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Unera is developed exclusively for residents and is completely free of charge. Elevate your case logs. Download Unera today. That's U-N-I-R-A, Unera. Hi, everyone. We're so excited to be returning to the BTK team this upcoming two years. While you may know us as your former HPV team, we're now transitioned to bring you exciting surgical oncology topics.
We've all been overwhelmed and overwhelmed with complex patients, challenging operative planning, and nuanced treatment regimens. Our goal with our episodes is to make these complicated topics approachable and clinically relevant. Additionally, we hope to highlight high-yield topics for shelf exams, the ab site, and the boards. So let's get started with some introductions. I'm Elizabeth Carpenter, one of the fourth-year general surgery residents at Brookery Medical Center in San Antonio, Texas.
I'm Lexi Adams. I'm also a general surgery resident at Brook Army Medical Center. I'm Connor Chick. I'm a former general surgery resident at BAMC, but now a first-year surgical oncology fellow at Ohio State. I'm Tim Breland. I'm a surgical oncologist at Brook Army Medical Center in San Antonio. We're really excited for this new set of topics for Surgeon. Unfortunately, we also are missing one of our team members here tonight, Dr. Dan Nelson. He just started his fellowship at MD Anderson for HPB.
All right, so let's go ahead and get started with a case to kick off this episode. So we have a 62-year-old male who presented to the ED with flank pain and hematuria with concern initially for nephrolithiasis confirmed on abdominal CT scan. His labs demonstrated a mild anemia but they were otherwise unremarkable.
Soon after, in the ER, the patient developed a low-grade fever, nausea, and thus the CT scan was repeated with IV and PO contrast. This study demonstrated an incidental finding of a heterogeneously enhancing mass on the gastric fundus that was consistent with a gym.
per the radiologist. This mass was approximately 3 centimeters with central ulceration. The patient was eventually discharged from the ER with a recommendation to follow up with you in your surgical oncology clinic for a full workup of this lesion. So Lexi, what would be your next step for workup of this tumor? So first, I would want to get an EGD with an EUS to make sure that it's consistent with a GIST. And my differential would include other masses such as eleomyoma.
lymphoma, adenocarcinoma. You could get an FNA, although a biopsy is not always required for this as long as the mass is consistent with the gist both radiographically and endoscopically. It typically appears smooth and submucosal on the EUS. So back to you, Beth. For extraluminologists, would you get a percutaneous biopsy? Typically, we don't, and that's due to both the risk of bleeding as well as intra-abdominal tumor dissemination.
Just a quick comment on that. Really, the main risk factor for recurrence of GIST, it has to do with size and mitotic rate, but the one that we can control is tumor rupture. So just to be very clear on that point. You really don't ever want to percutaneously biopsy anything. You might think is a gist because you can rupture it into the peritoneal cavity and seed it, like you mentioned.
Endoscopic biopsy, on the other hand, is different because it won't rupture into the lumen of the bowel or through the mucosa typically. So most of the biopsies are going to be done by EUS. Great. So just to talk a little more about the epidemiology of GISTs, so Connor, what is the epidemiologic background of these tumors? Yeah, so older literature used to describe these as pretty rare. In some reports, as few as 0.8 per 100,000.
But more recent and smaller autopsy studies suggest that subclinical tumors might be present at up to 25% of patients who are over 50 years old. It is important to note that these tumors can occur anywhere in the GI tract.
The most common site is the stomach, and that's the one that we think about the most, followed by small intestine. And all the other sites are very rare. Of the rare ones, the more common ones are duodenum and rectum. And then extremely rare sites would be esophagus, colon, appendix. or even extraintestinal or mesenteric sites. Beth, why can these occur anywhere in the GI tract?
So just some mesenchymal tumors, these were historically characterized as spindle cell neoplasms of smooth muscle origin. So this is why in older textbooks, you may find these tumors within sarcoma chapters, or even in newer textbooks, honestly. from the interstitial cells of Cajal, the pacemakers of the GI tract. And so this is why you can find them anywhere along the GI tract is because of these cells that are present all along those areas.
So just to continue on with the case, Lexi, your pathology from the EGD returns with spindle cells, confirming your preoperative suspicion of a GIST. Additionally, histopathology demonstrates a positive CD117, a positive PDGFRA. and a negative dog one. Is there anything else you want to complete your workup? So we'll get a little more into the histopathology later on in the podcast, but...
In regards to other workup, because the mass is greater than two centimeters, we need to get a CT chest. Also, they are typically avid on PET CT, but we usually reserve that in case of suspicion for metastatic disease. so yeah i think that your the workup so far is reasonable keep in mind that if the patient presents with a mass this was asymptomatic but
Let's say on the endoscopy, they see an ulcer over the top of it or some stigmata that may have bled a little bit or something like that. You don't really need any of this. So on EUS, if it looks like it's arising from the muscular layer. It's not a mucosal tumor. It's not adenocarcinoma. It's in the stomach. What else could it really be, right? And whatever it is, you're going to cut it out. So don't get too spun up on the workup of a...
small, resectable gist, just go take it out. Particularly when it's in the body of the stomach, it's a very simple thing to do, to just kind of do a partial gastrectomy. You know, we don't get too spun up about this stuff until we start talking about medical therapy, really. And so, you know, we'll get into when we use neoadjuvant.
And that's going to be where all the rest of this becomes interesting. Right. So a gastricist is three centimeters of the body. Now, you know, one of the themes for test taking is that. The most common things in gist are actually all the favorable things. So the most common site is gastric and that's favorable. We'll talk about the exons later. The most common exon is 11. That's the good one. So, and the most common site. the stomach is the body which is the easiest to resect so
Your run-of-the-mill gist is going to be some random thing found. Either they got put on a blood thinner because they have AFib or had a PE, and then they started bleeding. And it turns out, oh, they had a gist that had never bled before, but it bled once they got put on a blood thinner. or incidentally found on a CT scan like this, right? And don't overthink it. You know, this is one of these diseases where, you know, everybody makes fun of me because I love neoadjuvant, but...
This is a surgical disease for the most part, right? You just go cut the thing out and half of them are going to come back with a mitotic rate that's low and it's going to be less than five centimeters. It's going to be in the body of the stomach. There's nothing more to do. Just cut it out and you've cured the patient.
before we get too spun up about all the details and workup of gist, keep in mind that most of the time you're just going to go whack it out with a little partial gastrectomy and the patient's going to move on with their life. Dr. Breland, just because this is something that I think can be very confusing to junior residents, can you just review again why exactly a tumor of the muscular layer of the organ can bleed?
Yeah, I think it just has to get big enough that it stretches the mucosa and then causes an ulcer. And then it's probably not the tumor that bleeds. It's the submucosal vessels that are disrupted by stretching. Or there's some distortion of the lumen enough that it causes an ulceration or something like that.
Again, most of them won't bleed. The ones that are the easiest are these really exophytic tumors that you go in and you're like... that's barely even connected to the stomach and you just literally have to take like one centimeter of stomach and there's like a golf ball hanging off the back of the stomach kind of and those are going to be the favorable really easy to resect ones so
You know, the ones that bleed are probably going to be bigger and they're going to be a little bit less exophytic and somehow, some way push up on the mucosa enough to cause some ulceration. And just to define exophytic for our more junior listeners, it's really going to be pertaining to the growth of a tumor outward as opposed to endophytic, which would be growth of a tumor inward. It's a dangler. That's the term for it.
So, again, that's kind of the run-of-the-mill simple stuff, right? Now, the real consideration comes in when there's some reason you don't want to operate right away, right? So let's say it's like... You know, it's a larger gist and it's close to the GE junction. And man, if you go in to staple that thing off, you know, you're going to narrow the cardia and you're just like, man, if I could get that thing to shrink, surgery would be a lot easier.
Now we start talking about medical therapies. So the majority, you know, we're going to talk about the genes here. In fact. Connor, why don't you kind of launch us off into the genotyping of these gists and try to understand, you know, which mutations portend what prognosis and how it affects therapy. Okay, so the important things to know in terms of genotyping with GIST. So the majority of GIST are going to express a mutation in CKIT, also known as KIT.
also known as CD117. And so when you see those, either C-kit or CD117 on a test, those are the same thing. That is a receptor tyrosine kinase. So it sits in the cell membrane. there's multiple domains of that receptor tyrosine kinase including the juxta membrane domain which is encoded by exon 11. and so we talked about exon 11 already that's the most common and the one that has
where mutation in that exon has the best prognosis. There's an extracellular membrane domain encoded by exon 9, which is the second most common, slightly less good prognosis. And then... The tyrosine kinase domains are encoded by exon 13 and 17, though those are more rare. Some gists, as opposed to the CKID mutation, express a mutation in the platelet-derived growth factor receptor A or alpha, so PDGFRA. That's also a receptor tyrosine kinase, but the ligand is platelet-derived growth factor.
Exon 18 mutations in that gene are seen in certain gastric gists, and that'll be important in discussing other therapies soon. Occasionally, we'll have gists that express neither KIT nor PDGFRA mutations, and these are called wild-type gists. Those are most often seen in SDH mutations. So, you know, more common ones being SDHB and SDHD. And those are, those, those gists in those syndromes tend to be associated with mutations in BRAF.
KRAS or NF1. So all that is kind of, you know, word salad, whatever. So, you know, people think that we get way too excited about this stuff, but. The reality is you got to know nine and 11 because it affects the therapy. So, you know, we're going to talk, I think in the next episode, a little bit more about the papers on the medical therapies, but.
The Exon 11 responds really well to Gleevec. Everybody should at least know what Gleevec is. And you can use a lower dose and you almost certainly are going to respond. Exon 9. does not respond as well, and you double the dose, and they still don't respond that well. And then the other ones are a mixed bag. But because it really affects therapy, it's really important.
So again, if you want to use, let's say this just as in a spot where you just can't resect it easily and you really need it to shrink. If it has an exon 11 mutation, you can give them Glee back and it will start shrinking within 48 hours. So there are studies that you can do a PET scan before they start Gleevec and do it literally three days after, and there will be a change in the tumor within just a few days. I mean, most people wait a week, but there's...
some papers that describe it even at 72 hours, and they'll have real change on a PET scan if they're going to respond to Gleevec. So it works very quickly and it works very well. And you can predict that by knowing the axon. So that's why it's important. So, you know, I try not to get too lost in the weeds, but at least no nine and 11. One of my other favorite things about gist is that the thing they stain gist for is called dog one.
And that's because it stands for diagnosis of GIST. So if you can remember that, you can remember what it's staying for and get an abcite question, right? Yeah. Speaking of abcite, Lexi, what genetic syndromes are tend to be associated with GISTs? So we have neurofibromatosis, NF1, and then we have Carney's triad, which, good trivia, that includes gastric gist, pulmonary chondroma, and extraadrenal paraganglioma.
And then another small variation on that is the Carnie-Stratakis syndrome, and that's just impaired ganglioma. And then you also have von Hippel-Lindau as well. Okay, great. So now that we've gone over all those things, let's go back to our case and let's talk about the staging of our patient's tumor. So just to review, this is a gastric gist of approximately 3 centimeters. Lexi, is there anything else you need to know to be able to stage this lesion?
So I would want to know if there's any evidence of regional lymph node involvement as well as any evidence of metastasis. I would also want to know what the mitotic rate of the tumor was because it's unique to just that the staging will be dependent on that factor.
Just to be clear, lymph node involvement is very rare. So it can happen, but it's very rare with a run-of-the-mill gist. So I don't look so much at the lymph nodes, but you do want to look at the liver because they can certainly metastasize. Thanks for bringing that up, Dr. Breland. So, for this patient, there's no regional lymph node involvement or metastasis, but the mitotic rate is seen to be over 5 mitoses per 50 high-powered field.
So greater than 5 is considered a high mitotic rate. So gastric and omentilgists, they have a separate staging classification than other sites that include small intestine and colorectal, and that's important. distinction from other staging systems for other cancers. So it would be a T2 tumor given that the tumor is two centimeters, so falls within the...
greater than two but less than five centimeters. It's N0 and M0 and has a high mitotic rate, which this makes it a stage two tumor. I would encourage you always to just pull up the NCCN guidelines and this will help. you figure out which stage your patients belong in. Just of note, like Dr. Breeland said, nodal involvement's extremely rare, but if there is nodal involvement, it makes it a stage four disease, even if there's no other evidence of distant metastasis.
Like any other malignancy, staging is incredibly important for prognosis for GIST. Both the size and mitotic rate predicts the risk of recurrence, and it's important to help us figure out the future medical therapy. So Connor, is there another tool besides just the NCCN guidelines that can help us determine a recurrence for these patients based on some of the factors we discussed? Yeah, there is. So there was a nomogram developed.
at Memorial Sloan Kettering that assigns point values for the size of the tumor in centimeters, the mitotic rate, and the site. And when you follow that nomogram, it gives you a probability of two-year and five-year recurrence-free survival. and we'll link this paper in the show notes so i guess my comment on staging would be that in the pre-operative setting i don't actually care that much right so
That's where things get a little bit confusing. We talk a lot about staging, but that's mostly to decide on adjuvant therapy. But as a surgeon, what I care about is, is this easy to resect or not easy to resect? And again, if it's... not easy to resect, you know, you're going to have to justify giving medical therapy. So probably you'd have to have, you know, a T2 or bigger or a high mitotic rate or something like that. But if it's, you know.
The reasons it'd be hard to resect are usually because it's invading another organ or something like that. And in those cases, or it's going to need a Whipple because it's a duodenal gist. And if you get it to resect or shrink back, you might... be able to just do a segmental or a side bite or something. But as a surgeon up front, that's what I care about. Is it easy to resect or hard to resect? And then if it's hard to resect, what's the axon?
And so the staging is really more after you resect or the medical oncologist to decide whether or not the recurrence risk is high enough to justify adjuvant therapy. So again... You know, the easy numbers to remember in your head, if it's a gastric gist, it's five and five. So it's not greater than five and as a mitotic rate of five or more, then you're done. You just resect and they're considered.
cured because their risk of recurrence is so low based on that msk algorithm or nomogram and then it's you know basically over five and over five they're going to get adjuvant therapy for stomach and then for basically everything else it's going to be lower, meaning that the threshold to give adjuvant therapy is lower. So for small bowel, you know, it's kind of two and five.
for the mitotic rate and size, for things like rectal and the more high-risk ones, probably everybody's going to get some adjuvant therapy, again, depending on their mutations. Okay, awesome. Thank you, Dr. Brill, and those are really clinically relevant points. Now, a word from our sponsor, Unera. Residency is busy, insanely busy. There are so many tasks vying for your time. For me, one of the most painful was logging cases.
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So just to summarize, at this point in our case, we have a patient with a gastric gist of approximately 3 centimeters, stage 2 given the high mitotic rate. Connor, how do you want to proceed with this patient? Yeah, so... This case is relatively straightforward in terms of decision-making, right? So this is a resectable tumor and given that it's three centimeters in size and it bled, you know, we would recommend upfront resection in general.
You know, we talked about how these just can be incidentally found. If they, if you find one less than two centimeters and it's asymptomatic, you can consider just observing because these small gastric just have such a good prognosis and tend to be very slow growing.
If the tumor is less than two centimeters, but it's symptomatic, meaning in most cases, when it's that small, it means bleeding. You can consider endoscopic resection, but for more than two centimeters in general, you're going to need a surgical resection. when we're talking about just in the in the stomach most often this is going to be a wedge resection
The reason for that is that we really only need grossly negative margins as opposed to when we do gastrectomies for adenocarcinoma where you have to plan for a five centimeter surgical margin. So again, really the goal is to get... grossly negative margins and not rupture the tumor capsule like dr vila mentioned earlier even if you do get a microscopically positive margin we generally don't re-resect those yeah and there's there's one reason for that is that
Again, often these are exophytic, meaning they've like grown out the wall of the stomach. And so what's your margin going to be? the peritoneal cavity, you know, like they may have serosa, but sometimes the tumor is eroded even through the serosa. And so you're, you know, it's basically tumor right out to the peritoneal cavity.
And so they're going to call that an R1 resection potentially because there is no margin to take there. And even on the stomach, on the gastric side, there's just no evidence, as long as you don't rupture the tumor, that there's any...
real extent of invasion. So it's not like these tumors like adenocarcinoma kind of work their way into the tissue. They just sort of push everything out of the way. So as long as you... get a grossly negative margin there's really no reason to even have them look at the margin in the microscope even though they do it anyway
Connor, can you go over the difference between R0, R1, and R2 resections? I think this is super important as we have our next two years on surgical oncology because this comes up again and again. Yeah, so R0 means microscopically negative margin. R1 means a grossly negative margin, but a microscopically positive margin.
And then R2 is where you have a grossly positive margin where essentially you know that you're cutting through tumor. And I would add that R1 can even be more complicated for tumors such as pancreas cancer. Less than one millimeter is considered R1. It's not always just microscopically positive, but sometimes it's within one millimeter. Sorry to make it more complicated. Thanks for clarifying that.
And on theme with how gists are different from adenocarcinoma, we generally don't do lymphadenectomy as part of an operation for a gist. With the one caveat that sometimes in SDH-deficient gists, you can...
find these enlarged nodes, those should be resected, but that's a pretty rare consideration. In general, you run to the mill gist, you're not going to plan to do a lymphadenectomy. Dr. Breeland, can you talk about whether we should... plan to do this minimally evasively does it have to be done open yeah i mean i think you interestingly you mentioned endoscopic resection so i'll touch on that in a second but yeah i mean i think the vast majority of these are going to be mis because
It really is a very straightforward operation. You just kind of like grab the stomach next to the gist, pull it out, fire a stapler, fire another stapler to kind of finish your wedge. and put it in a bag and you're done. I mean, it's, you know, it's usually like a 30, 40 minute operation.
Again, for the run of the mill gastric gist. So I do think that most of these should be done MIS. The key is not to rupture it. So, you know, particularly as robotic, you don't have haptic feedback. You got to be really careful grabbing the actual tumor itself. You want to, you know, avoid doing.
that kind of a no touch technique you brought up endoscopic that's kind of a newer thing that you know our our gi group is doing but you know i kind of joke with them i'm like you know it it's they it's not that easy for them to do endoscopically and like there's a risk that they rupture the stomach and all this stuff because they have to open the mucosa go through the mucosa cut out the muscular layer of the stomach and then rely on the serosa and then they'll like do some sort of endoscope
closure of the mucosa. And I'm like, okay, yeah. Or I could just take them to the operating room, fire a stapler twice, and they go home the next day. And there's like so little risk. So, you know, now I think if you're up by the GE junction or in some difficult area to resect, then endoscopic resection is a consideration. But again, if it's like sitting in the body of the stomach, it's just...
unless they have a hostile abdomen. I did have a patient recently that I sent for endoscopic because he had had like four X-laps and I was like, there's no way I'm getting an MIS. And, you know, so in that case, I think it's reasonable. But just don't overthink it a little bit with gist. They're pretty easy to cut out. So just kind of cut it out. All right. So I think we've kind of beat the surgical.
horse to death here so let's talk a little bit about medical therapy which i know all the surgery residents are excited about but lexi talk to me about what the mainstay of treatment for gist are and when it works so i think we've kind of
mentioned this a little bit before, but Gleevec is the one medication you definitely want to know, even for the ab site. As far as neoadjuvant therapy, we alluded to this, but if it's a really big tumor and it's going to affect your surgical plan, you could attempt to shrink it.
It's really close to something that you would rather preserve, such as the sphincters if it's a rectal gist, the G-junction if it's in the stomach. If that would affect the ultimate surgical planning, you would want to give it up front before you go and resect it. Yeah, and just to hammer the point home, so Gleevec or imatinib is the generic name, is really the mainstay of adjuvant or sometimes neoadjuvant therapy for GISTs. Imatinib is a selective inhibitor of the KIT protein tyrosine kinases.
We know, as we said, there's a better response rate when you have an exon 11 mutation. And we know there's improved recurrence-free survival as well. So that's for exon 11. If you have an exon 9 mutation, there's actually... clinical trial data that shows that getting a higher dose of imatinib is is required in order to to achieve similar similar outcomes
And like Dr. Vila mentioned earlier, even then, it may not be quite as good just because of the biology of having an exon 9 versus an 11 mutation. Something else to think about when you're giving this in the neoadjuvant setting or potentially the metastatic setting is resistance.
to tyrosine kinase inhibitors resistance in general is defined by clinical progression during this for the first six months of therapy and most often this is seen with the pdgfra exon 18 mutation wild type just can also develop resistance in particular patients that have been on the same therapy for more than six months if they develop progression you may want to think about escalating your dose or changing the agent depending on the cloud situation.
Yeah, and that exon 18 PDGFR, the thing to remember for the ab site is D842V if you really want to get 100 on the ab site. But those are highly resistant. They're an interesting mutation because... Some company developed a very specific drug to basically treat that one mutation.
And then the drug is incredibly expensive because so few patients have it. And the drug company had to spend a lot of money developing this drug. So they made it very, very expensive. But it works really well for that mutation. So it's an interesting kind of example of modern medicine where... you know, this orphan kind of group of patients that had this highly resistant mutation. And some company, you know, developed a very specific inhibitor for that and it works. And so...
You know, that's just kind of where we're getting in surgical oncology a little bit is that, you know, we can figure out exactly what your mutation is and then potentially give you a drug that. works exactly for that mutation. So anyway, the story of D842V is interesting whether or not you want to remember that one mutation.
One other key thing on neoadjuvant is how much neoadjuvant to give. Basically what you do is you just scan the patient at some interval every two months or so, every three months, and then once their tumor stops shrinking, you operate. So if their tumor is decreasing in size, you just keep giving the Gleevec. And then somewhere along the way, it'll kind of stop shrinking. And it may all be dead at that point.
but it may all be necrotic, but you're not really getting any more benefit. That usually happens around the six month mark, but eventually it'll just kind of stop shrinking. And once you see that on two interval scans, you operate. Yeah. So we talked about imatinib, but there's some other... tyrosine kinase inhibitors out there too. Beth can you go over those real quick?
Yeah, absolutely. So much less commonly heard about than Gleevec, but several alternative agents. So Sinitinib is a multi-targeted tyrosine kinase inhibitor that can control progressive disease in patients with Gleevec resistance. So, and this may also be a better first-line therapy in patients with SDH-deficient GIST with a higher response rate in exon 9 versus 11 kit mutations. The medication that Dr. Greenland alluded to...
Avrapritinib is the FDA-approved medication for the PDGFRA exon 18 mutation. So if you identify early Gleevec resistance, you should consider this genotyping study in the event they are candidate for this agent. Yeah. And in reality, the metastatic setting too, I mean, there's, there's a whole bunch of tyrosine kinase inhibitors that you can use as, you know, third, fourth, fifth lines, but that obviously gets very into the weeds. Dr. Freeland, do you have any other closing remarks for us?
No, I mean, I think the key points clinically, you know, for the ab site, you got to remember all this stuff, but clinically, you know, just think about, is this going to be easy to cut out or not? If it's easy to cut out, just go cut it out. If it's not, then you need to start getting into the genotyping.
you know if they have an exon 11 then you're going to have a good chance of response the other thing that comes up sometimes is that particularly small biologists will erode into the into the lumen sometimes and cause a fistula So you can actually get a tumor fistula from a small biologist. And those are fairly difficult to deal with sometimes because they get very inflamed and everything around them sort of sticks to them.
And sometimes they're really close to key structures and they can be difficult to deal with. Every once in a while, you'll also get just like a massive small biologist that is almost like a sarcoma that takes up half the abdomen.
And that's where, again, neoadjuvant, I think, is useful. The tough thing if they have the fistula is trying to get them through any sort of neoadjuvant if they're having fevers and these kind of things. So sometimes those are just difficult cases that you just have to take to the operating room.
You know, I think that in the last 10 years, just in my time from training to now, it's really changed quite a bit because we have all these effective therapies. And it's remarkable when they work there, they just like melt the tumor. And so if you have a duodenal gist that's, you know, going to impinge on the ampulla and you're like, man, I'm going to have to do a Whipple.
try to use neoadjuvant. You know, in 70% of the patients, you're going to have great response with neoadjuvant, and it may save the patient a more morbid operation. Awesome. So let's finish up with some ab site highlights and takeaways, especially as the ab site creeps up. So Connor, where do gists most commonly arise from? Most commonly in the stomach followed by a small intestine.
Okay, awesome. And then Lexi, gists are caused by activating mutations in what two common genes? Most common are KIT and PGF-RA. We should know that GISTs have a wide spectrum of clinical presentations, so this can be microtumors found on autopsy or rapidly progressive with widespread metastases. Risk of recurrence is independently predicted by a few items. Connor, what would those be? yeah so it's size mitotic rate and the site the primary site
Specific mutations help to predict response to TKI therapy. We won't go over those again. Please see the rest of the episode. Neoadjuvant therapy can help facilitate a few items. Lexi, when would you especially consider neoadjuvant therapy? Again, if it changes the operation you're going to do, such as avoiding the Whipple, trying to shrink it away from the GE junction or the sphincters.
All right, guys. Thanks so much for joining us as we discuss GIST tumors and our clinical case. Join us next time where we're going to talk about landmark trials in GIST. Be sure to check out our website at www.behindthenife.org for more great content. You can also follow us on Twitter at Behind the Knife and Instagram at Behind the Knife Podcast. If you like what you hear, please take a minute to leave us a review.
Content produced by Behind the Knife is intended for health professionals and is for educational purposes only. We do not diagnose, treat, or offer patient-specific advice. Thank you for listening. Until next time, dominate the day. you