Gastric Cancer最新文献

{"title":"Clinical impact of primary and secondary KIT mutations on the efficacy of molecular-targeted therapies in gastrointestinal stromal tumors.","authors":"Kota Kawabata, Tsuyoshi Takahashi, Toshirou Nishida, Yukinori Kurokawa, Kazuyoshi Yamamoto, Takuro Saito, Kota Momose, Kotaro Yamashita, Koji Tanaka, Tomoki Makino, Ryohei Kawabata, Atsushi Takeno, Kiyokazu Nakajima, Seiichi Hirota, Hidetoshi Eguchi, Yuichiro Doki","doi":"10.1007/s10120-025-01639-1","DOIUrl":"10.1007/s10120-025-01639-1","url":null,"abstract":"<p><strong>Background: </strong>Gastrointestinal stromal tumors (GISTs) are commonly driven by primary mutations in KIT or PDGFRA. Imatinib is the first-line therapy for GISTs. However, secondary mutations frequently emerge during imatinib treatment, contributing to resistance and influencing the efficacy of subsequent tyrosine kinase inhibitors, such as sunitinib and regorafenib. This study aimed to investigate the clinical relevance of both primary and secondary KIT mutations in treating and prognosing unresectable or recurrent GISTs.</p><p><strong>Methods: </strong>Ninety patients with unresectable or recurrent GISTs treated at our institution between 2000 and 2017 were retrospectively analyzed. Genetic testing was performed before the initial drug administration to guide first-line imatinib therapy based on the primary mutation profile. In 64 imatinib-resistant patients, additional genetic testing was conducted on tissues obtained from resistant lesions. Treatment response and prognosis were compared across mutational profiles.</p><p><strong>Results: </strong>The most common primary mutation was KIT exon 11 (76.7%), followed by exon 9 (12.2%). Patients with exon 9 mutations showed superior progression-free survival with sunitinib than those with exon 11 mutations. Among patients with exon 11 primary mutations, secondary mutations were identified in 79.2%, predominantly in KIT exon 13/14 (47.9%) or 17/18 (31.3%). Sunitinib was more effective in patients with secondary exon 13/14 mutations, whereas regorafenib was significantly more effective in those with exon 17/18 mutations.</p><p><strong>Conclusions: </strong>Secondary KIT mutations play a crucial role in imatinib resistance and the efficacy of second- and third-line therapies. Genetic profiling at the initial diagnosis and at the time of resistance may provide more personalized and effective treatment strategies.</p>","PeriodicalId":12684,"journal":{"name":"Gastric Cancer","volume":" ","pages":"899-910"},"PeriodicalIF":5.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12378141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144690015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dihydrotestosterone-androgen receptor signaling suppresses EBV-positive gastric cancer through DNA demethylation-mediated viral reactivation.","authors":"Miyeon Cho, Hyeji Byun, Sun Hee Lee, Sohyun Youn, Inuk Jung, Joohee Jung, Junho Lee, Hyosun Cho, Hyojeung Kang","doi":"10.1007/s10120-025-01626-6","DOIUrl":"10.1007/s10120-025-01626-6","url":null,"abstract":"<p><strong>Background: </strong>Our Kaplan-Meier analysis reveals that gastric cancer patients with high androgen receptor (AR) expression demonstrate poorer survival outcomes compared to those with low AR expression, particularly in patients with characteristics typical of EBV-positive gastric cancer. However, the molecular mechanisms driving this seemingly contradictory relationship have remained poorly understood, as our experimental findings suggest AR signaling actually suppresses tumor growth in EBVaGC.</p><p><strong>Methods: </strong>The study utilized AR-positive EBV-infected gastric cancer cell lines treated with dihydrotestosterone (DHT) to investigate molecular pathways. Comprehensive analyses included examination of apoptosis, miRNA expression, signaling pathways, DNA methylation patterns, and viral gene expression. In vivo validation was performed using xenograft models with MKN1-EBV and SNU719 cells to assess tumor growth and immune response.</p><p><strong>Results: </strong>DHT treatment triggered early apoptosis through upregulation of pro-apoptotic miRNAs, particularly miR-204-5p, while activating the PI3K-Akt pathway and enhancing DNA damage response through increased phosphorylation of key proteins. The treatment reduced DNMT3A expression, leading to genome-wide DNA demethylation and increased expression of both lytic (BZLF1) and latent (EBNA1, LMP1) EBV genes. Xenograft studies confirmed these findings, showing reduced tumor growth, increased lymphocyte infiltration, and enhanced viral gene expression specifically in AR-positive tumors.</p><p><strong>Conclusion: </strong>The study reveals that AR signaling suppresses EBV-positive gastric cancer by modulating both cellular apoptosis and EBV reactivation through epigenetic mechanisms. These findings suggest that AR agonists might have therapeutic potential in treating AR-positive EBV-associated gastric cancer.</p>","PeriodicalId":12684,"journal":{"name":"Gastric Cancer","volume":" ","pages":"776-798"},"PeriodicalIF":5.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of nodal dissection for locoregional gastric neuroendocrine carcinoma: a multicenter retrospective observational study.","authors":"Yukinori Yamagata, Mitsuhiro Furuta, Akifumi Notsu, Hirofumi Yasui, Rie Makuuchi, Takanobu Yamada, Michihiro Ishida, Kunihiro Tsuji, Shigeaki Baba, Noriaki Tokumoto, Shusuke Haruta, Masaya Watanabe, Takuya Hamakawa, Yasuyuki Kawachi, Norihiko Sugisawa, Hiroshi Yabusaki, Ryohei Kawabata, Yukinori Kurokawa, Narikazu Boku, Masanori Terashima, Nozomu Machida, Takaki Yoshikawa","doi":"10.1007/s10120-025-01636-4","DOIUrl":"10.1007/s10120-025-01636-4","url":null,"abstract":"<p><strong>Background: </strong>Gastric neuroendocrine carcinoma (NEC) is a rare and aggressive malignancy for which no standard treatment has been established for locoregional disease. This multicenter retrospective study aimed to evaluate the prognostic relevance and therapeutic efficacy of lymph node dissection in this setting.</p><p><strong>Methods: </strong>A total of 118 patients with gastric NEC or mixed adenoneuroendocrine carcinoma (MANEC) who underwent gastrectomy with lymph node dissection were analyzed. Survival outcomes, clinicopathological factors, and the therapeutic value index of each lymph node station were assessed. Lymph node involvement was classified using both the pathological N category and the extent of nodal involvement based on the dissection area (pND).</p><p><strong>Results: </strong>The 5-year overall survival and 3-year recurrence-free survival rates were 56.7% and 63.4%, respectively. Prognostic stratification using pND provided clearer separation than using the conventional pN category. Multivariate analysis identified older age, female sex, and pND2 (metastasis to D2 area nodes) as independent unfavorable prognostic factors. The therapeutic value index for lymph nodes in the D1 area was high (35.0, based on 5-year overall survival), whereas the index for D2 nodes was markedly lower (6.8). Notably, these indices remained consistent across histological subtypes, showing similar values between NEC and MANEC. Postoperative chemotherapy and surgical complications did not significantly affect survival outcomes.</p><p><strong>Conclusions: </strong>Perigastric (D1) lymph node dissection appears to provide meaningful survival benefit in locoregional gastric NEC, whereas the additional value of D2 dissection is limited. These findings support consideration of a more selective surgical approach, though further validation is needed.</p>","PeriodicalId":12684,"journal":{"name":"Gastric Cancer","volume":" ","pages":"1004-1016"},"PeriodicalIF":5.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YAP as a therapeutic target to reverse trastuzumab resistance.","authors":"Ah-Rong Nam, Kyoung-Seok Oh, Ju-Hee Bang, Yoojin Jeong, Sea Young Choo, Hyo Jung Kim, Su In Lee, Jae-Min Kim, Jeesun Yoon, Tae-Yong Kim, Do-Youn Oh","doi":"10.1007/s10120-025-01630-w","DOIUrl":"10.1007/s10120-025-01630-w","url":null,"abstract":"<p><strong>Background: </strong>Trastuzumab resistance in HER2-positive cancers remains a significant clinical challenge with limited therapeutic options. Although the tumor-promoting role of the Yes-associated protein (YAP) pathway is well established, its role in trastuzumab resistance remains unclear.</p><p><strong>Methods: </strong>We established four trastuzumab-resistant (HR) cell lines (NCI-N87HR, SNU216HR, SNU2670HR, and SNU2773HR) from HER2-positive gastric cancer and biliary tract cancer cell lines. YAP pathway activation was assessed using Phospho-RTK arrays, bulk RNA-Seq, and immunofluorescence. Antitumor effects of YAP targeting were evaluated with MTT assays, cell-cycle analysis, migration assays, RT-qPCR, ELISA, and xenograft models of SNU-2773 and SNU-2773HR cells. Immune modulation by YAP was studied through co-culture experiments with human PBMCs and cancer cells, followed by flow cytometry analysis of immune markers.</p><p><strong>Results: </strong>Upregulation and activation of the YAP/TAZ pathway were observed in HR cells, indicated by elevated ROR2 levels and nuclear translocation of YAP. This activation, driven by YAP/TEAD-dependent Wnt5a expression, suggests a positive-feedback mechanism that amplifies YAP activity. Elevated YAP and TEAD levels were observed in patient tumor tissues during disease progression following HER2-targeted therapies. Targeting YAP disrupted its oncogenic effects and restored sensitivity to trastuzumab, increased activation of CD4⁺ and CD8⁺ T cells in PBMCs, likely via PD-L1 downregulation and enhanced immunogenic cell death. Verteporfin, a YAP-TEAD inhibitor, effectively reduced tumor growth and increased apoptosis in mouse models bearing HR tumors.</p><p><strong>Conclusions: </strong>Targeting the ROR2-YAP/TEAD axis presents a promising therapeutic approach to overcome trastuzumab resistance in HER2-positive cancers, offering a potential strategy for enhancing treatment efficacy and improving clinical outcomes.</p>","PeriodicalId":12684,"journal":{"name":"Gastric Cancer","volume":" ","pages":"799-813"},"PeriodicalIF":5.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12379669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nuclear export of transmembrane protein PROM2 is specially regulated by CRM1 and affects the sensitivity of ferroptosis in gastric cancer.","authors":"Panpan Zhang, Wenbo Lin, Ting Wu, Shihao Rao, Danwei Huang, Jing Wu, Tao Tao, Jingjing Hou","doi":"10.1007/s10120-025-01642-6","DOIUrl":"10.1007/s10120-025-01642-6","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) exhibits high mortality and poor prognosis, with ferroptosis playing a critical role in its progression. More recent research suggests that PROM2 are closely associated with MVBs (Multivesicular Bodies) which is essential to ferroptosis, and may represent key molecules involved in the resistance of tumor cells to ferroptosis.</p><p><strong>Methods: </strong>The study employed RSL3-induced ferroptosis models to analyze mitochondrial damage, ROS accumulation, and iron dysregulation. PROM2 expression was assessed under varying RSL3 concentrations and durations. Co-immunoprecipitation and structural modeling elucidated the CRM1-PROM2 interaction. Clinical correlations were evaluated using GC tissue samples. In vivo animal experiments tested the effects of PROM2 and CRM1 inhibition on tumor growth.</p><p><strong>Results: </strong>RSL3 inhibits cell proliferation and induces ferroptosis in GC cells, concomitant with increased PROM2 expression. PROM2 Knockdown potentiates ferroptosis sensitivity and augments RSL3-induced cell death. Clinically, elevated PROM2 correlates with poor prognosis in GC patients. In vivo, PROM2 inhibition suppresses xenograft tumor growth and enhances ferroptosis susceptibility. Mechanistically, PROM2 interacts with CRM1 whose inhibition by LMB (Leptomycin B) impairs cell proliferation and promotes ferroptosis. Nucleocytoplasmic translocation of PROM2 is CRM1-dependent, and CRM1 expression positively correlates with PROM2 in GC tissues. CRM1 depletion synergizes with RSL3 to suppress tumor growth in xenograft models.</p><p><strong>Conclusions: </strong>These findings delineate a CRM1-PROM2 signaling axis that governs ferroptosis sensitivity in GC, wherein CRM1-mediated nuclear export of PROM2 during ferroptosis represents a critical regulatory node. Targeting this axis may offer novel diagnostic and therapeutic strategies for GC and other malignancies.</p>","PeriodicalId":12684,"journal":{"name":"Gastric Cancer","volume":" ","pages":"837-851"},"PeriodicalIF":5.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating peritoneal elastic laminal invasion to improve stratification of patients with pT3 gastric cancer.","authors":"Daiki Terajima, Motohiro Kojima, Shingo Sakashita, Tetsuro Taki, Takahiro Kinoshita, Genichiro Ishii, Naoya Sakamoto","doi":"10.1007/s10120-025-01627-5","DOIUrl":"10.1007/s10120-025-01627-5","url":null,"abstract":"<p><strong>Background: </strong>Elastic laminal invasion (ELI), defined as tumor invasion beyond the peritoneal elastic lamina, may affect gastric cancer (GC) prognosis, though limited data exist on this relationship.</p><p><strong>Methods: </strong>We retrospectively reviewed representative pathological slides from 396 patients with pT3 or pT4a GC who underwent curative resection to assess the association between ELI and relapse-free survival (RFS) and overall survival (OS).</p><p><strong>Results: </strong>The 5-year RFS of pT3 GC with negative ELI was 85.9%, which was better than the 55.9% of that of ELI-positive pT3 (P < 0.001) or pT4a (51.3%) GC (P < 0.001). Similarly, the 5-year OS of ELI-negative pT3 GC was 90.4%, while the corresponding values for ELI-positive pT3 and pT4a were 67.0% (P < 0.001) and 63.6% (P < 0.001), respectively. Multivariate analysis revealed that the most significant prognostic factors for RFS were pT factors (i.e., pT3 with ELI/pT4), tumor size (≥ 80 mm), and nodal metastasis. We subdivided our cohort of patients with pathological stage II (pT3N0, pT3N1) GC into ELI-negative and ELI-positive subgroups, and found that the ELI-negative ones had better RFS percentages than those who were ELI-positive or stage III (P = 0.002 and P < 0.001, respectively).</p><p><strong>Conclusions: </strong>ELI-positive pT3 GC has a worse prognosis than its ELI-negative counterpart, comparable to that of pT4a. These findings suggest a need to revisit the pT grading system in GC.</p>","PeriodicalId":12684,"journal":{"name":"Gastric Cancer","volume":" ","pages":"862-871"},"PeriodicalIF":5.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144698352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating boron neutron capture therapy as a potential treatment for unresectable gastrointestinal stromal tumors.","authors":"Seita Hagihara, Jun Arima, Yasuhiko Ueda, Yosuke Inomata, Takafumi Shima, Minoru Suzuki, Sang-Woong Lee, Kohei Taniguchi","doi":"10.1007/s10120-025-01633-7","DOIUrl":"10.1007/s10120-025-01633-7","url":null,"abstract":"<p><strong>Background: </strong>Boron neutron capture therapy selectively delivers the boron isotope ¹⁰B to tumors, where neutron irradiation induces a nuclear reaction that generates particle radiation, eradicating cancer cells. Imatinib and other drug therapies remain standard treatments for recurrent and unresectable gastrointestinal stromal tumors; however, their efficacy is limited by drug resistance. Therefore, developing novel therapeutic strategies for unresectable gastrointestinal stromal tumors is essential. This study aimed to investigate the therapeutic potential of boron neutron capture therapy for recurrent and unresectable gastrointestinal stromal tumors.</p><p><strong>Methods: </strong>The GIST-T1 cell line and its imatinib-resistant variant (GIST-T1/IM-R) were utilized to assess boronophenylalanine uptake and evaluate boron neutron capture therapy efficacy in both in vitro and in vivo models.</p><p><strong>Results: </strong>Boronophenylalanine was substantially incorporated into GIST-T1 and GIST-T1/IM-R cells. Boron neutron capture therapy significantly reduced survival fractions in both cell lines compared to neutron irradiation alone. In the GIST-T1 mouse model, high boronophenylalanine uptake was observed 3 h post-administration, resulting in significant tumor growth suppression following boron neutron capture therapy. Elevated expression of cleaved PARP, Caspase-3, Caspase-8, and γH2AX significantly increased in GIST-T1 tumors post-boron neutron capture therapy.</p><p><strong>Conclusions: </strong>The results indicate that boron neutron capture therapy suppresses tumor growth by inducing extrinsic apoptosis through severe DNA damage. This study suggests that boron neutron capture therapy is a promising alternative treatment for gastrointestinal stromal tumors, particularly for cases exhibiting resistance to conventional therapies.</p>","PeriodicalId":12684,"journal":{"name":"Gastric Cancer","volume":" ","pages":"924-934"},"PeriodicalIF":5.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144495863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Positive association between anti-Helicobacter pylori IgG antibody titers and atrophic gastritis in a Latvian cohort.","authors":"Joo Hyun Lim, Inese Poļaka, Danute Ražuka-Ebela, Inga Bogdanova, Sergei Parshutin, Mārcis Leja, Jin Young Park","doi":"10.1007/s10120-025-01629-3","DOIUrl":"10.1007/s10120-025-01629-3","url":null,"abstract":"<p><strong>Background: </strong>Although H. pylori is the most important risk factor for gastric cancer, the role of anti-H. pylori antibody titers in gastric carcinogenesis has not been investigated outside Asia. We aimed to analyze the relationship between H. pylori antibody titers and the risk of gastric precancerous lesions in a Caucasian population.</p><p><strong>Methods: </strong>We analyzed the GISTAR pilot study data on participants from Latvia with available anti-H. pylori IgG antibody serology and histopathological information. Participants were classified into four groups according to antibody titer: low-negative (LN), high-negative (HN), low-positive (LP), and high-positive (HP). Odds ratios (ORs) for atrophic gastritis among the 4 groups were compared using logistic regression.</p><p><strong>Results: </strong>Among a total of 1725 individuals, 970 with available histopathological information were included. A total of 738 individuals (76.1%) had histologically diagnosed atrophic gastritis. Risk of histological atrophic gastritis for each group compared to LN was as follows: HN (OR, 1.52; 95% confidence interval (CI) 0.85-2.72), LP (OR 2.04; 95% CI 1.25-3.32), and HP (OR, 2.47; 95% CI 1.50-4.07). Antibody titer as a continuous variable showed a positive relationship with histological atrophic gastritis (OR 1.09 per 10 EIU; 95% CI 1.04-1.14). The positive relationship was clearer among those aged ≥ 50 years.</p><p><strong>Conclusions: </strong>Anti-H. pylori antibody titer was positively related to the risk of atrophic gastritis in a middle-aged Caucasian population, suggesting its potential complementary role in gastric cancer risk stratification in a European setting where upper endoscopic examination is less routinely available.</p>","PeriodicalId":12684,"journal":{"name":"Gastric Cancer","volume":" ","pages":"749-759"},"PeriodicalIF":5.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The oncogenic role of hypomethylated ZNF793 in gastric carcinoma: a focus on cell survival and stemness.","authors":"Lingyan Jin, Hye-Yeong Jin, Meihui Li, Younghoon Kim, Nam-Yun Cho, Jeong Mo Bae, Gyeong Hoon Kang","doi":"10.1007/s10120-025-01632-8","DOIUrl":"10.1007/s10120-025-01632-8","url":null,"abstract":"<p><strong>Background: </strong>Although genome-wide promoter CpG island hypermethylation of Epstein-Barr virus-associated gastric carcinoma (EBV GC) is well known, ZNF793 is rarely methylated in EBV GC but is frequently methylated in other molecular subtypes of GC, including microsatellite instability-high GC. Based on the hypothesis that ZNF793 may be important for cell survival and stemness in EBV GC, the oncogenic role of ZNF793 was investigated.</p><p><strong>Methods: </strong>ZNF793 expression was knocked out and then restored in EBV and non-EBV GC cell lines, and its effects on cell proliferation, cell migration, cell invasion, tumor sphere formation, and xenograft tumor formation were assessed.</p><p><strong>Results: </strong>ZNF793 knockout significantly suppressed the migration, invasion, proliferation, and stemness in GC cells with ZNF793 expression. Additionally, ZNF793 knockout significantly inhibited tumor growth in a xenograft tumor model.</p><p><strong>Conclusions: </strong>These results suggest that ZNF793 plays an oncogenic role in not only EBV GC but also other subtypes of GC and may be a potential therapeutic target.</p>","PeriodicalId":12684,"journal":{"name":"Gastric Cancer","volume":" ","pages":"814-824"},"PeriodicalIF":5.1,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12378280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144368784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter to the Editor: Intraoperative corticosteroid administration for resectable gastric cancer: a multicenter, randomized, open‑label, phase II/III study.","authors":"Gökhan Çolak, Bilgin Demir","doi":"10.1007/s10120-025-01652-4","DOIUrl":"https://doi.org/10.1007/s10120-025-01652-4","url":null,"abstract":"","PeriodicalId":12684,"journal":{"name":"Gastric Cancer","volume":" ","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}