Stomach cancer overview
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahad Hasan, M.D.[2] Omer Kamal, M.D.[3], Parminder Dhingra, M.D. [4], Mohammed Abdelwahed M.D[5]
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Overview
Stomach cancer (gastric cancer) is a malignant neoplasm arising from the stomach, of which more than 90% are adenocarcinomas; less common types include gastric lymphoma, gastrointestinal stromal tumor, and neuroendocrine tumors. Gastric cancer is the fifth most commonly diagnosed cancer and the fifth leading cause of cancer death worldwide, with an estimated 968,350 new cases and 659,853 deaths in 2022. Age-standardized incidence and mortality have declined for decades as Helicobacter pylori prevalence has fallen, but incidence remains highest in East Asia, Eastern Europe, and parts of Central and South America. In the United States, the median age at diagnosis is 68 years, men are affected nearly twice as often as women, and early-onset disease (diagnosis before age 50) is rising. Billroth performed the first successful gastrectomy for gastric cancer in 1881.
Gastric adenocarcinoma develops through two biologically distinct pathways. The intestinal type arises through the Correa cascade (chronic gastritis → atrophic gastritis → intestinal metaplasia → dysplasia → carcinoma), which is overwhelmingly initiated by chronic H. pylori infection. The diffuse type usually arises de novo and is centered on loss of E-cadherin; its hereditary form, hereditary diffuse gastric cancer, is caused by germline CDH1 pathogenic variants. H. pylori, an IARC Group 1 carcinogen, is associated with about 90% of non-cardia cancers. Other risk factors include tobacco smoking, heavy alcohol use, high-salt and salt-preserved foods, processed meat, obesity, prior partial gastrectomy, autoimmune gastritis/pernicious anemia, and family history; cardia and gastroesophageal junction cancers are more closely linked to obesity and gastroesophageal reflux disease. About 10% of cases show familial clustering, but only 1–3% are attributable to known germline variants. The Cancer Genome Atlas (TCGA) defines four molecular subtypes: Epstein-Barr virus–positive, microsatellite instability-high, genomically stable, and chromosomal instability. Gastric cancer is classified by anatomic site, TNM stage, histology (Laurén and WHO), macroscopic pattern (Borrmann and Paris), and molecular subtype, but only stage and predictive biomarkers currently change management.
Early gastric cancer is often asymptomatic. Advanced disease presents with abdominal pain, weight loss, early satiety, bloating, dysphagia, hematemesis, or melena. Signs of advanced or metastatic disease include Virchow's node, Sister Mary Joseph nodule, Blumer's shelf, the Leser-Trelat sign, and Trousseau's syndrome. Gastric cancer must be differentiated from gastric lymphoma, gastric metastasis, gastritis, benign gastric ulcer, and Ménétrier's disease. Endoscopic screening every 2–3 years is suggested in high-incidence regions, whereas in low-incidence regions such as the United States it is reserved for defined high-risk groups. Upper endoscopy with biopsy is the diagnostic test of choice. Staging uses the AJCC/UICC 8th edition TNM system, with separate clinical (cTNM), pathological (pTNM), and post-neoadjuvant (ypTNM) stage groups. Endoscopic ultrasonography is the most reliable method for assessing depth of invasion, contrast-enhanced CT evaluates distant spread, PET/CT helps characterize CT-detected lymphadenopathy, and staging laparoscopy detects occult peritoneal disease before neoadjuvant therapy. Stage is the strongest determinant of prognosis: five-year survival exceeds 90% for treated early gastric cancer but is poor for disseminated disease.
Endoscopic resection by endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) is the treatment of choice for early gastric cancer meeting Japanese Gastric Cancer Association criteria. Gastrectomy with D2 lymphadenectomy is standard for potentially curable T2–T4 tumors, and laparoscopic and robot-assisted approaches are oncologically equivalent to open surgery. For resectable cT2 or higher or node-positive disease, perioperative chemotherapy with FLOT (fluorouracil, leucovorin, oxaliplatin, and docetaxel) is the preferred standard, and the addition of durvalumab improved event-free and overall survival in the MATTERHORN trial. For unresectable, recurrent, or metastatic disease, first-line systemic therapy is a fluoropyrimidine plus platinum backbone guided by biomarker testing: a PD-1 inhibitor (nivolumab or pembrolizumab) for HER2-negative tumors, trastuzumab (with pembrolizumab if PD-L1-positive) for HER2-positive tumors, and zolbetuximab for claudin 18.2-positive tumors. Later-line options include ramucirumab with or without paclitaxel, trastuzumab deruxtecan, and trifluridine/tipiracil. Palliative gastrectomy is not routinely recommended. Primary prevention centers on H. pylori eradication, smoking cessation, and a diet low in salt and rich in fruits and vegetables.
Historical perspective
John Jones was the first to perform a gastric resection in animals. In 1881, Billroth’s first human surgery. In 1897, Schlatter has done the first esophago-enterostomy after gastrectomy. Between 1884 to 1929, Finney’s and Rienhoff were the first to perform partial gastrectomy showing less side effects and less mortality rates.
Classification
No single scheme captures all clinically relevant information about gastric cancer. In current practice, a gastric adenocarcinoma is described along several complementary axes:[1][2]
- Anatomic site: non-cardia (true gastric) versus gastroesophageal junction (GEJ) tumors, with Siewert subtyping for junctional tumors
- Extent of disease: the AJCC/UICC 8th-edition TNM system, with separate clinical (cTNM), pathologic (pTNM), and post-neoadjuvant (ypTNM) stage groups
- Histology: the Laurén types and the WHO histologic subtypes
- Macroscopic pattern: the Borrmann classification for advanced tumors and the Paris/superficial classification for early tumors
- Molecular subtype: the TCGA and ACRG genomic classifications, plus the predictive biomarkers HER2, PD-L1, mismatch repair/microsatellite instability (MMR/MSI), and claudin 18.2 (CLDN18.2)
- Precursor lesions: gastric dysplasia graded by the WHO two-tier system and the Vienna classification
Only TNM stage and the predictive biomarkers currently change management. Histologic and molecular subtypes remain mainly descriptive and prognostic.[3][4]
Pathophysiology
Gastric adenocarcinoma develops through two biologically distinct pathways. The intestinal-type pathway is driven by inflammation and progresses stepwise through the Correa cascade. It is overwhelmingly initiated by Helicobacter pylori. The diffuse-type pathway is largely de novo and is centered on loss of E-cadherin (CDH1).[4][5][6] H. pylori is a WHO Group 1 carcinogen. Only about 1–3% of infected individuals develop cancer, which reflects the combined effect of bacterial virulence (particularly CagA), host genetics, and environmental cofactors.[4][7]
The 2014 The Cancer Genome Atlas (TCGA) classification sits on top of the Lauren histologic dichotomy. It defines four subtypes:
- Chromosomal instability (CIN)
- Microsatellite instability (MSI)
- Epstein-Barr virus–positive (EBV+)
- Genomically stable (GS)
These subtypes are independently prognostic and underpin the biomarkers that direct targeted therapy and immunotherapy: mismatch repair (MMR)/MSI, HER2, PD-L1, and EBV.[8][9][10]
About 10% of gastric cancers show familial aggregation, but only 1–3% are attributable to known germline variants. The most important of these is hereditary diffuse gastric cancer (HDGC), caused by germline CDH1 pathogenic variants. Contemporary penetrance estimates for HDGC are substantially lower than historical figures.[4][2][11]
Causes
Gastric adenocarcinoma results from an interaction between chronic infection, environmental and dietary exposures, host genetic susceptibility, and, in a small minority, high-penetrance germline variants. Chronic Helicobacter pylori infection, an IARC group 1 carcinogen, is the dominant modifiable cause. It accounts for approximately 75% of attributable risk overall and approximately 90% of non-cardia (distal) cancers.[4][12] Most intestinal-type cancers arise through the stepwise Correa cascade (chronic gastritis → atrophic gastritis → intestinal metaplasia → dysplasia → carcinoma). Diffuse-type cancers frequently arise without a recognizable precancerous lesion. When diffuse-type cancer is hereditary, it is driven by germline CDH1 (E-cadherin) inactivation.[13] About 10% of cases show familial clustering, but only about 1–3% are attributable to a known heritable germline variant.[2] The TCGA molecular classification (EBV-positive, MSI, genomically stable, chromosomal instability) has superseded older, undifferentiated oncogene lists as the framework for molecular etiology.[8]
Differential diagnosis
Stomach cancer must be differentiated from other diseases presenting with episodic abdominal pain, weight loss and loss of appetite such as gastric lymphoma, gastric metastasis, gastritis, benign gastric ulcer, Menetrier's disease.
Epidemiology and Demographics
Gastric cancer is the fifth most commonly diagnosed cancer and the fifth leading cause of cancer death worldwide. GLOBOCAN estimated 968,350 new cases and 659,853 deaths in 2022.[14][9] Age-standardized incidence and mortality have declined for more than half a century, mainly because Helicobacter pylori prevalence has fallen and food refrigeration and preservation have improved. Absolute case numbers keep rising because of population growth and aging.[12] Incidence is highest in East Asia, Eastern Europe, and parts of Central and South America. In the United States, about 30,300 new cases are diagnosed each year, the median age at diagnosis is 68 years, and incidence in men is nearly twice that in women.[9] Cardia and non-cardia gastric cancer are epidemiologically distinct diseases. The incidence of early-onset disease (diagnosis before age 50) is rising in several low-incidence countries, including the United States.[4][9]
Risk Factors
Risk for gastric adenocarcinoma (>90% of stomach cancers) is dominated by chronic Helicobacter pylori infection. H. pylori is an IARC Group 1 carcinogen and is associated with roughly 90% of non-cardia (gastric body and antrum) cancers.[15][9] It drives the stepwise Correa cascade: chronic gastritis → atrophic gastritis → intestinal metaplasia → dysplasia → carcinoma.[4][12]
Other modifiable risk factors are tobacco smoking, heavy alcohol use, high dietary salt and salt-preserved foods, processed meat, and obesity. Nonmodifiable factors include older age, male sex, high-risk ancestry or immigration from high-incidence regions, prior partial gastrectomy, prior abdominal radiotherapy, autoimmune gastritis/pernicious anemia, and inherited predisposition. The most important inherited cause is a germline CDH1 pathogenic variant causing hereditary diffuse gastric cancer (HDGC).[9]
Risk-factor profiles differ by anatomic site and histology:
- Non-cardia, intestinal-type cancer is overwhelmingly H. pylori–driven and arises from precancerous mucosal lesions.
- Cardia/gastroesophageal junction (GEJ) cancer is more closely linked to obesity and gastroesophageal reflux disease (GERD).[12]
- Diffuse-type cancer can arise without a precursor inflammatory field. This includes the hereditary (CDH1) form.[16]
Screening
Gastric cancer screening aims to detect adenocarcinoma at an early, curable stage and to identify gastric premalignant conditions along the Correa cascade: atrophic gastritis (AG), gastric intestinal metaplasia (GIM), and dysplasia.[17]
How a population is screened depends on how common gastric cancer is in that region:
- High-incidence regions: endoscopic screening every 2–3 years is suggested.
- Low-incidence regions: general-population screening is not recommended.[18]
- United States: screening endoscopy is considered only for defined high-risk groups.[19]
Upper endoscopy (EGD) is the preferred screening test.[19] In the Korean national program, EGD was associated with lower gastric cancer mortality, whereas the upper GI series (UGIS) was not.[20]
The only randomized trial reported so far found a non-significant reduction in non-cardia gastric cancer mortality with endoscopic screening.[21]
Natural history, Complications and Prognosis
If left untreated, the five-year survival rates of gastric cancer range from almost no survival for patients with disseminated disease to almost 50% survival for patients with localized distal gastric cancers confined to resectable regions. Higher recurrence rates are seen in those who have piecemeal or incomplete resections. Depending on the extent of the tumor at the time of diagnosis, the prognosis may vary. However, the prognosis is generally regarded as poor. Complications of gastric cancer are ascites, gastrointestinal bleeding, distant metastasis to other organs, weight loss, recurrence of cancer, and treatment complications. The prognosis of patients with gastric cancer is related to tumor extent that includes direct tumor extension and lymph nodes involvement. The five-year survival rate for treated early gastric cancer is over 90 percent; nearly 100 percent for mucosal tumors, and 80 to 90 percent for submucosal tumors.
Staging
Gastric adenocarcinoma is staged with the tumor–node–metastasis (TNM) system maintained jointly by the American Joint Committee on Cancer (AJCC) and the Union for International Cancer Control (UICC). The current standard is the AJCC 8th edition, implemented January 1, 2018. It is the version used in the NCCN Gastric Cancer Guidelines.[22][3]
The 8th edition uses the same T, N, and M definitions in every setting. It provides three separate stage-grouping schemata for different points in care:
- clinical (cTNM), before treatment
- pathological (pTNM), after upfront resection
- post-neoadjuvant pathological (ypTNM), after preoperative therapy and resection[23][16]
Stage determines the main treatment choice: endoscopic resection, surgery alone, perioperative multimodality therapy, or palliative systemic therapy. Stage is also the strongest determinant of prognosis.[9]
History and Symptoms
Symptoms of stomach cancer include abdominal pain, bloating, weight loss, hematemesis, melena, and dysphagia. Twenty-five percent of patients have a history of gastric ulcer
Physical Examination
Patients with stomach cancer generally appear weak. Common physical examination findings include abdominal distention, palpation of an abdominal mass, and pallor. Leser-Trelat sign and presence of Virchow's node (left supraclavicular lymphadenopathy), Sister Mary Joseph nodule (visible periumbilical nodule), Blumer's shelf (rectal mass/shelf on rectal exam) and/or Trousseau's syndrome (migratory phlebitis) on physical examination are highly suggestive of stomach cancer
Laboratory findings
Laboratory findings in gastric cancer include anemia of chronic disease on complete blood count, liver function tests may reveal abnormalities in liver function tests, antigens such as carcinoembryonic antigen, glycoprotein CA 125, carbohydrate antigen 19-9, cancer antigen 72-4, alpha-fetoprotein
Endoscopy and Biopsy
Biopsy may be helpful in the diagnosis of stomach cancer. It has a sensitivity of 98% to diagnose gastric cancer but may be negative in linitis plastica. It is commonly used nowadays as first line of treatment for superficial lesions.
Chest X-Ray
Chest x-ray may show spread to the lungs as a cannon-ball appearance on radiography. Advanced gastric carcinoma may be visible on an abdominal x-ray as an uneven stomach contours or small masses indenting the stomach contours
CT
Abdominal CT scan may be helpful in the diagnosis of stomach cancer. It is used to evaluate metastatic disease, especially hepatic or adnexal metastases, ascites, or distant nodal spread. Integrated PET/CT imaging can be useful to confirm malignant involvement of CT-detected lymphadenopathy. A negative PET CT is not helpful, since even large tumors with a diameter of several centimeters may not be visible on PET scan if the tumor cells have a fairly low metabolic activity.
MRI
MRI has better soft tissue sensitivity than CT.Individual layers may be better differentiated on MRI compared with CT. Hence, better T staging of stomach cancer. Water or effervescent granules are used to distend stomach to perform MRI
Echocardiography/Ultrasound
Endoscopic ultrasonography (EUS) is the most reliable diagnostic technique for evaluation of the depth of invasion of primary gastric cancers. Endoscopic ultrasonography is not the procedure of choice for detecting nodal spread.
Other imaging findings
Barium studies may be diagnostic of stomach cancer. The sensitivity of barium meals may be 14%. False-negative barium studies can occur in 50 percent of cases. There are three types of early gastric cancer which include polypoid, ulcerated, and superficial.
Other diagnostic studies
Laparoscopy has the advantage of directly visualizing the liver surface, the peritoneum, and local lymph nodes. Diagnostic laparoscopy is especially important for patients who are being considered for a trial of neoadjuvant therapy.
Medical therapy
The optimal therapy for stomach cancer depends on the stage at diagnosis and, in advanced disease, increasingly on molecular biomarkers. For patients with resectable disease, perioperative chemotherapy with the FLOT regimen (fluorouracil, leucovorin, oxaliplatin, and docetaxel) is the preferred standard for medically fit patients, having demonstrated superior overall survival compared with the older epirubicin-based ECF/ECX regimen (median overall survival 50 versus 35 months) in the phase 3 FLOT4-AIO trial.[24] The addition of perioperative immunotherapy with durvalumab to FLOT improved event-free survival (HR 0.71) and, at the final analysis, overall survival (HR 0.78; 95% CI 0.63–0.96; p=0.021) in the phase 3 MATTERHORN trial; no overall survival advantage was seen in the diffuse-type subgroup.[25][26][3] Adjuvant chemoradiotherapy and adjuvant chemotherapy with S-1 or capecitabine plus oxaliplatin remain acceptable options, particularly where perioperative therapy was not given. Medical therapy is also indicated for patients with unresectable or recurrent disease, after non-curative R2 resection, unresectable T4b disease, extensive nodal disease, hepatic metastases, peritoneal dissemination, or other M1 disease. Response to treatment should be evaluated by examinations such as CT scan, endoscopy, and contrast radiography. For unresectable, recurrent, or metastatic disease, systemic therapy is guided by biomarker testing for HER2 overexpression, programmed death-ligand 1 (PD-L1) combined positive score (CPS), claudin 18.2 (CLDN18.2), and mismatch repair/microsatellite instability (MMR/MSI) status. First-line therapy uses a fluoropyrimidine plus platinum backbone, to which a PD-1 inhibitor (nivolumab or pembrolizumab) is added in HER2-negative disease, trastuzumab is added in HER2-positive disease (with pembrolizumab for PD-L1–positive HER2-positive tumors), and zolbetuximab is added for CLDN18.2-positive tumors. For locally advanced unresectable and metastatic tumors, the goals of chemotherapy include palliation of symptoms, improvement in quality of life, and prolongation of survival; later-line options include ramucirumab with or without paclitaxel, trastuzumab deruxtecan for HER2-positive disease, and trifluridine/tipiracil.
Surgery
Surgery remains the only potentially curative treatment for stomach cancer and is central to the multidisciplinary management of gastric cancer. Endoscopic resection is the treatment of choice for early gastric cancer meeting absolute or expanded indication criteria, as defined by the Japanese Gastric Cancer Association (JGCA) 2021 (6th edition) treatment guidelines.[27] Methods for endoscopic resection include endoscopic mucosal resection (EMR) and endoscopic submucosal dissection (ESD). Side effects of endoscopy include bleeding and perforation. For T1 tumors, a gross resection margin of 2 cm should be obtained. A proximal margin of at least 3 cm is recommended for T2 or deeper tumors with an expansive growth pattern and 5 cm for those with an infiltrative growth pattern. For tumors invading the esophagus, a 5-cm margin is not necessarily required, but intraoperative frozen section examination of the resection line is preferred to confirm an R0 resection.
Lymph node dissection is defined by extent. D1 lymphadenectomy refers to dissection of only the perigastric lymph nodes (stations 1-7). D1+ lymphadenectomy adds stations 8a, 9, and (for total gastrectomy) 11p to the D1 dissection and is used for cT1 tumors not indicated for D1 alone. D2 lymphadenectomy is an extended lymph node dissection that additionally removes nodes along the hepatic, left gastric, celiac, and splenic arteries, and, when indicated, the splenic hilum; it is the standard of care for potentially curable T2-T4 tumors. D3 (super-extended) dissection adds D2 plus removal of nodes within the porta hepatis and para-aortic regions; prophylactic para-aortic dissection added to D2 did not improve survival in the randomized JCOG9501 trial and is not routinely recommended outside clinical trials.[28]
Laparoscopic and robot-assisted minimally invasive gastrectomy with D2 lymphadenectomy are now supported by long-term randomized data as oncologically equivalent, and in some outcomes superior, alternatives to open gastrectomy for both early and locally advanced gastric cancer.[29][30][31] For resectable locoregional adenocarcinoma (cT2 or higher, or node-positive), perioperative systemic chemotherapy with FLOT (fluorouracil, leucovorin, oxaliplatin, and docetaxel) — now increasingly combined with the anti-PD-L1 monoclonal antibody durvalumab — has replaced older anthracycline-based (ECF/MAGIC) regimens as the perioperative standard of care.[24][25] For metastatic disease, gastrectomy is not routinely recommended for palliation alone, based on the randomized REGATTA trial, and first-line systemic therapy — chemotherapy plus the anti-PD-1 monoclonal antibody nivolumab in appropriate candidates — is preferred over surgery-first approaches.[32][33]
Primary prevention
Effective measures for the primary prevention of stomach cancer include smoking cessation, eradication of Helicobacter pylori infection, and having a balanced diet rich in fruits and vegetables. In areas of low gastric cancer, incidence and screening for gastric cancer with upper endoscopy should be reserved for specific high-risk subgroups. Individuals at increased risk for gastric cancer include gastric adenomas, pernicious anemia, gastric intestinal metaplasia, familial adenomatous polyposis, Lynch syndrome, Peutz-Jeghers syndrome, Juvenile polyposis syndrome.
Secondary prevention
Gastric cancer secondary prevention is indicated for all patients after gastric surgeries. Physical examination, complete blood count, imaging or endoscopy are indicated to decrease chances of recurrence.
References
- ↑ Van Cutsem E, Sagaert X, Topal B, Haustermans K, Prenen H (2016). "Gastric cancer". Lancet. 388 (10060): 2654–2664. doi:10.1016/S0140-6736(16)30354-3. PMID 27156933.
- ↑ 2.0 2.1 2.2 Smyth EC, Nilsson M, Grabsch HI, van Grieken NC, Lordick F (2020). "Gastric cancer". Lancet. 396 (10251): 635–648. doi:10.1016/S0140-6736(20)31288-5. PMID 32861308 Check
|pmid=value (help). - ↑ 3.0 3.1 3.2 National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology: Gastric Cancer. Version 4.2026. 2026. NCCN
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Sundar R, Nakayama I, Markar SR, Shitara K, van Laarhoven HWM, Janjigian YY, Smyth EC (2025). "Gastric cancer". Lancet. 405 (10494): 2087–2102. doi:10.1016/S0140-6736(25)00052-2. PMID 40319897 Check
|pmid=value (help). - ↑ Gawron AJ, Shah SC, Altayar O, Davitkov P, Morgan D, Turner K, Mustafa RA (2020). "AGA Technical Review on Gastric Intestinal Metaplasia—Natural History and Clinical Outcomes". Gastroenterology. 158 (3): 705–731.e5. doi:10.1053/j.gastro.2019.12.001. PMID 31816300.
- ↑ Bessède E, Dubus P, Mégraud F, Varon C (2015). "Helicobacter pylori infection and stem cells at the origin of gastric cancer". Oncogene. 34 (20): 2547–55. doi:10.1038/onc.2014.187.
- ↑ Duan Y, Xu Y, Dou Y, Xu D (2025). "Helicobacter pylori and gastric cancer: mechanisms and new perspectives". J Hematol Oncol. 18 (1): 10. doi:10.1186/s13045-024-01654-2.
- ↑ 8.0 8.1 Cancer Genome Atlas Research Network (2014). "Comprehensive molecular characterization of gastric adenocarcinoma". Nature. 513 (7517): 202–9. doi:10.1038/nature13480. PMC 4170219. PMID 25079317.
- ↑ 9.0 9.1 9.2 9.3 9.4 9.5 9.6 Patel AK, Sethi NS, Park H (2026). "Gastric Cancer: A Review". JAMA. 335 (5): 439–450. doi:10.1001/jama.2025.20034. PMID 41499132 Check
|pmid=value (help). - ↑ Walch HS, Borpatragohain R, Jee J, et al. (2025). "Clinical implications of The Cancer Genome Atlas molecular classification system in esophagogastric cancer". Clin Cancer Res. 31 (10): 1912–1921. doi:10.1158/1078-0432.CCR-24-3473. PMID 40299774 Check
|pmid=value (help). - ↑ Ryan CE, Fasaye GA, Gallanis AF, et al. (2024). "Germline CDH1 variants and lifetime cancer risk". JAMA. 332 (9): 722–729. doi:10.1001/jama.2024.10852.
- ↑ 12.0 12.1 12.2 12.3 Thrift AP, Wenker TN, El-Serag HB (May 2023). "Global burden of gastric cancer: epidemiological trends, risk factors, screening and prevention". Nat Rev Clin Oncol. 20 (5): 338–349. doi:10.1038/s41571-023-00747-0. PMID 36959359 Check
|pmid=value (help). - ↑ Decourtye-Espiard L, Guilford P (April 2023). "Hereditary diffuse gastric cancer". Gastroenterology. 164 (5): 719–735. doi:10.1053/j.gastro.2023.01.038. PMID 36740198 Check
|pmid=value (help). - ↑ Bray F, Laversanne M, Sung H, Ferlay J, Siegel RL, Soerjomataram I, Jemal A (2024). "Global cancer statistics 2022: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries". CA Cancer J Clin. 74 (3): 229–263. doi:10.3322/caac.21834. PMID 38572751 Check
|pmid=value (help). - ↑ IARC Working Group on the Evaluation of Carcinogenic Risks to Humans (1994). Schistosomes, liver flukes and Helicobacter pylori. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. 61. Lyon: International Agency for Research on Cancer. PMID 7715068.
- ↑ 16.0 16.1 Hirata Y, Noorani A, Song S, Wang L, Ajani JA (2023). "Early stage gastric adenocarcinoma: clinical and molecular landscapes". Nat Rev Clin Oncol. 20 (7): 453–469. doi:10.1038/s41571-023-00767-w. PMC 11869628 Check
|pmc=value (help). PMID 37264184 Check|pmid=value (help). - ↑ Morgan DR, Corral JE, Li D, Montgomery EA, Riquelme A, Kim JJ, Sauer B, Shah SC (2025). "ACG Clinical Guideline: Diagnosis and Management of Gastric Premalignant Conditions". Am J Gastroenterol. 120 (4): 709–737. doi:10.14309/ajg.0000000000003350. PMID 40072510 Check
|pmid=value (help). - ↑ Dinis-Ribeiro M, Libânio D, Uchima H, Spaander MCW, Bornschein J, Matysiak-Budnik T, Tziatzios G, Santos-Antunes J, Areia M, Chapelle N, Esposito G, Fernandez-Esparrach G, Kunovsky L, Garrido M, Tacheci I, Link A, Marcos P, Marcos-Pinto R, Moreira L, Pereira AC, Pimentel-Nunes P, Romanczyk M, Fontes F, Hassan C, Bisschops R, Feakins R, Schulz C, Triantafyllou K, Carneiro F, Kuipers EJ (2025). "Management of epithelial precancerous conditions and early neoplasia of the stomach (MAPS III): European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter and Microbiota Study Group (EHMSG) and European Society of Pathology (ESP) Guideline update 2025". Endoscopy. 57 (5): 504–554. doi:10.1055/a-2529-5025. PMID 40112834 Check
|pmid=value (help). - ↑ 19.0 19.1 Shah SC, Wang AY, Wallace MB, Hwang JH (2025). "AGA Clinical Practice Update on Screening and Surveillance in Individuals at Increased Risk for Gastric Cancer in the United States: Expert Review". Gastroenterology. 168 (2): 405–416.e1. doi:10.1053/j.gastro.2024.11.001. PMID 39718517 Check
|pmid=value (help). - ↑ Jun JK, Choi KS, Lee HY, Suh M, Park B, Song SH, Jung KW, Lee CW, Choi IJ, Park EC, Lee D (2017). "Effectiveness of the Korean National Cancer Screening Program in Reducing Gastric Cancer Mortality". Gastroenterology. 152 (6): 1319–1328.e7. doi:10.1053/j.gastro.2017.01.029. PMID 28147224.
- ↑ Liu M, Yang W, Guo C, Liu Z, Li F, Liu A, Yang H, Shen L, Wu Q, Duan L, Wang H, Tian H, Shi C, Pan Y, Liu Y, Liu F, Cai H, He Z, Ke Y (2026). "Effect of endoscopic screening for non-cardia gastric cancer: a 12-year report of a population-based randomized trial". BMC Med. 24: 529. doi:10.1186/s12916-026-05043-z. PMID 42410417 Check
|pmid=value (help). - ↑ Amin MB, Edge SB, Greene FL, et al. (eds.) (2017). AJCC Cancer Staging Manual (8th ed.). New York: Springer.
- ↑ In H, Ravetch E, Langdon-Embry M, Palis B, Ajani JA, Hofstetter WL, Kelsen DP, Sano T (2018). "The newly proposed clinical and post-neoadjuvant treatment staging classifications for gastric adenocarcinoma for the American Joint Committee on Cancer (AJCC) staging". Gastric Cancer. 21 (1): 1–9. doi:10.1007/s10120-017-0765-y. PMID 28948368.
- ↑ 24.0 24.1 Al-Batran SE, Homann N, Pauligk C, Goetze TO, Meiler J, Kasper S, Kopp HG, Mayer F, Haag GM, Luley K, Lindig U, Schmiegel W, Pohl M, Stoehlmacher J, Folprecht G, Probst S, Prasnikar N, Fischbach W, Mahlberg R, Trojan J, Koenigsmann M, Martens UM, Thuss-Patience P, Egger M, Block A, Heinemann V, Illerhaus G, Moehler M, Schenk M, Kullmann F, Behringer DM, Heike M, Pink D, Teschendorf C, Löhr C, Bernhard H, Schuch G, Rethwisch V, von Weikersthal LF, Hartmann JT, Kneba M, Daum S, Schulmann K, Weniger J, Belle S, Gaiser T, Oduncu FS, Güntner M, Hozaeel W, Reichart A, Jäger E, Kraus T, Mönig S, Bechstein WO, Schuler M, Schmalenberg H, Hofheinz RD (May 2019). "Perioperative chemotherapy with fluorouracil plus leucovorin, oxaliplatin, and docetaxel versus fluorouracil or capecitabine plus cisplatin and epirubicin for locally advanced, resectable gastric or gastro-oesophageal junction adenocarcinoma (FLOT4): a randomised, phase 2/3 trial". Lancet. 393 (10184): 1948–1957. doi:10.1016/S0140-6736(18)32557-1. PMID 30982686.
- ↑ 25.0 25.1 Janjigian YY, Al-Batran SE, Wainberg ZA, Kim YW, Elimova E, Barros-Sotolongo A, Boku N, Chao J, Ho G, Lorenzen S, Aprile G, Chau I, Sun W, Kim JG, Rueschoff J, Chen LT, Bhagia P, Zhao J, Watson P, Molife LR, Shitara K (2025). "Perioperative Durvalumab in Gastric and Gastroesophageal Junction Cancer". N Engl J Med. 393 (3): 217–230. doi:10.1056/NEJMoa2503701. PMID 40454643 Check
|pmid=value (help). Vancouver style error: initials (help) - ↑ Janjigian YY, Al-Batran SE, Wainberg ZA, et al. (September 2026). "Perioperative durvalumab plus fluorouracil, leucovorin, oxaliplatin, and docetaxel for resectable gastric and gastro-oesophageal junction adenocarcinoma (MATTERHORN): final results of overall survival and event-free survival by pathological response in a global, randomised, double-blind, placebo-controlled, multicentre, phase 3 trial". Lancet. 408 (10560): 1114–1128. doi:10.1016/S0140-6736(26)01254-7. PMID 42716074 Check
|pmid=value (help). - ↑ Japanese Gastric Cancer Association (2023). "Japanese Gastric Cancer Treatment Guidelines 2021 (6th edition)". Gastric Cancer. 26 (1): 1–25. doi:10.1007/s10120-022-01331-8. PMC 9813208 Check
|pmc=value (help). PMID 36342574 Check|pmid=value (help). - ↑ Sasako M, Sano T, Yamamoto S, Kurokawa Y, Nashimoto A, Kurita A; et al. (2008). "D2 lymphadenectomy alone or with para-aortic nodal dissection for gastric cancer". N Engl J Med. 359 (5): 453–62. doi:10.1056/NEJMoa0707035. PMID 18669424.
- ↑ Son SY, Hur H, Hyung WJ, Park YK, Lee HJ, An JY, Kim W, Kim HI, Kim HH, Ryu SW, Kim MC, Kong SH, Cho GS, Kim JJ, Park DJ, Ryu KW, Kim YW, Kim JW, Lee JH, Yang HK, Han SU (2022). "Laparoscopic vs Open Distal Gastrectomy for Locally Advanced Gastric Cancer: 5-Year Outcomes of the KLASS-02 Randomized Clinical Trial". JAMA Surg. 157 (10): 879–886. doi:10.1001/jamasurg.2022.2749. PMC 9301593 Check
|pmc=value (help). PMID 35857305 Check|pmid=value (help). - ↑ Huang C, Liu H, Hu Y, Sun Y, Su X, Cao H, Hu J, Wang K, Suo J, Tao K, He X, Wei H, Ying M, Hu W, Du X, Yu J, Zheng C, Liu F, Li Z, Zhao G, Zhang J, Chen P, Li G (2022). "Laparoscopic vs Open Distal Gastrectomy for Locally Advanced Gastric Cancer: Five-Year Outcomes From the CLASS-01 Randomized Clinical Trial". JAMA Surg. 157 (1): 9–17. doi:10.1001/jamasurg.2021.5104. PMC 8529527 Check
|pmc=value (help). PMID 34668963 Check|pmid=value (help). - ↑ Hu Y, Hyung WJ, Huang H, Huang C, Yang HK, Sun Y, Park YK, Su X, Lee HJ, Cao H, An JY, Hu J, Kim W, Wang K, Kim HI, Suo J, Kim HH, Tao K, Ryu SW, He X, Hur H, Wei H, Kim MC, Kong SH, Ying M, Cho GS, Hu W, Kim JJ, Du X, Park DJ, Yu J, Ryu KW, Liu H, Kim YW, Li Z, Kim JW, Ji J, Lee JH, Li G, Han SU (2025). "Long-term outcomes of laparoscopic distal gastrectomy for locally advanced gastric cancer: An individual patient data meta-analysis of KLASS-02 and CLASS-01 randomized controlled trials". Chin J Cancer Res. 37 (3): 365–376. doi:10.21147/j.issn.1000-9604.2025.03.06. PMC 12240251 Check
|pmc=value (help). PMID 40642493 Check|pmid=value (help). - ↑ Fujitani K, Yang HK, Mizusawa J, Kim YW, Terashima M, Han SU, Iwasaki Y, Hyung WJ, Takagane A, Park DJ, Yoshikawa T, Hahn S, Nakamura K, Park CH, Kurokawa Y, Bang YJ, Park BJ, Sasako M, Tsujinaka T (2016). "Gastrectomy plus chemotherapy versus chemotherapy alone for advanced gastric cancer with a single non-curable factor (REGATTA): a phase 3, randomised controlled trial". Lancet Oncol. 17 (3): 309–318. doi:10.1016/S1470-2045(15)00553-7. PMID 26822397.
- ↑ Janjigian YY, Shitara K, Moehler M, Garrido M, Salman P, Shen L, Wyrwicz L, Yamaguchi K, Skoczylas T, Campos Bragagnoli A, Liu T, Schenker M, Yanez P, Tehfe M, Kowalyszyn R, Karamouzis MV, Bruges R, Zander T, Pazo-Cid R, Hitre E, Feeney K, Cleary JM, Poulart V, Cullen D, Lei M, Xiao H, Kondo K, Li M, Ajani JA (2021). "First-line nivolumab plus chemotherapy versus chemotherapy alone for advanced gastric, gastro-oesophageal junction, and oesophageal adenocarcinoma (CheckMate 649): a randomised, open-label, phase 3 trial". Lancet. 398 (10294): 27–40. doi:10.1016/S0140-6736(21)00797-2. PMID 34102137 Check
|pmid=value (help).