Blood Research最新文献

{"title":"Abnormal expression of <i>H-Ras</i> induces S-phase arrest and mitotic catastrophe in human T-lymphocyte leukemia.","authors":"Jorge A Zamora-Domínguez,&nbsp;Irma Olarte-Carrillo,&nbsp;Rubén Ruiz-Ramos,&nbsp;Christian Ramos-Peñafiel,&nbsp;Luis A Jiménez-Zamudio,&nbsp;Ethel A García-Latorre,&nbsp;Federico Cruz Centeno,&nbsp;Adolfo Martínez-Tovar","doi":"10.5045/br.2023.2022143","DOIUrl":"https://doi.org/10.5045/br.2023.2022143","url":null,"abstract":"<p><strong>Background: </strong>Leukemia is a neoplasm with high incidence and mortality rates. Mitotic death has been observed in tumor cells treated with chemotherapeutic agents. Ras family proteins participate in the transduction of signals involved in different processes, such as proliferation, differentiation, survival, and paradoxically, initiation of cell death.</p><p><strong>Methods: </strong>This study investigated the effect of <i>H-Ras</i> expression on human T-cell acute lymphoblastic leukemia MOLT-4 cells. Cells were electroporated with either wild-type (Ras^wt) or oncogenic mutant in codon 12 exon 1 (Ras^mut) versions of <i>H-Ras</i> gene and stained for morphological analysis. Cell viability was assessed using trypan blue staining and cell cycle analysis using flow cytometry. <i>H-Ras</i> gene expression was determined using quantitative real-time reverse transcription polymerase chain reaction. The <i>t</i>, ANOVA, and Scheffe tests were used for statistical analysis.</p><p><strong>Results: </strong>Human T-cell acute lymphoblastic leukemia MOLT-4 cells showed nuclear fragmentation and presence of multiple nuclei and micronuclei after transfection with either wt or mutant <i>H-Ras</i> genes. Cell cycle analysis revealed a statistically significant increase in cells in the S phase when transfected with either wt (83.67%, <i>P</i><0.0005) or mutated (81.79%, <i>P</i><0.0001) <i>H-Ras</i> genes. Although similar effects for both versions of <i>H-Ras</i> were found, cells transfected with the mutated version died at 120 h of mitotic catastrophe.</p><p><strong>Conclusion: </strong>Transfection of human T-cell acute lymphoblastic leukemia MOLT-4 cells with either normal or mutated <i>H-Ras</i> genes induced alterations in morphology, arrest in the S phase, and death by mitotic catastrophe.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":null,"pages":null},"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/7e/26/br-58-1-20.PMC10063590.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9581888","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":"CD5+ follicular lymphoma rapidly transformed to high-grade B-cell lymphoma with double-hit: from <i>BCL2</i> to <i>MYC</i> disruption.","authors":"Eva Soler-Espejo,&nbsp;Javier Marco-Ayala,&nbsp;Tzu-Hua Chen-Liang,&nbsp;María José López-Poveda,&nbsp;Raúl Teruel-Montoya,&nbsp;Francisco José Ortuño","doi":"10.5045/br.2023.2023039","DOIUrl":"https://doi.org/10.5045/br.2023.2023039","url":null,"abstract":"REFERENCES 1. Rapaport SI, Ames SB, Duvall BJ. A plasma coagulation defect in systemic lupus erythematosus arising from hypoprothrombinemia combined with antiprothrombinase activity. Blood 1960;15: 212-27. 2. Kim JS, Kim MJ, Bae EY, Jeong DC. Pulmonary hemorrhage in pediatric lupus anticoagulant hypoprothrombinemia syndrome. Korean J Pediatr 2014;57:202-5. 3. Mazodier K, Arnaud L, Mathian A, et al. Lupus anticoagulanthypoprothrombinemia syndrome: report of 8 cases and review of the literature. Medicine (Baltimore) 2012;91:251-60. 4. Komvilaisak P, Wisanuyotin S, Jettrisuparb A, Wiangnon S. Lupus anticoagulant-hypoprothrombinemia syndrome (LAC-HPS) in children with systemic lupus erythematosus: report of 3 cases. J Pediatr Hematol Oncol 2017;39:e521-4. 5. Yacobovich JR, Uziel Y, Friedman Z, Radnay J, Wolach B. Diffuse muscular haemorrhage as presenting sign of juvenile systemic lupus erythematosus and lupus anticoagulant hypoprothrombinaemia syndrome. Rheumatology (Oxford) 2001;40:585-7. 6. Sakamoto A, Ogura M, Hattori A, et al. Lupus anticoagulant hypoprothrombinemia syndrome associated with bilateral adrenal haemorrhage in a child: early diagnosis and intervention. Thromb J 2021;19:19. 7. Jaeger U, Kapiotis S, Pabinger I, Puchhammer E, Kyrle PA, Lechner K. Transient lupus anticoagulant associated with hypoprothrombinemia and factor XII deficiency following adenovirus infection. Ann Hematol 1993;67:95-9. 8. Appert-Flory A, Fischer F, Amiral J, Monpoux F. Lupus anticoagulant-hypoprothrombinemia syndrome (HLAS): report of one case in a familial infectious context. Thromb Res 2010; 126:e139-40. 9. Schmugge M, Tölle S, Marbet GA, Laroche P, Meili EO. Gingival bleeding, epistaxis and haematoma three days after gastroenteritis: the haemorrhagic lupus anticoagulant syndrome. Eur J Pediatr 2001;160:43-6. 10. Baca V, Montiel G, Meillón L, et al. Diagnosis of lupus anticoagulant in the lupus anticoagulant-hypoprothrombinemia syndrome: report of two cases and review of the literature. Am J Hematol 2002;71:200-7. 11. Bajaj SP, Rapaport SI, Fierer DS, Herbst KD, Schwartz DB. A mechanism for the hypoprothrombinemia of the acquired hypoprothrombinemia-lupus anticoagulant syndrome. Blood 1983; 61:684-92. 12. Becton DL, Stine KC. Transient lupus anticoagulants associated with hemorrhage rather than thrombosis: the hemorrhagic lupus anticoagulant syndrome. J Pediatr 1997;130:998-1000. 13. Bowles L, Platton S, Yartey N, et al. Lupus anticoagulant and abnormal coagulation tests in patients with Covid-19. N Engl J Med 2020;383:288-90. CD5+ follicular lymphoma rapidly transformed to high-grade B-cell lymphoma with double-hit: from BCL2 to MYC disruption","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":null,"pages":null},"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/a4/09/br-58-1-79.PMC10063588.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9228257","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":"Can the bone marrow harvest volume be reduced safely in hematopoietic stem cell transplantation with pediatric sibling donors?","authors":"Awatif AlAnazi,&nbsp;Amer Nadeem,&nbsp;Khawar Siddiqui,&nbsp;Ali AlAhmari,&nbsp;Ibrahim Ghemlas,&nbsp;Abdullah AlJefri,&nbsp;Hawazen AlSaedi,&nbsp;Saadiya Khan,&nbsp;Mouhab Ayas","doi":"10.5045/br.2023.2022167","DOIUrl":"https://doi.org/10.5045/br.2023.2022167","url":null,"abstract":"<p><strong>Background: </strong>Reduced harvest volumes in pediatric donors appear to have the potential to reduce donor-associated risks while maintaining engraftment in recipients; however, the allowable harvest volume reduction remains undefined.</p><p><strong>Methods: </strong>We retrospectively analyzed the data pairs of 553 bone marrow (BM) harvests from pediatric (age at harvest <18 yr) sibling donors and clinical outcomes of 553 pediatric (age at infusion <14 yr) transplant-naïve recipients to assess the optimal BM harvest volume needed from pediatric donors to obtain the desired CD34+ cell count (≥3.0×10⁶ cells per kg of recipient weight), and to study its impact on the clinical outcomes of transplantation in pediatric recipients.</p><p><strong>Results: </strong>The minimum desired CD34+ cell count of ≥3.0×10⁶ per kg of recipient weight was achieved for 506 (95.3%) of donor-recipient pairs. The median CD34+ cell yield was 6.4×10⁶ per kg of recipient weight (range, 1.2‒33.8×10⁶) in donors younger than 5 years old at harvest, 4.7×10⁶ (range, 0.3‒28.5×10⁶) in donors aged 5‒10 years and 2.1×10⁶ (range, 0.3‒11.3×10⁶) in donors older than 10 years (<i>P</i><0.001).</p><p><strong>Conclusion: </strong>The infused CD34+ cell dose (×10⁶ cells/kg of recipient weight) had no impact on GRFS; however, a CD34+ cell dose of ＞7×10⁶ cells/kg of recipient weight did not improve hematopoietic recovery.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":null,"pages":null},"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/41/47/br-58-1-28.PMC10063592.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9581889","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":"Anaplastic diffuse large B-cell lymphoma: a deceptive morphology.","authors":"Priyadharshini Sivasubramaniam,&nbsp;Aishwarya Ravindran","doi":"10.5045/br.2023.2022247","DOIUrl":"https://doi.org/10.5045/br.2023.2022247","url":null,"abstract":"An elderly male without significant past medical history presented with cervical lymphadenopathy. Labs showed anemia (Hb 7.6 g/dL) and elevated WBC count (16×10 9 /L) with neutrophilia. Limited core biopsy revealed partial nodal involvement by an overtly malignant proliferation with marked anaplasia including multinucleated forms (A, B) and appeared to display a somewhat cohesive pattern of growth suggestive of an epithelioid neoplasm. Flow cytometry showed no immunophenotypic evidence of lymphoma. The primary differential diagnosis based on these findings included a poorly-differentiated carcinoma versus melanoma, however, immunostains for keratin, Melan A and SOX10 were negative. CD45 was only performed subsequently due to receipt of the case for hematopathologist evaluation given the lymphadenopathy. Surprisingly, the anaplastic tumor cells (A ×40; B ×200; C ×400) were diffusely CD45-positive; subsequent immunostains revealed positivity","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":null,"pages":null},"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/b0/7b/br-58-1-1.PMC10063593.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9283128","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":"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":null,"pages":null},"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":"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":null,"pages":null},"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":null,"pages":null},"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":null,"pages":null},"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":"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":null,"pages":null},"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":"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":null,"pages":null},"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}