Leukemia Research Reports最新文献

{"title":"Cup-like nuclei in adult B-cell acute lymphoblastic leukemia with the translocation (4;11)(q21;q23)","authors":"Yuyang Lu,&nbsp;Xinran Feng,&nbsp;Fengyu Chen","doi":"10.1016/j.lrr.2024.100463","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100463","url":null,"abstract":"<div><p>Cuplike Nuclei(CLN) cells, particularly rare in Acute Lymphoblastic Leukemia(ALL), have been documented in only few cases to date. A recent study has revealed a correlation between CLN and IKZF1 deletions in pediatric B-ALL. This study introduces a case of CLN in adult B-ALL with a translocation (4;11)(q21;q23), while discussing the current relevant literature on the subject. Through this examination, several unique characteristics of CLN cells in both ALL and Acute Myeloid Leukemia are highlighted. It is essential to accumulate further data to confirm these distinctive traits, and investigate the potential association between CLN and cytogenetic/molecular abnormalities.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100463"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000530/pdfft?md5=5858aaae09370ebe47b10a263fd4f1b3&pid=1-s2.0-S2213048924000530-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141084644","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":"FIRST SINGLE-CENTER EXPERIENCE WITH LUSPATERCEPT THERAPY IN LOW-RISK MYELODYSPLASTIC SYNDROME (LR-MDS) PATIENTS WITH TRANSFUSION DEPENDENCE REFRACTORY TO ERYTHROPOIETIN THERAPY","authors":"A. Jonasova ,&nbsp;L. Minarik","doi":"10.1016/j.lrr.2024.100444","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100444","url":null,"abstract":"<div><h3>Introduction</h3><p>Luspatercept is a recent breakthrough in the therapy of anemia in low-risk MDS.</p></div><div><h3>Methods</h3><p>From January 2021 to October 2023, 44 patients (median age 77, M/F 25/19, WHO 2016 classification: MDS-RS-MLD 28, MDS-MLD -4, RARS-T 8, CMML- 0 2, 5q- + RS 2, IPSS-R: very low 2, low 33, Intermediate 9, IPSS-M (35 pts): very low + low 18, moderate low 11, moderate high 2, high 2, very high 2) were treated with luspatercept. Median follow-up was 13 months (range 1-42). The median number of cycles was 15 (2-42). Transfusion dependency (TD) before luspatercept initiation ranged from 2 transfusion units (TU) to 12 TU/8 weeks. All patients were tested for <em>SF3B1</em> mutation.</p></div><div><h3>Results</h3><p>We evaluated 42 patients. Twenty-four (57 %) patients reached TI (&gt;12weekes), 6 (14 %) patients have had a reduction in transfusion need (HI, according to IWG criteria 2006). There were differences in response according to transfusion burden. Significant more responders belonged to lower IPSS-R, IPSS-M categories. In 17 patients, we added ESA (± <u>prednisone)</u>, which led to the improvement of response in 12 cases with 9 TI. Four patients died (2-disease progression, 2 for comorbidity). There were no adverse effects of Grade II or more.</p></div><div><h3>Conclusions</h3><p>We did observed better responses in patients bearing single mutation in <em>SF3B1</em>, in lower IPSS-R and IPSS-M risk categories, patients with LTB and lower initial baseline EPO levels. The higher response rate in our follow-up may be influenced by the combination with ESA and rapid dose escalation.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100444"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000347/pdfft?md5=1b7441e2a9653431cdf33e47754dc6b8&pid=1-s2.0-S2213048924000347-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140103893","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":"Diagnostic challenges in classification of plasmacytoid dendritic cell proliferation associated with acute myeloid leukemia in the context of secondary-type mutations","authors":"Iran Rashedi ,&nbsp;Yasmeen Abulkhair ,&nbsp;Eric Diehl ,&nbsp;Hong Chang","doi":"10.1016/j.lrr.2024.100480","DOIUrl":"10.1016/j.lrr.2024.100480","url":null,"abstract":"","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"22 ","pages":"Article 100480"},"PeriodicalIF":0.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000700/pdfft?md5=3172dfc2a3e647cdf8499ed2843b484b&pid=1-s2.0-S2213048924000700-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142271782","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 follow-up of efficacy and safety in elderly patients with chronic myeloid leukemia treated with intermittent low dose dasatinib therapy","authors":"Masahiro Imamura ,&nbsp;Yusuke Nakamura ,&nbsp;Daisuke Hidaka ,&nbsp;Reiki Ogasawara ,&nbsp;Kohei Okada ,&nbsp;Junichi Sugita ,&nbsp;Shuichi Ota","doi":"10.1016/j.lrr.2024.100452","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100452","url":null,"abstract":"<div><p>Intermittent low dose dasatinib therapy brought about a beneficial effect in elderly patients with chronic-phase chronic myeloid leukemia (CML-CP) without inducing severe adverse events (AEs). An 85-year-old male patient, who received twice-weekly, thrice-weekly, or four-times-weekly administration of 20 mg/day dasatinib after once-weekly administration, achieved a major molecular response two years after the start of dasatinib treatment and later sometimes achieved a deep molecular response, maintaining the efficacy for 11 years. The mean daily dose ranged from 5.7 mg to 11.4 mg. Furthermore, a 79-year-old male patient, who received thrice-weekly or every other day administration of 20 mg/day dasatinib after once-weekly administration, achieved a deep molecular response at four and half years after the start of dasatinib treatment. The mean daily dose is 8.6 mg. Intermittent low dose dasatinib therapy appears to be feasible in elderly patients with CML-CP. The goal of treatment in elderly patients with CML-CP appears to be different from that in younger patients, since they often suffer from serious AEs in the case of standard dose tyrosine kinase inhibitor therapy, followed by the dose reduction or cessation of treatment.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100452"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000426/pdfft?md5=462f4213710ba69f39849c2a008dab4a&pid=1-s2.0-S2213048924000426-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139992805","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":"Late-onset Familial Hemophagocytic Lymphohistiocytosis in a survivor of Hodgkin's Lymphoma","authors":"Mirza Rameez Samar,&nbsp;Daania Shoaib,&nbsp;Nida e Zehra,&nbsp;Munira Moosajee","doi":"10.1016/j.lrr.2023.100394","DOIUrl":"10.1016/j.lrr.2023.100394","url":null,"abstract":"<div><p>Hemophagocytic Lymphohistiocytosis is an inflammatory condition which results in over activation of the immune system. It could be either sporadic or familial. The familial subtype is linked with various genetic mutations and is commonly a disease of the young. Here we report a case of HLH in an adult, occurring in the background of a successfully treated hematological malignancy. Upon workup, he was also found to have pathogenic STXBP2 mutation, suggesting HLH of familial origin. To date, only few cases of adult-onset familial HLH have been brought to light.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100394"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048923000341/pdfft?md5=0c2bb1c1935904886b32a1fbbda5c361&pid=1-s2.0-S2213048923000341-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135510425","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":"Central nervous system relapse after combination therapy including polatuzumab vedotin in patients with diffuse large B-cell lymphoma","authors":"Yoshikazu Hori,&nbsp;Hiroki Hosoi,&nbsp;Toshiki Mushino,&nbsp;Yuka Okabe,&nbsp;Ayaka Sakaki,&nbsp;Kikuaki Yoshida,&nbsp;Yuichi Tochino,&nbsp;Yusuke Yamashita,&nbsp;Takashi Sonoki","doi":"10.1016/j.lrr.2024.100467","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100467","url":null,"abstract":"<div><p>Preventing central nervous system (CNS) relapse is a major challenge in the treatment of diffuse large B-cell lymphoma (DLBCL). However, no previous studies have examined the efficacy of polatuzumab vedotin (PV)-containing regimens in preventing CNS relapse in patients with DLBCL. Here, we report two cases of CNS relapse after PV-containing chemotherapy for DLBCL. CNS relapse developed during combination therapy with PV, bendamustine, and rituximab (PV-BR) in one patient and six months after PV-BR in the other patient. PV-containing chemotherapy may be ineffective as a prophylaxis against CNS relapse; therefore, additional strategies for preventing CNS relapse in DLBCL patients are required.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100467"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000578/pdfft?md5=babcc8510ff43c91a9ccbb0e28e154bc&pid=1-s2.0-S2213048924000578-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141291578","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 PROGNOSTIC IMPACT OF ERYTHROID DYSPLASIA IN APLASTIC ANEMIA AND MYELODYSPLASTIC NEOPLASMS WITH SINGLE-LINEAGE DYSPLASIA","authors":"T. Maeda ,&nbsp;A. Matsuda ,&nbsp;J. Kanda ,&nbsp;H. Kawabata ,&nbsp;T. Ishikawa ,&nbsp;K. Tohyama ,&nbsp;A. Kitanaka ,&nbsp;K. Araseki ,&nbsp;K. Shimbo ,&nbsp;T. Hata ,&nbsp;T. Suzuki ,&nbsp;H. Kayano ,&nbsp;K. Usuki ,&nbsp;M. Shindo-Ueda ,&nbsp;N. Arima ,&nbsp;M. Nohgawa ,&nbsp;A. Ohta ,&nbsp;S. Chiba ,&nbsp;Y. Miyazaki ,&nbsp;S. Nakao ,&nbsp;K. Mitani","doi":"10.1016/j.lrr.2024.100415","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100415","url":null,"abstract":"<div><h3>Introduction</h3><p>While genetic aberrations are becoming increasingly critical in disease classification, morphological abnormalities defined by a 10% threshold in each lineage continue to play a significant role as a diagnostic tool for myelodysplastic neoplasms (MDS). However, erythroid lineage dysplasia has been reported in some cases of aplastic anemia (AA), a phenomenon noted as common in the UK guidelines.</p></div><div><h3>Methods</h3><p>We assessed the impact of erythroid dysplasia on the survival in AA patients enrolled in an ongoing prospective registry, central morphological review (blinded), and follow-up study of AA and MDS conducted by the Japanese National Research Group on Idiopathic Bone Marrow Failure Syndromes. Furthermore, we compared the prognosis of AA patients with erythroid dysplasia with that of patients diagnosed in the same study with MDS presenting with single-lineage erythroid dysplasia (“MDS-SLED”). According to this study's definition, the criteria for excluding MDS are stringent, considering both bone marrow cellularity and megakaryocyte counts. Therefore, AA is not diagnosed when a decrease is not observed in the megakaryocyte count.</p></div><div><h3>Results</h3><p>The study included a total of 32 cases of AA with erythroid dysplasia, 56 cases of AA without dysplasia, and 47 cases of MDS-SLED. The overall survival or leukemia-free survival showed no significant difference between AA patients with and without erythroid dysplasia (both p=0.14). Nevertheless, distinct differences were seen between AA with erythroid dysplasia and those diagnosed with MDS-SLED (both p&lt;0.0001).</p></div><div><h3>Conclusions</h3><p>Erythroid dysplasia should not exclude an AA diagnosis. In particular, megakaryocyte count plays an important role in differentiating between MDS from AA.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100415"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000050/pdfft?md5=7573e4ade75876432a3b6af05c0b0267&pid=1-s2.0-S2213048924000050-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140103396","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":"MACHINE-LEARNING-BASED PREDICTIVE CLASSIFIER FOR BONE MARROW FAILURE SYNDROME USING COMPLETE BLOOD COUNT AND CELL POPULATION DATA","authors":"J. Seo ,&nbsp;C. Lee ,&nbsp;Y. Koh ,&nbsp;C.H. Sun ,&nbsp;J.-M. Lee ,&nbsp;H. An ,&nbsp;M. Kim","doi":"10.1016/j.lrr.2024.100419","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100419","url":null,"abstract":"<div><h3>Introduction</h3><p>Accurate risk assessment of bone marrow failure syndrome (BMFS) is crucial for early diagnosis and intervention.</p></div><div><h3>Methods</h3><p>We used complete blood count (CBC) data to develop a predictive model for BMFS. Retrospective CBC data were collected from Seoul National University Hospital and Seoul St. Mary's Hospital of the Catholic Medical Center in South Korea. We developed binary classifiers for aplastic anaemia (AA) and myelodysplastic syndrome (MDS) and generated a BMFS classifier to determine the maximum probability. Classifiers were developed using multiple feature sets consisting of 13, 17, 25, or 28 CBC features to ensure applicability to various CBC testing settings. Performance was evaluated using the area under the receiver operating characteristic curve (AUROC).</p></div><div><h3>Results</h3><p>XGBoost achieved the best AUROCs, 0·953–0·961 for the AA classifier and 0·910–0·935 for the MDS classifier, across multiple CBC feature sets. The BMFS classifier, combining the AA and MDS classifiers, demonstrated an AUROC of 0·915–0·936. When using cut-off probabilities to achieve a 95% sensitivity, the specificities ranged from 68% to 79%. External validation on an independent dataset yielded an AUROC of 0·932–0·942, a sensitivity of 93–96%, and a specificity of 65–82% at the aforementioned cut-offs.</p></div><div><h3>Conclusions</h3><p>Our predictive model provides a practical guide for diagnosing BMFS based on basic demographics and CBC data available during the first clinical encounter. It provides a reliable risk assessment tool for primary physicians, facilitating a more effective triage, timely referrals, and improved patient care.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100419"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000098/pdfft?md5=19ebce038be1abecd2d1fc4fb7c72b94&pid=1-s2.0-S2213048924000098-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140103420","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":"MITOTIC PERTURBATION IS A KEY MECHANISM OF ACTION OF DECITABINE IN MYELOID TUMOR TREATMENT","authors":"T. Yabushita ,&nbsp;T. Chinen ,&nbsp;D. Kitagawa ,&nbsp;T. Kitamura ,&nbsp;S. Goyama","doi":"10.1016/j.lrr.2024.100446","DOIUrl":"https://doi.org/10.1016/j.lrr.2024.100446","url":null,"abstract":"<div><h3>Introduction</h3><p>Decitabine (DAC) is an epigenetic drug clinically used for the treatment of myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). However, its exact mechanism of action is unclear.</p></div><div><h3>Methods</h3><p>To uncover the mechanisms underlying resistance to HMA, we performed genome-scale CRISPR activation screen using murine MDS/AML cells expressing ASXL1 and SETBP1 mutants (cSAM).</p></div><div><h3>Results</h3><p>Our genome-wide CRISPR-dCas9 activation screen using MDS-derived AML cells indicates that mitotic regulation is critical for DAC resistance. DAC strongly induces abnormal mitosis (abscission failure or tripolar mitosis) in human myeloid tumors at clinical concentrations, especially in those with TP53 mutations or antecedent hematological disorders. This DAC-induced mitotic disruption and apoptosis are significantly attenuated in DNMT1-depleted cells. In contrast, overexpression of Dnmt1, but not the catalytically inactive mutant, enhances DAC-induced mitotic defects in myeloid tumors. We also demonstrate that DAC-induced mitotic disruption is enhanced by pharmacological inhibition of the ATR-CLSPN-CHK1 pathway. In addition, transcriptome and metabolome analyses combined with our screen revealed the involvement of cholesterol metabolism in DAC resistance. Inhibition of cholesterol synthesis using statins delayed mitotic progression, suggesting that cholesterol is also important for proper mitosis. Moreover, co-treatment with DAC and statin caused mitotic catastrophe and showed synergistic growth-inhibitory effects in leukemia cells.</p></div><div><h3>Conclusions</h3><p>These data challenge the current assumption that DAC inhibits leukemogenesis through DNMT1 inhibition and subsequent DNA hypomethylation and highlight the potent activity of DAC to disrupt mitosis through aberrant DNMT1-DNA covalent bonds.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"21 ","pages":"Article 100446"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000360/pdfft?md5=2b1491f56cdd45cbc1b15efc15f2ef43&pid=1-s2.0-S2213048924000360-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140103895","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 ZMYND11::MBTD1 fusion gene following chemotherapy and radiotherapy for breast cancer: A case report","authors":"Hidetsugu Kawai ,&nbsp;Sawako Shiraiwa ,&nbsp;Daisuke Ogiya ,&nbsp;Masako Toyosaki ,&nbsp;Shinichiro Machida ,&nbsp;Rikio Suzuki ,&nbsp;Makoto Onizuka ,&nbsp;Yoshiaki Ogawa ,&nbsp;Hiroshi Kawada","doi":"10.1016/j.lrr.2024.100478","DOIUrl":"10.1016/j.lrr.2024.100478","url":null,"abstract":"<div><p>The t(10;17)(p15;q21) translocation is a very rare recurrent cytogenetic aberration, and produced <em>ZMYND11::MBTD1</em> fusion gene. To date, nine cases of acute leukemia with the t(10;17)(p15;q21) translocation have been reported, but the case of AML with <em>ZMYND11::MBTD1</em> after chemotherapy and radiotherapy have not been reported. Epirubicin-based chemotherapy or radiotherapy for breast cancer increases the risk of developing secondary leukemia. We report a case of AML with the <em>ZMYND11::MBTD1</em> fusion gene that developed after epirubicin-based chemotherapy and radiotherapy for breast cancer. previous chemotherapy and radiotherapy may be associated with poor prognosis of AML with <em>ZMYND11/MBTD1</em>.</p></div>","PeriodicalId":38435,"journal":{"name":"Leukemia Research Reports","volume":"22 ","pages":"Article 100478"},"PeriodicalIF":0.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2213048924000682/pdfft?md5=ce7223922598a44c6fcf072460505d41&pid=1-s2.0-S2213048924000682-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142049343","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}