BJC reports最新文献

{"title":"Assessing the risk of second primary lung cancer in women after previous breast cancer.","authors":"Yuanhui Huang, Jenny J Lin, Juan P Wisnivesky, Chung Yin Kong, Keith Sigel","doi":"10.1038/s44276-025-00151-4","DOIUrl":"10.1038/s44276-025-00151-4","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer (BC) survivors may be at increased risk of developing second cancers compared to those without BC diagnosis due to shared risk factors and potential carcinogenic effects of cancer therapy. Lung cancer (LC) is the most common second primary cancer among BC survivors. This study aimed to evaluate the association between BC and the subsequent incidence of LC.</p><p><strong>Methods: </strong>Women aged 55-74 were identified from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. The risk of incident LC was compared by BC status using a multivariable Cox regression model with BC and smoking exposures incorporated as time-updated variables.</p><p><strong>Results: </strong>75,951 females from the PLCO trial were identified, with 5808 diagnosed with BC after enrollment. The unadjusted incidence rate (IR) of the second LC was significantly higher among BC survivors than non-BC participants (231 vs. 172 per 100,000 person-years). The adjusted hazard ratio (HR) for the second primary LC associated with BC diagnosis was 1.24 (95% CI: 1.03-1.49).</p><p><strong>Conclusions: </strong>BC diagnosis was an independent risk factor for the development of second primary LC. Consequently, BC survivors may derive benefits from enhanced LC screening interventions.</p>","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"3 1","pages":"33"},"PeriodicalIF":0.0,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of HER2 amplification or overexpression with overall survival in advanced upper gastrointestinal adenocarcinomas.","authors":"Minggui Pan, Arun Dang, Tina Huang, Jack Stover, Meng M Tong, Chen Jiang, Ninah S Achacoso, Jeffrey Bien, Aleyda V Solorzano, Pamela Tse, Elaine Chung, Vishnu P Kanakaveti, Dean Felsher, George A Fisher, Sachdev Thomas, Laurel Habel","doi":"10.1038/s44276-025-00148-z","DOIUrl":"10.1038/s44276-025-00148-z","url":null,"abstract":"<p><strong>Background: </strong>Advanced esophageal (EAC), gastroesophageal junction (GEJAC) and gastric (GAC) adenocarcinomas with HER2 amplification or overexpression (HER2+) are routinely treated with trastuzumab. However, it remains unclear if HER2+ is associated with superior overall survival (OS).</p><p><strong>Methods: </strong>The cohort included recurrent or de novo metastatic GAC, GEJAC and EAC from Kaiser Permanente Northern California. We used Cox regression modelling to examine association between HER2+ and OS, adjusting for demographics, performance status, CCI, receipt of chemotherapy and p53 (mutp53), KRAS (mutKRAS), CDKN2A, PIK3CA co-mutations and MYC amplification.</p><p><strong>Results: </strong>Of 875 total eligible patients, 173 had EAC, 276 had GEJAC and 426 had GAC. HER2+ was associated with better OS among the full cohort (HR = 0.74, 95% CI [0.60-0.93]), among EAC (HR = 0.62; [95% CI, 0.40-0.96]) and GEJAC (HR = 0.59; [95% CI, 0.38-0.87]), but not among GAC (HR = 0.89; [95% CI, 0.59-1.35]) patients. GEJAC had better OS than EAC (HR = 0.68, [95% CI, 0.54-0.86]). Trastuzumab treatment was associated with better OS (HR = 0.40, 95% CI [0.21-0.77]). In addition, HER2+ was associated with better OS across the molecular subgroups except that of KRAS mutation (mutKRAS). Our data also show that GEJAC, EAC and GAC were differentially associated with mutp53, mutKRAS and MYC amplification.</p><p><strong>Conclusion: </strong>HER2+ and treatment with trastuzumab in HER2+ patients were associated with superior OS in upper gastrointestinal adenocarcinomas across molecular subgroups except that of mutKRAS. These results reaffirm the importance of anti-HER2 treatment in HER2+ patients and provide insight on the prognostic and biological divergence among these anatomically linked upper gastrointestinal adenocarcinomas.</p>","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"3 1","pages":"31"},"PeriodicalIF":0.0,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increasing incidence of early-onset kidney cancer in young adults aged <50 years in England: an analysis of the national cancer registration data by age and gender, 1985-2020.","authors":"Anjum Memon, Yalda Salari, Manraj Bawa, Paimaun Zakikhani","doi":"10.1038/s44276-025-00149-y","DOIUrl":"https://doi.org/10.1038/s44276-025-00149-y","url":null,"abstract":"<p><strong>Background: </strong>The incidence of kidney cancer, which is 34% attributable to obesity and smoking, has been steadily increasing over the past few decades in many countries in Europe, North America and Oceania. In recent years, there have been several reports of increasing incidence of early-onset cancer in young adults aged <50 years. We conducted a retrospective population-based cohort study to examine whether there have been changes in the incidence of kidney cancer in England during the past four decades.</p><p><strong>Methods: </strong>Individual-level, national (population-based) cancer registration data for patients diagnosed with kidney cancer (ICD-10 code, C64) in England from 1985-2020 were obtained from the Office for National Statistics/Public Health England. Average annual incidence rates (AAIR) were calculated by two age categories (<50, 50+ years) and gender during the six five-year time periods (1985-89 to 2010-14) and the recent six-year period (2015-20). The percentage change in the incidence rates in each age group and gender was calculated as the change in the AAIR from the first (1985-89) to the last time period (2015-20). The Average Annual Percentage Change (AAPC, year-on-year increase in incidence rates during 1985-2000) was estimated using the slope of the linear trend line fitted to the incidence rates by year of diagnosis.</p><p><strong>Results: </strong>During the 36-year study period (1985-2020), a total of 206,816 cases (62.4% males, 37.6% females) of kidney cancer were registered in England. In young adults aged <50 years, the AAIRs (per 100,000 population) increased by 157% in males and 133% in females (from 1.4 in 1985-89 to 3.6 in 2015-20 in males and from 0.9 in 1985-89 to 2.1 in 2015-20 in females). In older adults aged 50+ years, the AAIRs increased by 127% in males and 144% in females (from 24.5 in 1985-89 to 55.5 in 2015-20 in males and from 11.9 in 1985-89 to 29.0 in 2015-20 in females). The AAPC during the 36-year period was 5.0% in people aged <50 years compared to 4.7% in those aged 50+ years.</p><p><strong>Conclusion: </strong>There has been a steady and substantial increase in the incidence of kidney cancer in England over the past four decades. This was partly driven by the largest and unexpected increase in the incidence of early-onset kidney cancer in young adults aged <50 years, which was steepest in males. Some of this increase is in analogy with the increasing prevalence of obesity; nevertheless, other causes driving this increase in early-onset kidney cancer in young adults remain elusive and need further investigation.</p>","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"3 1","pages":"32"},"PeriodicalIF":0.0,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078672/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144083101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genomics and integrative clinical data machine learning scoring model to ascertain likely Lynch syndrome patients.","authors":"Ramadhani Chambuso, Takudzwa Nyasha Musarurwa, Alessandro Pietro Aldera, Armin Deffur, Hayli Geffen, Douglas Perkins, Raj Ramesar","doi":"10.1038/s44276-025-00140-7","DOIUrl":"10.1038/s44276-025-00140-7","url":null,"abstract":"<p><strong>Background: </strong>Lynch syndrome (LS) screening methods include multistep molecular somatic tumor testing to distinguish likely-LS patients from sporadic cases, which can be costly and complex. Also, direct germline testing for LS for every diagnosed solid cancer patient is a challenge in resource limited settings. We developed a unique machine learning scoring model to ascertain likely-LS cases from a cohort of colorectal cancer (CRC) patients.</p><p><strong>Methods: </strong>We used CRC patients from the cBioPortal database (TCGA studies) with complete clinicopathologic and somatic genomics data. We determined the rate of pathogenic/likely pathogenic variants in five (5) LS genes (MLH1, MSH2, MSH6, PMS2, EPCAM), and the BRAF mutations using a pre-designed bioinformatic annotation pipeline. Annovar, Intervar, Variant Effect Predictor (VEP), and OncoKB software tools were used to functionally annotate and interpret somatic variants detected. The OncoKB precision oncology knowledge base was used to provide information on the effects of the identified variants. We scored the clinicopathologic and somatic genomics data automatically using a machine learning model to discriminate between likely-LS and sporadic CRC cases. The training and testing datasets comprised of 80% and 20% of the total CRC patients, respectively. Group regularisation methods in combination with 10-fold cross-validation were performed for feature selection on the training data.</p><p><strong>Results: </strong>Out of 4800 CRC patients frorm the TCGA datasets with clinicopathological and somatic genomics data, we ascertained 524 patients with complete data. The scoring model using both clinicopathological and genetic characteristics for likely-LS showed a sensitivity and specificity of 100%, and both had the maximum accuracy, area under the curve (AUC) and AUC for precision-recall (AUCPR) of 1. In a similar analysis, the training and testing models that only relied on clinical or pathological characteristics had a sensitivity of 0.88 and 0.50, specificity of 0.55 and 0.51, accuracy of 0.58 and 0.51, AUC of 0.74 and 0.61, and AUCPR of 0.21 and 0.19, respectively.</p><p><strong>Conclusions: </strong>Simultaneous scoring of LS clinicopathological and somatic genomics data can improve prediction and ascertainment for likely-LS from all CRC cases. This approach can increase accuracy while reducing the reliance on expensive direct germline testing for all CRC patients, making LS screening more accessible and cost-effective, especially in resource-limited settings.</p>","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"3 1","pages":"30"},"PeriodicalIF":0.0,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12053672/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144060156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Case report of three patients with end-stage recurrent glioblastoma treated with meldonium.","authors":"Sandra Bien-Möller, Martin E Weidemeier, Josefine Radke, Jörg Baldauf, Stefan Engeli, Mladen V Tzvetkov, Henry W S Schroeder","doi":"10.1038/s44276-025-00124-7","DOIUrl":"https://doi.org/10.1038/s44276-025-00124-7","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma is the most aggressive primary brain tumor in adults. The prognosis is still very poor with a median survival time less than a year. A growing body of data supports the role for fatty acid oxidation (FAO) in the aggressive behavior of glioblastoma. We have previously shown that meldonium, an orally active compound that impairs FAO, caused significant growth reduction of glioblastoma in mice. Here, we report three cases of experimental meldonium-containing therapy in end-stage recurrent glioblastoma patients.</p><p><strong>Methods: </strong>Three end-stage glioblastoma patients, who had second relapse tumor progression after standard of care therapy, received 500 mg meldonium twice a day on the top of the existing therapy regimen. Tolerability and treatment outcomes were monitored.</p><p><strong>Results: </strong>Meldonium was well tolerated by all three patients. One patient experienced long-term growth arrest and maintained clinically stable disease status, currently 24 months into treatment with meldonium. In contrast, the other two patients passed away.</p><p><strong>Conclusions: </strong>The case reports presented here suggest good tolerability and the potential for meldonium to improve outcome in glioblastoma patients. Controlled clinical trials need to follow to evaluate systematically possible benefits from the integration of meldonium into standard glioblastoma treatment protocols.</p>","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"3 1","pages":"29"},"PeriodicalIF":0.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037855/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer risk according to lifestyle risk score trajectories: a population-based cohort study.","authors":"Thi Minh Thu Khong, Thi Tra Bui, Hee-Yeon Kang, Eunjung Park, Moran Ki, Yoon-Jung Choi, Byungmi Kim, Jin-Kyoung Oh","doi":"10.1038/s44276-025-00141-6","DOIUrl":"https://doi.org/10.1038/s44276-025-00141-6","url":null,"abstract":"<p><strong>Background: </strong>While individual lifestyle behaviors have been associated with cancer risk, combined impact of these factors remains understudied. This research explores relationships between lifestyle risk score trajectories and cancer risk within the Korean population.</p><p><strong>Methods: </strong>A cohort of 3,451,189 cancer-free men and women who participated in a health examination between 2002 and 2003, provided by the National Health Insurance, was studied. Lifestyle risk score trajectories were determined using group-based trajectory modeling based on total score of four modifiable unhealthy behaviors: current smoking, heavy alcohol drinking, excess body weight, and physical inactivity repeatedly observed three times between 2002 and 2007. Scores ranged between 0 (low risk) and 8 (high risk). The Cox proportional hazards model was applied to examine the association between these trajectories and cancer incidence.</p><p><strong>Results: </strong>During the follow-up time (2008-2019), 312,075 cancer cases were identified. Among men, seven trajectories were identified, and trajectories of high lifestyle risk scores increased cancer risk of all cancer combined, cancer subgroupings, upper aero-digestive, stomach, colorectal, liver, gallbladder, pancreatic, lung, and bladder cancer, but inverse relation was observed for prostate cancer. Among women, four trajectory groups showed similar trends.</p><p><strong>Conclusions: </strong>Maintaining a healthy lifestyle and avoiding unhealthy behaviors are essential for cancer prevention.</p>","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"3 1","pages":"28"},"PeriodicalIF":0.0,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12032105/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144048284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic reprogramming in glioblastoma: a rare case of recurrence to scalp metastasis.","authors":"Amir Barzegar Behrooz, Hamid Latifi-Navid, Narges Zolfaghari, Somayeh Piroozmand, Ahmad Pour-Rashidi, Mahsa Bourbour, Fatemeh Jusheghani, Mahmoud Aghaei, Negar Azarpira, Fatemeh Mollasalehi, Sedigheh Alamdar, Ahmad Nasimian, Jabar Lotfi, Shahla Shojaei, Elham Nazar, Saeid Ghavami","doi":"10.1038/s44276-025-00134-5","DOIUrl":"https://doi.org/10.1038/s44276-025-00134-5","url":null,"abstract":"<p><strong>Background: </strong>Glioblastoma (GB), an aggressive brain malignancy with a poor prognosis of 1.5-2 years, rarely exhibits extracranial metastasis (ECM). However, metabolic reprogramming has emerged as a key driver of GB progression and invasiveness. This study presents a rare case of recurrent GB with scalp metastasis, exploring how metabolic shifts enable GB cells to evade treatment and adapt to hostile environments, offering insights for developing innovative therapies.</p><p><strong>Methods: </strong>Tandem mass spectrometry (MS/MS) was employed to analyze amino acid profiles in both the recurrent and metastatic stages of GB. Systems biology approaches were used to uncover genetic alterations and metabolic reprogramming associated with the progression from recurrence to metastasis.</p><p><strong>Results: </strong>Our analysis revealed distinct amino acid utilization patterns in a patient with a molecular phenotype of wild-type IDH-1&2, TERT mutation, non-mutated BRAF and EGFR, and non-methylated MGMT. During recurrence and metastasis, significant differences in amino acid profiles were observed between blood and cerebrospinal fluid (CSF) samples. Additionally, protein-protein interaction (PPI) analysis identified key genomic drivers potentially responsible for the transition from recurrent to metastatic GB.</p><p><strong>Conclusions: </strong>Beyond established risk factors such as craniotomy, biopsies, ventricular shunting, and radiation therapy, our findings suggest that metabolic reprogramming plays a crucial role in the transition from recurrent to metastatic GB. Targeting these metabolic shifts could provide new avenues for managing and preventing extracranial metastasis in GB, making this an important focus for future research.</p>","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"3 1","pages":"27"},"PeriodicalIF":0.0,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12022025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144005451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Monitoring circulating tumor DNA by recurrent hotspot mutations in bladder cancer.","authors":"Shigehiro Tsukahara, Masaki Shiota, Takashi Matsumoto, Dai Takamatsu, Shohei Nagakawa, Nozomi Noda, Shinya Matsumoto, Mikako Yagi, Takeshi Uchiumi, Yuya Kunisaki, Dongchon Kang, Masatoshi Eto","doi":"10.1038/s44276-025-00143-4","DOIUrl":"https://doi.org/10.1038/s44276-025-00143-4","url":null,"abstract":"<p><strong>Background: </strong>Liquid biopsy can evaluate minimally residual disease. Hotspot mutations are also common in non-coding regions among the MIBC patients. We evaluated the status of MIBC with hotspot mutations with cfDNA.</p><p><strong>Methods: </strong>Tumor and blood from MIBC patients were collected prospectively. We evaluate the VAF of mutations (TERT, PLEKHS1, ADGRG6 and WDR74) with digital PCR in tumor and cfDNA as somatic mutation. We originally designed and validated primers and probes. VAF of cfDNA and clinical imaging were matched. This study was approved by the Institutional Review Board (#2022-157).</p><p><strong>Result: </strong>37 MIBC patients were enrolled and 28 (76%) patients had any hotspot. Among the 21 patients of follow-up cohort, cfDNA predicted recurrence 58 days earlier than the diagnosis by CT scan. Furthermore, the detection of ctDNA at the first visit after radical cystectomy was associated with recurrence free survival (P = 0.0043) and overall survival (P = 0.017). The patient who received neoadjuvant chemotherapy (NAC) and diagnosed as ypT0 belonged to the nonrecurrence group with negative ctDNA.</p><p><strong>Conclusion: </strong>Hotspot mutation is promising biomarker to predict earlier recurrence than CT-scan. Multiple detection of mutations in cfDNA contributes to reliable recurrence prediction.</p>","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"3 1","pages":"26"},"PeriodicalIF":0.0,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12022302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144057412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the effect of differing centre hydration and anti-emetic policies on acute gastrointestinal and renal toxicities in the De-ESCALaTE trial.","authors":"Anthony Kong, Matthew Hazell, Gulnaz Iqbal, Janet Dunn, Hisham Mehanna","doi":"10.1038/s44276-025-00132-7","DOIUrl":"https://doi.org/10.1038/s44276-025-00132-7","url":null,"abstract":"<p><strong>Background: </strong>The De-ESCALaTE trial confirmed the superiority of cisplatin over cetuximab in combination with radiotherapy for the treatment of low risk HPV+ oropharyngeal cancer (HPV + OPC). However, there were concerns about certain toxicities with the use of cisplatin, in particular nausea, vomiting, dehydration and renal toxicities.</p><p><strong>Methods: </strong>The De-ESCALaTE trial collected data on several centre level policies on hydration and anti-emetic use. Univariable and backwards stepwise multivariable logistic regression models were used to model the association between centre level policy variables and severe adverse events (SAEs) of interest and severe (grade 3-5) acute toxicities of interest. In addition, the predictive performance of each model was assessed.</p><p><strong>Results: </strong>Centre level policies including the use of a triple anti-emetics regimen pre and post chemotherapy, increased volumes of IV fluids given before and during cisplatin chemotherapy as well as oral fluids advised post chemotherapy, were all associated with a reduced odds of SAEs of interest. Only a policy to give diuretics was associated with a reduction of severe (grade 3-5) acute toxicities of interest.</p><p><strong>Conclusions: </strong>For centres with HPV + OPC patients undergoing chemoradiation, we recommend the use of specific hydration and anti-emetic policies to reduce the rates of relevant SAEs and severe acute toxicities.</p>","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"3 1","pages":"25"},"PeriodicalIF":0.0,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12019484/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144057308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Younger-onset type 2 diabetes associated with increased long-term cancer risk in Chinese adults: A 30-year follow-up of the Da Qing Diabetes Study.","authors":"Siyao He, Xin Qian, Jinping Wang, Xiaoxia Shen, Yali An, Bo Zhang, Bo Chen, Hui Li, Xiaoping Chen, Yanyan Chen, Yang Wang, Chenggang Jin, Qiuhong Gong, Guangwei Li","doi":"10.1038/s44276-025-00142-5","DOIUrl":"https://doi.org/10.1038/s44276-025-00142-5","url":null,"abstract":"<p><strong>Background: </strong>We investigated the association between younger-onset type 2 diabetes, duration of diabetes, and cancer risk based on data from the Da Qing Diabetes Prevention Outcome Study (DQDPOS).</p><p><strong>Methods: </strong>The analysis recruited 620 younger-onset (age≤50 years) and 649 older-onset (age>50 years) patients with type 2 diabetes, and 310 younger non-diabetes controls (age≤50 years). Multiple regression analysis was used to test the influence of younger-onset diabetes and duration of diabetes on the long-term risk of cancer.</p><p><strong>Results: </strong>The annual incidence of all cancer among the non-diabetes, younger-, and older-onset type 2 diabetes was significantly different (3.7, 5.5, and 4.0/1000 person-years, respectively). The standard Cox analysis revealed that the patients with younger-onset diabetes had a significantly higher risk of cancer than those with older-onset diabetes (hazard ratio [HR]:1.81; 95% confidence interval [CI]:1.20-2.73) and younger non-diabetic controls (HR:2.43; 95% CI:1.34-4.41) after adjustment for diabetes duration and other confounders. Stepwise general linear regression model analysis revealed that a longer diabetes-free time was associated with longer lifetime cancer-free years (partial R² = 0.36, p < 0.001), in addition to the non-modifiable predictor duration of diabetes.</p><p><strong>Conclusions: </strong>Younger-onset type 2 diabetes was significantly associated with an increased risk of cancer beyond the influence of diabetes duration.</p>","PeriodicalId":519964,"journal":{"name":"BJC reports","volume":"3 1","pages":"24"},"PeriodicalIF":0.0,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12015435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144001901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}