Cancer Prevention Research最新文献

Construction and validation of a novel forecasting nomogram to the risk of colorectal adenomas: preventing colorectal cancer at its origin 构建和验证新型结直肠腺瘤风险预测提名图：从源头预防结直肠癌

IF 3.3 3区医学

Cancer Prevention Research Pub Date : 2024-09-17 DOI: 10.1158/1940-6207.capr-24-0066

Mao Li, Mingyu Cui, Xiaobin Zhou, Ying Song

{"title":"Construction and validation of a novel forecasting nomogram to the risk of colorectal adenomas: preventing colorectal cancer at its origin","authors":"Mao Li, Mingyu Cui, Xiaobin Zhou, Ying Song","doi":"10.1158/1940-6207.capr-24-0066","DOIUrl":"https://doi.org/10.1158/1940-6207.capr-24-0066","url":null,"abstract":"Colorectal adenomas are responsible for the origin of most colorectal cancers (CRC). Early detection together with active intervention of colorectal adenomas plays a crucial role in the prevention of colorectal cancer. This study aimed to construct and validate a new nomogram for the forecasting of the risk of colorectal adenomas based on lifestyle risk factors that could offer potential benefits for CRC prevention. Colonoscopy reports, pathology reports, physical factors, family history, personal history of disease, diet, and lifestyle habits were collected from 1133 subjects who underwent complete colonoscopy. All subjects were divided into the training cohort (n = 792) and the validation cohort (n = 341). A nomogram predicting the risk of colorectal adenoma development was constructed using the training cohort and the C-index was calculated. The predictive accuracy and clinical applicability of the nomogram were verified in the validation cohort. The nomogram was constructed by 6 statistically significant variables selected from 18 health factors, including advanced age, male, smoking, drinking, pickles, and irregular defecation. The C-index of the training cohort was 0.778 and the C-index of the validation cohort was 0.754. The calibration curve and decision curve analysis (DCA) also confirmed that the model has good predictive ability and high profit. The nomogram constructed in this study was validated and can be applied to predicting the occurrence risk of colorectal adenoma. The model can guide the identification of patients with non-symptomatic colorectal adenomas and the recognition of high-risk individuals for whom a colonoscopy is advisable.","PeriodicalId":9373,"journal":{"name":"Cancer Prevention Research","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142257568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Colon Age: A Metric for Whether and How to Screen Male Veterans for Early-Onset Colorectal Cancer. 结肠年龄：是否及如何筛查男性退伍军人早期结直肠癌的标准。

IF 3.3 3区医学

Cancer Prevention Research Pub Date : 2024-05-17 DOI: 10.1158/1940-6207.CAPR-23-0544

T. Imperiale, Laura J Myers, Barry C. Barker, Timothy E Stump, Joanne Daggy

{"title":"Colon Age: A Metric for Whether and How to Screen Male Veterans for Early-Onset Colorectal Cancer.","authors":"T. Imperiale, Laura J Myers, Barry C. Barker, Timothy E Stump, Joanne Daggy","doi":"10.1158/1940-6207.CAPR-23-0544","DOIUrl":"https://doi.org/10.1158/1940-6207.CAPR-23-0544","url":null,"abstract":"We aimed to develop a metric for estimating risk for early-onset colorectal cancer (EOCRC) to help decide whether and how to screen persons < age 50. We used risk prediction models derived and validated on male Veterans to calculate the relative risks (RRs) for 6 scenarios: one low-risk scenario (no risk factors present), four intermediate risk scenarios (some factors present), and one high-risk scenario (all factors present) for three age groups (35-39, 40-44, and 45-49 years). For each scenario, we estimated absolute CRC risk using SEER CRC incidence rates and each scenario's RR. We identified the current SEER 5-year age group to which the revised estimate was closest and refer to the midpoint of this group as the \"colon age\". When the revised estimate was ≥ that for 50-54-year-olds and for 70-74-year-olds, respective recommendations were made for (any) CRC screening and screening with colonoscopy. Among the scenarios, there was inconsistency between the two models for the 35-39 and 40-44 age groups, with only the 15-variable model recommending screening for the higher-risk 35-to-39-year-olds. Both models recommended screening for some intermediate risk and high-risk 40-44-year-olds. The models were well-aligned on whether and how to screen most 45-49-year-olds. Using risk factors for EOCRC with CRC incidence rates, \"colon age\" may be useful for shared decision making about whether and how to screen male Veterans < 50 years. For 45-49-year-olds, the 7-variable model may be preferred by patients, providers, and health systems.","PeriodicalId":9373,"journal":{"name":"Cancer Prevention Research","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140963649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effect of Clonal Hematopoiesis Mutations and Canakinumab Treatment on Incidence of Solid Tumors in the CANTOS Randomized Clinical Trial 克隆性造血突变和卡那单抗治疗对 CANTOS 随机临床试验中实体瘤发病率的影响

IF 3.3 3区医学

Cancer Prevention Research Pub Date : 2024-05-03 DOI: 10.1158/1940-6207.capr-23-0342

Janghee Woo, Tingting Zhai, Fang Yang, Huilei Xu, Margaret L. Healey, Denise P. Yates, Michael T. Beste, David P. Steensma

{"title":"Effect of Clonal Hematopoiesis Mutations and Canakinumab Treatment on Incidence of Solid Tumors in the CANTOS Randomized Clinical Trial","authors":"Janghee Woo, Tingting Zhai, Fang Yang, Huilei Xu, Margaret L. Healey, Denise P. Yates, Michael T. Beste, David P. Steensma","doi":"10.1158/1940-6207.capr-23-0342","DOIUrl":"https://doi.org/10.1158/1940-6207.capr-23-0342","url":null,"abstract":"Clonal hematopoiesis (CH) is more common in older persons and has been associated with an increased risk of hematological cancers and cardiovascular diseases. The most common CH mutations occur in the DNMT3A and TET2 genes and result in increased pro-inflammatory signaling. The Canakinumab Anti-inflammatory Thrombosis Outcome Study (CANTOS, NCT01327846) evaluated the neutralizing anti-IL-1β antibody canakinumab in 10,061 randomized patients with a history of myocardial infarction and persistent inflammation; DNA samples were available from 3,923 patients for targeted genomic sequencing. We examined the incidence of non-hematological malignancy by treatment assignment and CH mutations and estimated the cumulative incidence of malignancy events during trial follow-up. Patients with TET2 mutations treated with canakinumab had the lowest incidence of non-hematological malignancy across cancer types. The cumulative incidence of at least one reported malignancy was lower for patients with TET2 mutations treated with canakinumab vs those treated with placebo. These findings support a potential role for canakinumab in cancer prevention and provide evidence of IL-1β blockade cooperating with CH mutations to modify the disease course.","PeriodicalId":9373,"journal":{"name":"Cancer Prevention Research","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140835611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Diet modulates the gut microbiome, metabolism, and mammary gland inflammation to influence breast cancer risk 饮食调节肠道微生物组、新陈代谢和乳腺炎症，从而影响乳腺癌风险

IF 3.3 3区医学

Cancer Prevention Research Pub Date : 2024-05-03 DOI: 10.1158/1940-6207.capr-24-0055

Alana A. Arnone, Adam S. Wilson, David R. Soto-Pantoja, Katherine L. Cook

{"title":"Diet modulates the gut microbiome, metabolism, and mammary gland inflammation to influence breast cancer risk","authors":"Alana A. Arnone, Adam S. Wilson, David R. Soto-Pantoja, Katherine L. Cook","doi":"10.1158/1940-6207.capr-24-0055","DOIUrl":"https://doi.org/10.1158/1940-6207.capr-24-0055","url":null,"abstract":"Several studies have indicated a strong link between obesity and the risk of breast cancer. Obesity decreases gut microbial biodiversity and modulates Bacteroidetes-to-Firmicutes proportional abundance, suggesting that increased energy-harvesting capacity from indigestible dietary fibers and elevated lipopolysaccharide bioavailability may promote inflammation. To address the limited evidence linking diet-mediated changes in the gut microbiota to breast cancer risk, we aimed to determine how diet affects the microbiome and breast cancer risk. Female 3-week-old BALB/c mice were fed six different diets (control, high-sugar, lard, coconut oil, lard+flaxseed oil, and lard+safflower oil) for 10 weeks. Fecal 16s sequencing was performed for each group. Diet shifted fecal microbiome populations and modulated mammary gland macrophage infiltration. Fecal conditioned media shifted macrophage polarity and inflammation. In our DMBA-induced breast cancer model, diet differentially modulated tumor and mammary gland metabolism. We demonstrated how dietary patterns change metabolic outcomes, and gut microbiota, which may contribute to breast tumor risk. Furthermore, we showed the influence of diet on metabolism, inflammation, and macrophage polarity. This study suggests that dietary-microbiome interactions are key mediators of breast cancer risk.","PeriodicalId":9373,"journal":{"name":"Cancer Prevention Research","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140835602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

On the Hunt for the Missed Genetic Causes of Multiple Primary Tumors 寻找多发性原发性肿瘤被遗漏的遗传原因

IF 3.3 3区医学

Cancer Prevention Research Pub Date : 2024-05-02 DOI: 10.1158/1940-6207.capr-24-0115

Fiona Chan-Pak-Choon, William D. Foulkes

引用次数: 0

Economic Considerations for Implementing Tobacco Cessation Programs in Cancer Care Settings 在癌症护理机构实施戒烟计划的经济考虑因素

IF 3.3 3区医学

Cancer Prevention Research Pub Date : 2024-05-02 DOI: 10.1158/1940-6207.capr-24-0122

Ramzi G. Salloum, Kimberly A. Shoenbill, Adam O. Goldstein

引用次数: 0

Stool protein mass spectrometry identifies biomarkers for the early detection of diffuse-type gastric cancer 粪便蛋白质谱法确定早期检测弥漫型胃癌的生物标记物

IF 3.3 3区医学

Cancer Prevention Research Pub Date : 2024-04-26 DOI: 10.1158/1940-6207.capr-23-0449

Chi-Lee C. Ho, Michael B. Gilbert, Guillaume Urtecho, Hyoungjoo Lee, David A. Drew, Samuel J. Klempner, Jin S. Cho, Thomas J. Ryan, Naryan Rustgi, Hyuk Lee, Jeeyun Lee, Alexander Caraballo, Marina V. Magicheva-Gupta, Carmen Rios, Alice E. Shin, Yuen-Yi Tseng, Jeremy L. Davis, Daniel C. Chung, Andrew T. Chan, Harris H. Wang, Sandra Ryeom

{"title":"Stool protein mass spectrometry identifies biomarkers for the early detection of diffuse-type gastric cancer","authors":"Chi-Lee C. Ho, Michael B. Gilbert, Guillaume Urtecho, Hyoungjoo Lee, David A. Drew, Samuel J. Klempner, Jin S. Cho, Thomas J. Ryan, Naryan Rustgi, Hyuk Lee, Jeeyun Lee, Alexander Caraballo, Marina V. Magicheva-Gupta, Carmen Rios, Alice E. Shin, Yuen-Yi Tseng, Jeremy L. Davis, Daniel C. Chung, Andrew T. Chan, Harris H. Wang, Sandra Ryeom","doi":"10.1158/1940-6207.capr-23-0449","DOIUrl":"https://doi.org/10.1158/1940-6207.capr-23-0449","url":null,"abstract":"There is a high unmet need for early detection approaches for diffuse gastric cancer (DGC). We examined whether the stool proteome of mouse models of GC or individuals with hereditary diffuse GC (HDGC) have utility as biomarkers for early detection. Proteomic mass spectrometry of stool from a genetically engineered mouse model driven by oncogenic KrasG12D and loss of p53 and Cdh1 in gastric parietal cells (known as TCON mice) identified differentially abundant proteins compared to littermate controls. Immunoblot assays validated a panel of proteins including actinin alpha 4 (ACTN4), N-acylsphingosine amidohydrolase 2 (ASAH2), dipeptidyl peptidase 4 (DPP4), and valosin-containing protein (VCP) as enriched in TCON stool compared to littermate control stool. Immunofluorescence analysis of these proteins in TCON stomach sections revealed increased protein expression as compared to littermate controls. Proteomic mass spectrometry of stool obtained from HDGC patients with CDH1 mutations identified increased expression of ASAH2, DPP4, VCP, lactotransferrin (LTF), and tropomyosin-2 (TPM2) relative to stool from healthy sex and age-matched donors. Chemical inhibition of ASAH2 using C6-urea ceramide was toxic to GC cell lines and patient derived-GC organoids. This toxicity was reversed by adding downstream products of the S1P synthesis pathway, suggesting a dependency on ASAH2 activity in GC. An exploratory analysis of the HDGC stool microbiome identified features which correlated with patient tumors. Here we provide evidence supporting the potential of analyzing stool biomarkers for the early detection of DGC.","PeriodicalId":9373,"journal":{"name":"Cancer Prevention Research","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140802262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Germline Testing identifies Pathogenic/Likely Pathogenic Variants in Patients with Pancreatic Neuroendocrine Tumors. 种系检测确定胰腺神经内分泌肿瘤患者的致病性/可能致病性变异。

IF 3.3 3区医学

Cancer Prevention Research Pub Date : 2024-04-25 DOI: 10.1158/1940-6207.CAPR-23-0483

Chirayu Mohindroo, Seyda Baydogan, Parul Agarwal, Robin D Wright, Laura R Prakash, Maureen E Mork, Alison P Klein, Dan Laheru, Jess Maxwell, Matthew H G Katz, Arvind Dasari, Michael P Kim, Jin He, Florencia McAllister, A. De Jesus-Acosta

{"title":"Germline Testing identifies Pathogenic/Likely Pathogenic Variants in Patients with Pancreatic Neuroendocrine Tumors.","authors":"Chirayu Mohindroo, Seyda Baydogan, Parul Agarwal, Robin D Wright, Laura R Prakash, Maureen E Mork, Alison P Klein, Dan Laheru, Jess Maxwell, Matthew H G Katz, Arvind Dasari, Michael P Kim, Jin He, Florencia McAllister, A. De Jesus-Acosta","doi":"10.1158/1940-6207.CAPR-23-0483","DOIUrl":"https://doi.org/10.1158/1940-6207.CAPR-23-0483","url":null,"abstract":"10% of pancreatic neuroendocrine tumors (pNETs) are related to inherited syndromes (MEN1, MEN4, VHL, NF1, TSC). Growing evidence suggests that clinically sporadic pNETs can also harbor germline pathogenic variants. In this study, we report the prevalence of pathological/likely pathological germline variants (P/LP) in a high-risk cohort and an unselected cohort. We collected clinical data of patients with pNETs seen at MD Anderson Cancer Center (MDACC) and Johns Hopkins Hospital (JHH). High-risk cohort included (n=132) patients seen at MDACC who underwent germline testing for high-risk criteria (early onset, personal or family history of cancer and syndromic features) between 2013-2019. Unselected cohort (n=106) patients seen at JHH who underwent germline testing following their diagnosis of pNETs between 2020 to 2022. In the high-risk cohort (n=132), 33% (n=44) had P/LP variants. The majority of the patients had P/LP variants in MEN1 56% (n=25), followed by DNA repair pathways 18% (n=8), and 7 %(n=3) in MSH2 (Lynch Syndrome). Patients with P/LP were younger (45 years vs 50 years; p=0.002). In the unselected cohort (n=106), 21% (n=22) had P/LP. The majority were noted in DNA repair pathways 40% (n=9) and MEN1 36% (n=8). Multifocal tumors correlated with the presence of P/LP (p=0.0035). MEN1 germline P/LP variants correlated with younger age (40 vs 56 years) (p=0.0012). presence of multifocal tumors (p<0.0001), and WHO grade 1 histology (p=0.0078). P/LP variants are prevalent in patients with clinically sporadic pNET irrespective of high-risk features. The findings support upfront universal germline testing in all pNET patients.","PeriodicalId":9373,"journal":{"name":"Cancer Prevention Research","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140657702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nfe2l2/NRF2 deletion attenuates tumorigenesis and increases bacterial diversity in a mouse model of Lynch syndrome. 在林奇综合征小鼠模型中，Nfe2l2/NRF2缺失可减轻肿瘤发生并增加细菌多样性。

IF 3.3 3区医学

Cancer Prevention Research Pub Date : 2024-04-22 DOI: 10.1158/1940-6207.CAPR-23-0478

Felix Haller, K. Jimenez, Maximilian Baumgartner, M. Lang, Anton Klotz, M. Jambrich, Georg Busslinger, Leonhard Müllauer, V. Khare, C. Gasche

{"title":"Nfe2l2/NRF2 deletion attenuates tumorigenesis and increases bacterial diversity in a mouse model of Lynch syndrome.","authors":"Felix Haller, K. Jimenez, Maximilian Baumgartner, M. Lang, Anton Klotz, M. Jambrich, Georg Busslinger, Leonhard Müllauer, V. Khare, C. Gasche","doi":"10.1158/1940-6207.CAPR-23-0478","DOIUrl":"https://doi.org/10.1158/1940-6207.CAPR-23-0478","url":null,"abstract":"Lynch syndrome (LS) is the most prevalent heritable form of colorectal cancer (CRC). Its early onset and high lifetime risk for CRC emphasize the necessity for effective chemoprevention. NFE2L2 (NRF2) is often considered a potential druggable target, and many chemopreventive compounds do induce NRF2. However, while NRF2 counteracts oxidative stress, it is also overexpressed in CRC and may promote tumorigenesis. Herein, we evaluated the role of NRF2 in prevention of LS-associated neoplasia. We found an increased levels of NRF2 in intestinal epithelia of mice with intestinal epithelial-specific Msh2 deletion (MSH2ΔIEC) as compared to C57BL/6 (wild type) mice, as well as an increase in downstream NRF2 targets Nqo1 and Gclc. Likewise, NRF2 levels were increased in human MSH2-deficient LS tumors compared to healthy controls. In silico analysis of a publicly accessible RNA-sequencing LS dataset also found an increase in downstream NRF2 targets. Upon crossing MSH2ΔIEC with Nrf2null mice (MSH2ΔIECNrf2null), we unexpectedly found reduced tumorigenesis in MSH2ΔIECNrf2null compared to MSH2ΔIEC after 40 weeks. This occurred despite an increase in oxidative damage in MSH2ΔIECNrf2null mice. Loss of NRF2 impaired proliferation as seen by Ki67 intestinal staining and in organoid cultures. This was accompanied by diminished WNT/β-catenin signaling. Apoptosis was unaffected. Microbial alpha-diversity increased over time with loss of NRF2 based upon 16S rRNA gene amplicon sequencing of murine fecal samples. Altogether, we show that NRF2 protein levels are increased in MSH2-deficiency and associated neoplasia, but loss of NRF2 attenuates tumorigenesis. Activation of NRF2 may not be a feasible strategy for chemoprevention in LS.","PeriodicalId":9373,"journal":{"name":"Cancer Prevention Research","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140677489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Prevalence of H. pylori and gastric intestinal metaplasia in BRCA1 and BRCA2 carriers BRCA1 和 BRCA2 携带者中幽门螺杆菌和胃肠化生的发病率

IF 3.3 3区医学

Cancer Prevention Research Pub Date : 2024-04-20 DOI: 10.1158/1940-6207.capr-24-0039

Blake A. Niccum, Sarah Coughlin, Daniel Clay, Jordan Heiman, Kole H. Buckley, Michaela Dungan, Michael G. Daniel, Jose Ruiz, Kara N. Maxwell, Susan M. Domchek, Galen Leung, Nuzhat A. Ahmad, Gregory G. Ginsberg, Michael L. Kochman, Bryson W. Katona

{"title":"Prevalence of H. pylori and gastric intestinal metaplasia in BRCA1 and BRCA2 carriers","authors":"Blake A. Niccum, Sarah Coughlin, Daniel Clay, Jordan Heiman, Kole H. Buckley, Michaela Dungan, Michael G. Daniel, Jose Ruiz, Kara N. Maxwell, Susan M. Domchek, Galen Leung, Nuzhat A. Ahmad, Gregory G. Ginsberg, Michael L. Kochman, Bryson W. Katona","doi":"10.1158/1940-6207.capr-24-0039","DOIUrl":"https://doi.org/10.1158/1940-6207.capr-24-0039","url":null,"abstract":"BRCA1 and BRCA2 carriers may be at increased risk for gastric cancer (GC), however the mechanisms of gastric carcinogenesis remain poorly understood. We sought to determine the prevalence of GC risk factors Helicobacter pylori (H. pylori) infection and gastric intestinal metaplasia (GIM) among BRCA1/2 carriers to gain insight into the pathogenesis of GC in this population. 100 unselected BRCA1/2 carriers undergoing endoscopic ultrasound from 3/2022-3/2023 underwent concomitant upper endoscopy with non-targeted gastric antrum and body biopsies. The study population (70% women; mean age: 60.1) included 66% BRCA2 carriers. H. pylori was detected in one (1%) individual, 7 (7%) had GIM, 2 (2%) had autoimmune atrophic gastritis, and no GCs were diagnosed. Among BRCA1/2 carriers, H. pylori prevalence was low and GIM prevalence was similar to the general population, however identification of H. pylori or GIM may help inform future GC risk management strategies in BRCA1/2 carriers.","PeriodicalId":9373,"journal":{"name":"Cancer Prevention Research","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140624729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0