Episode two of the Gastritis and Gastric Cancers chapter works through the four gastric tumor families where histology and molecular driver are the discriminator: adenocarcinoma by Lauren type, MALT versus large B-cell lymphoma, the three gastric neuroendocrine tumors, and GIST as the model targeted-therapy cancer. Each tumor's biology drives its staging and its drug. Board-relevant triggers, molecular markers, and treatment sequences throughout. Topics covered Gastric adenocarcinoma and the Lauren classification Hereditary diffuse gastric cancer and CDH1 Adenocarcinoma staging and molecular profiling MALT versus large B-cell gastric lymphoma Three types of gastric neuroendocrine tumor GIST molecular biology and risk stratification Targeted therapy sequences (FLOT, R-CHOP, TKIs) Key decisions Intestinal-type adenocarcinoma arises from the H. pylori atrophy cascade; diffuse type comes from E-cadherin/CDH1 loss, signet-ring cells, and worse prognosis. Signet-ring histology in a 30s-40s patient with a first-degree relative triggers germline CDH1 testing and prophylactic total gastrectomy. Linitis plastica gives a rigid non-distensible leather-bottle stomach; superficial forceps biopsies miss it because cells sit deep, so non-diagnostic superficial biopsies mandate deeper sampling. Resectable disease gets perioperative FLOT plus D2 dissection; metastatic disease is profiled for HER2, PD-L1, MMR/MSI, and claudin 18.2. MALT lymphoma is H. pylori-driven and eradication is curative in most early stomach-confined cases, but t(11;18) marks non-responders needing radiation or rituximab. Large B-cell lymphoma gets R-CHOP, never antibiotics alone. Gastric NETs sort by gastrin: type 1 from atrophic gastritis (high gastrin, high pH), type 2 from ZES/MEN1 (high gastrin, low pH), both low-risk; type 3 is gastrin-independent on normal mucosa with normal gastrin and is the dangerous one, resected like adenocarcinoma. A normal gastrin flags the highest-risk NET. GIST arises from interstitial cells of Cajal as a fourth-layer (muscle) hypoechoic mass, CD117/DOG1 positive, with no nodal spread so no lymphadenectomy. Rule of fives (size and mitotic count) plus small-bowel site and rupture stratify risk; resect gastric GISTs over 2 cm. GIST drug follows the mutation: KIT-mutant responds to imatinib (exon 11 best, exon 9 higher dose), PDGFRA D842V needs avapritinib, and resistance sequence is imatinib then sunitinib then regorafenib then ripretinib. For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: [email protected]. (00:00) - Introduction: histology and driver as discriminator (00:33) - Adenocarcinoma and the Lauren split (03:58) - Staging and molecular profiling to therapy (06:12) - Gastric lymphoma: MALT versus large B-cell (09:31) - Neuroendocrine tumors sorted by gastrin (12:25) - GIST: molecular biology, ultrasound, and drugs (16:11) - Recap by histology and driver

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