Tumour Virus Research最新文献

{"title":"Clinical performance of the SureX PCR HPV test versus hybrid capture assays (DH2/careHPV) in primary cervical cancer screening","authors":"Yumei Ouyang ,&nbsp;Guzhanuer Abuduxikuer ,&nbsp;Tangnuer Abulimiti ,&nbsp;Guligeina Abudurexiti ,&nbsp;Qian Zhuo ,&nbsp;Wenyun Li ,&nbsp;Kadeliya Muhetaer ,&nbsp;Shaliya Abuduwufu ,&nbsp;Gulixian Tuerxun ,&nbsp;Remila Rezhake ,&nbsp;Guzhalinuer Abulizi","doi":"10.1016/j.tvr.2025.200319","DOIUrl":"10.1016/j.tvr.2025.200319","url":null,"abstract":"<div><h3>Background</h3><div>Evaluating novel human papillomavirus (HPV) tests in well-designed, population-based screening studies is essential for ensuring the benefits of cervical cancer screening.</div></div><div><h3>Methods</h3><div>8638 women aged over 25 years from China underwent HPV screening using a PCR-based full genotyping HPV assay (SureX HPV), alongside hybrid-capture HPV tests (DH2/careHPV) and cytology. Any abnormal results triggered colposcopy and biopsy if indicated. Screening performance was evaluated for detecting cervical intraepithelial neoplasia grade 2 or worse (CIN2+) and CIN3+.</div></div><div><h3>Results</h3><div>The high-risk HPV (hrHPV) positive rate by SureX HPV was significantly higher than by careHPV (11.0 % vs. 8.2 %, <em>P</em> &lt;0.01) but similar to DH2 HPV (12.0 % vs. 11.5 %, <em>P</em> =0.34). The overall agreement rates between SureX HPV and careHPV/DH2 HPV were 93.5 % (Kappa=0.63) and 94.0 % (Kappa=0.71). For CIN2+ detection, SureX HPV showed not-significantly higher sensitivity than careHPV (91.2 % vs 82.5 %, <em>P</em> =0.18) but lower specificity (91.2 % vs. 93.1 %, <em>P</em> &lt;0.01). Compared to DH2, SureX HPV demonstrated comparable sensitivity (95.7 % for both, <em>P</em> =1.0) and specificity (89.5 % vs. 90.2 %, <em>P</em> =0.21). Similar patterns were observed for CIN3+ detection. The area under the receiver operating characteristic curve (AUC) for the SureX HPV was similar to hybrid-capture HPV tests (<em>P</em> &gt;0.05 for both) and significantly higher than the cytology (ASC-US+) test for CIN2+/CIN3+ detection (<em>P</em> &lt;0.05 for both).</div></div><div><h3>Conclusions</h3><div>The PCR-based SureX HPV test demonstrated good concordance with well-validated hybrid-capture HPV tests in detecting hrHPV and CIN2+/CIN3+. Despite its slightly suboptimal specificity, SureX HPV could be an alternative in primary screening due to its full genotyping capability.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200319"},"PeriodicalIF":4.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intraperitoneal delivery of cannabidiol (CBD) and Δ9-tetrahydocannabinol (THC) promotes papillomavirus infections in athymic nude mice","authors":"Sarah A. Brendle ,&nbsp;Jingwei Li ,&nbsp;Dongxiao Sun ,&nbsp;Junjia Zhu ,&nbsp;Angela N. Henderson-Redmond ,&nbsp;Daniel J. Morgan ,&nbsp;Karla K. Balogh ,&nbsp;Danielle Covington ,&nbsp;Debra A. Shearer ,&nbsp;Jiafen Hu","doi":"10.1016/j.tvr.2024.200307","DOIUrl":"10.1016/j.tvr.2024.200307","url":null,"abstract":"<div><div>We used our mouse papillomavirus (MmuPV1) model to test the hypothesis that two primary psychoactive ingredients of marijuana, Δ⁹-tetrahydrocannabinol (THC) and cannabidiol (CBD), promote papillomavirus persistence in the oral mucosa of infected mice. We conducted intraperitoneal (ip) injections of a moderate dose (3 mg/kg) of either CBD and/or THC in both male and female athymic nude mice and followed the mice up to 20 weeks post-infection. These doses are comparable to what is estimated for human conventional cannabis consumption. All mice were infected with MmuPV1 in the oral cavity at week 4 post-ip delivery of CBD, THC, or a combination of THC and CBD (T + C). THC and CBD were detected in the blood of treated mice for up to 72 h after ip injection. Significantly higher levels of viral DNA were detected in males from both CBD and T + C-treated groups compared to those in the control group at 9- 10-and 12-weeks post infection. A marginally increased viral RNA was also detected in the infected tongues of males in all tested groups compared to that in males in the vehicle control group; the opposite was observed in females. We detected significantly higher levels of dermal dendritic cells (CD205⁺CD11c⁺), granulocytes (Ly6G⁺), but macrophages (F4-80+) recruited to the infected tongues of CBD-treated females. Our findings suggest that CBD may play a role in promoting MmuPV1 persistence in the oral cavity.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200307"},"PeriodicalIF":4.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11731512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856753","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":"Clinical indications for host-cell DNA methylation markers in cervical screening and management of cervical intraepithelial neoplasia: A review","authors":"S. Dick ,&nbsp;D.A.M. Heideman ,&nbsp;J. Berkhof ,&nbsp;R.D.M. Steenbergen ,&nbsp;M.C.G. Bleeker","doi":"10.1016/j.tvr.2024.200308","DOIUrl":"10.1016/j.tvr.2024.200308","url":null,"abstract":"<div><div>DNA methylation of host-cell genes is an epigenetic process that regulates gene expression and is associated with cervical cancer development. Studies on the natural history of cervical intraepithelial neoplasia (CIN) and the molecular alterations associated with cervical carcinogenesis led to the identification of several host-cell DNA methylation markers. Over the past years, various studies on methylation markers have shown promising results in terms of diagnostic and prognostic value to improve cervical cancer screening and management of CIN. This review provides an overview of the clinical indications of host-cell DNA methylation markers in cervical screening and management of CIN, and outlines avenues for further applications.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200308"},"PeriodicalIF":4.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11728911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856752","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":"Drosophila model of HPV18-Induced pathogenesis reveals a role for E6 oncogene in regulation of NF-κB and Wnt to inhibit apoptosis","authors":"Mojgan Padash Barmchi ,&nbsp;Rami N. Hassan ,&nbsp;Mehrnaz Afkhami ,&nbsp;John P. Masly ,&nbsp;Harrison Brown ,&nbsp;Quincy P. Collins ,&nbsp;Michael J. Grunsted","doi":"10.1016/j.tvr.2025.200316","DOIUrl":"10.1016/j.tvr.2025.200316","url":null,"abstract":"<div><div>Cancers caused by high-risk human papillomavirus (HPV) remain a significant health threat resulting in more than 300,000 deaths, annually. Persistent expression of two HPV oncogenes, E6 and E7, are necessary for cancer development and progression. E6 has several functions contributing to tumorigenesis one of which is blocking programmed cell death, apoptosis. The detailed mechanism of anti-apoptosis function of E6 is not fully understood. Here, using a <em>Drosophila</em> model of HPV18E6 and the human UBE3A-induced pathogenesis, we show that anti-apoptotic function of E6 is conserved in <em>Drosophila</em>. We demonstrate that the <em>Drosophila</em> homologs of human NF-κB transcription factors, Dorsal and Dif are proapoptotic. They induce the expression of Wingless (Wg, the <em>Drosophila</em> homolog of human Wnt), leading to apoptosis. Our results indicate that E6 oncogene inhibits apoptosis by downregulating the expression of Wg, Dorsal, and Dif. Additionally, we find that Dorsal and Dif, not only promote apoptosis but also regulate autophagy and necrosis. Dorsal promotes autophagy while Dif counteracts it, inducing the formation of acidic vacuoles and necrosis. Interestingly, although E6 blocks the proapoptotic function of Dorsal and Dif, it lacks the ability to interfere with their role in apoptosis-independent cell death. Given the high conservation of NF-κB transcription factors our results provide new insight into potential mechanisms mediated by NF-κB to intervene with cell immortalization action of E6 oncoprotein in HPV-infected cells.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200316"},"PeriodicalIF":4.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143617835","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":"The oncogenic role of the NSD histone methyltransferases in head and neck and cervical cancers","authors":"Lavinia Ghiani,&nbsp;Susanna Chiocca","doi":"10.1016/j.tvr.2024.200301","DOIUrl":"10.1016/j.tvr.2024.200301","url":null,"abstract":"<div><div>Understanding the role of NSD proteins in virus-induced cancers could reveal new therapeutic strategies. Targeting NSD proteins may not only disrupt the epigenetic changes triggered by viruses but also help restore normal cellular function. For instance, developing NSD inhibitors could counteract abnormal histone modifications caused by viral infections and slow cancer progression. Our review on the NSD protein family emphasizes its critical role in epigenetic regulation and cancer progression, also in virus-induced cancers. As research on the molecular mechanisms of NSD proteins advances, these proteins are emerging as promising candidates for targeted cancer therapies, particularly in cancers driven by histone modifications and transcriptional dysregulation.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200301"},"PeriodicalIF":4.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683330/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792704","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":"Too many cooks in the kitchen: HPV driven carcinogenesis – The result of collaboration or competition?","authors":"Weimer Kathleen","doi":"10.1016/j.tvr.2024.200311","DOIUrl":"10.1016/j.tvr.2024.200311","url":null,"abstract":"<div><div>Infection by Human Papillomaviruses accounts for the most widespread sexually transmitted infection worldwide. Clinical presentation of these infections can range from subclinical and asymptomatic to anogenital cancers, with the latter associated with persistent infection over a significant period of time. Of the over 200 isotypes of the human virus identified, a subset of these has been characterized as high-risk due to their ability to induce oncogenesis. At the core of Papillomavirus pathogenesis sits three virally encoded oncoproteins: E5, E6, and E7. In this review we will discuss the respective roles of these proteins and how they contribute to carcinogenesis, evaluating key distinguishing features that separate them from their low-risk counterparts. Furthermore, we will consider the complex relationship between this trio and how their interwoven functional networks underpin the development of cancer.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200311"},"PeriodicalIF":4.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753912/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142904032","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":"Fibroblasts regulate the transcriptional signature of human papillomavirus-positive keratinocytes","authors":"Claire D. James ,&nbsp;Rachel L. Lewis ,&nbsp;Austin J. Witt ,&nbsp;Christiane Carter ,&nbsp;Nabiha M. Rais ,&nbsp;Xu Wang ,&nbsp;Molly L. Bristol","doi":"10.1016/j.tvr.2024.200302","DOIUrl":"10.1016/j.tvr.2024.200302","url":null,"abstract":"<div><div>Persistent human papillomavirus (HPV) infection is necessary but insufficient for viral oncogenesis. Additional contributing co-factors, such as immune evasion and viral integration have been implicated in HPV-induced cancer progression. It is widely accepted that HPV + keratinocytes require co-culture with fibroblasts to maintain viral DNA as episomes. How fibroblasts regulate viral episome maintenance is a critical knowledge gap. Here we present comprehensive RNA sequencing and proteomic analysis demonstrating that coculture with fibroblasts is supportive of the viral life cycle, and is confirmatory of previous observations. Novel observations suggest that errors in “cross-talk” between fibroblasts and infected keratinocytes may regulate HPV integration and drive oncogenic progression. Our co-culture models offer new insights into HPV-related transformation mechanisms.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200302"},"PeriodicalIF":4.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699615/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142819715","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":"The impact of DNA tumor viruses in low-to-middle income countries (LMICS): A literature review","authors":"","doi":"10.1016/j.tvr.2024.200289","DOIUrl":"10.1016/j.tvr.2024.200289","url":null,"abstract":"<div><p>DNA viruses are common in the human population and act as aetiological agents of cancer on a large scale globally. They include the human papillomaviruses (HPV), Epstein-Barr virus (EBV), Kaposi sarcoma-associated herpesvirus (KSHV), hepatitis viruses, and human polyomaviruses. Oncogenic viruses employ different mechanisms to induce cancer. Notably, cancer only develops in a minority of individuals who are infected, usually following protracted years of chronic infection. The human papillomaviruses (HPVs) are associated with the highest number of cancer cases, including cervical cancer and other epithelial malignancies. Hepatitis B virus (HBV) and the RNA virus hepatitis C (HCV) are significant contributors to hepatocellular cancer (HCC). Other oncoviruses include Epstein-Barr virus (EBV), Kaposi sarcoma-associated herpes virus (KSHV), human T-cell leukemia virus (HTLV-I), and Merkel cell polyomavirus (MCPyV). The identification of these infectious agents as aetiological agents for cancer has led to reductions in cancer incidence through preventive interventions such as HBV and HPV vaccination, HPV-DNA based cervical cancer screening, antiviral treatments for chronic HBV and HCV infections, and screening of blood for transfusion for HBV and HCV. Successful efforts to identify additional oncogenic viruses in human cancer may provide further understanding of the aetiology and development of cancer, and novel approaches for prevention and treatment. Cervical cancer, caused by HPV, is the leading gynaecological malignancy in LMICs, with high age-standardised incidence and mortality rates, HCC due to HBV is an important cause of cancer deaths, and the burden of other cancer attributable to infections continues to rise globally. Hence, cancers attributable to DNA viruses have become a significant global health challenge. These viruses hence warrant continued attention and interrogation as efforts to understand them further and device further preventive interventions are critical.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"18 ","pages":"Article 200289"},"PeriodicalIF":4.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666679024000132/pdfft?md5=80e4f481a18359eac895e3e2cb06f042&pid=1-s2.0-S2666679024000132-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141560346","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":"JC virus small tumor antigen promotes S phase entry and cell cycle progression","authors":"Renato Biffi ,&nbsp;Stefanie W. Benoit ,&nbsp;Ilker K. Sariyer ,&nbsp;Mahmut Safak","doi":"10.1016/j.tvr.2024.200298","DOIUrl":"10.1016/j.tvr.2024.200298","url":null,"abstract":"<div><div>The early coding region of JC virus (JCV) encodes several regulatory proteins including large T antigen (LT-Ag), small t antigen (Sm t-Ag) and T’ proteins because of the alternative splicing of the pre-mRNA. LT-Ag plays a critical role in cell transformation by targeting the key cell cycle regulatory proteins including p53 and pRb, however, the role of Sm t-Ag in this process remains elusive. Here, we investigated the effect of Sm t-Ag on the cell cycle progression and demonstrated that it facilitates S phase entry and exit when cells are released from G0/G1 growth arrest. Examination of the cell cycle stage specific expression profiles of the selected cyclins and cyclin-dependent kinases, including those active at the G1/S and G2/M transition state, demonstrated a higher level of early expression of these regulators such as cyclin B, cycling E, and Cdk2. In addition, analysis of the effect of Sm t-Ag on the growth promoting pathways including those active in the PI3K/Akt/mTOR axis showed substantially higher levels of the phosphorylated-Akt, -Gsk3-β and -S6K1 in Sm t-Ag-positive cells. Collectively, our results demonstrate that Sm t-Ag promotes cell cycle progression by activating the growth promoting pathways through which it may contribute to LT-Ag-mediated cell transformation.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"18 ","pages":"Article 200298"},"PeriodicalIF":4.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142717194","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":"DNA methylation at individual CpG-sites of EPB41L3, HTERT and FAM19A4 are useful for detection of cervical high-grade squamous intraepithelial lesions (HSIL) or worse: Analysis of individual CpG-sites outperforms averaging","authors":"Monica Molano ,&nbsp;Dorothy A. Machalek ,&nbsp;Samuel Phillips ,&nbsp;Grace Tan ,&nbsp;Suzanne M. Garland ,&nbsp;David Hawkes ,&nbsp;Prisha Balgovind ,&nbsp;Reza Haqshenas ,&nbsp;Steve G. Badman ,&nbsp;John Bolnga ,&nbsp;Josephine Gabuzzi ,&nbsp;Zure Kombati ,&nbsp;Gloria M. Munnull ,&nbsp;Julia ML. Brotherton ,&nbsp;Marion Saville ,&nbsp;John M. Kaldor ,&nbsp;Pamela J. Toliman ,&nbsp;Andrew J. Vallely ,&nbsp;Gerald L. Murray","doi":"10.1016/j.tvr.2024.200288","DOIUrl":"10.1016/j.tvr.2024.200288","url":null,"abstract":"<div><p>Global methylation analysis of gene promoters is promising for detection of high-grade squamous intraepithelial lesions or worse (HSIL+) in high-risk human papillomavirus (hrHPV)-positive women. However, diagnostic performance of methylation data at individual CpG-sites is limited. We explored methylation for predicting HSIL+ in self- and clinician-collected samples from Papua New Guinea.</p><p>Methylation of <em>EPB41L3</em> (1–6 CpG-sites), <em>hTERT</em> (1–10 CpG-sites) and <em>FAM19A4</em> (1–5 CpG-sites) was assessed through pyrosequencing from 44 HPV+ samples (4 cancers, 19 HSIL, 4 low-grade squamous intraepithelial lesions (LSIL), 17 normal). New primers were designed for <em>FAM19A4</em> directed to the first exon region not explored previously.</p><p>In clinician-collected samples, methylation at CpG-sites 4 and 5 of <em>EPB41L3</em> were the best HSIL predictors (AUC &gt;0.83) and CpG-site 4 for cancer (0.925). Combination of <em>EPB41L3</em> sites 2/4 plus <em>FAM19A4</em> site 1 were the best HSIL+ markers [100% sensitivity, 63.2% specificity].</p><p>Methylation at CpG-site 5 of <em>FAM19A4</em> was the best HSIL predictor (0.67) in self-collected samples, and CpG-sites 1 and 3 of <em>FAM19A4</em> for cancer (0.77). Combined, <em>FAM19A4</em> site 1 plus HPV 16/18 detection yielded sensitivity of 82.6% and specificity of 61.9%.</p><p>In conclusion, methylation at individual CpG-sites of <em>EPB41L3</em> and <em>FAM19A4</em> outperformed global analysis and improved HSIL+ detection, warranting further investigation.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"18 ","pages":"Article 200288"},"PeriodicalIF":4.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666679024000120/pdfft?md5=211b8be54b2e08277c81b68123f37b1d&pid=1-s2.0-S2666679024000120-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141499638","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}