Cancer Epidemiology Biomarkers & Prevention最新文献

{"title":"Clonal Hematopoiesis of Indeterminate Potential as a Predictor of Colorectal Cancer Risk: Insights from the UK Biobank Cohort.","authors":"Yongfeng Liu, Zhihui Xi, Jianlong Zhou, Fa Ling, Yucheng Zhang, Huajie Xie, Jiabin Zheng, Baijin Xia, Huolun Feng, Yong Li","doi":"10.1158/1055-9965.EPI-24-1342","DOIUrl":"10.1158/1055-9965.EPI-24-1342","url":null,"abstract":"<p><strong>Background: </strong>Clonal hematopoiesis of indeterminate potential (CHIP) has been shown to be associated with the occurrence of solid tumors, but its relationship with colorectal cancer still needs to be studied.</p><p><strong>Methods: </strong>We conducted a prospective matched case-control study using data from the UK Biobank, including 5,310 incident colorectal cancer cases and 26,550 controls matched for age, sex, and body mass index.</p><p><strong>Results: </strong>Analysis of the UK Biobank data revealed that the presence of CHIP was associated with an increased risk of colorectal cancer. The odds ratio (OR) for colorectal cancer in the presence of CHIP was 1.20 (P = 0.006). This association remained significant even after excluding participants with a family history of bowel cancer (multivariate OR, 1.19; P = 0.007). Subgroup analyses demonstrated that CHIP independently increased the risk of colorectal cancer in females (multivariate OR, 1.25; P = 0.018) and in individuals older than 60 years (multivariate OR, 1.17; P = 0.046). Gene-specific analyses revealed that mutations in TET2 and ATM were particularly significant in relation to colorectal cancer risk, with an OR of 1.62 (P = 0.002) for TET2 and 2.98 (P < 0.001) for ATM.</p><p><strong>Conclusions: </strong>Our findings indicate that CHIP is associated with an increased risk of colorectal cancer, particularly in individuals more than 60 years of age or in females.</p><p><strong>Impact: </strong>Screening for CHIP in the population may improve the early detection and diagnosis rates of colorectal cancer.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"405-411"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142968828","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}

{"title":"Chronic Health Conditions among LGBTQ+ Cancer Survivors: Letter.","authors":"Di Zhao, Jie Liu","doi":"10.1158/1055-9965.EPI-24-1737","DOIUrl":"10.1158/1055-9965.EPI-24-1737","url":null,"abstract":"","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":"34 3","pages":"448"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536393","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}

{"title":"Differential DNA Methylation in the Benign and Cancerous Prostate Tissue of African American and European American Men.","authors":"Meytal Chernoff, Kathryn Demanelis, Marc Gillard, Dayana Delgado, Kevin J Gleason, Meritxell Oliva, Lin Chen, Anthony Williams, Russel Z Szmulewitz, Donald J Vander Griend, Brandon L Pierce","doi":"10.1158/1055-9965.EPI-24-0288","DOIUrl":"10.1158/1055-9965.EPI-24-0288","url":null,"abstract":"<p><strong>Background: </strong>African American (AA) men are at increased risk of prostate cancer compared with European American (EA) men. Biological mechanisms, including epigenetics, likely contribute to this disparity, but prior studies have been limited by sample size, candidate gene approaches, or lack of epigenome-wide DNA methylation (DNAm) data.</p><p><strong>Methods: </strong>To improve our understanding of these mechanisms, we compared DNAm features distinguishing tumor and paired histologically benign tissue from 76 AA and 75 EA patients with prostate cancer. We generated genome-wide array-based DNAm data and conducted differential methylation analyses comparing tumor and benign tissues in each ancestry group. We then examined the predictive ability of our identified sites and differential methylation by ancestry group.</p><p><strong>Results: </strong>We identified 90,747 and 98,929 differentially methylated CpGs in AA and EA, respectively, with 76,400 common to both groups. We identified 6,267 genes with differentially methylated promoters common to both ancestries and 639 and 1,301 genes unique to AA and EA respectively, as well as differentially methylated pathways. Only 10 CpGs were needed to distinguish tumor from benign based on a receiver operating characteristic curve (AUC > 0.9), with differentially methylated CpGs in one ancestry accurately predicting tumor versus benign in the other group. We also identified ancestry-associated CpGs (89 in tumor, 423 in benign).</p><p><strong>Conclusions: </strong>Methylation features distinguishing tumor and benign were similar for EA and AA men; however, subtle differences were identified.</p><p><strong>Impact: </strong>Differences in tumor and ancestry-associated CpGs may reveal differential tumor growth strategies, an important area for future disparities research.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"428-438"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12707997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-FDX1 Autoantibody as a Potential Biomarker for Non-Small Cell Lung Cancer Detection.","authors":"Jing Li, Xiaobin Cao, Lulu Zhang, Aichen Liu, Siyu Liu, Fengqi Chen, Yutong Li, Hanke Ma, Wenke Sun, Songyun Ouyang, Liping Dai, Jingjing Liu","doi":"10.1158/1055-9965.EPI-24-1096","DOIUrl":"10.1158/1055-9965.EPI-24-1096","url":null,"abstract":"<p><strong>Background: </strong>Autoantibodies can be readily identified prior to biopsy and may serve as valuable biomarkers for cancer detection. Ferredoxin 1 (FDX1) is a key regulator in the process of cuproptosis and affects the prognosis of lung cancer. In this study, we investigated whether the anti-FDX1 autoantibody could serve as a novel biomarker for the detection of non-small cell lung cancer (NSCLC).</p><p><strong>Methods: </strong>A total of 1,155 plasma samples were divided into the verification and validation groups. The expression levels of the anti-FDX1 autoantibody in 414 patients with NSCLC, 327 patients with benign pulmonary nodules (BPN), and 414 normal controls (NC) were detected using ELISA. Western blotting and immunofluorescence analyses were performed to confirm the ELISA results.</p><p><strong>Results: </strong>Plasma anti-FDX1 autoantibody levels were significantly higher in patients with NSCLC than in patients with BPN and NCs in the verification and validation groups. The ELISA results were confirmed by Western blotting and immunofluorescence. The anti-FDX1 autoantibody distinguished NSCLC from NC and BPN with an AUC (95% confidence interval) of 0.806 (0.772-0.839) and 0.627 (0.584-0.670), respectively.</p><p><strong>Conclusions: </strong>Our study demonstrated the potential benefits of the anti-FDX1 autoantibody as a novel biomarker for NSCLC detection.</p><p><strong>Impact: </strong>These findings suggested that the anti-FDX1 autoantibody may facilitate the detection of NSCLC.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"439-447"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853087","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}

{"title":"Red Meat, Poultry, and Fish Consumption and the Risk of Liver Cancer: A Prospective Cohort Study of 0.5 Million Chinese Adults.","authors":"Chun-Rui Wang, Dong Cai, Kun He, Jie-Jun Hu, Xin Dai, Qian Zhu, Guo-Chao Zhong","doi":"10.1158/1055-9965.EPI-24-1158","DOIUrl":"10.1158/1055-9965.EPI-24-1158","url":null,"abstract":"<p><strong>Background: </strong>Epidemiological evidence on meat consumption and liver cancer risk is limited and inconclusive; moreover, no prospective study has been conducted to investigate this association in China. Hence, we performed this study to examine the association of red meat, poultry, and fish consumption with the risk of liver cancer in a Chinese population.</p><p><strong>Methods: </strong>A total of 510,048 Chinese adults of ages 30 to 79 years were included and were followed up through December 31, 2016. Red meat, poultry, and fish consumption was evaluated using an interviewer-administered laptop-based questionnaire. HRs and 95% confidence intervals (CI) for liver cancer incidence were calculated using Cox regression.</p><p><strong>Results: </strong>Over a mean follow-up of 9.94 years, 1,906 liver cancer cases were observed. Each 50 g/day increase in red meat (HR 0.72; 95% CI, 0.49-1.05), poultry (HR 0.93; 95% CI, 0.83-1.03), and fish (HR 0.95; 95% CI, 0.85-1.05) consumption was not associated with the risk of liver cancer in the whole study population; however, subgroup analysis revealed an inverse association with poultry consumption in rural residents but not in urban residents (Pinteraction = 0.046). The initial associations did not change materially in a series of sensitivity analyses.</p><p><strong>Conclusions: </strong>Red meat and fish consumption is not associated with the risk of liver cancer in this Chinese population. The inverse association with poultry consumption in Chinese rural residents should be interpreted with caution.</p><p><strong>Impact: </strong>This is the first prospective study examining the association between meat consumption and the risk of liver cancer in the Chinese population.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"412-419"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876011","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}

{"title":"Epidemiology and Clinical Outcomes of Childhood Central Nervous System Cancers in a Large Low/Middle-Income Country Pediatric Oncology Center: A Report on 5,051 Kids.","authors":"Eslam Maher, Mohamed Kamal, Moatasem El-Ayadi, Amal Refaat, Abdelrahman Enayet, Mohamed El-Beltagy, Eman Eldebawy, Hala Taha, Madiha Awad, Mohamed S Zaghloul","doi":"10.1158/1055-9965.EPI-24-1188","DOIUrl":"10.1158/1055-9965.EPI-24-1188","url":null,"abstract":"<p><strong>Background: </strong>Central nervous system (CNS) tumors are the leading cause of cancer-related deaths in children. Although most cases come from low- and middle-income countries (LMIC) where their prognosis is worse, few epidemiologic studies are conducted in these regions.</p><p><strong>Methods: </strong>We conducted a registry-based cohort study for childhood CNS tumors at Children's Cancer Hospital, Egypt, over 15 years. Unified treatment protocols were implemented. Survival analyses were conducted using the Kaplan-Meier function. Cases were additionally annotated using the International Classification of Childhood Cancer-3 classification.</p><p><strong>Results: </strong>In total, 5,051 children ≤18 years of age were identified, accounting for 20% of all childhood cancers treated at Children's Cancer Hospital, Egypt. The most common tumor sites were the posterior fossa (36.8%) and brainstem (17.7%). Pathologies were predominantly astrocytic (n = 1,360; 26.9%) and embryonal (n = 1,003; 19.9%) in origin. The 5-year overall survival (OS) and event-free survival for all cases were 64.6% and 51.8%, respectively. More specifically, 1,421 low-grade gliomas were identified, with a 5-year OS of 91.1%. Medulloblastoma (n = 801) recorded a 5-year OS of 66%. The entity with the worst prognosis was diffuse intrinsic pontine glioma (n = 633), with a 5-year OS of 3.2%.</p><p><strong>Conclusions: </strong>We report on a large number of childhood CNS tumors from an LMIC. This study underscores the need to understand the burden of childhood brain tumors and its outcomes in resource-constrained settings.</p><p><strong>Impact: </strong>This study reports on the epidemiology and clinical outcomes of 5,000+ children with CNS tumors from a specialized LMIC center. Despite the lack of many sophisticated and advanced facilities, LMICs can improve the clinical end-results with experience and augmented efforts.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"420-427"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142833909","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}

{"title":"Epidemiologic Studies of Biomarkers and Their Role in Carcinogenesis: The Need for a Formal Causal Inference Approach.","authors":"Frances E M Albers, S Ghazaleh Dashti, Brigid M Lynch","doi":"10.1158/1055-9965.EPI-24-1758","DOIUrl":"10.1158/1055-9965.EPI-24-1758","url":null,"abstract":"<p><p>In this issue of Cancer Epidemiology, Biomarkers & Prevention, Brantley and colleagues investigated the relationships between estrogen metabolites and postmenopausal breast cancer, using data from a nested case-control study within the Nurses' Health Study. One study aim was to investigate the extent to which estrogen metabolism patterns provided further insights into mechanisms in breast cancer development beyond the role of estradiol. In this editorial, we describe the challenges in interpreting results from observational studies of biomarkers and their role in carcinogenesis due to: (i) a general lack of clarity in the research question, (ii) the limits of current knowledge about the complex underlying causal structure involving interrelated biomarkers, and (iii) the limitations in existing data sources (e.g., biomarkers measured at a single time point). We propose that applying a formal causal inference framework in these studies could be a step forward in improving their rigor, by enabling researchers to be more explicit about the causal effects of interest and the assumptions made, and to advocate for the improvement of future studies. See related article by Brantley et al., p. 375.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":"34 3","pages":"373-374"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536399","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}

{"title":"Chronic Health Conditions among LGBTQ+ Cancer Survivors: Reply.","authors":"Austin R Waters, Erin E Kent, Hazel B Nichols, Kelly Tan","doi":"10.1158/1055-9965.EPI-24-1788","DOIUrl":"10.1158/1055-9965.EPI-24-1788","url":null,"abstract":"","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":"34 3","pages":"449"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12998150/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating Estrogen Metabolites and Risk of Breast Cancer among Postmenopausal Women in the Nurses' Health Study.","authors":"Kristen D Brantley, Regina G Ziegler, Neal E Craft, Susan E Hankinson, A Heather Eliassen","doi":"10.1158/1055-9965.EPI-24-0577","DOIUrl":"10.1158/1055-9965.EPI-24-0577","url":null,"abstract":"<p><strong>Background: </strong>Estradiol and estrone are well-established risk factors for postmenopausal breast cancer. Experimental evidence suggests that specific estrogen metabolites, produced via irreversible hydroxylation of estrone and estradiol at position 2 or 16, may independently influence carcinogenesis.</p><p><strong>Methods: </strong>We performed a nested case-control study of breast cancer (328 breast cancer cases; 639 controls) among postmenopausal women within the Nurses' Health Study to examine the role of estrogens and estrogen metabolites (jointly referred to as EM). Plasma concentrations of each EM (unconjugated + conjugated forms) were measured by LC-MS/MS. Multivariable conditional logistic regression, adjusting for breast cancer risk factors, estimated relative risks (RR) and 95% confidence intervals of breast cancer across quintiles of individual EM, EM pathways, and pathway ratios. Associations by estrogen receptor (ER) and progesterone receptor (PR) status were analyzed by unconditional logistic regression.</p><p><strong>Results: </strong>Estradiol and estrone were strongly associated with increased breast cancer risk [estradiol: RRQ5 vs. Q1 (95% confidence interval) = 2.64 (1.64-4.26); estrone: 2.78 (1.74-4.45); both P-trends <0.001]. The 2-hydroxylation pathway was strongly associated with risk [RRQ5 vs. Q1 = 3.09 (1.81-5.27); P-trend <0.001] and remained so after adjusting for unconjugated estradiol [RRQ5 vs. Q1 = 2.23 (1.25-3.96); P-trend = 0.01]. Although the 16-hydroxylation pathway was modestly associated with risk [RRQ5 vs. Q1 = 1.62 (1.03-2.54); P-trend = 0.01], the association was attenuated after unconjugated estradiol adjustment [RRQ5 vs. Q1 = 1.24 (0.77-1.99); P-trend = 0.19]. Similar positive associations with the 2-pathway and 16-pathway were observed for ER+/PR+ and ER-/PR- tumors.</p><p><strong>Conclusions: </strong>In this cohort of postmenopausal women, 2-hydroxylation of estrone and estradiol was associated with increased breast cancer risk, independent of unconjugated estradiol.</p><p><strong>Impact: </strong>These results highlight the need to revisit the role of estrogen metabolism in breast cancer etiology and prevention. See related In the Spotlight, p. 367.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"375-384"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11865363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasma n-3 Polyunsaturated Fatty Acid Levels and Colorectal Cancer Risk in the UK Biobank: Evidence of Nonlinearity, as Well as Tumor Site- and Sex-Specificity.","authors":"Joanna Aldoori, Michael A Zulyniak, Giles J Toogood, Mark A Hull","doi":"10.1158/1055-9965.EPI-24-1154","DOIUrl":"10.1158/1055-9965.EPI-24-1154","url":null,"abstract":"<p><strong>Background: </strong>The relationship between omega-3 polyunsaturated fatty acid (n-3 PUFA) intake and colorectal cancer risk is unclear. Blood n-3 PUFA concentration is a biomarker of dietary n-3 PUFA intake. We examined the relationship between plasma n-3 PUFA concentrations and colorectal cancer risk in UK Biobank (UKBB) participants.</p><p><strong>Methods: </strong>We analyzed the relationship between tertiles (T) of plasma total n-3 PUFAs and n-3 PUFA docosahexaenoic acid (DHA) levels, and overall colorectal cancer (also stratified by tumor location and sex) risk. Cox proportional hazards regression models were adjusted for clinical covariates. Nonlinearity was tested by restricted cubic splines.</p><p><strong>Results: </strong>There were 2,602 incident colorectal cancer cases in 234,598 UKBB participants with baseline plasma fatty acid data (mean follow-up 13.4 years). There was an inverse association between the plasma total n-3 PUFA level [T2 HR = 0.88 (95% confidence interval, 0.80-0.97) compared with the T1 reference; T3 = 0.91 (0.83-1.00)], as well as the plasma DHA concentration [T2 = 0.89 (0.80-0.98); T3 = 0.91 (0.82-1.00)], and colorectal cancer risk. The relationship was nonlinear [P for nonlinearity = 0.14 (total n-3 PUFAs) and 0.008 (DHA)], with a plateau effect at the highest n-3 PUFA concentrations. The relationship was more pronounced for proximal colon cancer [T2 = 0.82 (0.69-0.97); T3 = 0.76 (0.64-0.90) for DHA] and was evident for males [T2 = 0.84 (0.74-0.95); T3 = 0.89 (0.78-1.00)], but not for females.</p><p><strong>Conclusions: </strong>Higher plasma n-3 PUFAs are associated with reduced colorectal cancer risk in the UKBB.</p><p><strong>Impact: </strong>Nonlinearity, as well as tumor site and sex specificities, of the inverse relationship between plasma n-3 PUFA levels and colorectal cancer risk, if confirmed in other diverse populations, has significant implications for nutritional prevention guidelines.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"394-404"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863467","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}