly easy to recognize. We've subclassified these tumors. This is a papillary type one, papillary type two, and at the conference we recommended that we report these types. Grade appears to be more important, but on the left is a type one, which is basophilic small cells. On the right is type two, eosinophilic moratipia. I've never seen a metastatic lesion on a pure type one, whereas the metastatic lesions tend to be type two. Here's a chromophobe renal cell carcinoma. Classic plant cell-like appearance. Again, 95% of these tumors do very well. Those with necrosis or sort of comatoid differentiation, advanced stage, those are the important features and should be, of course, reported. Now why is this important for us to report? Actually, there was controversy amongst even pathologists whether it mattered to subtype or not. And it was clear by the consensus conference that the majority greater than 90% said yes because of the prognostic differences between these tumors, even for more local advanced stages. There are some new subtypes that you'll see in surgical pathology reports. One of them is clear cell papillary or clear cell tubular papillary. Not a very good name. It's confusing because you think, is it a mixed tumor? What is it? Well, it is a distinct entity and different from clear cell and different from papillary. It tends to be low grade, not very aggressive. Most patients are cured. There's a single report of a metastatic lesion. But this probably will be the third most common subtype in renal cell carcinoma as we go and study this more. I just wanted to present photos of the more, the rare variants and going from the upper left translocation associated across the musinous tubular spindle cell, tubular cystic and then renal medullary or collecting duct. And again, it's critical that pathologists understand the spectrum of these lesions and give you the appropriate diagnosis. Moving on to stage or grade. Some major changes were made at the Consensus Conference and the number one was to drop the term Furman. Really, it is a nuclear grade on the nuclear size and not a nuclear grade and thus really should be designated as really the ice upgrade. And that was a recommendation that was made. I do have a picture of Dr. Skinner and I give him the credit for really developing the first and most comprehensive grading system. As you know, he's a urologist, recently retired from USC, but as a resident at Mass General wrote a very good paper on grading in renal cell carcinoma and really it was kind of lost in the literature and not even cited by Furman. I've had the opportunity to talk with Dr. Skinner and he made sure to say to mention Dr. Compton who was a pathologist on this study. Now here's the outcome in our series of the various grades. One and two cluster together, they're significantly different but marginally and the big drop off occurs between two and three and three and four. Here's other features that we talked about at the Consensus Conference and interesting, a lot of these features are particularly necrosis. 30% of pathologists, urologic pathologists didn't mention it in their path report and I think that's a mistake and the Consensus was there also that this needed to be reported and put in the report. Fat Invasion we'll talk a little about and then the patterns of differentiation. Here's tumor necrosis. It really has characteristic features, coagulum, apoptotic debris and it occurs about 20% of grade three tumors very rare in grade two. So if you're seeing reports that have grade two and 30% of the tumors have necrosis in them they're probably looking at other degenerative features that aren't true tumor necrosis and something to talk about with the pathologist. If you look at the outcome in clear cell renal cell carcinoma the drop off in outcome is significant given a tumor that has necrosis versus one that doesn't. This outcome difference is also important in chromophore renal cell carcinoma, similar drop off in survival, important in papillary but not like clear cell and chromophore. I got a phone call from one of the other pathologists from New Zealand, Brett Delaun, who's done a lot in the pathology of renal cell and said what happens if you combine necrosis and grade into a single system. So what we did was we took the data and grouped patients based on their ice upgrade and the presence or absence of necrosis and on sarcomatoid differentiation present or absent and you created nine groups based on those features and you can see the proportion of clear cells grade two that had necrosis was only about 2% of patients. Now if you take those groups and you stratify them with a combination of grade and necrosis you see a catheter and myer curve that stratifies out like this. So grade one and two is one and two tumors without necrosis, grade three and four groups grade, groups three and four are renal cell grade two with necrosis and grade three without necrosis and then six fives, excuse me, five, six, seven, eight is where necrosis appears. So now you're able to stratify those curves based on a grading system that incorporates necrosis. The point, at this point this system is being validated has not been put into practice but it may be dependent on its validation. Here's a common feature degeneration in a low grade renal cell carcinoma, a lot of fibrin that has been misinterpreted as necrosis and that may drive up the presence of necrosis in reports in low grade lesions. Moving on to fat invasion, historically we've been always focused as pathologists on that peripheral perinephric fat and for some reason we weren't paying attention to the renal sinus fat and that's where all the lymphatics and the venous drainage occurs and not until recently worked by Houston Thompson at Mayo and Dr. Steve Bonsib at the University of Louisiana, Louisiana State really have turned our attention to the renal sinus fat. This is a retrospective study looking at outcomes in patients that had perinephric versus renal sinus and this is really not going back to the old cases where they weren't paying attention to renal sinus and may not have sampled it. We still see a difference in outcome so it is important. If you go back to T1 patients that died of renal cell carcinoma that really shouldn't, we actually had the opportunity to go back to this gross specimen, put more tissue in and look at the renal sinus fat and patients that died of renal cell carcinoma really should not have and you see that those patients we missed sinus fat invasion. It was there in the majority of patients and was overlooked and I think that occurred at most institutions, again we're not paying attention to that pathologic feature. In fact, Dr. Bonsip says that T tumors don't really exist that if you sample that renal sinus fat in very large renal cells you'll nearly always find fat invasion. Those patients are always PT3 not PT2. Here's some photographs of the various patterns of renal sinus fat invasion. Often that renal cell has a capsule and a close interface with the renal sinus fat and that is not invasion. There's no pushing to it without invading. Finally, I want to finish up on sarcomatoid renal cell carcinoma. Here's a large sarcomatoid mass actually composed of bone. Here's a chromophobe with a spindle cell component and essential that we recognize this as pathologist because of its impact on outcome and you see that grade four without sarcomatoid does significantly worse or actually with sarcomatoid does significantly worse than grade four without and if you look at the subtypes once you've had sarcomatoid differentiation it doesn't matter what the underlying subtype is it has a very aggressive outcome and I'll actually finish with that and since I'm in Iowa in Chicago I'll put American Gothic there. Thank you.