International Journal of Cancer最新文献

{"title":"Differences in the incidence and mortality of digestive cancer between Global Cancer Observatory 2020 and Global Burden of Disease 2019","authors":"Ziqing Yu,&nbsp;Xiaoyin Bai,&nbsp;Runing Zhou,&nbsp;Gechong Ruan,&nbsp;Mingyue Guo,&nbsp;Wei Han,&nbsp;Shiyu Jiang,&nbsp;Hong Yang","doi":"10.1002/ijc.34740","DOIUrl":"10.1002/ijc.34740","url":null,"abstract":"<p>The burden of digestive cancers is increasing worldwide. The Global Cancer Observatory (GLOBOCAN) 2020 and the Global Burden of Disease (GBD) 2019 are two primary cancer databases, which have a significant impact on policy formulation and resource allocation. We aim to compare the incidence and mortality of digestive cancers between them. Digestive cancer (esophageal, stomach, colorectal, liver, gallbladder and pancreatic cancer) incidence was obtained from the Cancer Today and GBD 2019 result tool. The top five countries with the most or minor difference between GLOBOCAN 2020 and GBD 2019 in age-standardized incidence rates (ASIRs) of digestive cancers were identified. A systematic search on the incidence of specific digestive cancer in selected countries from PubMed and Embase was conducted, and 20 of 281 publications were included. The most significant differences in digestive cancers incidence were commonly found in Asian countries (70%), particularly Indonesia, Vietnam and Myanmar, located in Southeast Asia. The ASIRs for most digestive cancers, except liver cancer, in GLOBOCAN 2020 were higher than those in GBD 2019. Gallbladder cancer had the highest average ratio, followed by liver cancer. The most commonly used standard population was Segi's standard population, followed by the World Health Organization standard population. The data sources nor the processing methods of GLOBOCAN 2020 and GBD 2019 were not similar. Low- and middle-income countries without population-based cancer registries were more likely to have selection bias in data collection and amplify regional variations of etiological factors. Better judgments on the quality of cancer data can be made.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"154 4","pages":"615-625"},"PeriodicalIF":6.4,"publicationDate":"2023-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41090540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to “Surveillance of premalignant gastric cardia lesions: A population-based prospective cohort study in China”","authors":"","doi":"10.1002/ijc.34735","DOIUrl":"10.1002/ijc.34735","url":null,"abstract":"<p>Gu J, Xie S, Wang S, et al. Surveillance of premalignant gastric cardia lesions: A population-based prospective cohort study in China. <i>Int J Cancer</i>. 2021;149(9):1639-1648. doi:10.1002/ijc.33720</p><p>The cumulative rate for the incidence of gastric cardia adenocarcinoma (GCA) for patients with a baseline diagnosis of atrophic carditis (AC)/cardia intestinal metaplasia (CIM) was included as 1.58% in the published version.</p><p>This should be corrected to 2.17% at all instances in text and in Tables 2 and 3.</p><p>This correction does not change the main results and conclusions of the article.</p><p>We apologize for this error.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"154 1","pages":"E1"},"PeriodicalIF":6.4,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.34735","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41095167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Telomere dysfunction in Tert knockout mice delays BrafV600E-induced melanoma development","authors":"Jinglong Zhang,&nbsp;Fan Zhang,&nbsp;Kenneth I. Porter,&nbsp;Panshak P. Dakup,&nbsp;Shuwen Wang,&nbsp;Gavin P. Robertson,&nbsp;Shobhan Gaddameedhi,&nbsp;Jiyue Zhu","doi":"10.1002/ijc.34713","DOIUrl":"10.1002/ijc.34713","url":null,"abstract":"Telomerase activation is a crucial step in melanomagenesis, often occurring because of ultraviolet radiation (UVR)-induced mutations at the telomerase gene (TERT) promoter and rendering TERT transcription in response to the activated Raf-MAP kinase pathway by BRAFV600E mutation. Due to the excessively long telomeres in mice, this process does not occur during melanomagenesis in mouse models. To investigate the impact of telomere dysfunction on melanomagenesis, BrafV600E was induced in generations 1 and 4 (G1 and G4) of Tert-/- mice. Our findings revealed that, regardless of UVR exposure, melanoma development was delayed in G4 mice, which had shorter telomeres compared to G1 and wild-type C57BL/6J (G0) mice. Moreover, many G4 tumors displayed an accumulation of excessive DNA damage, as evidenced by increased γH2A.X staining. Tumors from UVR-exposed mice exhibited elevated p53 protein expression. Cultured tumor cells isolated from G4 mice displayed abundant chromosomal fusions and rearrangements, indicative of telomere dysfunction in these cells. Additionally, tumor cells derived from UVB-exposed mice exhibited constitutively elevated expression of mutant p53 proteins, suggesting that p53 was a target of UVB-induced mutagenesis. Taken together, our findings suggest that telomere dysfunction hampers melanomagenesis, and targeting telomere crisis-mediated genomic instability may hold promise for the prevention and treatment of melanoma.","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"154 3","pages":"548-560"},"PeriodicalIF":6.4,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.34713","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41095263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor cell-expressed lipolysis-stimulated lipoprotein receptor negatively regulates T-cell function","authors":"Masashi Funauchi,&nbsp;Satoshi Serada,&nbsp;Kosuke Hiramatsu,&nbsp;Eiji Funajima,&nbsp;Mizuki Kanda,&nbsp;Yoshikazu Nagase,&nbsp;Satoshi Nakagawa,&nbsp;Tomoharu Ohkawara,&nbsp;Minoru Fujimoto,&nbsp;Yuji Suzuki,&nbsp;Yutaka Ueda,&nbsp;Tadashi Kimura,&nbsp;Tetsuji Naka","doi":"10.1002/ijc.34738","DOIUrl":"10.1002/ijc.34738","url":null,"abstract":"<p>Lipolysis-stimulated lipoprotein receptor (LSR) is known as a lipoprotein receptor. LSR is expressed in various solid tumors, including epithelial ovarian, gastric, and colon cancers. High LSR expression is significantly associated with poor prognosis, but its role in cancer has not been fully elucidated. LSR belongs to the Ig protein superfamily, which is conserved in B7 family. Here, we assessed LSR as a novel immune checkpoint molecule. We developed a novel anti-LSR antibody (#27-6 mF-18) that defects antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity activity. The #27-6 mF-18 cross-reacts with both human and mouse LSR. We found that LSR was expressed on 4T1 murine breast cancer cell line. The #27-6 mF-18 exhibited antitumor effects against the 4T1 syngeneic tumor model, a poor immunogenic model refractory to treatment with anti-PD-1 or anti-CTLA-4 antibodies. Compared with control antibody-treated mice, mice treated with #27-6 mF-18 showed significantly increased numbers of CD8⁺ T cells and a ratio of activated CD8⁺ T cells infiltrated in the tumor tissue. This antitumor effect was abrogated by CD8⁺ T-cell depletion through anti-CD8 antibody treatment, indicating that LSR negatively regulates tumor immunity by repressing CD8⁺ T cells. These findings show that LSR negatively regulates T-cell immune activity. LSR targeting could provide immune checkpoint inhibitors for cancer immunotherapy.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"154 3","pages":"425-433"},"PeriodicalIF":6.4,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41097808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Geographic, sex and socioeconomic disparities in esophageal cancer incidence in China: A population-based study","authors":"Xianhui Ran,&nbsp;Hongmei Zeng,&nbsp;Rongshou Zheng,&nbsp;Kexin Sun,&nbsp;Bingfeng Han,&nbsp;Shaoming Wang,&nbsp;Ru Chen,&nbsp;Li Li,&nbsp;Wenqiang Wei,&nbsp;Jie He","doi":"10.1002/ijc.34730","DOIUrl":"10.1002/ijc.34730","url":null,"abstract":"<p>Geographic and sex differences in esophageal cancer have been reported in China, but data are lacking at the local level. We aimed to investigate geographic and sex disparities in esophageal cancer incidence among Chinese counties and whether county-level socioeconomic status was associated with these variations. We obtained esophageal cancer data from 2015 to 2017 for 782 counties from population-based cancer registries in China. We calculated age-standardized incidence rates and male-to-female incidence rate ratios (IRRs) by county. We performed hotspot analysis to identify geographical clusters. We used negative binomial regression models to analyze the association between incidence rates and county-level socioeconomic factors. There were significant geographic disparities in esophageal cancer incidence, with 8.1 times higher rate in the 90th-percentile county than in the 10th-percentile county (23.7 vs 2.9 per 100 000 person-years). Clusters of elevated rates were prominent across north-central China. Nationally, men had 2.9 times higher incidence of esophageal cancer than women. By county, the male-to-female IRRs ranged from 1.1 to 21.1. Clusters of high male-to-female IRRs were observed in northeast China. Rurality (IRR 1.16, 95% CI 1.10-1.22), per capita gross domestic product (IRR 0.95, 0.92-0.98) and percentage of people with a high school diploma (IRR 0.86, 0.84-0.87) in a county were significantly associated with esophageal cancer incidence. The male-to-female IRRs were higher in counties with higher socioeconomic status. Substantial differences in incidence rates and sex ratios of esophageal cancer exist between Chinese counties, and county-level socioeconomic status was associated with these variations. These findings may inform interventions to reduce these disparities.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"154 3","pages":"477-487"},"PeriodicalIF":6.4,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41093908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating interactions of polygenic risk scores and NAT2 genotypes with tobacco smoking in bladder cancer risk","authors":"Pranoti Pradhan,&nbsp;Guochong Jia,&nbsp;Nikhil K. Khankari,&nbsp;Wei Zheng","doi":"10.1002/ijc.34736","DOIUrl":"10.1002/ijc.34736","url":null,"abstract":"<p>Tobacco smoking is the most important risk factor for bladder cancer. Previous studies have identified the <i>N</i>-acetyltransferase (<i>NAT2</i>) gene in association with bladder cancer risk. The <i>NAT2</i> gene encodes an enzyme that metabolizes aromatic amines, carcinogens commonly found in tobacco smoke. In our study, we evaluated potential interactions of tobacco smoking with <i>NAT2</i> genotypes and polygenic risk score (PRS) for bladder cancer, using data from the UK Biobank, a large prospective cohort study. We used Cox proportional hazards models to measure the strength of the association. The PRS was derived using genetic risk variants identified by genome-wide association studies for bladder cancer. With an average of 10.1 years of follow-up of 390 678 eligible participants of European descent, 769 incident bladder cancer cases were identified. Current smokers with a PRS in the highest tertile had a higher risk of developing bladder cancer (HR: 6.45, 95% CI: 4.51-9.24) than current smokers with a PRS in the lowest tertile (HR: 2.41, 95% CI: 1.52-3.84; <i>P for additive interaction</i> = &lt;.001). A similar interaction was found for genetically predicted metabolizing <i>NAT2</i> phenotype and tobacco smoking where current smokers with the slow <i>NAT2</i> phenotype had an increased risk of developing bladder cancer (HR: 5.70, 95% CI: 2.64-12.30) than current smokers with the fast <i>NAT2</i> phenotype (HR: 3.61, 95% CI: 1.14-11.37; <i>P for additive interaction</i> = .100). Our study provides support for considering both genetic and lifestyle risk factors in developing prevention measures for bladder cancer.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"154 2","pages":"210-216"},"PeriodicalIF":6.4,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41096324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anal cancer screening results from 18-to-34-year-old men who have sex with men living with HIV","authors":"Yuxin Liu,&nbsp;Swati Bhardwaj,&nbsp;Keith Sigel,&nbsp;John Winters,&nbsp;Joseph Terlizzi,&nbsp;Michael M. Gaisa","doi":"10.1002/ijc.34734","DOIUrl":"10.1002/ijc.34734","url":null,"abstract":"<p>Men who have sex with men living with HIV (MSM LWH) are at highest risk for human papillomavirus (HPV)-associated anal cancer. There is no consensus on the optimal screening initiation age. This study aimed to assess the prevalence and severity of anal HPV disease among MSM LWH under the age of 35, which is a currently proposed screening age threshold. Between 2014 and 2020, 1255 18-to-34-year-old MSM LWH underwent anal cytology screening. 916 were co-tested for high-risk HPV (HR-HPV). 467 underwent high-resolution anoscopy (HRA) and biopsy. Cancer registry data were queried. Predictors of abnormal cytology (ie, ≥ASCUS) and histological high-grade squamous intraepithelial lesions (HSIL) were evaluated using unadjusted logistic regression models. Median age was 28 years (range, 18-34). 19% received at least one dose of HPV vaccine. Abnormal cytology rate was 65%. HR-HPV and HPV16 prevalence were 87% and 30%. Biopsy results were benign (10%), LSIL (43%) and HSIL (47%). No cases of prevalent or incident anal cancers were detected. Findings were similar between age subgroups (18-24, 25-29 and 30-34) except for a higher prevalence of AIN 3 in the 30-34 group (19%). Abnormal cytology was significantly associated with HR-HPV infection. Histological HSIL was associated with HR-HPV infection and cytological LSIL or worse. The absence of anal cancer in a large cohort of MSM LWH under the age of 35, despite high prevalence of anal HR-HPV infection and precancer, supports an age-based anal cancer screening strategy for MSM LWH.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"154 1","pages":"21-27"},"PeriodicalIF":6.4,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41098643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atypical (non-V600E) BRAF mutations in metastatic colorectal cancer in population and real-world cohorts","authors":"Emerik Osterlund,&nbsp;Ari Ristimäki,&nbsp;Markus J. Mäkinen,&nbsp;Soili Kytölä,&nbsp;Juha Kononen,&nbsp;Per Pfeiffer,&nbsp;Leena-Maija Soveri,&nbsp;Mauri Keinänen,&nbsp;Halfdan Sorbye,&nbsp;Luís Nunes,&nbsp;Tapio Salminen,&nbsp;Lasse Nieminen,&nbsp;Aki Uutela,&nbsp;Päivi Halonen,&nbsp;Annika Ålgars,&nbsp;Jari Sundström,&nbsp;Raija Kallio,&nbsp;Raija Ristamäki,&nbsp;Annamarja Lamminmäki,&nbsp;Hanna Stedt,&nbsp;Eetu Heervä,&nbsp;Teijo Kuopio,&nbsp;Tobias Sjöblom,&nbsp;Helena Isoniemi,&nbsp;Bengt Glimelius,&nbsp;Pia Osterlund","doi":"10.1002/ijc.34733","DOIUrl":"10.1002/ijc.34733","url":null,"abstract":"<p><i>BRAF</i>-V600E mutation (mt) is a strong negative prognostic and predictive biomarker in metastatic colorectal cancer (mCRC). Non-V600Emt, designated atypical <i>BRAF</i>mt (a<i>BRAF</i>mt) are rare, and little is known about their frequency, co-mutations and prognostic and predictive role. These were compared between mutational groups of mCRC patients collected from three Nordic population-based or real-world cohorts. Pathology of a<i>BRAF</i>mt was studied. The study included 1449 mCRC patients with 51 (3%) a<i>BRAF</i>mt, 182 (13%) <i>BRAF-</i>V600Emt, 456 (31%) <i>RAS</i>&amp;<i>BRAF</i> wild-type (wt) and 760 (52%) <i>RAS</i>mt tumours. a<i>BRAF</i>mt were seen in 2% of real-world and 4% of population-based cohorts. Twenty-six different a<i>BRAF</i>mt were detected, 11 (22%) class 2 (serrated adenocarcinoma in 2/9 tested), 32 (64%) class 3 (serrated in 15/25) and 4 (8%) unclassified. a<i>BRAF</i>mt patients were predominantly male, had more rectal primaries, less peritoneal metastases, deficient mismatch repair in one (2%), and better survival after metastasectomy (89% 5-year overall survival [OS]-rate) compared with <i>BRAF</i>-V600Emt. a<i>BRAF</i>mt and <i>BRAF</i>-V600Emt had poorer performance status and received fewer treatment lines than <i>RAS</i>&amp;<i>BRAF</i>wt and <i>RAS</i>mt. OS among a<i>BRAF</i>mt (median 14.4 months) was longer than for <i>BRAF-</i>V600Emt (11.2 months), but shorter than for <i>RAS</i>&amp;<i>BRAF</i>wt (30.5 months) and <i>RAS</i>mt (23.4 months). Addition of bevacizumab trended for better OS for the a<i>BRAF</i>mt. Nine patients with a<i>BRAF</i>mt received cetuximab/panitumumab without response. a<i>BRAF</i>mt represents a distinct subgroup differing from other <i>RAS</i>/<i>BRAF</i> groups, with serrated adenocarcinoma in only half. OS for patients with a<i>BRAF</i>mt tumours was slightly better than for <i>BRAF</i>-V600Emt, but worse than for <i>RAS</i>mt and <i>RAS</i>&amp;<i>BRAF</i>wt. a<i>BRAF</i>mt should not be a contraindication for metastasectomy.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"154 3","pages":"488-503"},"PeriodicalIF":6.4,"publicationDate":"2023-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.34733","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41091931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"21-gene expression assay and clinical outcomes of premenopausal patients with hormone receptor-positive breast cancer","authors":"Jaewon Hyung,&nbsp;Sae Byul Lee,&nbsp;Jisun Kim,&nbsp;Hee Jeong Kim,&nbsp;BeomSeok Ko,&nbsp;Jong Won Lee,&nbsp;Byung-Ho Son,&nbsp;Hee Jin Lee,&nbsp;Gyungyub Gong,&nbsp;Hyehyun Jeong,&nbsp;Jae Ho Jeong,&nbsp;Jeong Eun Kim,&nbsp;Jin-Hee Ahn,&nbsp;Kyung Hae Jung,&nbsp;Sung-Bae Kim","doi":"10.1002/ijc.34728","DOIUrl":"10.1002/ijc.34728","url":null,"abstract":"<p>The prognostic role of the recurrence score (RS) based on the 21-gene expression assay in premenopausal women is not well delineated, and we investigated the association of outcomes and the RS in premenopausal patients who had 21-gene expression assay at Asan Medical Center, Seoul, Korea, between June 2005 and July 2018. Invasive breast cancer-free survival (IBCFS) by STEEP version 2.0 was compared according to the RS and clinical risk factors. A total of 554 patients were included in our study and 116 patients (20.9%) had age &lt;40 years, 238 patients (43.0%) had luminal B subtype (Ki67 ≥ 20%), and 83 patients (15.0%) had RS &gt;25. All patients received adjuvant tamoxifen ± chemotherapy. Overall, patients with RS &gt;25 showed trend toward worse IBCFS from multivariable analysis (adjusted HR 1.89 [95% CI: 0.95-3.73], <i>P</i> = .069). When comparing outcomes according to age and luminal subtypes, patients with luminal B subtype and age &lt;40 years (n = 60) showed significantly worse outcomes compared to the others (luminal A or luminal B + age ≥40 years, n = 494; adjusted HR 2.95 [95% CI: 1.49-5.82], log-rank <i>P</i> &lt; .001). Among patients with luminal B subtype and age &lt;40 years, there was no significant association observed between IBCFS and the RS (log-rank <i>P</i> = .51). In conclusion, while RS &gt;25 showed association with poor outcomes in premenopausal women, it may have less prognostic significance among those with luminal B subtype and age &lt;40 years.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"154 4","pages":"748-756"},"PeriodicalIF":6.4,"publicationDate":"2023-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10339061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"State of the science and future directions for research on HIV and cancer: Summary of a joint workshop sponsored by IARC and NCI","authors":"Eric A. Engels,&nbsp;Meredith S. Shiels,&nbsp;Ruanne V. Barnabas,&nbsp;Julia Bohlius,&nbsp;Paul Brennan,&nbsp;Jessica Castilho,&nbsp;Stephen J. Chanock,&nbsp;Megan A. Clarke,&nbsp;Anna E. Coghill,&nbsp;Jean-Damien Combes,&nbsp;Scott Dryden-Peterson,&nbsp;Gypsyamber D'Souza,&nbsp;Satish Gopal,&nbsp;Antoine Jaquet,&nbsp;Kathryn Lurain,&nbsp;Alain Makinson,&nbsp;Jeffrey Martin,&nbsp;Mazvita Muchengeti,&nbsp;Robert Newton,&nbsp;Fred Okuku,&nbsp;Jackson Orem,&nbsp;Joel M. Palefsky,&nbsp;Ramya Ramaswami,&nbsp;Hilary A. Robbins,&nbsp;Keith Sigel,&nbsp;Sylvia Silver,&nbsp;Gita Suneja,&nbsp;Robert Yarchoan,&nbsp;Gary M. Clifford","doi":"10.1002/ijc.34727","DOIUrl":"10.1002/ijc.34727","url":null,"abstract":"<p>An estimated 38 million people live with human immunodeficiency virus (HIV) worldwide and are at excess risk for multiple cancer types. Elevated cancer risks in people living with HIV (PLWH) are driven primarily by increased exposure to carcinogens, most notably oncogenic viruses acquired through shared transmission routes, plus acceleration of viral carcinogenesis by HIV-related immunosuppression. In the era of widespread antiretroviral therapy (ART), life expectancy of PLWH has increased, with cancer now a leading cause of co-morbidity and death. Furthermore, the types of cancers occurring among PLWH are shifting over time and vary in their relative burden in different parts of the world. In this context, the International Agency for Research on Cancer (IARC) and the US National Cancer Institute (NCI) convened a meeting in September 2022 of multinational and multidisciplinary experts to focus on cancer in PLWH. This report summarizes the proceedings, including a review of the state of the science of cancer descriptive epidemiology, etiology, molecular tumor characterization, primary and secondary prevention, treatment disparities and survival in PLWH around the world. A consensus of key research priorities and recommendations in these domains is also presented.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"154 4","pages":"596-606"},"PeriodicalIF":6.4,"publicationDate":"2023-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.34727","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10261251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}