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Results indicate synergistic risk and support PARP-inhibitor exploration to prevent progression.",{"@graph":14,"@context":73},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/research-report/","Research & 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is the study aiming to clarify about H. pylori and hereditary cancer risk?","Question",{"text":63,"@type":64},"The study aims to clarify the molecular link between H. pylori infection, BRCA1/2 pathogenic variants, gastric cancer development, and higher incidence in HBOC families.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"What did the study find about gastric cancer incidence in HBOC families with BRCA1/2 variants?",{"text":68,"@type":64},"It found a higher gastric cancer incidence in HBOC families carrying germline pathogenic variants of BRCA1/2 compared with non-HBOC families (2.95% vs 0.78%).",{"name":70,"@type":61,"acceptedAnswer":71},"How do the results support a preventive or therapeutic role for PARP inhibitors?",{"text":72,"@type":64},"The findings suggest that therapeutic agents targeting BRCA1/2 pathogenic variants could help avoid gastric cancer development in HBOC families, and that PARP inhibitors may potentially inhibit gastric cancer development and progression with gBRCA1/2 variants.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},330934,1790103880,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,111,115,120,123,127],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & 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Linked With Hereditary Breast  \nand Ovarian Cancer  \nTakuma Hayashia, e, Kenji Sanob, Mako Okadaa, Takashi Urac, Ikuo Konishia, d  \nAbstract  \nBackground: Helicobacter pylori (H. pylori), a bacterium which chronically infects the stomach of approximately half the world’s population, is a risk factor for the development of gastric cancer (GC) . However, the underlying mechanism whereby H. pylori infection induces GC development remains unclear. Intermittent injection of the H. pylori cytotoxin-associated gene A antigen (CagA) protein into its host cell inhibits nuclear translocation of BRCA1/BRCA2, DNA repair proteins involved in the development of breast cancer/ovarian cancer. Interestingly, hereditary breast and ovarian cancer (HBOC) syndrome is associated with GC development. Here, we aimed to clarify the molecular link between H. pylori infection, BRCA1/2 pathogenic variants (PVs), GC and higher GC incidence in HBOC families.  \nMethods: We retrospectively reviewed data from Japanese patients undergoing precision treatment using cancer genomic medicine.  \nResults: We found a higher GC incidence in HBOC families having germline pathogenic variants (GPVs) of BRCA1/2 (2.95% vs. 0.78% in non-HBOC families) . Next, we found that 96.1% of H. pylori-infected patients received cancer genomic medicine for advanced GC, and > 16% advanced GC patients had gBRCA2 PVs. Furthermore, expressing wild-type BRCA1/2 in Gan mice (a mouse model of human GC) inhibited GC development. Thus, gBRAC1/2 PVs and H. pylori infection synergistically increase the risk of GC development.  \nConclusion: Our study highlights the need to investigate the potential of therapeutic agents against BRCA1/2 PVs to avoid the development of GC in HBOC families. In addition, our results suggest that poly (ADP-ribose) polymerase (PARP) inhibitors could potentially inhibit GC development and progression with gBRCA1/2 PVs.  \nManuscript submitted March 18, 2024, accepted May 17, 2024 Published online July 5, 2024  \naCancer Medicine, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan  \nbPathological Division, Shinshu University Hospital, Matsumoto,, Nagano 390-0877, Japan  \ncMedical Oncology, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan  \ndKyoto University School of Medicine, Kyoto 606-8507, Japan eCorresponding Author: Takuma Hayashi, Cancer Medicine, National Hospital Organization Kyoto Medical Center, Fushimi-ku, Kyoto 612-8555, Japan. [Email: yoyoyo224@hotmail.com](Email: yoyoyo224@hotmail.com)  \ndoi: [https://doi.org/10.14740/wjon1871](https://doi.org/10.14740/wjon1871)  \nKeywords: Gastric cancer; Helicobacter pylori; BRCA1; BRCA2; HBOC  \nIntroduction  \nDuring gastric cancer (GC) development, external stimuli turn mucosal epithelial cells into cancer precursor cells, which are further transformed into cancerous cells that proliferate uncontrollably [1] . As the tumor grows due to cancer cell proliferation, GC cells gradually infiltrate the submucosa, muscularis propria, and serosa [2, 3] . Then, GC cells crossing outside theserosa get scattered within the abdomen and pelvis, resulting in peritoneal dissemination. In addition, these GC cells directly infiltrate the large intestine, pancreas, diaphragm, and liver, all near the stomach [4] and/or invade lymph vessels and blood vessels, resulting in distant metastasis in multiple organs. Notably, a type of stomach cancer, scirrhous GC, spreads while making the stomach wall hard and thick [5]. Furthermore, scirrhous GC (which is also a refractory malignant tumor) is difficult to diagnose by endoscopic examination.  \nEast Asian countries (Japan, China, and South Korea) have the highest incidence of GC worldwide with > 50,000 GC deaths annually recorded in Japan [6] . Helicobacter pylori (H. pylori), a pathogenic bacterium that chronically infects the human gastric mucosa, is estimated to in","cbCaipWn5XSoNttO","https://ap.wps.com/l/cbCaipWn5XSoNttO","pdf",3184735,"English","# Abstract\n## Background\n## Methods\n## Results\n## Conclusion\n# Introduction","[{\"question\":\"What is the study aiming to clarify about H. pylori and hereditary cancer risk?\",\"answer\":\"The study aims to clarify the molecular link between H. pylori infection, BRCA1/2 pathogenic variants, gastric cancer development, and higher incidence in HBOC families.\"},{\"question\":\"What did the study find about gastric cancer incidence in HBOC families with BRCA1/2 variants?\",\"answer\":\"It found a higher gastric cancer incidence in HBOC families carrying germline pathogenic variants of BRCA1/2 compared with non-HBOC families (2.95% vs 0.78%).\"},{\"question\":\"How do the results support a preventive or therapeutic role for PARP inhibitors?\",\"answer\":\"The findings suggest that therapeutic agents targeting BRCA1/2 pathogenic variants could help avoid gastric cancer development in HBOC families, and that PARP inhibitors may potentially inhibit gastric cancer development and progression with gBRCA1/2 variants.\"}]","Hereditary Gastric Cancer Is Linked With Hereditary Breast and Ovarian Cancer - Abstract | PDF",1789990774,23]