Blood Research最新文献

{"title":"Effects of immune system cells in GvHD and corresponding therapeutic strategies.","authors":"Maryam Jadid Tavaf,&nbsp;Mahboobeh Ebrahimi Verkiani,&nbsp;Fateme Poorhoseini Hanzaii,&nbsp;Mina Soufi Zomorrod","doi":"10.5045/br.2023.2022192","DOIUrl":"https://doi.org/10.5045/br.2023.2022192","url":null,"abstract":"<p><p>Allogeneic tissue transplantation is one of the most effective treatments for several diseases and injuries, in particular, malignant and non-malignant hematological conditions. Following this procedure, transplanted tissue encounters various complications, one of the most serious being graft-versus-host disease (GvHD). The management of GvHD directly affects the success of transplantation and the survival rate of the patient; therefore, many studies have focused on GvHD prevention and control. This review briefly explains the transplantation process, causes of graft rejection, and importance of the human leukocyte antigen system. Initially, we address the pathophysiology and immunobiology of GvHD, the cells involved in this complication, the differences between chronic and acute GvHD, and the importance of graft-versus-leukemia. Interestingly, various types of immune cells are involved in GvHD pathogenesis. After explaining how these cells affect the GvHD process, we discuss the studies conducted to control and reduce GvHD symptoms.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"58 1","pages":"2-12"},"PeriodicalIF":2.2,"publicationDate":"2023-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/11/1f/br-58-1-2.PMC10063589.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9581903","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":"High rate of hepatitis B reactivation during tyrosine kinase inhibitor treatment among patients with chronic myeloid leukemia in Korea.","authors":"Jee Hyun Kong,&nbsp;Jae Yeon Jang,&nbsp;Tae Hwa Ko,&nbsp;Seong Hee Kang,&nbsp;Yundeok Kim","doi":"10.5045/br.2022.2022099","DOIUrl":"https://doi.org/10.5045/br.2022.2022099","url":null,"abstract":"Median age (yr) 52 (20–91) Sex male (N, %) 1,386 (60.8) Median duration of TKI treatment, months (range) 51.3 (1–160.5) TKI Imatinib, N (%) 1,563 (68.6) Dasatinib, N (%) 825 (36.2) Nilotinib, N (%) 678 (29.8) Radotinib, N (%) 154 (6.8) N of TKIs 1 TKI, N (%) 1,552 (68.1) 2 TKIs, N (%) 533 (23.4) 3 TKIs, N(%) 171 (7.5) 4 TKIs, N (%) 22 (1.0) HBV infection, N (%) 143 (6.3) HBV reactivation, N (% of HBV carrier) 33 (23.1) During imatinib, N 24 During dasatinib, N 6 During nilotinib, N 1 During radotinib, N 0 HBV reactivation events/1,000 patients-year Imatinib, events/1,000 patients-year 3.5 Dasatinib, events/1,000 patients-year 3.0 Nilotinib, events/1,000 patients-year 0.6 Radotinib, events/1,000 patients-year 0 Median interval (mo) from TKI initiation to HBV reactivation, (range) 2 (0–67) Death, N (%) 466 (20.5)","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"57 4","pages":"290-293"},"PeriodicalIF":2.2,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/05/7e/br-57-4-290.PMC9812728.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10364761","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":"Various inclusions in chronic lymphocytic leukemia/small lymphocytic lymphoma.","authors":"Verónica Roldán Galiacho,&nbsp;Ana Lobo Olmedo,&nbsp;Javier Arzuaga Mendez,&nbsp;Juan Carlos García-Ruiz","doi":"10.5045/br.2022.2022120","DOIUrl":"https://doi.org/10.5045/br.2022.2022120","url":null,"abstract":"(A) Globular inclusions in peripheral blood lymphocytes in a 67-year-old woman with 5-year history of CLL managed with a “watch and wait” approach. Other findings included increased lymphocyte count of 270×10 9 /L, hemoglobin of 110 g/L, and platelets of 78×10 9 /L. Serum lactate dehydrogenase level was normal. Positron emission tomography/ computed tomography revealed multiple adenopathies with low SUV and no evidence of transformation. (B) Multiple crystalline inclusions in peripheral blood lymphocytes in a 60-year-old asymptomatic woman with axillary lymphadenopathies. Laboratory evaluations revealed the following: hemoglobin of 132 g/L, platelets of 212×10 9 /L, and lymphocytes of 3.7×10 9 /L. B-cells revealed clonal CLL phenotype on flow cytometry. Lymph node biopsy revealed lymphoid infiltrate with low Ki67 and positivity for CD20, CD23, and CD5. A diagnosis of SLL was established","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"57 4","pages":"247"},"PeriodicalIF":2.2,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2f/04/br-57-4-247.PMC9812721.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10589508","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":"Erratum.","authors":"","doi":"10.5045/br.2022.2022089e1","DOIUrl":"https://doi.org/10.5045/br.2022.2022089e1","url":null,"abstract":"","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"57 4","pages":"297"},"PeriodicalIF":2.2,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2c/c6/br-57-4-297.PMC9812730.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10643566","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":"Red blood cells from COVID-19 patients suffer from increased oxidative stress and may have increased lactate influx.","authors":"Edel Mullen,&nbsp;Stephen Bergin,&nbsp;Geraldine Healy,&nbsp;John Quinn,&nbsp;Siobhan Glavey,&nbsp;Philip Thomas Murphy","doi":"10.5045/br.2022.2022084","DOIUrl":"https://doi.org/10.5045/br.2022.2022084","url":null,"abstract":"TO THE EDITOR: Coronavirus disease (COVID-19) is caused by SARS-CoV-2, a novel, highly infectious, single stranded RNA virus. An inappropriate immune response characterised by the excess production of pro-inflammatory cytokines (‘cytokine storm’) is common in severe cases of COVID-19 [1]. Such severe disease is frequently complicated by coagulopathy, often progressing to DIC and multi-organ failure [2]. The ‘cytokine storm’ accompanying severe COVID-19 as well as increased serum ferritin levels may be important sources of endogenous oxidative stress [3, 4] Such excess oxidative stress may lead to tissue damage in the lungs and elsewhere by generation of reactive oxygen species (ROS) [5]. The potential role of red blood cells (RBCs) in the pathophysiology of COVID-19, especially their possible contribution to hypoxia and to the thrombotic complications remains uncertain. Both anemia and increase in RBC distribution width have now been associated with increased mortality in hospitalized patients with SARS-CoV-2 infection [6, 7]. In addition, increased oxidation of structural proteins and impairment of membrane lipid homeostasis is reported in RBCs of COVID-19 positive patients, which may alter RBC deformability, potentially contributing to the thromboembolic complications seen in severe forms of COVID-19 infection [8]. To further investigate the possible role of RBC dysfunction in COVID-19, we measured ROS in RBCs of patients infected with COVID-19 at our hospital and the effect of the anti-oxidant N-acetyl cysteine (NAC). To look for evidence of increased adherence of RBCs to endothelial cells (ECs) and platelets in COVID-19 which might contribute to thrombosis, we measured RBC surface expression of adhesion molecules CD44, CD242 (ICAM-4) and CD47, as these red blood cell surface proteins have been implicated in interactions with blood vessels and/or platelets [9]. We also measured surface expression of CD147, as a surrogate marker of the lactate transporter monocarboxylate transporter 1 (MCT1) [10].","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"57 4","pages":"294-296"},"PeriodicalIF":2.2,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e7/29/br-57-4-294.PMC9812725.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10643568","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":"FVIII inhibitor surveillance in children with hemophilia A in Indonesia: a report from the Indonesian Pediatric Hematology-Oncology Working Group.","authors":"Novie A Chozie,&nbsp;Djajadiman Gatot,&nbsp;Bambang Sudarmanto,&nbsp;Susi Susanah,&nbsp;Rini Purnamasari,&nbsp;Pudjo Hagung Widjajanto,&nbsp;Susanto Nugroho,&nbsp;Olga Rasiyanti,&nbsp;Dian Puspitasari,&nbsp;Muhammad Riza,&nbsp;Maria C Shanty Larasati,&nbsp;Sri Suryo Adiyanti,&nbsp;Made Citra Saraswati,&nbsp;Fitri Primacakti","doi":"10.5045/br.2022.2022153","DOIUrl":"https://doi.org/10.5045/br.2022.2022153","url":null,"abstract":"<p><strong>Background: </strong>Factor VIII (FVIII) inhibitor diagnosis and surveillance in Indonesia are challenging owing to geographic conditions and the lack of laboratory facilities nationwide for inhibitor assays. This study aimed to determine the prevalence of FVIII inhibitors in children diagnosed with hemophilia A (HA) in Indonesia.</p><p><strong>Methods: </strong>A cross-sectional study was conducted in 12 hospitals in eight provinces of Indonesia between 2020 and 2021. Factor VIII inhibitor screening was performed in a central hemostasis laboratory for all children with HA (≤18 yr) who had received a minimum of 10 exposure days to clotting factor concentrates. The FVIII inhibitor titer was determined using the Bethesda assay.</p><p><strong>Results: </strong>Children (388) were enrolled in this study, including 219 (56.4%), 131 (33.8%), and 38 (9.4%) with severe, moderate, and mild HA, respectively. The prevalence of children who developed FVIII inhibitors was 37 out of 388 (9.6%). Factor VIII inhibitors were found in 25/219 (11.4%) severe, 11/131 (8.3%) moderate, and 1/38 (2.6%) children with mild HA. Thirteen children had low-titer inhibitors and 24 had high-titer inhibitors, with a median of 9.44 (1.48‒412.0) Bethesda Units. Among 13 children with low-titer inhibitors, eight underwent a confirmation test, of which five tested negative and were classified as transient. A significant difference in annual joint bleeding rate was found between patients with low and high inhibitor titers and those without inhibitors (<i>P</i>＜0.001).</p><p><strong>Conclusion: </strong>Factor VIII inhibitor prevalence in Indonesia was relatively low. However, the risk factors that may contribute to FVIII inhibitor development among Indonesian patients require further study.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"57 4","pages":"272-277"},"PeriodicalIF":2.2,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7a/97/br-57-4-272.PMC9812731.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9204823","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":"Prognostic impact of total body irradiation dose in pediatric acute lymphoblastic leukemia patients treated with allogeneic hematopoietic stem cell transplantation in second complete remission.","authors":"Wonjin Jang,&nbsp;Suejung Jo,&nbsp;Jae Won Yoo,&nbsp;Seongkoo Kim,&nbsp;Jae Wook Lee,&nbsp;Pil-Sang Jang,&nbsp;Nack-Gyun Chung,&nbsp;Bin Cho","doi":"10.5045/br.2022.2022174","DOIUrl":"https://doi.org/10.5045/br.2022.2022174","url":null,"abstract":"<p><strong>Background: </strong>Allogeneic HSCT may improve survival in pediatric ALL patients who relapse. In this study, we analyzed the outcome and prognostic factors of 62 ALL patients (35 male, 56.5%) who received allogeneic HSCT in second complete remission (CR) at our institution between April 1st 2009 and December 31st 2019.</p><p><strong>Methods: </strong>The median time from diagnosis to relapse was 35.1 months (range, 6.0‒113.6 mo). Fifty-three patients (85.5%) experienced bone marrow relapse only. The number of patients who received transplant according to each donor type was as follows: HLA matched family donor 17 (27.4%), matched unrelated donor (UD) 22 (35.5%), mismatched donor 23 (37.1%). All patients received HSCT with a myeloablative conditioning, 58 patients (93.5%) with the incorporation of TBI [31 patients 12 Gray (Gy), 24 patients 13.2 Gy, 3 patients 8 Gy].</p><p><strong>Results: </strong>The 5-year event-free survival (EFS), and overall survival of the study group was 41.3±6.3% (26/62), and 42.3±6.6% (27/62), respectively. The cumulative incidence of relapse and transplant-related mortality was 57.1±6.4% and 1.6±1.6%, respectively. Infant ALL, shorter time from diagnosis to relapse, and TBI dose of 12 Gy, rather than 13.2 Gy, resulted in significantly worse EFS. In multivariate analysis, infant ALL and TBI dose of 12 Gy during conditioning predicted significantly lower EFS.</p><p><strong>Conclusion: </strong>In our study group, treatment with a higher dose of TBI during conditioning resulted in better EFS for ALL patients who underwent HSCT in second CR. Further study is needed to determine potential long-term complications associated with a higher TBI dose.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"57 4","pages":"256-263"},"PeriodicalIF":2.2,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8d/06/br-57-4-256.PMC9812732.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9204825","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":"Rapid development of lower leg compartment syndrome following firearm injury in a patient with moderate hemophilia B.","authors":"Jelena Bodrozic,&nbsp;Danijela Lekovic,&nbsp;Igor Koncar,&nbsp;Natasa Sulović Dzelatović,&nbsp;Predrag Miljic","doi":"10.5045/br.2022.2022112","DOIUrl":"https://doi.org/10.5045/br.2022.2022112","url":null,"abstract":"REFERENCES 1. Graux C, Cools J, Melotte C, et al. Fusion of NUP214 to ABL1 on amplified episomes in T-cell acute lymphoblastic leukemia. Nat Genet 2004;36:1084-9. 2. Ragg S, Zehentner BK, Loken MR, Croop JM. Evidence for BCR/ABL1-positive T-cell acute lymphoblastic leukemia arising in an early lymphoid progenitor cell. Pediatr Blood Cancer 2019;66:e27829. 3. Govaerts I, Jacobs K, Vandepoel R, Cools J. JAK/STAT pathway mutations in T-ALL, including the STAT5B N642H mutation, are sensitive to JAK1/JAK3 inhibitors. Hemasphere 2019;3:e313. 4. Sharma P, Rana S, Sreedharanunni S, et al. An evaluation of a fluorescence in situ hybridization strategy using air-dried blood and bone-marrow smears in the risk stratification of pediatric B-lineage acute lymphoblastic leukemia in resource-limited settings. J Pediatr Hematol Oncol 2021;43:e481-5. 5. Graux C, Stevens-Kroef M, Lafage M, et al. Heterogeneous patterns of amplification of the NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia. Leukemia 2009;23:125-33. 6. Deenik W, Beverloo HB, van der Poel-van de Luytgaarde SC, et al. Rapid complete cytogenetic remission after upfront dasatinib monotherapy in a patient with a NUP214-ABL1-positive T-cell acute lymphoblastic leukemia. Leukemia 2009;23:627-9. 7. Li X, Ping N, Wang Y, et al. Case report: a case with Philadelphia chromosome positive T-cell lymphoblastic lymphoma and a review of literature. Front Oncol 2021;10:584149. 8. Jain P, Kantarjian H, Jabbour E, et al. Clinical characteristics of Philadelphia positive T-cell lymphoid leukemias-(De novo and blast phase CML). Am J Hematol 2017;92:E3-4. 9. Ballerini P, Busson M, Fasola S, et al. NUP214-ABL1 amplification in t(5;14)/HOX11L2-positive ALL present with several forms and may have a prognostic significance. Leukemia 2005; 19:468-70. 10. Barber KE, Martineau M, Harewood L, et al. Amplification of the ABL gene in T-cell acute lymphoblastic leukemia. Leukemia 2004;18:1153-6. 11. Kim HJ, Woo HY, Koo HH, Tak EY, Kim SH. ABL oncogene amplification with p16(INK4a) gene deletion in precursor T-cell acute lymphoblastic leukemia/lymphoma: report of the first case. Am J Hematol 2004;76:360-3. 12. Chen Y, Zhang L, Huang J, et al. Dasatinib and chemotherapy in a patient with early T-cell precursor acute lymphoblastic leukemia and NUP214-ABL1 fusion: a case report. Exp Ther Med 2017;14:3979-84. 13. Peterson JF, Pitel BA, Smoley SA, et al. Detection of a cryptic NUP214/ABL1 gene fusion by mate-pair sequencing (MPseq) in a newly diagnosed case of pediatric T-lymphoblastic leukemia. Cold Spring Harb Mol Case Stud 2019;5:a003533. 14. De Keersmaecker K, Lahortiga I, Graux C, et al. Transition from EML1-ABL1 to NUP214-ABL1 positivity in a patient with acute T-lymphoblastic leukemia. Leukemia 2006;20:2202-4. 15. Bernasconi P, Calatroni S, Giardini I, et al. ABL1 amplification in T-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet 2005;162:146-50.","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"57 4","pages":"281-284"},"PeriodicalIF":2.2,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b8/3e/br-57-4-281.PMC9812729.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10634863","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":"NK-cell trogocytosis of CD19 antigen: a rare B-ALL MRD mimicker.","authors":"Devasis Panda,&nbsp;Amardeep Pathak,&nbsp;Narender Tejwani,&nbsp;Anurag Mehta","doi":"10.5045/br.2022.2022235","DOIUrl":"https://doi.org/10.5045/br.2022.2022235","url":null,"abstract":"","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"57 4","pages":"249"},"PeriodicalIF":2.2,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/9b/f2/br-57-4-249.PMC9812724.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10643567","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":"Epigenetic and genetic investigation of SOCS-1 gene in patients with multiple myeloma.","authors":"Fatıma Ceren Tuncel,&nbsp;Istemi Serin,&nbsp;Sacide Pehlivan,&nbsp;Yasemin Oyaci,&nbsp;Mustafa Pehlivan","doi":"10.5045/br.2022.2022097","DOIUrl":"https://doi.org/10.5045/br.2022.2022097","url":null,"abstract":"<p><strong>Background: </strong>The suppressor of cytokine signaling-1 (SOCS-1) functions to induce an appropriate immune response and is an essential physiological regulator of interferon signaling. DNA methylation involves adding a methyl group to the carbon 5 position of cytosine. Besides comparing SOCS-1 gene methylation status between patients with multiple myeloma (MM) and healthy controls, this study also aimed to demonstrate the effect of SOCS-1 gene distribution and the effect of methylation of SOCS-1 on progression-free survival (PFS) and overall survival (OS).</p><p><strong>Methods: </strong>This study included 120 patients diagnosed with MM between January 2018 and 2020 and 80 healthy individuals. The distribution of the SOCS-1 genotypes was statistically compared between MM patients and healthy controls. Additionally, the statistically significant effects of these genotypes on survival were examined.</p><p><strong>Results: </strong>The CA/CA genotype of SOCS-1 was significantly higher in healthy controls (<i>P</i>=0.001), while the Del/Del genotype was significantly higher in patients with MM (<i>P</i>=0.034). The percent methylated reference (PMR) value of the SOCS-1 gene was significantly higher in the healthy controls (median, 43.48; range, 2.76‒247.75; <i>P</i>=0.001). Patients with a PMR value of ≥43.48 were 3.125 times more likely to develop progression than those with a PMR value of ＜43.48.</p><p><strong>Conclusion: </strong>The effects of SOCS-1 polymorphisms on the pathogenesis of.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"57 4","pages":"250-255"},"PeriodicalIF":2.2,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/77/a0/br-57-4-250.PMC9812727.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10628163","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}