Leukemia Research Reports最新文献

{"title":"Avapritinib treatment of aggressive systemic mastocytosis with a novel KIT exon 17 mutation","authors":"Lyndsey Sandow ,&nbsp;Ajia Town ,&nbsp;Michael C. Heinrich","doi":"10.1016/j.lrr.2023.100409","DOIUrl":"https://doi.org/10.1016/j.lrr.2023.100409","url":null,"abstract":"<div><h3>Background</h3><p>Systemic mastocytosis is a rare hematologic malignancy that leads to the accumulation of neoplastic mast cells in the bone marrow, visceral organs, and skin. Mutations in the receptor tyrosine kinase, KIT are seen in most patients with systemic mastocytosis. The most common mutation is a gain of function mutation in KIT D816V. Avapritinib is a highly selective KIT D816V inhibitor approved for the treatment of advanced systemic mastocytosis. Recent studies have also suggested that avapritinib is active across other KIT mutations located in exon 11 and exon 17.</p></div><div><h3>Case Presentation</h3><p>A 68 year old woman was referred for a history of lymphadenopathy and diarrhea and was ultimately found to have systemic mastocytosis with involvement in her bone marrow, gastrointestinal tract, liver, and spleen. The bone marrow biopsy reveled a novel KIT p.D816-N822delinsMIDSI mutation in exon 17. The patient was started on avapritinib leading to significant decrease in the frequency of her diarrhea and a significant reduction in her tryptase levels. Her course was complicated by arthralgias leading to a decrease in her avapritinib dose and ultimately a degranulation episode requiring hospitalization. Following dose re-escalation, patient has remained clinically stable without any further adverse events.</p></div><div><h3>Conclusion</h3><p>We report a case of aggressive systemic mastocytosis with a novel KIT mutation on exon 17 treated with avapritinib leading to a sustained response. While avapritinib is known as a potent inhibitor against the D816V mutation, our case suggests that it may also be effective against other rare KIT mutations in systemic mastocytosis offering more potential treatment options in patients with rare mutations.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100409"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048923000493/pdfft?md5=0eee6858a41cb33a1be31e66b68a4b0d&pid=1-s2.0-S2213048923000493-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139108503","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":"Plasma cell leukemia with soft tissue involvement; reporting a rare case","authors":"Ahmed Bendari ,&nbsp;Rahaf M. Abu Khalaf ,&nbsp;Sunder Sham ,&nbsp;Reham Al-Refai ,&nbsp;Oana Vele ,&nbsp;Alyssa Yurovitsky","doi":"10.1016/j.lrr.2024.100411","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100411","url":null,"abstract":"<div><p>Plasma cell leukemia (PCL) is a rare aggressive variant of multiple myeloma. PCL is diagnosed when clonal plasma cells constitute more than 20 % of the total circulating leukocytes or when the absolute plasma cell count exceeds 2 × 10⁹ /L. Extramedullary involvement including cavity effusion is frequently seen at the time of diagnosis. However, soft tissue involvement is rarely encountered with only one published case in the English literature. We report a 74-year-old man, who presented with progressive shortness of breath over a few months. Laboratory studies showed leukocytosis (32 × 109 /L) with 26 % peripheral plasmacytoid cells and significantly elevated lactate dehydrogenase (&gt; 2500 U/L). Serum protein electrophoresis detected a monoclonal IgG lambda band. A 7.4 cm left hilar mass, bilateral pleural effusion, and multiple fluorodeoxyglucose (FDG)-avid subcutaneous nodules in the pelvic and gluteal regions were demonstrated on imaging. Gluteal nodule biopsy revealed diffuse infiltrative CD138+ and MUM1+ cells with aberrant CD4, CD30, and BCL2 expression. The Ki-67 proliferation index was 70 %. Bone marrow biopsy showed sheets of atypical plasma cells with lambda-restriction and CD138 and MUM1 expression without cyclin D1 and CD20 expression. These cells comprise approximately 70–80 % of the bone marrow cellularity. A similar immunophenotype was demonstrated in peripheral and bone marrow flow cytometry. Molecular and cytogenetics showed an abnormal clone with a complex karyotype including monosomy 13 and 14q deletion. Overall, these findings are consistent with a plasma cell neoplasm. Our case study illustrates soft tissue involvement in PCL, which is rarely seen.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100411"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000013/pdfft?md5=be4ca13748083953664037e163c94181&pid=1-s2.0-S2213048924000013-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139433843","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":"Acute myeloid leukemia with a novel AKAP9::PDGFRA fusion transformed from essential thrombocythemia: A case report and mini review","authors":"Yavuz Sahin ,&nbsp;Jianming Pei ,&nbsp;Don A. Baldwin ,&nbsp;Nashwa Mansoor ,&nbsp;Lori Koslosky ,&nbsp;Peter Abdelmessieh ,&nbsp;Y. Lynn Wang ,&nbsp;Reza Nejati ,&nbsp;Joseph. R. Testa","doi":"10.1016/j.lrr.2024.100465","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100465","url":null,"abstract":"<div><p>Acute myeloid leukemia (AML) is a heterogeneous hematological malignancy associated with various combinations of gene mutations, epigenetic abnormalities, and chromosome rearrangement-related gene fusions. Despite the significant degree of heterogeneity in its pathogenesis, many gene fusions and point mutations are recurrent in AML and have been employed in risk stratification over the last several decades. Gene fusions have long been recognized for understanding tumorigenesis and their proven roles in clinical diagnosis and targeted therapies. Advances in DNA sequencing technologies and computational biology have contributed significantly to the detection of known fusion genes as well as for the discovery of novel ones. Several recurring gene fusions in AML have been linked to prognosis, treatment response, and disease progression. In this report, we present a case with a long history of essential thrombocythemia and hallmark <em>CALR</em> mutation transforming to AML characterized by a previously unreported <em>AKAP9::PDGFRA</em> fusion gene. We propose mechanisms by which this fusion may contribute to the pathogenesis of AML and its potential as a molecular target for tyrosine kinase inhibitors.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100465"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000554/pdfft?md5=61cd70a7f26e97e6afe74f7343ef5f35&pid=1-s2.0-S2213048924000554-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141250067","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":"Venetoclax for an ATRA and ATO resistance acute promyelocytic leukemia patient with TNRC18::RARA fusion gene","authors":"Weina Li ,&nbsp;Haijie Li ,&nbsp;Xueyan Chen ,&nbsp;Yan Zheng","doi":"10.1016/j.lrr.2024.100482","DOIUrl":"10.1016/j.lrr.2024.100482","url":null,"abstract":"<div><div>Variant acute promyelocytic leukemia (APL) poses diagnostic and therapeutic challenges primarily because of the absence of <em>PML::RARA.</em> This report presents the case of a patient diagnosed with <em>all-trans</em> retinoic acid (ATRA)-resistant APL harboring the <em>TNRC18::RARA</em> fusion gene. After treatment with venetoclax, azacitidine, and ATRA, the patient achieved complete remission. The patient also developed pulmonary tuberculosis and a multidrug-resistant infection, which improved considerably after antituberculosis treatment and carrimycin, respectively.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"22 ","pages":"Article 100482"},"PeriodicalIF":0.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142319538","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 ROLE OF LET-7/HMGA2 LINKAGE IN THE PATHOGENESIS AND PROGNOSIS OF MYELODYSPLASTIC NEOPLASMS","authors":"D. Vlachopoulou ,&nbsp;C.-N. Kontandreopoulou ,&nbsp;P.T. Diamantopoulos ,&nbsp;S. Syriopoulou ,&nbsp;C. Stafylidis ,&nbsp;P. Katsiampoura ,&nbsp;A. Galanopoulos ,&nbsp;M. Dimou ,&nbsp;P. Panayiotidis ,&nbsp;N.-A. Viniou","doi":"10.1016/j.lrr.2024.100428","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100428","url":null,"abstract":"<div><h3>Introduction</h3><p>MicroRNAs (miRNAs),are significant regulators of human hematopoietic stem cells. Their deregulation contributes to hematological malignancies.The let-7 family has been found frequently deregulated in malignancies.In MDS various alterations of miRNAs have been reported.High Mobility Group AT-Hook 2 (HMGA2) protein functions as a transcriptional regulator. In this study, we investigated the HMGA2 expression in MDS and specifically in patients with fibrosis we studied the prognostic significance of four members of the let-7 family (let-7a, let-7b, let-7c, let-7d).</p></div><div><h3>Methods</h3><p>RNA extraction, reverse transcription, anda SYBR Green based real-time PCR were performed for the absolute quantification of HMGA2, using standard protocols. After RNA polyadenylation and reverse transcription with an oligo-dT adapter primer, miRNAs transcript levels were determined using the SYBR Green chemistry. IBM SPSS statistics, version 26 (IBM Corporation, North Castle, NY, USA) was used for the analysis.</p></div><div><h3>Results</h3><p>HMGA2 gene expression was investigated in 78 patients with MDS, whereas transcript levels of four members of the let-7 family (let-7a, let-7b, let-7c, let-7d) were analyzed in 11 patients with fibrosis. Let-7a transcript levels were significantly higher in MDS patients who developed acute myeloid leukemia (AML) compared to the group that did not (p=0.0141). Let-7d presented a negative correlation (p=0.0408). A moderate (p =0.0483) negative correlation of HMGA2 with let-7c, and a strong positive correlation (p =0.0481) with let-7d, were observed.</p></div><div><h3>Conclusions</h3><p>In literature, the let-7/HMGA2 linkage could be a signature in MDS pathogenesis. Let-7a level was found higher in transformation to AML,defining it as a poor prognostic factor, in contrast with the protective role of high let-7d.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100428"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000189/pdfft?md5=5918d5e24efc7086c03e1df509bcef87&pid=1-s2.0-S2213048924000189-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140103588","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":"PREDICTION OF POST-TRANSPLANT RELAPSE IN THE MYELODYSPLASTIC SYNDROMES VIA EVALUATION OF STEM CELLS","authors":"S. Chung ,&nbsp;B. Kroger ,&nbsp;Y. Huang ,&nbsp;A. Son ,&nbsp;P. Carlsgaard ,&nbsp;L. Pop ,&nbsp;R. Vittrup ,&nbsp;F. Kalkan ,&nbsp;A. Cherukuri ,&nbsp;D. Sallman ,&nbsp;R. Tamari ,&nbsp;C. Gurnari ,&nbsp;J. Maciejewski ,&nbsp;Y. Madanat","doi":"10.1016/j.lrr.2024.100434","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100434","url":null,"abstract":"<div><h3>Introduction</h3><p>Allogeneic stem cell transplant (alloSCT) remains the only curative treatment for the myelodysplastic syndromes (MDS), but relapse is common. Studies using error-corrected sequencing (ECS) on bulk bone marrow (BM) have shown that molecular residual disease is predictive of relapse. But the sensitivity of this approach is limited, and it is not known what cells give rise to relapse.</p></div><div><h3>Methods</h3><p>To test our hypothesis that hematopoietic stem cells (HSCs) drive post-transplant relapse, we developed a protocol to perform ECS on as few as &lt;25 HSCs. We used this new tool to ask if post-transplant relapse originates from MDS HSCs, and whether their persistence predicts for relapse. We also sought to determine if curing MDS requires eradication of MDS HSCs, or whether they are simply suppressed by graft-versus-tumor effect.</p></div><div><h3>Results</h3><p>We sequenced HSCs, multipotent progenitors (MPPs), restricted progenitors, and bulk BM from 33 MDS patients who underwent alloSCT (with an additional 20 specimens to be presented). Persistence of mutations in HSCs/MPPs in the first 120 days post-transplant was 100% specific and 84% sensitive for relapse, while detection of mutations in bulk BM was only 41% sensitive and 85% specific (Figure). Average time from mutation detection in HSCs/MPPs to relapse was 6.9 months.</p></div><div><h3>Conclusions</h3><p>In conclusion, we have shown for the first time that relapse of MDS after allogeneic transplant is driven by failure to eradicate MDS HSCs, and that detection of MDS HSCs early after transplant is highly predictive for relapse. This can identify patients who may benefit from early post-transplant interventions to forestall relapse.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100434"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000244/pdfft?md5=5c20ca020c976ddcb1410b50e5ea0d5c&pid=1-s2.0-S2213048924000244-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140103600","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":"A novel mutation of LYST and haemophagocytic lymphohistiocytosis as the first symptom in children with ph+ALL: A case report and literature review","authors":"Tiantian Wang ,&nbsp;Xuhui liu ,&nbsp;Li Lin ,&nbsp;Renzhi Pei ,&nbsp;Ying Lu","doi":"10.1016/j.lrr.2024.100481","DOIUrl":"10.1016/j.lrr.2024.100481","url":null,"abstract":"<div><div>Haemophagocytic lymphohistiocytosis (HLH) is a rare disorder. This study sheds light on a rare and intriguing case of HLH as the initial symptom in a child with Philadelphia chromosome-positive acute lymphoblastic leukaemia (ph+ALL). This case report, accompanied by a comprehensive literature review, highlights the diagnostic challenges and treatment complexities encountered in the management of such rare manifestations. Moreover, the identification of a novel mutation in the <em>LYST</em> gene adds a unique genetic perspective to the understanding of HLH pathogenesis, potentially opening avenues for further research in this area.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"22 ","pages":"Article 100481"},"PeriodicalIF":0.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142421070","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":"An uncommon triad of myelodysplastic syndrome, Crohn's disease and autoimmune hepatitis: A case report and review of the literature","authors":"Arij Cheffai,&nbsp;Wiem Boufrikha,&nbsp;Rim Rakez,&nbsp;Amina Ben Ghechir,&nbsp;Mohamed Adnène Laatiri","doi":"10.1016/j.lrr.2024.100487","DOIUrl":"10.1016/j.lrr.2024.100487","url":null,"abstract":"<div><div>Myelodysplastic syndrome (MDS) is associated with an autoimmune disease (AD) in 10 to 20% of cases. Crohn's disease (CD) is not a common autoimmune manifestation reported with MDS. The triad made up of MDS, CD and another autoimmune manifestation is even more unusual. To our knowledge, only four cases with this triad have been reported in the literature to date, and ours is the fifth. It's about a 50-year-old man with a history of autoimmune hepatitis who was diagnosed, five years later, with MDS with multilineage dysplasia. He was started on Azacitidine three weeks before retaining the diagnosis of an associated CD.</div></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"22 ","pages":"Article 100487"},"PeriodicalIF":0.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142660224","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":"Long-term hematologic response after azacitidine treatment in a lower-risk myelodysplastic syndrome patient: A case report","authors":"Konstantinos Loukidis ,&nbsp;Marcel Tschopp","doi":"10.1016/j.lrr.2024.100412","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100412","url":null,"abstract":"<div><p>We report results of a 65-year-old patient with lower-risk myelodysplastic syndrome and multilineage dysplasia treated with hypomethylating agents. After failure of erythropoietin and thalidomide, the patient received azacitidine and achieved hematological remission for 95 months. In 2016, the treatment was switched to decitabine with promising results. These data showed that azacitidine used as a third-line treatment resulted in an exceptionally long-lasting positive hematological response after standard first- and second-line therapies had failed. Additionally, the patient experienced a good quality of life with no complications related to profound cytopenia, and continues to do so at the time of this report's preparation.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100412"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000025/pdfft?md5=e72361bbaa948ac9ce896da14d682999&pid=1-s2.0-S2213048924000025-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139436101","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":"PROVIDING TIMELY PATIENT-CENTERED MOLECULAR DIAGNOSTIC TESTING FOR PATIENTS WITH ACUTE MYELOID LEUKEMIA: A QUALITY IMPROVEMENT STUDY","authors":"A. Qureshi ,&nbsp;J. Ho ,&nbsp;L. Schenkel ,&nbsp;B. Chin-Yee ,&nbsp;U. Deotare ,&nbsp;A. Meybodi ,&nbsp;L. Saini ,&nbsp;B. Sadikovic ,&nbsp;I. Chin-Yee","doi":"10.1016/j.lrr.2024.100422","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100422","url":null,"abstract":"<div><h3>Introduction</h3><p>At many centers, molecular diagnostic (MD) testing for Acute Myeloid Leukemia (AML) struggles to meet turn-around-time (TAT) required for therapeutic decision-making. At our tertiary referral centre, TAT for MD (karyotyping and next-generation sequencing [NGS]) exceeded 4 weeks, resulting in a 'quality gap' in our care pathway for AML. The goal of our study was to improve TAT for MD to optimize care for patients with AML/MDS.</p></div><div><h3>Methods</h3><p>A multidisciplinary team (hematologists, laboratory scientists, and hematopathologists) defined target TATs for each MD test based on guidelines and available therapies. TAT was evaluated from time of bone marrow to MD reporting. Retrospective review from 2021-2022 was performed to establish baseline time points to compare to post-intervention TATs. Root cause analysis was performed through stakeholder interviews to identify areas contributing to delays in TAT. The primary outcome was the ability to meet target TAT for MD.</p></div><div><h3>Results</h3><p>Baseline TAT for cytogenetics and NGS varied widely and exceeded targets (Figure 1). Root cause analysis identified lack standardized ordering and testing for patients with AML due to inconsistent decision-maker awareness. Laboratory factors included batching and lack prioritization of AML samples. Interventions included a standardized AML testing algorithm triggered reflexively by flow cytometry at the time diagnosis. Impact of laboratory triggered algorithm for AML testing is shown in Figure 1.</p></div><div><h3>Conclusions</h3><p>Shared decision-making between hematologists and laboratory practitioners to develop an algorithm for reflex testing and treatment of AML improved TAT. Further improvements are underway to acheive targets, and lessons will be used to inform care pathways for AML/MDS.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100422"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000128/pdfft?md5=c7c6e8b1ab03b7c7ac343da1529bcfcf&pid=1-s2.0-S2213048924000128-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140103266","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}