Pub Date : 2023-12-31Epub Date: 2023-10-19DOI: 10.5045/br.2023.2023125
Myung-Won Lee, Jeong Suk Koh, Sora Kang, Hyewon Ryu, Ik-Chan Song, Hyo-Jin Lee, Hwan-Jung Yun, Seon Young Kim, Seong Soo Kim, Deog-Yeon Jo
Background: Although atherosclerosis is likely to be involved in the development of arterial thrombotic events in patients with essential thrombocythemia (ET), abdominal aortic calcification (AAC) has rarely been investigated. We evaluated the prevalence and clinical relevance of AAC at the time of ET diagnosis.
Methods: This retrospective study included patients newly diagnosed with ET who underwent abdominal computed tomography (CT) at the time of diagnosis between January 2002 and December 2021 at Chungnam National University Hospital, Daejeon, Korea. CT images were reviewed and an aortic calcification score was assigned.
Results: Of the 94 patients (median age, 62 yr; range, 18‒90 yr), AAC was detected in 62 (66.0%). AAC was most commonly mild (33.0%), followed by moderate (22.7%) and severe (5.3%). Old age [odds ratio (OR), 34.37; 95% confidence interval (CI), 12.32‒95.91; P＜0.001] was an independent risk factor for AAC. The patients with AAC had a higher WBC count (11.8±4.7 vs. 9.7±2.9×109/L, P=0.017), higher neutrophil-to-lymphocyte ratio (4.3±2.7 vs. 3.1±1.5, P=0.039), and higher JAK2V617F positivity (81.5% vs. 58.8%, P=0.020) compared to those without AAC. AAC was an independent risk factor for arterial thrombotic vascular events that occurred before or at diagnosis of ET (OR, 4.12; 95% CI, 1.11‒15.85; P=0.034).
Conclusion: AAC is common in patients with ET and is associated with arterial thrombotic events.
{"title":"Abdominal aortic calcification in patients newly diagnosed with essential thrombocythemia.","authors":"Myung-Won Lee, Jeong Suk Koh, Sora Kang, Hyewon Ryu, Ik-Chan Song, Hyo-Jin Lee, Hwan-Jung Yun, Seon Young Kim, Seong Soo Kim, Deog-Yeon Jo","doi":"10.5045/br.2023.2023125","DOIUrl":"10.5045/br.2023.2023125","url":null,"abstract":"<p><strong>Background: </strong>Although atherosclerosis is likely to be involved in the development of arterial thrombotic events in patients with essential thrombocythemia (ET), abdominal aortic calcification (AAC) has rarely been investigated. We evaluated the prevalence and clinical relevance of AAC at the time of ET diagnosis.</p><p><strong>Methods: </strong>This retrospective study included patients newly diagnosed with ET who underwent abdominal computed tomography (CT) at the time of diagnosis between January 2002 and December 2021 at Chungnam National University Hospital, Daejeon, Korea. CT images were reviewed and an aortic calcification score was assigned.</p><p><strong>Results: </strong>Of the 94 patients (median age, 62 yr; range, 18‒90 yr), AAC was detected in 62 (66.0%). AAC was most commonly mild (33.0%), followed by moderate (22.7%) and severe (5.3%). Old age [odds ratio (OR), 34.37; 95% confidence interval (CI), 12.32‒95.91; <i>P</i>＜0.001] was an independent risk factor for AAC. The patients with AAC had a higher WBC count (11.8±4.7 vs. 9.7±2.9×10<sup>9</sup>/L, <i>P</i>=0.017), higher neutrophil-to-lymphocyte ratio (4.3±2.7 vs. 3.1±1.5, <i>P</i>=0.039), and higher <i>JAK2</i>V617F positivity (81.5% vs. 58.8%, <i>P</i>=0.020) compared to those without AAC. AAC was an independent risk factor for arterial thrombotic vascular events that occurred before or at diagnosis of ET (OR, 4.12; 95% CI, 1.11‒15.85; <i>P</i>=0.034).</p><p><strong>Conclusion: </strong>AAC is common in patients with ET and is associated with arterial thrombotic events.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":" ","pages":"173-180"},"PeriodicalIF":2.2,"publicationDate":"2023-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10758625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49683468","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}
Pub Date : 2023-12-31Epub Date: 2023-10-19DOI: 10.5045/br.2023.2023178
Verónica Roldán Galiacho, Paula Zoco Gallardo, Laura Zaldumbide Dueñas, Bernabé Dávila De Las Fuentes, Juan Carlos García-Ruiz
{"title":"Flower-shaped lymphocytes in CD5+ diffuse large B-cell lymphoma's leukemic phase.","authors":"Verónica Roldán Galiacho, Paula Zoco Gallardo, Laura Zaldumbide Dueñas, Bernabé Dávila De Las Fuentes, Juan Carlos García-Ruiz","doi":"10.5045/br.2023.2023178","DOIUrl":"10.5045/br.2023.2023178","url":null,"abstract":"","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":" ","pages":"165"},"PeriodicalIF":2.2,"publicationDate":"2023-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10758631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49683469","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}
Sadiq Khalaf Ali, Saad Abdulbaqi Alomar, Hussam Mahmood Salih, Nooran Salem Yaseen
the potential to escalate to a maximum of 25 mg bid. However, in contrast to decitabine, greater caution is necessary when combined with intensive cytotoxic chemotherapy. Thus, further research is needed to determine the appropriate dosing. In summary, our case highlights that the combination of ruxolitinib and AML-style cytotoxic chemotherapy is an attractive option for older patients with post-MPN AML. Given the heterogeneity of this population and the lack of treatment options, further exploration of the role of ruxolitinib in combination with cytotoxic chemotherapy is required.
{"title":"A challenging diagnosis of hepatosplenic T cell lymphoma in a 10-year-old child.","authors":"Sadiq Khalaf Ali, Saad Abdulbaqi Alomar, Hussam Mahmood Salih, Nooran Salem Yaseen","doi":"10.5045/br.2023.2023132","DOIUrl":"https://doi.org/10.5045/br.2023.2023132","url":null,"abstract":"the potential to escalate to a maximum of 25 mg bid. However, in contrast to decitabine, greater caution is necessary when combined with intensive cytotoxic chemotherapy. Thus, further research is needed to determine the appropriate dosing. In summary, our case highlights that the combination of ruxolitinib and AML-style cytotoxic chemotherapy is an attractive option for older patients with post-MPN AML. Given the heterogeneity of this population and the lack of treatment options, further exploration of the role of ruxolitinib in combination with cytotoxic chemotherapy is required.","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"58 3","pages":"157-161"},"PeriodicalIF":2.2,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/6a/67/br-58-3-157.PMC10548286.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41154967","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}
Pub Date : 2023-09-30Epub Date: 2023-07-24DOI: 10.5045/br.2023.2023112
Jian Li, Merit Hanna
A 67-year-old patient received rituximab and bendamustine for follicular lymphoma and achieved complete response two years prior to developing moderate anaemia (94 g/L) and thrombocytopenia (44×10 9 /L). Blood film showed circulating nucleated red cells and proerythroblasts with dysplasia (A, B). Diagnostic bone marrow aspirate was a dry tap. Trephine imprints showed 42% nucleated red cells with significant dysplasia such as binucleation, nuclear irregularity and cytoplasmic vacuoles (C). Immature erythroblasts were increased but comprised ＜ 30% of nucleated cells. There was minimal maturation beyond the proerythroblast phase. Trephine core was hypercellular with abnormal megakaryocytes and erythroblasts (D). The latter showed weak membranous staining with anti-CD117 (E) and variable patterns of glycophorin A (F). Intra-sinusoidal infiltration of proerythroblasts were highlighted. There was no evidence for increased myeloblasts, granulocytic
{"title":"Intrasinusoidal proerythroblast infiltration in therapy related myeloid neoplasm.","authors":"Jian Li, Merit Hanna","doi":"10.5045/br.2023.2023112","DOIUrl":"10.5045/br.2023.2023112","url":null,"abstract":"A 67-year-old patient received rituximab and bendamustine for follicular lymphoma and achieved complete response two years prior to developing moderate anaemia (94 g/L) and thrombocytopenia (44×10 9 /L). Blood film showed circulating nucleated red cells and proerythroblasts with dysplasia (A, B). Diagnostic bone marrow aspirate was a dry tap. Trephine imprints showed 42% nucleated red cells with significant dysplasia such as binucleation, nuclear irregularity and cytoplasmic vacuoles (C). Immature erythroblasts were increased but comprised ＜ 30% of nucleated cells. There was minimal maturation beyond the proerythroblast phase. Trephine core was hypercellular with abnormal megakaryocytes and erythroblasts (D). The latter showed weak membranous staining with anti-CD117 (E) and variable patterns of glycophorin A (F). Intra-sinusoidal infiltration of proerythroblasts were highlighted. There was no evidence for increased myeloblasts, granulocytic","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":" ","pages":"126"},"PeriodicalIF":2.2,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/98/ec/br-58-3-126.PMC10548291.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9858742","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}
Pub Date : 2023-09-30Epub Date: 2023-08-25DOI: 10.5045/br.2023.2023120
Suji Park, Jae-Ryong Shim, Ji Hyun Lee, Jin-Yeong Han
REFERENCES 1. Swerdlow SH, Campo E, Pileri SA, et al. The 2016 revision of the World Health Organization classification of lymphoid neoplasms. Blood 2016;127:2375-90. 2. Dores GM, Matsuno RK, Weisenburger DD, Rosenberg PS, Anderson WF. Hairy cell leukaemia: a heterogeneous disease? Br J Haematol 2008;142:45-51. 3. Tiacci E, Trifonov V, Schiavoni G, et al. BRAF mutations in hairy-cell leukemia. N Engl J Med 2011;364:2305-15. 4. Cortazar JM, DeAngelo DJ, Pinkus GS, Morgan EA. Morphological and immunophenotypical features of hairy cell leukaemia involving lymph nodes and extranodal tissues. Histopathology 2017;71:112-24. 5. Hammond WA, Swaika A, Menke D, Tun HW. Hairy cell lymphoma: a potentially under-recognized entity. Rare Tumors 2017;9:6518. 6. Rosen DS, Smith S, Gurbuxani S, Yamini B. Extranodal hairy cell leukemia presenting in the lumbar spine. J Neurosurg Spine 2008;9:374-6. 7. Choi WW, Weisenburger DD, Greiner TC, et al. A new immunostain algorithm classifies diffuse large B-cell lymphoma into molecular subtypes with high accuracy. Clin Cancer Res 2009;15:5494-502. 8. Chadha P, Rademaker AW, Mendiratta P, et al. Treatment of hairy cell leukemia with 2-chlorodeoxyadenosine (2-CdA): longterm follow-up of the Northwestern University experience. Blood 2005;106:241-6. 9. Saven A, Burian C, Koziol JA, Piro LD. Long-term follow-up of patients with hairy cell leukemia after cladribine treatment. Blood 1998;92:1918-26. Co-existence of RUNX1-RUNX1T1 and BCR-ABL1 in acute myeloid leukemia: a case report
{"title":"Co-existence of <i>RUNX1-RUNX1T1</i> and <i>BCR-ABL1</i> in acute myeloid leukemia: a case report.","authors":"Suji Park, Jae-Ryong Shim, Ji Hyun Lee, Jin-Yeong Han","doi":"10.5045/br.2023.2023120","DOIUrl":"10.5045/br.2023.2023120","url":null,"abstract":"REFERENCES 1. Swerdlow SH, Campo E, Pileri SA, et al. The 2016 revision of the World Health Organization classification of lymphoid neoplasms. Blood 2016;127:2375-90. 2. Dores GM, Matsuno RK, Weisenburger DD, Rosenberg PS, Anderson WF. Hairy cell leukaemia: a heterogeneous disease? Br J Haematol 2008;142:45-51. 3. Tiacci E, Trifonov V, Schiavoni G, et al. BRAF mutations in hairy-cell leukemia. N Engl J Med 2011;364:2305-15. 4. Cortazar JM, DeAngelo DJ, Pinkus GS, Morgan EA. Morphological and immunophenotypical features of hairy cell leukaemia involving lymph nodes and extranodal tissues. Histopathology 2017;71:112-24. 5. Hammond WA, Swaika A, Menke D, Tun HW. Hairy cell lymphoma: a potentially under-recognized entity. Rare Tumors 2017;9:6518. 6. Rosen DS, Smith S, Gurbuxani S, Yamini B. Extranodal hairy cell leukemia presenting in the lumbar spine. J Neurosurg Spine 2008;9:374-6. 7. Choi WW, Weisenburger DD, Greiner TC, et al. A new immunostain algorithm classifies diffuse large B-cell lymphoma into molecular subtypes with high accuracy. Clin Cancer Res 2009;15:5494-502. 8. Chadha P, Rademaker AW, Mendiratta P, et al. Treatment of hairy cell leukemia with 2-chlorodeoxyadenosine (2-CdA): longterm follow-up of the Northwestern University experience. Blood 2005;106:241-6. 9. Saven A, Burian C, Koziol JA, Piro LD. Long-term follow-up of patients with hairy cell leukemia after cladribine treatment. Blood 1998;92:1918-26. Co-existence of RUNX1-RUNX1T1 and BCR-ABL1 in acute myeloid leukemia: a case report","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":" ","pages":"151-155"},"PeriodicalIF":2.2,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d1/25/br-58-3-151.PMC10548288.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10423130","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}
Pub Date : 2023-09-30Epub Date: 2023-08-25DOI: 10.5045/br.2023.2023136
Dong Hyun Kim, Ja Min Byun, Dong-Yeop Shin, Inho Kim, Sung-Soo Yoon, Youngil Koh
Age 62 74 Gender F M MPN type Essential thrombocythemia Polycythemia vera AML diagnosis Feb 2019 Mar 2019 JAK2 status Negative Positive Other molecular status Complex karyotype, TP53, ROS1, FGFR4 mutations Not assessed Treatment 5+2 induction chemotherapy with ruxolitinib 5+2 induction chemotherapy with ruxolitinib Response to induction Complete remission Partial remission Response to consolidation Not assessed (EOT) Not assessed (EOT) EOT reason Septic pneumonia Deteriorated condition Duration of response 3 months + 24 months + OS 3 months 24 months + Outcome Deceased Medically stable after EOT
{"title":"Concomitant ruxolitinib with cytarabine-based induction chemotherapy in secondary acute myeloid leukemia evolving from myeloproliferative neoplasm.","authors":"Dong Hyun Kim, Ja Min Byun, Dong-Yeop Shin, Inho Kim, Sung-Soo Yoon, Youngil Koh","doi":"10.5045/br.2023.2023136","DOIUrl":"10.5045/br.2023.2023136","url":null,"abstract":"Age 62 74 Gender F M MPN type Essential thrombocythemia Polycythemia vera AML diagnosis Feb 2019 Mar 2019 JAK2 status Negative Positive Other molecular status Complex karyotype, TP53, ROS1, FGFR4 mutations Not assessed Treatment 5+2 induction chemotherapy with ruxolitinib 5+2 induction chemotherapy with ruxolitinib Response to induction Complete remission Partial remission Response to consolidation Not assessed (EOT) Not assessed (EOT) EOT reason Septic pneumonia Deteriorated condition Duration of response 3 months + 24 months + OS 3 months 24 months + Outcome Deceased Medically stable after EOT","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":" ","pages":"155-157"},"PeriodicalIF":2.2,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ff/9b/br-58-3-155.PMC10548284.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10423129","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}
Background: Pulmonary thromboembolism (PTE) is a significant contributing factor to vascular diseases. This study aimed to determine the prevalence of pulmonary thromboembolism and its predisposing factors in patients with COVID-19.
Methods: This cross-sectional study included 284 patients with COVID-19 who were admitted to Nemazee Teaching Hospital (Shiraz, Iran) between June and August 2021. All patients were diagnosed with COVID-19 by a physician based on clinical symptoms or positive polymerase chain reaction (PCR) test results. The collected data included demographic data and laboratory findings. Data were analyzed using the SPSS software. P≤0.05 was considered statistically significant.
Results: There was a significant difference in the mean age between the PTE group and non-PTE group (P=0.037). Moreover, the PTE group had a significantly higher prevalence of hypertension (36.7% vs. 21.8%, P=0.019), myocardial infarction (4.5% vs. 0%, P=0.006), and stroke (23.9% vs. 4.9%, P=0.0001). Direct bilirubin (P=0.03) and albumin (P=0.04) levels significantly differed between the PTE and non-PTE groups. Notably, there was a significant difference in the partial thromboplastin time (P=0.04) between the PTE and non-PTE groups. A regression analysis indicated that age (OR, 1.02; 95% CI, 1.00‒1.004; P=0.005), blood pressure (OR, 2.07; 95% CI, 1.12‒3.85; P=0.02), heart attack (OR, 1.02; 95% CI, 1.28‒6.06; P=0.009), and albumin level (OR, 0.39; 95% CI, 0.16‒0.97; P=0.04) were all independent predictors of PTE development.
Conclusion: Regression analysis revealed that age, blood pressure, heart attack, and albumin levels were independent predictors of PTE.
{"title":"Investigating the prevalence of and predictive and risk factors for pulmonary embolism in patients with COVID-19 in Nemazee Teaching Hospital.","authors":"Mahnaz Yadollahi, Hessam Hosseinalipour, Muhammad Alinaqi, Mehrdad Karajizadeh, Mehrdad Jowkar, Kazem Jamali, Maryam Yadollahi, Pooria Fazeli","doi":"10.5045/br.2023.2023076","DOIUrl":"10.5045/br.2023.2023076","url":null,"abstract":"<p><strong>Background: </strong>Pulmonary thromboembolism (PTE) is a significant contributing factor to vascular diseases. This study aimed to determine the prevalence of pulmonary thromboembolism and its predisposing factors in patients with COVID-19.</p><p><strong>Methods: </strong>This cross-sectional study included 284 patients with COVID-19 who were admitted to Nemazee Teaching Hospital (Shiraz, Iran) between June and August 2021. All patients were diagnosed with COVID-19 by a physician based on clinical symptoms or positive polymerase chain reaction (PCR) test results. The collected data included demographic data and laboratory findings. Data were analyzed using the SPSS software. <i>P</i>≤0.05 was considered statistically significant.</p><p><strong>Results: </strong>There was a significant difference in the mean age between the PTE group and non-PTE group (<i>P</i>=0.037). Moreover, the PTE group had a significantly higher prevalence of hypertension (36.7% vs. 21.8%, <i>P</i>=0.019), myocardial infarction (4.5% vs. 0%, <i>P</i>=0.006), and stroke (23.9% vs. 4.9%, <i>P</i>=0.0001). Direct bilirubin (<i>P</i>=0.03) and albumin (<i>P</i>=0.04) levels significantly differed between the PTE and non-PTE groups. Notably, there was a significant difference in the partial thromboplastin time (<i>P</i>=0.04) between the PTE and non-PTE groups. A regression analysis indicated that age (OR, 1.02; 95% CI, 1.00‒1.004; <i>P</i>=0.005), blood pressure (OR, 2.07; 95% CI, 1.12‒3.85; <i>P</i>=0.02), heart attack (OR, 1.02; 95% CI, 1.28‒6.06; <i>P</i>=0.009), and albumin level (OR, 0.39; 95% CI, 0.16‒0.97; <i>P</i>=0.04) were all independent predictors of PTE development.</p><p><strong>Conclusion: </strong>Regression analysis revealed that age, blood pressure, heart attack, and albumin levels were independent predictors of PTE.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":" ","pages":"127-132"},"PeriodicalIF":2.2,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/14/f4/br-58-3-127.PMC10548293.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9823324","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}
Pub Date : 2023-09-30Epub Date: 2023-07-27DOI: 10.5045/br.2023.2023097
Seong-Ho Kang, Ji Seon Choi
Background: Epigenetic studies, particularly research on microRNA (miRNA), have flourished. The abnormal expression of miRNA contributes to the development of hematologic malignancies. miR-765 has been reported to inhibit cell proliferation by downregulating proteolipid protein 2 (PLP2), which causes apoptosis. We investigated miR-765 dysregulation in myelodysplastic syndromes (MDS).
Methods: We compared the expression profiles of miR-765 in 65 patients with MDS and 11 controls. Cell proliferation and apoptosis assays were performed to determine the in vitro effects of miR-765 on leukemia cells transfected with the miR-765 mimic. Reverse transcription quantitative PCR (RT-qPCR) and western blotting were performed to examine the targets of miR-765.
Results: We found that miR-765 levels were upregulated 10.2-fold in patients with MDS compared to controls. In refractory cytopenia with multilineage dysplasia, the percentage of patients with elevated miR-765 levels was significantly higher than in other forms of MDS. Experiments with leukemia cells revealed that transfection with a miR-765 mimic inhibited cell proliferation and induced apoptosis. RT-qPCR and western blotting demonstrated that the target of miR-765 was PLP2.
Conclusion: These findings imply that upregulation of miR-765 induces apoptosis via downregulation of PLP2 and may have a role in MDS pathogenesis.
{"title":"MicroRNA-765 is upregulated in myelodysplastic syndromes and induces apoptosis via PLP2 inhibition in leukemia cells.","authors":"Seong-Ho Kang, Ji Seon Choi","doi":"10.5045/br.2023.2023097","DOIUrl":"10.5045/br.2023.2023097","url":null,"abstract":"<p><strong>Background: </strong>Epigenetic studies, particularly research on microRNA (miRNA), have flourished. The abnormal expression of miRNA contributes to the development of hematologic malignancies. miR-765 has been reported to inhibit cell proliferation by downregulating proteolipid protein 2 (PLP2), which causes apoptosis. We investigated miR-765 dysregulation in myelodysplastic syndromes (MDS).</p><p><strong>Methods: </strong>We compared the expression profiles of miR-765 in 65 patients with MDS and 11 controls. Cell proliferation and apoptosis assays were performed to determine the <i>in vitro</i> effects of miR-765 on leukemia cells transfected with the miR-765 mimic. Reverse transcription quantitative PCR (RT-qPCR) and western blotting were performed to examine the targets of miR-765.</p><p><strong>Results: </strong>We found that miR-765 levels were upregulated 10.2-fold in patients with MDS compared to controls. In refractory cytopenia with multilineage dysplasia, the percentage of patients with elevated miR-765 levels was significantly higher than in other forms of MDS. Experiments with leukemia cells revealed that transfection with a miR-765 mimic inhibited cell proliferation and induced apoptosis. RT-qPCR and western blotting demonstrated that the target of miR-765 was PLP2.</p><p><strong>Conclusion: </strong>These findings imply that upregulation of miR-765 induces apoptosis via downregulation of PLP2 and may have a role in MDS pathogenesis.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":" ","pages":"133-137"},"PeriodicalIF":2.2,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e7/7a/br-58-3-133.PMC10548289.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9930594","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}
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