Gastritis, Gastric Cancers, and Submucosal Tumors: Gastric Tumors: Diagnosis and Drug Choice

0:00Welcome to Board Pearls. This is episode two of two of the Gastritis, Gastric Cancers, and Submucosal Tumors chapter, in the Stomach and Small Bowel Disorders module. This episode is the tumors of the stomach: adenocarcinoma, lymphoma, neuroendocrine tumors, and gastrointestinal stromal tumors, GIST. A man with gastric adenocarcinoma shows how the histologic type is used, what on the exam changes the plan, how staging proceeds, and which molecular tests choose the drug, and a young woman with a stiff stomach shows the diffuse type. A woman with mucosa-associated lymphoid tissue, MALT, lymphoma shows why antibiotics can cure it and which genetic test predicts when they won't, and a man with a large ulcerated mass shows the aggressive lymphoma. A man with small polyps on atrophic mucosa and a woman with a single large mass show the neuroendocrine tumor types, and why a normal gastrin is a warning. And a woman with a bleeding submucosal mass shows why endoscopic ultrasound is the key test for GIST, how risk is judged, and why the mutation chooses the drug.

1:07Here's the first patient. A sixty-seven-year-old man has three months of early satiety, then vomiting after meals, and twenty pounds of weight loss. He has iron deficiency anemia. He smoked for forty years, and he grew up in a family that heavily salted and preserved its food. On exam he's thin, with a firm node above his left clavicle. Endoscopy shows an ulcerated mass in the antrum narrowing the pylorus. Biopsies show a gland-forming adenocarcinoma.

1:35He has gastric adenocarcinoma, and the pathologist's first classification, the Lauren type, matters because the two types are almost different diseases, with different workups and operations. Intestinal type forms gland-like structures. It develops through the H. pylori cascade: gastritis, atrophy, intestinal metaplasia, dysplasia, then cancer. It occurs mostly in older patients, more often men, usually in the distal stomach. It's the type that makes gastric cancer so much more common in East Asia, Eastern Europe, and parts of Latin America.

2:11The two types also differ in their molecular path. Intestinal type gathers mutations in APC, p53, and KRAS, telomerase activation, and MLH1 hypermethylation along the way, and a subset amplifies HER2. Diffuse type forms no glands. It's made of poorly cohesive cells, including signet ring cells, that infiltrate the wall. It occurs at younger ages, equally in men and women, at similar rates worldwide, and carries a worse prognosis. It arises through loss of E-cadherin, inherited from a germline CDH1 mutation or acquired in the tumor. H. pylori, especially strains carrying cagA, is a class one carcinogen for both types.

2:56His tumor forms glands, so it's intestinal type, and his risk factors fit: older age, male sex, smoking, a high-salt preserved diet, and very likely long-standing H. pylori. The rest of the list is atrophic gastritis from H. pylori or autoimmune disease; extensive or incomplete intestinal metaplasia; adenomatous gastric polyps; prior partial gastrectomy, especially with a Billroth two reconstruction; a first-degree relative with gastric cancer; a diet low in fruit and vegetables or high in processed meat; and, for cancers of the cardia, obesity.

3:32His presentation shows how far the cancer has gone. He's presenting late because early gastric cancer is usually silent, and about four in five early cancers cause no symptoms or only ulcer-like dyspepsia. Patients usually present with alarm features. They're weight loss, dysphagia from a tumor near the junction, vomiting from an antral tumor blocking the outlet, as in him, and overt or occult bleeding, which explains his iron deficiency.

3:57His exam changes the plan before any scan. A hard left supraclavicular node is Virchow's node, a sign of distant spread. The other landmarks of spread are Sister Mary Joseph's nodule, a periumbilical deposit; Blumer's shelf, a pelvic peritoneal deposit felt on rectal exam; and a Krukenberg tumor, signet ring metastases to the ovaries, usually both. Paraneoplastic signs include migratory superficial thrombophlebitis, called Trousseau syndrome; acanthosis nigricans; and the sudden eruption of many seborrheic keratoses, the sign of Leser-Trelat. So his node is biopsied first, because if it holds cancer, his disease is metastatic.

4:42In a patient without that node, staging runs in a fixed order. Endoscopy with biopsy makes the diagnosis. Endoscopic ultrasound gives the most accurate depth and nodal staging. T one is confined to the mucosa or submucosa, T two reaches the muscularis propria, T three the subserosa, and T four goes through the serosa or into neighboring organs. Depth and nodes decide whether a cancer can be removed through the scope or needs perioperative chemotherapy and surgery.

5:10The rest of staging looks for spread the scope can't see. Computed tomography, CT, of the chest, abdomen, and pelvis looks for distant spread, most often to the liver and peritoneum, and positron emission tomography with CT, PET-CT, helps in selected patients. Before any curative operation, staging laparoscopy with peritoneal washings looks for peritoneal spread that CT misses, especially in diffuse-type tumors and tumors through the serosa.

5:40His supraclavicular node contains adenocarcinoma. He has metastatic disease, so surgery for cure is off the table, and the molecular profile decides treatment.

5:52Every advanced tumor gets the full molecular profile at diagnosis, because each result chooses a drug. HER2 is tested by immunohistochemistry, with fluorescence in situ hybridization, FISH, for equivocal results. Programmed death-ligand one, PD-L1, is reported as a combined positive score. Microsatellite instability or mismatch repair deficiency is tested, along with Epstein-Barr virus status and claudin eighteen point two.

6:22Each result has a matching treatment. HER2-positive tumors, immunohistochemistry three plus, or two plus with FISH amplification, get trastuzumab added to first-line chemotherapy, with pertuzumab or trastuzumab deruxtecan later. PD-L1-positive tumors benefit from adding pembrolizumab or nivolumab to chemotherapy, more so as the score rises. Nivolumab's label doesn't strictly require a score threshold, though it works best at higher scores.

6:51Two more results have their own drugs. Tumors with microsatellite instability or mismatch repair deficiency respond remarkably well to checkpoint inhibitors, so pembrolizumab alone is indicated regardless of PD-L1, and withholding it because PD-L1 is low is a classic trap. Claudin eighteen point two-positive tumors can get zolbetuximab, an antibody against that protein, added to chemotherapy.

7:15His tumor is HER2-positive, so he starts first-line chemotherapy with trastuzumab. Five-year survival in advanced disease is only about ten to fifteen percent, which is why prevention, eradicating H. pylori and surveying premalignant stomachs, matters so much.

7:33His diagnosis also changes his family's risk. His children and siblings are first-degree relatives of a gastric cancer patient, so they're on the list for H. pylori testing and treatment. Family history is also a modifier that can move a relative with metaplasia into surveillance. A family with several gastric cancers, especially diffuse type at young ages, needs referral for genetic testing.

7:56Had his cancer been caught earlier, the stage would have set a different plan. An early cancer confined to the mucosa or submucosa, differentiated, not ulcerated, under two centimeters, and without lymphovascular invasion, can be removed endoscopically, by mucosal resection or submucosal dissection, with curative intent in selected cases.

8:17Locally advanced resectable cancer gets chemotherapy around surgery. It's perioperative fluorouracil, leucovorin, oxaliplatin, and docetaxel, FLOT, before and after surgery, which replaced older epirubicin-based regimens because it improved overall survival and pathologic response. A distal tumor with a clear proximal margin gets a subtotal gastrectomy, and a proximal or diffuse-type tumor gets a total gastrectomy, either way with a D two lymph node dissection. A patient who goes straight to surgery and has high-risk findings in the specimen gets adjuvant fluoropyrimidine-based chemoradiation.

8:56The second patient shows how the diffuse type changes the workup. A twenty-nine-year-old woman has dyspepsia and weight loss. Endoscopy shows a stiff stomach that barely distends with air, and biopsies show signet ring cell carcinoma, diffuse type. Her stiff, thickened stomach is linitis plastica, the diffuse variant in which signet ring cells infiltrate the whole wall. It makes up about a tenth of gastric adenocarcinomas, is often metastatic at diagnosis, and carries the worst prognosis.

9:27Her age and type trigger genetic testing. A young patient with diffuse type, or a family with several gastric cancers, triggers CDH1 genetic testing for hereditary diffuse gastric cancer, and carriers may need to consider prophylactic gastrectomy. Staging laparoscopy with cytology is especially important in her, and a total gastrectomy would be the operation if she's resectable.

9:50The third patient's gastric tumor is a lymphoma, and it's one that antibiotics can treat. A sixty-one-year-old woman has six months of dyspepsia. Endoscopy shows patchy red, nodular mucosa with a few shallow ulcers in the body of the stomach. Biopsies show marginal zone B-cell lymphoma of MALT type. H. pylori is present.

10:12She has gastric MALT lymphoma with H. pylori, and its pathogenesis is why antibiotics could cure her. A normal stomach has essentially no organized lymphoid tissue. Chronic H. pylori infection creates some, and in that acquired tissue, T cells that react to H. pylori help nearby B cells grow. Over years, a group of B cells can become a single clone and turn into a low-grade marginal zone lymphoma.

10:36Those malignant B cells still depend on help, at first. They need the H. pylori-driven T cells. Remove the bacterium and the help stops, and many of these lymphomas regress. That makes MALT lymphoma the only gastric malignancy in which antibiotics can be curative for early disease.

10:55Gastric lymphoma is less than five percent of gastric tumors, and its two main types are treated completely differently. MALT lymphoma is low grade and driven by H. pylori. Diffuse large B-cell lymphoma is aggressive, doesn't respond to eradication, and needs chemoimmunotherapy. So the first decision is which one she has.

11:15Her biopsy says MALT, and she's staged before treatment for two reasons. Staging shows whether the lymphoma is confined to the stomach wall, which decides whether antibiotics are likely to work. And it makes sure a large-cell lymphoma isn't hiding in the same stomach, because infiltration can extend beyond what mucosal biopsies show. She has endoscopic ultrasound for depth and nearby nodes, and CT of the chest, abdomen, and pelvis.

11:41One genetic test, also done at diagnosis, decides whether antibiotics can work. It's FISH for t eleven eighteen. The translocation fuses API2 and MALT1, and the fusion protein switches on nuclear factor kappa B permanently, so the lymphoma cells no longer need H. pylori-driven T-cell help. A translocation-positive MALT lymphoma doesn't respond to eradication, because the tumor no longer needs the signal being removed. The translocation is present in about thirty percent of gastric MALT lymphomas and is more common in those that don't respond, invade deeper, or involve nodes.

12:19Her endoscopic ultrasound shows lymphoma confined to the mucosa and submucosa with no nodes, her CT is clear, and her FISH is negative. She has early, localized, H. pylori-positive MALT lymphoma. Involved nodes would have meant stage two disease, which moves straight to second-line treatment.

12:37Her first-line treatment is H. pylori eradication. It produces complete histologic remission in about seventy to eighty percent of patients with disease confined to the stomach, and up to ninety percent in some series of early disease limited to the mucosa and submucosa without nodes. She takes optimized bismuth quadruple therapy for fourteen days. Eradication is confirmed by breath test or stool antigen at least four weeks after the antibiotics, with her proton pump inhibitor, PPI, held.

13:05Her response is judged by repeat endoscopy with biopsies, not by symptoms. Biopsies come three to six months after treatment, then every six months for two years, then yearly. Many patients in complete remission still have a small clonal B-cell population on sensitive polymerase chain reaction, PCR, clonality testing. That clone, without visible lymphoma on histology, doesn't predict relapse and doesn't change management. Her six-month biopsies show complete histologic remission.

13:37Antibiotics aren't enough for every patient, and four groups move to second-line treatment. They're t eleven eighteen lymphoma, which is independent of the bacterium; H. pylori-negative lymphoma, which has no bacterium to remove; stage two or higher disease; and disease that persists after eradication.

13:56Second-line treatment depends on the stage. For localized disease, stages one and two, involved-site radiation therapy, typically twenty-four to thirty gray, achieves high local control rates. For more advanced disease, it's rituximab alone or with chemotherapy such as chlorambucil, bendamustine, or fludarabine. Surgery has essentially no role, because less invasive treatment works and the disease is often multifocal.

14:21The fourth patient has the aggressive gastric lymphoma. A sixty-eight-year-old man has a large ulcerated mass in the body and antrum, and biopsies show sheets of large B cells that stain for CD20. That's diffuse large B-cell lymphoma, the most common primary gastric lymphoma. It can arise on its own or transform from a MALT lymphoma, particularly one with t eleven eighteen. At endoscopy it forms large ulcerated masses, protruding tumors, or multiple shallow ulcers, most often in the body and antrum.

14:53His staging is broader, because it behaves like a systemic lymphoma. It includes endoscopy and endoscopic ultrasound, CT, bone marrow aspiration and biopsy, examination of Waldeyer's ring, the tonsils and adenoids, and a serum lactate dehydrogenase, LDH, for prognosis.

15:14His treatment is chemoimmunotherapy, not antibiotics. It's R-CHOP, rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone, usually for six cycles, which cures more than seventy percent of localized disease. H. pylori is eradicated too, but eradication alone never controls a large-cell lymphoma.

15:34The fifth patient's tumors come from the stomach's hormone-sensing cells. A sixty-four-year-old man has an endoscopy for iron deficiency. In the body and fundus there are five small smooth polyps, the largest fourteen millimeters, on a background of pale, smooth mucosa without folds. The antrum looks normal. Biopsies of the polyps show a well-differentiated neuroendocrine tumor, and biopsies of the surrounding body show atrophic gastritis.

16:02He has gastric neuroendocrine tumors, and their origin explains how they're classified. Most gastric neuroendocrine tumors arise from enterochromaffin-like cells in the body and fundus, which grow in response to gastrin. So the key question about any gastric neuroendocrine tumor is whether gastrin is driving it, and that splits them into three types that predict behavior and treatment.

16:24The type comes from two measurements together, the fasting gastrin and the gastric pH. His gastrin is very high and his gastric pH is six. A high gastrin with a high pH means the stomach isn't making acid, so the antral G cells keep making gastrin, which is autoimmune atrophic gastritis, and his background biopsies confirm it. He has a type one tumor.

16:46The other two combinations define the other types. A high gastrin with a low pH means a gastrinoma driving both acid and tumor, type two. A normal gastrin means nothing drives the tumor except the tumor itself, type three. A PPI raises both gastrin and gastric pH on its own, so the numbers are read knowing whether he's on one, and off it when safe. That's also why the endoscopist biopsied the surrounding mucosa, because the polyps show what the tumor is, and the background shows why it's there.

17:16Type one is the most common, about four out of five gastric neuroendocrine tumors, and it's low risk. These tumors are usually under a centimeter, multiple, in the body and fundus on an atrophic background, with a low risk of malignancy. They secrete histamine, which the liver clears, so they don't cause carcinoid syndrome, and distant spread is uncommon.

17:38His tumors are managed by size. Tumors over one centimeter are removed endoscopically, by mucosal resection or submucosal dissection, and smaller ones are watched. So his fourteen-millimeter tumor is resected and the four small ones are left, with surveillance endoscopy, often yearly at first. Wide surgical resection is rarely needed.

18:01Removing the gastrin source is rarely worth it. Antrectomy, which removes the gastrin source, has been used historically but is reserved for very symptomatic or rapidly progressing disease. Gastrectomy to remove a small type one tumor is never right, because it doesn't touch the gastrin that will grow the next one. He also needs the rest of his autoimmune gastritis care: B12 and iron replaced, thyroid checked, and H. pylori tested.

18:27His pathology also carries a grade, which drives prognosis for every type. Grade one tumors have a Ki-67 under three percent and fewer than two mitoses per ten high-power fields. Grade two have a Ki-67 of three to twenty percent, or two to twenty mitoses. Grade three have a Ki-67 over twenty percent, or more than twenty mitoses. Beyond these well-differentiated tumors are high-grade neuroendocrine carcinomas, small-cell or large-cell type, treated with platinum-based chemotherapy like small cell lung cancer. His tumor is grade one, as most type one and type two tumors are, while type three tumors span all three grades.

19:07Type two tumors arise in Zollinger-Ellison syndrome, the gastrinoma patient whose gastrin is high but whose pH is low. They almost always occur with multiple endocrine neoplasia type one, MEN1. The gastrin effect on enterochromaffin-like cells is the same, but the stomach behind them is hyperplastic rather than atrophic, because the parietal cells are still there. Type two tumors are uncommon and carry a low risk of spread. The priority is the gastrinoma, the gastric tumors are handled like type one, and MEN1 means searching the parathyroids, pituitary, and pancreas.

19:42The sixth patient shows that type three is the dangerous one. A fifty-six-year-old woman has a single two-and-a-half centimeter ulcerated mass in her stomach on normal background mucosa. Biopsies show a neuroendocrine tumor, and her gastrin is normal. With no gastrin driving it, the tumor is growing autonomously.

20:00Type three behaves like a cancer. It's sporadic, arises from enterochromaffin cells, is usually single and larger than two centimeters, can sit anywhere in the stomach, and often has lymph node or liver metastases at diagnosis. It can cause an atypical carcinoid syndrome from histamine and serotonin. It's treated like gastric adenocarcinoma, with partial or total gastrectomy and regional lymph node dissection.

20:26Endoscopic resection has only a narrow place in type three. It's acceptable only for a small, low-grade type three tumor, under one to two centimeters, without nodes, and then submucosal dissection is preferred for better margins. At two and a half centimeters and ulcerated, she needs a gastrectomy.

20:45Her staging uses imaging built for neuroendocrine tumors. It's CT or magnetic resonance imaging, MRI, of the abdomen and pelvis; gallium sixty-eight DOTATATE PET-CT, the best test for neuroendocrine spread, which has replaced older octreotide scanning; and endoscopic ultrasound for depth and nodes.

21:06One familiar test helps less than expected. A twenty-four-hour urine five-hydroxyindoleacetic acid, five-HIAA, is most useful for midgut tumors with liver metastases. Foregut tumors like gastric ones lack the enzyme that converts the serotonin precursor to serotonin, so they make little of it.

21:25Spread is treated in steps. Octreotide or lanreotide is first-line for well-differentiated disease. Lutetium one seventy-seven DOTATATE is for progressive receptor-positive disease. Everolimus or sunitinib is used in selected cases. And resection, embolization, or ablation treats liver-dominant disease.

21:47The last patient's tumor sits under the lining, and its driver mutation picks her drug. A fifty-five-year-old woman has two days of black stools and a hemoglobin of eight. Endoscopy shows a six-centimeter round mass bulging into the stomach from under normal-looking mucosa, with a small oozing ulcer at its center. The bleeding is controlled endoscopically. A smooth mass under the lining with central ulceration and bleeding, in a young or middle-aged patient, is the typical presentation of GIST.

22:16Where GIST comes from explains where it appears and how it's driven. It arises from the interstitial cells of Cajal, the pacemaker cells that set the stomach's slow wave, or their precursors. So it appears wherever they live: most often the stomach, about sixty percent, then the small intestine, and less often the colon, rectum, esophagus, or omentum and mesentery.

22:41Its mutations divide it into groups. Most carry an activating KIT mutation, which stains as CD117. A minority have a PDGFRA mutation instead, and a similar minority have neither. That wild-type group includes succinate dehydrogenase-deficient tumors, as in the Carney triad and Carney-Stratakis syndrome, and those in neurofibromatosis type one, often multifocal in the small bowel.

23:06Confirming that her mass is a GIST takes endoscopic ultrasound, because it both locates the layer of origin and characterizes the lesion. The gastric wall appears as five layers. GIST arises from the fourth, the muscularis propria, where the interstitial cells of Cajal live, as a dark, hypoechoic mass continuous with that layer.

23:27The layer and echo pattern separate GIST from its mimics. A leiomyoma also arises from the muscularis propria but is more common in the esophagus. A lipoma usually arises from the submucosa and is bright, hyperechoic. Cysts are anechoic, and gastric varices show flow. Granular cell tumors arise from the submucosa, and ectopic pancreas usually sits in the wall of the antrum. Her mass is a six-centimeter hypoechoic lesion from the fourth layer.

23:56Her tissue is tested for the markers and the mutation. It comes from an endoscopic ultrasound-guided needle aspiration or biopsy. It's sent for CD117 and DOG1, positive in essentially all GISTs, and for KIT and PDGFRA mutation analysis, because the mutation decides treatment. Hers shows a KIT exon eleven mutation.

24:18With the diagnosis made, risk decides whether a small tumor needs surgery and whether imatinib follows surgery. Size and mitoses per fifty high-power fields matter most, captured by a rule of fives. Under five centimeters and under five mitoses is low risk, over five centimeters or over five mitoses is intermediate, and over both is high risk.

24:41Two more factors adjust that risk. Location adjusts it, because a gastric GIST behaves better than a small bowel GIST of the same size and count. And rupture, spontaneous or during surgery, makes any tumor high risk, because it seeds the peritoneum, which then becomes the main danger. A four-centimeter tumor with three mitoses that ruptures is treated as high risk.

25:04Size and site decide who needs surgery. Under the twenty twenty-three ACG guideline, gastric GISTs over two centimeters are resected, and so are all GISTs outside the stomach at any size, because the chance of spread rises with size. The operation is a wedge or partial resection with negative margins, without lymph node dissection, because GIST rarely spreads to regional nodes. Total gastrectomy is only for very large or awkwardly placed tumors.

25:33Small gastric GISTs have other options. A gastric GIST under two centimeters without high-risk ultrasound features, irregular borders, cystic spaces, echogenic foci, or a heterogeneous appearance, can be watched. An expert endoscopist can remove selected small gastric GISTs with full-thickness resection or submucosal tunneling. A small GIST outside the stomach is still resected.

25:59She has a wedge resection with clear margins and no rupture. Pathology shows a six-centimeter tumor with eight mitoses per fifty high-power fields, which is high risk.

26:09Her high risk decides what follows surgery. She gets adjuvant imatinib four hundred milligrams daily for three years after complete resection, which improves both recurrence-free and overall survival. Exon eleven mutations, like hers, respond best. Exon nine mutations need a higher dose, up to eight hundred milligrams daily. Imatinib can also be given before surgery to downstage a large or awkwardly placed tumor. She completes three years of imatinib and remains free of recurrence.

26:39The mutation can make imatinib useless. A patient whose GIST has spread to the liver and carries PDGFRA D842V is resistant to imatinib from the start, and the drug is avapritinib, which targets the activated kinase. Wild-type GISTs, succinate dehydrogenase-deficient or neurofibromatosis-related, often don't respond to imatinib either, though they tend to grow slowly.

27:03Metastatic GIST with the usual mutation follows a drug sequence. For metastatic GIST with the usual KIT mutation, imatinib is first-line and continued indefinitely, because it controls but doesn't eradicate the disease, and stopping it leads to progression. With resistance, the sequence is sunitinib, then regorafenib, then ripretinib, which covers a broad range of secondary KIT and PDGFRA resistance mutations.

27:28Here are the traps the boards set in these patients. Virchow's node isn't missed before surgery is planned. Staging laparoscopy isn't skipped before a curative operation. Advanced disease isn't treated without the full molecular profile, and a checkpoint inhibitor isn't withheld from a mismatch-repair-deficient tumor because of a low PD-L1. An early, small, differentiated cancer doesn't need a gastrectomy. Diffuse type gets a total gastrectomy, not a subtotal one. And CDH1 testing isn't missed in a young patient.

28:00The lymphoma traps follow. A gastric lymphoma isn't treated before MALT or large-cell is decided. The t eleven eighteen test isn't forgotten. Eradication doesn't cure translocation-positive, H. pylori-negative, or nodal MALT lymphoma. A persistent PCR clone isn't treated when the histology is clear. MALT lymphoma doesn't go to surgery, and large-cell lymphoma isn't treated with antibiotics alone.

28:24The neuroendocrine and GIST traps close the list. A gastric neuroendocrine tumor isn't treated before gastrin and pH are measured. Small type one tumors don't go to gastrectomy, and a type three tumor isn't treated like a type one. Urine five-HIAA isn't relied on for a foregut tumor. GIST mutation analysis isn't skipped, a lymph node dissection isn't done, and rupture makes any tumor high risk. Adjuvant imatinib isn't forgotten, it isn't stopped in metastatic disease, and it isn't given for PDGFRA D842V.

28:58So, start to finish. Gastric adenocarcinoma is intestinal type, following the H. pylori cascade in older patients, or diffuse type, younger and infiltrative, with CDH1 testing in a young patient or family cluster. Look for signs of spread, stage with endoscopy, endoscopic ultrasound, CT, and staging laparoscopy, and profile every advanced tumor for HER2, PD-L1, mismatch repair, Epstein-Barr virus, and claudin eighteen point two.

29:30Early differentiated lesions can be resected endoscopically. Locally advanced disease gets perioperative FLOT with gastrectomy and D two dissection. In metastatic disease, the profile chooses the drug.

29:43MALT lymphoma depends on H. pylori, so eradication cures most localized, translocation-negative disease, followed by biopsies. The rest gets radiation or rituximab, never surgery. Large-cell lymphoma needs R-CHOP.

30:00Type every gastric neuroendocrine tumor by gastrin and pH. Type one, high gastrin and high pH from autoimmune gastritis, is low risk, so resect over a centimeter and watch the rest. Type two, high gastrin and low pH with MEN1, is low risk, and the gastrinoma comes first. Type three, normal gastrin, is aggressive and treated like adenocarcinoma.

30:26GIST arises from the interstitial cells of Cajal, is a fourth-layer hypoechoic mass on endoscopic ultrasound, and is CD117 and DOG1 positive. Risk depends on size, mitoses, site, and rupture. Resect gastric GISTs over two centimeters and all non-gastric GISTs without node dissection. Give imatinib for three years after a high-risk resection, at a higher dose for exon nine, and give avapritinib for PDGFRA D842V.

30:58The next chapter is gastric and small bowel motility: gastroparesis, cyclic vomiting and cannabis hyperemesis, intestinal pseudo-obstruction, and functional dyspepsia.

31:09For the full chapter, the practice vignettes, and the topic-tagged question bank, head to board pearls dot com. You'll find the rest of the series on Apple Podcasts, Spotify, or wherever you listen to podcasts. That brings us to the end of episode two of two of chapter seven, and I'll see you in the next one.