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B‐cell lymphomas frequently (dys)regulate \u003Cjats:styled-content style=\"fixed-case\">BCR\u003C\u002Fjats:styled-content> signalling and thus take advantage of this pre‐existing pathway for B‐cell proliferation and survival. This has recently been underscored by clinical trials demonstrating that small molecules (fosfamatinib, ibrutinib, idelalisib) inhibiting \u003Cjats:styled-content style=\"fixed-case\">BCR\u003C\u002Fjats:styled-content>‐associated kinases (\u003Cjats:styled-content style=\"fixed-case\">SYK\u003C\u002Fjats:styled-content>,\u003Cjats:styled-content style=\"fixed-case\"> BTK\u003C\u002Fjats:styled-content>,\u003Cjats:styled-content style=\"fixed-case\"> PI\u003C\u002Fjats:styled-content>3K) have an encouraging clinical effect. Here we describe the current knowledge of the specific aspects of \u003Cjats:styled-content style=\"fixed-case\">BCR\u003C\u002Fjats:styled-content> signalling in diffuse large B‐cell lymphoma (\u003Cjats:styled-content style=\"fixed-case\">DLBCL\u003C\u002Fjats:styled-content>), follicular lymphoma, chronic lymphocytic leukaemia (\u003Cjats:styled-content style=\"fixed-case\">CLL\u003C\u002Fjats:styled-content>) and normal B cells. Multiple factors can contribute to \u003Cjats:styled-content style=\"fixed-case\">BCR\u003C\u002Fjats:styled-content> pathway (dys)regulation in these malignancies and the activation of ‘chronic’ or ‘tonic’ \u003Cjats:styled-content style=\"fixed-case\">BCR\u003C\u002Fjats:styled-content> signalling. In lymphoma B cells, the balance of initiation, amplitude and duration of \u003Cjats:styled-content style=\"fixed-case\">BCR\u003C\u002Fjats:styled-content> activation can be influenced by a specific immunoglobulin structure, the expression and mutations of adaptor molecules (like \u003Cjats:styled-content style=\"fixed-case\">GAB\u003C\u002Fjats:styled-content>1, \u003Cjats:styled-content style=\"fixed-case\">BLNK\u003C\u002Fjats:styled-content>,\u003Cjats:styled-content style=\"fixed-case\"> GRB\u003C\u002Fjats:styled-content>2, \u003Cjats:styled-content style=\"fixed-case\">CARD\u003C\u002Fjats:styled-content>11), the activity of kinases (like \u003Cjats:styled-content style=\"fixed-case\">LYN\u003C\u002Fjats:styled-content>,\u003Cjats:styled-content style=\"fixed-case\"> SYK\u003C\u002Fjats:styled-content>,\u003Cjats:styled-content style=\"fixed-case\"> PI\u003C\u002Fjats:styled-content>3K) or phosphatases (like \u003Cjats:styled-content style=\"fixed-case\">SHIP\u003C\u002Fjats:styled-content>‐1, \u003Cjats:styled-content style=\"fixed-case\">SHP\u003C\u002Fjats:styled-content>‐1 and \u003Cjats:styled-content style=\"fixed-case\">PTEN\u003C\u002Fjats:styled-content>) and levels of micro\u003Cjats:styled-content style=\"fixed-case\">RNA\u003C\u002Fjats:styled-content>s. We also discuss the crosstalk of \u003Cjats:styled-content style=\"fixed-case\">BCR\u003C\u002Fjats:styled-content> with other signalling pathways (\u003Cjats:styled-content style=\"fixed-case\">NF\u003C\u002Fjats:styled-content>‐κB, adhesion through integrins, migration and chemokine signalling) to emphasise that the ‘\u003Cjats:styled-content style=\"fixed-case\">BCR\u003C\u002Fjats:styled-content> inhibitors’ target multiple pathways interconnected with \u003Cjats:styled-content style=\"fixed-case\">BCR\u003C\u002Fjats:styled-content>, which might explain some of their clinical activity.\u003C\u002Fjats:p>",{"EN":111},"B‐cell receptor signalling and its crosstalk with other pathways in normal and malignant cells",{"VOID":113},"25080849",{"VOID":115},"10.1111\u002Fejh.12427","PUBLICATION","VERIFIED","Auto 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A, 1999, Accelerated emigration of B lymphocytes in the Xid mouse, J Immunol, 162, 4417, 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K, 2000, Genetic defect in human X‐linked agammaglobulinemia impedes a maturational evolution of pro‐B cells into a later stage of pre‐B cells in the B‐cell differentiation pathway, Blood, 96, 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Iron deficiency anemia (IDA) and beta‐thalassemia trait (B‐TT) are the most common causes of hypochromic microcytic anemias. Many indices have been defined to quickly discriminate these similar entities via parameters obtained from automated blood count analyzers. The purpose of the study was to evaluate the predictive value of these indices in differential diagnosis of IDA and B‐TT in adult cases.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Methods: \u003C\u002Fjats:bold> This study consists of 45 IDA cases, 36 women and nine men, whose mean age is 33.87 ± 11.59 (mean ± SD) (range 17–57 yr) and 66 B‐TT cases, 41 women and 25 men, whose mean age is 33.26 ± 13.36 (mean ± SD) (range 14–74 yr). IDA cases with Hb value <8.7 g\u002FdL have been excluded because these cases are not confused with B‐TT cases in practice. Patient groups have been evaluated according to red blood cell (RBC), red blood cell distribution width (RDW), Mentzer index, Shine and Lal indices, England and Fraser indices, Srivastava index, Green and King indices, RDW index and Ricerca index. Sensitivity, specificity, positive and negative predictive values and Youden’s index have been calculated.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Results: \u003C\u002Fjats:bold> Finally, none of these different formulations are superior to RBC value obtained from automated analyzers in adult cases with IDA and B‐TT.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Conclusions: \u003C\u002Fjats:bold> Total body iron status and hemoglobin A\u003Cjats:sub>2\u003C\u002Fjats:sub> level should be obtained for accurate differential diagnosis of IDA and B‐TT until more efficient tools develop.\u003C\u002Fjats:p>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\u003Cjats:p>\u003Cjats:bold>Mục tiêu: \u003C\u002Fjats:bold> Thiếu máu do thiếu sắt (IDA) và đặc điểm beta-thalassemia (B-TT) là nguyên nhân phổ biến nhất gây ra các dạng thiếu máu vi nhược sắc. Nhiều chỉ số đã được xác định để phân biệt nhanh chóng những thực thể tương tự này thông qua các thông số thu được từ máy phân tích công thức máu tự động. Mục đích của nghiên cứu là đánh giá giá trị tiên đoán của những chỉ số này trong chẩn đoán phân biệt IDA và B-TT ở các trường hợp người lớn.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Phương pháp: \u003C\u002Fjats:bold> Nghiên cứu bao gồm 45 trường hợp IDA, 36 phụ nữ và 9 nam giới, với độ tuổi trung bình là 33.87 ± 11.59 (trung bình ± SD) (phạm vi 17–57 tuổi) và 66 trường hợp B-TT, 41 phụ nữ và 25 nam giới, với độ tuổi trung bình là 33.26 ± 13.36 (trung bình ± SD) (phạm vi 14–74 tuổi). Những trường hợp IDA có giá trị Hb <8.7 g\u002FdL đã bị loại trừ vì những trường hợp này không gây nhầm lẫn với các trường hợp B-TT trong thực tế. Các nhóm bệnh nhân đã được đánh giá dựa trên số lượng tế bào máu đỏ (RBC), độ rộng phân bố tế bào máu đỏ (RDW), chỉ số Mentzer, các chỉ số Shine và Lal, chỉ số England và Fraser, chỉ số Srivastava, chỉ số Green và King, chỉ số RDW và chỉ số Ricerca. Độ nhạy, độ đặc hiệu, giá trị tiên đoán dương và âm, và chỉ số Youden đã được tính toán.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Kết quả: \u003C\u002Fjats:bold> Cuối cùng, không có bất kỳ một trong những công thức phân biệt này nào mạnh hơn giá trị RBC thu được từ các máy phân tích tự động trong các trường hợp người lớn bị IDA và B-TT.\u003C\u002Fjats:p>\u003Cjats:p>\u003Cjats:bold>Kết luận: \u003C\u002Fjats:bold> Tình trạng sắt toàn cơ thể và mức hemoglobin A\u003Cjats:sub>2\u003C\u002Fjats:sub> nên được thu thập để có chẩn đoán phân biệt chính xác giữa IDA và B-TT cho đến khi có các công cụ hiệu quả hơn phát triển.\u003C\u002Fjats:p>",{"EN":656,"VI":657},"Predictive value of discrimination indices in differential diagnosis of iron deficiency anemia and beta‐thalassemia trait","Giá trị tiên đoán của các chỉ số phân biệt trong chẩn đoán phân biệt thiếu máu do thiếu sắt và đặc điểm 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G, 1992, Automated measurement of red blood cell microcytosis and hypochromia in iron deficiency and beta‐thalassemia trait, Arch Pathol Lab Med, 116, 84",{},{"id":24,"text":805,"url":24,"identifiers":806},"10.1016\u002FS0140-6736(77)92128-6",{"doi":805},{"id":24,"text":808,"url":24,"identifiers":809},"10.1016\u002FS0140-6736(73)91856-4",{"doi":808},{"id":24,"text":811,"url":24,"identifiers":812},"10.1016\u002FS0140-6736(73)90637-5",{"doi":811},{"id":24,"text":814,"url":24,"identifiers":815},"Green R, 1989, A new red cell discriminant incorporating volume dispersion for differentiating iron deficiency anemia from thalassemia minor, Blood Cells, 15, 481",{},{"id":24,"text":817,"url":24,"identifiers":818},"10.1097\u002F00043426-199907000-00040",{"doi":817},{"id":24,"text":820,"url":24,"identifiers":821},"Ricerca BM, 1987, Differentiation of iron deficiency from thalassaemia trait: a new approach, Haematologica, 72, 409",{},{"id":823,"createTime":824,"updateTime":824,"relativeEntities":825,"slug":826,"properties":827,"entityType":116,"verifyStatus":117,"verifyTime":824,"verifyNote":118,"languages":840,"translateLanguages":24,"viewCount":25,"primaryUrl":841,"fullTextUrl":24,"authors":842,"publicationType":179,"publisherRelationship":905,"citationCount":955,"citationInfo":956,"publishDate":959,"publishYear":957,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":960,"openAccess":24,"references":961,"isForceReanalyzing":638},"70872f4f-57a4-4613-8441-861ded467fb1","2025-02-10T08:37:47.578+00:00",[],"Folate-deficient-human-lymphoblasts-Changes-in-deoxynucleotide-metabolism-and-thymidylate-cycle-activities",{"openalex":828,"mag":830,"abstract":832,"title":834,"pm":836,"doi":838},{"VOID":829},"W2064006613",{"VOID":831},"2064006613",{"EN":833},"\u003Cjats:p>\u003Cjats:bold>Abstract: \u003C\u002Fjats:bold> Peripheral blood lymphocytes of healthy volunteers cultured with phytohaemagglutinin in folate‐deficient medium exhibit megaloblastic maturation with reduced intracellular folate content. We have employed this \u003Cjats:italic>in vitro\u003C\u002Fjats:italic> model for megaloblastic maturation to determine accompanying changes in cellular thymidylate cycle activities and deoxynucleotide levels. Folate‐deficient cells exhibit a two‐fold increase in thymidine kinase and thymidylate synthase activities. These increased activities were reduced to those of folate‐replete cells by co‐culture of folate‐deficient cells with thymidine. Folate deficiency was accompanied by reduced cellular levels of thymidine triphosphate (TTP) and deoxyguanosine triphosphate (dGTP). Exogenous deoxyuridine produced no increase in the reduced levels of TTP of folate‐deficient cells but effected a two‐fold increase in cellular deoxycytidine triphosphate. Exogenous thymidine increased the reduced TTP levels of folate‐deficient cells and corrected the reduced dGTP level; the increase in cellular TTP accompanying exogenous thymidine was more pronounced in folate‐deficient cells. These \u003Cjats:italic>in vitro\u003C\u002Fjats:italic> findings are compatible with a block in \u003Cjats:italic>de novo\u003C\u002Fjats:italic> thymidylate synthesis and explain in part the reported \u003Cjats:italic>in vivo\u003C\u002Fjats:italic> changes for the deoxynucleotide pool in megaloblastic marrow cells due to folate or vitamin B12 deficiency.\u003C\u002Fjats:p>",{"EN":835},"Folate‐deficient human lymphoblasts: Changes in deoxynucleotide metabolism and thymidylate cycle activities",{"VOID":837},"1889478",{"VOID":839},"10.1111\u002Fj.1600-0609.1991.tb00131.x",[120],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1600-0609.1991.tb00131.x",[843,860,875,890],{"id":844,"sortIndex":25,"researcher":24,"roles":845,"affiliations":846,"properties":855,"displayName":857,"givenName":24,"familyName":24},"dead9a3e-a599-4fea-af59-0615c9395276",[],[847],{"id":848,"sortIndex":25,"affiliation":849,"properties":24},"8b686d63-1efe-409e-ac14-2245b4274b8f",{"id":848,"createTime":24,"updateTime":24,"relativeEntities":850,"slug":24,"properties":851,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":854,"statistic":24},[],{"title":852},{"EN":853},"Department of Haematology, and Department of Pathology & Immunology, Monash University Medical School, Alfred Hospital, Prahran, Australia",[],{"title":856,"openalex":858},{"EN":857},"Martin B Van Der Weyden",{"VOID":859},"A5110162373",{"id":861,"sortIndex":144,"researcher":24,"roles":862,"affiliations":863,"properties":870,"displayName":872,"givenName":24,"familyName":24},"5f7ae12a-2850-4d95-bb4e-3f51eb9adafe",[],[864],{"id":848,"sortIndex":25,"affiliation":865,"properties":24},{"id":848,"createTime":24,"updateTime":24,"relativeEntities":866,"slug":24,"properties":867,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":869,"statistic":24},[],{"title":868},{"EN":853},[],{"title":871,"openalex":873},{"EN":872},"Ronald J. 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IwataN. AraiT. YamauchiH. MaekawaT..Abnormal dNTP metabolism and effects of thymidine in megaloblastic anemia. 17th Congress of International Society of Hematology1978: p428(abstract).",{},{"id":24,"text":979,"url":24,"identifiers":980},"10.1038\u002F248602a0",{"doi":979},{"id":24,"text":982,"url":24,"identifiers":983},"10.1111\u002Fj.1365-2141.1978.tb03636.x",{"doi":982},{"id":24,"text":985,"url":24,"identifiers":986},"10.1111\u002Fj.1365-2141.1981.tb07200.x",{"doi":985},{"id":24,"text":988,"url":24,"identifiers":989},"10.1111\u002Fj.1600-0609.1975.tb01065.x",{"doi":988},{"id":24,"text":991,"url":24,"identifiers":992},"10.1111\u002Fj.1365-2141.1976.tb03571.x",{"doi":991},{"id":24,"text":994,"url":24,"identifiers":995},"10.1016\u002F0006-291X(79)90949-5",{"doi":994},{"id":24,"text":997,"url":24,"identifiers":998},"10.1016\u002F0014-2964(80)90116-4",{"doi":997},{"id":24,"text":1000,"url":24,"identifiers":1001},"Hayman RJ, 1980, Phytohemagglutinin‐stimulated normal human peripheral blood lymphocytes in folate‐depleted medium: an in vitro model for megaloblastic hemopoiesis, Blood, 55, 863, 10.1182\u002Fblood.V55.5.863.863",{"doi":1002},"10.1182\u002Fblood.V55.5.863.863",{"id":24,"text":1004,"url":24,"identifiers":1005},"Tattersall MHN, 1973, Changes in the deoxy‐ribonucleoside triphosphate pools of mouse 5178 Y lymphoma cells following exposure to methotrexate or 5‐fluorouacil, Cancer Res, 33, 3086",{},{"id":24,"text":1007,"url":24,"identifiers":1008},"Young GJ, 1984, 5‐adenosylhomocysteine hydrolase inactivation and purine toxicity in cultured human T‐ and B‐lymphoblasts, J Lab Clin Med, 104, 86",{},{"id":24,"text":1010,"url":24,"identifiers":1011},"Hallam LJ, 1987, Vitamin B12‐responsive neonatal megaloblastic anemia and homocystinuria with associated reduced methionine synthase activity, Blood, 69, 1128, 10.1182\u002Fblood.V69.4.1128.1128",{"doi":1012},"10.1182\u002Fblood.V69.4.1128.1128",{"id":24,"text":1014,"url":24,"identifiers":1015},"10.1016\u002F0003-2697(78)90696-6",{"doi":1014},{"id":24,"text":1017,"url":24,"identifiers":1018},"Roberts D., 1971, Methotrexate and cytosine arabino‐side modulation of thymidylate synthase activity in CCRR‐CEM cells, Cancer Res, 31, 457",{},{"id":24,"text":1020,"url":24,"identifiers":1021},"10.1016\u002F0003-2697(65)90120-X",{"doi":1020},{"id":24,"text":1023,"url":24,"identifiers":1024},"10.1016\u002F0006-2952(79)90640-3",{"doi":1023},{"id":24,"text":1026,"url":24,"identifiers":1027},"10.1016\u002F0005-2787(79)90495-7",{"doi":1026},{"id":24,"text":1029,"url":24,"identifiers":1030},"Iwata N., 1982, Characteristic abnormality of deoxynucleoside triphosphate metabolism in megaloblastic anemia, Blood, 60, 918, 10.1182\u002Fblood.V60.4.918.918",{"doi":1031},"10.1182\u002Fblood.V60.4.918.918",{"id":24,"text":1033,"url":24,"identifiers":1034},"Sakamoto S., 1975, Thymidylate synthetase activity in bone marrow cells in pernicious anemia, Blood, 46, 699, 10.1182\u002Fblood.V46.5.699.699",{"doi":1035},"10.1182\u002Fblood.V46.5.699.699",{"id":24,"text":1037,"url":24,"identifiers":1038},"10.1111\u002Fj.1600-0609.1990.tb00413.x",{"doi":1037},{"id":24,"text":1040,"url":24,"identifiers":1041},"10.1042\u002Fbj1960225",{"doi":1040},{"id":24,"text":1043,"url":24,"identifiers":1044},"10.1042\u002Fbj1940451",{"doi":1043},{"id":24,"text":1046,"url":24,"identifiers":1047},"10.1111\u002Fj.1600-0609.1989.tb01231.x",{"doi":1046},{"id":1049,"createTime":1050,"updateTime":1050,"relativeEntities":1051,"slug":1052,"properties":1053,"entityType":116,"verifyStatus":117,"verifyTime":1066,"verifyNote":118,"languages":1067,"translateLanguages":24,"viewCount":25,"primaryUrl":1068,"fullTextUrl":24,"authors":1069,"publicationType":179,"publisherRelationship":1155,"citationCount":1204,"citationInfo":1205,"publishDate":1209,"publishYear":1206,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1210,"openAccess":24,"references":1211,"isForceReanalyzing":638},"fec92b78-1c38-4aec-bde3-8a2aa497de8d","2025-02-10T08:37:40.608+00:00",[],"Incidence-of-myelodysplastic-syndromes-in-a-Swedish-population",{"openalex":1054,"mag":1056,"abstract":1058,"title":1060,"pm":1062,"doi":1064},{"VOID":1055},"W2077411388",{"VOID":1057},"2077411388",{"EN":1059},"\u003Cjats:p>\u003Cjats:bold>Abstract: \u003C\u002Fjats:bold> The myelodysplastic syndromes (MDS) have attracted great interest during the last decade. Unfortunately there is not much material published concerning the incidence of these conditions. We present epidemiologic data on MDS based on case registration of patients in a well‐defined population and as a comparison similar data on acute myeloid leukaemia (AML). Between the years 1978–1992 we registered 120 cases of MDS and 146 cases of AML. The median age for all the MDS cases was 74.1 years for men and 78.2 years for women. Among haematologists there is a suspicion that the incidence of MDS is rising. Our study does not support this opinion. We have divided the study period into 5‐year periods and the crude incidence has been 3.2, 4.1 and 3.5\u002F100 000\u002Fyear for each period. In the age group over 70 years MDS was more frequent than AML and in the last 5‐year period the incidence was 15.0\u002F100 000\u002Fyear for MDS compared to 10.2\u002F100 000\u002Fyear for AML. In conclusion MDS is quite common among elderly people and there is no evidence for a rising incidence during the last 15 years.\u003C\u002Fjats:p>",{"EN":1061},"Incidence of myelodysplastic syndromes in a Swedish 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The permeability of red blood cells (RBCs) to thiol containing compounds, reduced glutathione (GSH) and N‐acetyl cysteine (NAC), has been studied in control adult and neonatal cells and after oxidative stress. NAC penetrates the cell membrane easily while GSH hardly permeates. We measured their capacity to enhance intracellular non‐protein thiols (NPSH), after inducing damage to the membrane by formation of defects. Diamide, phenazine methosulfate (PMS) and t‐butyl hydroperoxide (BHP) were chosen as exogenous oxidants, each inducing damage by a different mechanism. Our data indicate that although neonatal cells are more sensitive to oxidative stress, only membrane damage induced by diamide, renders adult and neonatal cells permeable to GSH. NAC treatment enhances thiol levels in cells exposed to oxidizing agents, as well as in control cells.\u003C\u002Fjats:p>",{"EN":1907},"Red blood cell permeability to thiol compounds following oxidative stress",{"VOID":1909},"8898929",{"VOID":1911},"10.1111\u002Fj.1600-0609.1996.tb01370.x","2025-01-04T23:38:16.791+00:00",[120],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1600-0609.1996.tb01370.x",[1916,1933,1950,1965,1982,1997,2014],{"id":1917,"sortIndex":25,"researcher":24,"roles":1918,"affiliations":1919,"properties":1928,"displayName":1930,"givenName":24,"familyName":24},"dc5c7a30-d634-4f87-9b5a-976deaf8fb7e",[],[1920],{"id":1921,"sortIndex":25,"affiliation":1922,"properties":24},"056bcf05-11b8-4751-8eda-acf4ef085074",{"id":1921,"createTime":24,"updateTime":24,"relativeEntities":1923,"slug":24,"properties":1924,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1927,"statistic":24},[],{"title":1925},{"EN":1926},"Dr Kaufmann Haematology Laboratory, Physiology Department, Beer-Sheva, Israel.",[],{"title":1929,"openalex":1931},{"EN":1930},"Dalia Mazor",{"VOID":1932},"A5022232175",{"id":1934,"sortIndex":144,"researcher":24,"roles":1935,"affiliations":1936,"properties":1945,"displayName":1947,"givenName":24,"familyName":24},"23c0666d-d4af-42cb-b1c8-d274a162579a",[],[1937],{"id":1938,"sortIndex":25,"affiliation":1939,"properties":24},"ed0f961f-af89-477c-bb95-f0f7cb01c18e",{"id":1938,"createTime":24,"updateTime":24,"relativeEntities":1940,"slug":24,"properties":1941,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1944,"statistic":24},[],{"title":1942},{"EN":1943},"The Dr Kaufmann Haematology Laboratory, Physiology Department, Faculty of Health Sciences, Ben‐Gurion University of the Negev, Beer‐Sheva, Israel",[],{"title":1946,"openalex":1948},{"EN":1947},"Erez Golan",{"VOID":1949},"A5080093637",{"id":1951,"sortIndex":163,"researcher":24,"roles":1952,"affiliations":1953,"properties":1960,"displayName":1962,"givenName":24,"familyName":24},"04ba9677-4f14-4b90-b98b-c125cf76eb19",[],[1954],{"id":1938,"sortIndex":25,"affiliation":1955,"properties":24},{"id":1938,"createTime":24,"updateTime":24,"relativeEntities":1956,"slug":24,"properties":1957,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1959,"statistic":24},[],{"title":1958},{"EN":1943},[],{"title":1961,"openalex":1963},{"EN":1962},"V. 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methods",{},{"id":24,"text":2123,"url":24,"identifiers":2124},"10.1016\u002F0167-4889(89)90241-3",{"doi":2123},{"id":24,"text":2126,"url":24,"identifiers":2127},"10.1016\u002F0006-2952(91)90674-T",{"doi":2126},{"id":24,"text":2129,"url":24,"identifiers":2130},"10.1111\u002Fj.1423-0410.1994.tb00327.x",{"doi":2129},{"id":24,"text":2132,"url":24,"identifiers":2133},"10.1159\u002F000204383",{"doi":2132},{"id":24,"text":2135,"url":24,"identifiers":2136},"10.1016\u002FS0021-9258(19)77815-6",{"doi":2135},{"id":24,"text":2138,"url":24,"identifiers":2139},"10.1016\u002F0278-6222(88)90002-2",{"doi":2138},{"id":24,"text":2141,"url":24,"identifiers":2142},"10.1016\u002F0005-2736(83)90009-3",{"doi":2141},{"id":24,"text":2144,"url":24,"identifiers":2145},"10.1016\u002F0005-2736(86)90108-2",{"doi":2144},{"id":24,"text":2147,"url":24,"identifiers":2148},"10.3109\u002F10715769209049184",{"doi":2147},{"id":2150,"createTime":2151,"updateTime":2151,"relativeEntities":2152,"slug":2153,"properties":2154,"entityType":116,"verifyStatus":117,"verifyTime":2167,"verifyNote":118,"languages":2168,"translateLanguages":24,"viewCount":25,"primaryUrl":2169,"fullTextUrl":24,"authors":2170,"publicationType":179,"publisherRelationship":2299,"citationCount":2348,"citationInfo":2349,"publishDate":2353,"publishYear":2350,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":2354,"openAccess":24,"references":2355,"isForceReanalyzing":638},"f4ac9323-5d35-46dd-a8fa-19bb97396afb","2025-01-02T17:14:28.272+00:00",[],"-i-scp-IDH-scp-1-i-and-i-scp-IDH-scp-2-i-mutations-confer-an-adverse-effect-in-patients-with-acute-myeloid-leukemia-lacking-the-i-scp-NPM-scp-1-i-mutation",{"openalex":2155,"mag":2157,"abstract":2159,"title":2161,"pm":2163,"doi":2165},{"VOID":2156},"W2067190888",{"VOID":2158},"2067190888",{"EN":2160},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>We examined the incidence and prognostic effect of \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>1\u003C\u002Fjats:italic> and \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>2\u003C\u002Fjats:italic> mutations in 233 Japanese adults with acute myeloid leukemia (\u003Cjats:styled-content style=\"fixed-case\">AML\u003C\u002Fjats:styled-content>). \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>1\u003C\u002Fjats:italic> R132 mutations were detected in 20 (8.6%) patients with \u003Cjats:styled-content style=\"fixed-case\">AML\u003C\u002Fjats:styled-content>. \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>2\u003C\u002Fjats:italic> mutations were found in 19 (8.2%, 17 \u003Cjats:styled-content style=\"fixed-case\">R\u003C\u002Fjats:styled-content>140 and two \u003Cjats:styled-content style=\"fixed-case\">R\u003C\u002Fjats:styled-content>172) patients. \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>1\u003C\u002Fjats:italic> and \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>2\u003C\u002Fjats:italic> mutations were mutually exclusive and were associated with normal karyotype \u003Cjats:styled-content style=\"fixed-case\">AML\u003C\u002Fjats:styled-content>, cytogenetic intermediate‐risk group, and \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">NPM\u003C\u002Fjats:styled-content>1\u003C\u002Fjats:italic> mutations. Five‐year overall survival (\u003Cjats:styled-content style=\"fixed-case\">OS\u003C\u002Fjats:styled-content>) rates were significantly lower (15.6%) in patients harboring the \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>\u003C\u002Fjats:italic> mutations than in patients lacking the \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>\u003C\u002Fjats:italic> mutation (32.0%) in the entire cohort of \u003Cjats:styled-content style=\"fixed-case\">AML\u003C\u002Fjats:styled-content> (\u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">P\u003C\u002Fjats:styled-content> \u003C\u002Fjats:italic>=\u003Cjats:italic> \u003C\u002Fjats:italic>0.005). Among patients aged 59 yr or younger with \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>\u003C\u002Fjats:italic> mutations, 5‐yr \u003Cjats:styled-content style=\"fixed-case\">OS\u003C\u002Fjats:styled-content> in patients who underwent allogeneic stem cell transplantation (\u003Cjats:styled-content style=\"fixed-case\">SCT\u003C\u002Fjats:styled-content>) was significantly higher than that in those not receiving allogeneic \u003Cjats:styled-content style=\"fixed-case\">SCT\u003C\u002Fjats:styled-content> (50% vs. 10.6%, \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">P\u003C\u002Fjats:styled-content> \u003C\u002Fjats:italic>=\u003Cjats:italic> \u003C\u002Fjats:italic>0.020). Of 51 patients with \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">NPM\u003C\u002Fjats:styled-content>1\u003C\u002Fjats:italic> mutations, there was no significant difference in 5‐yr \u003Cjats:styled-content style=\"fixed-case\">OS\u003C\u002Fjats:styled-content> rates between patients with and those without the \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>\u003C\u002Fjats:italic> mutations. In contrast, among 175 patients lacking the \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">NPM\u003C\u002Fjats:styled-content>1\u003C\u002Fjats:italic> mutations, 5‐yr \u003Cjats:styled-content style=\"fixed-case\">OS\u003C\u002Fjats:styled-content> rate in patients with \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>\u003C\u002Fjats:italic> mutations was significantly lower than that in those without \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>\u003C\u002Fjats:italic> mutations (0% vs. 34.7%, \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">P\u003C\u002Fjats:styled-content> \u003C\u002Fjats:italic>= <0.001). These data suggest that \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>\u003C\u002Fjats:italic> mutations have an unfavorable effect in \u003Cjats:styled-content style=\"fixed-case\">AML\u003C\u002Fjats:styled-content>, especially \u003Cjats:styled-content style=\"fixed-case\">AML\u003C\u002Fjats:styled-content> with the \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">NPM\u003C\u002Fjats:styled-content>1\u003C\u002Fjats:italic> wild type and younger \u003Cjats:styled-content style=\"fixed-case\">AML\u003C\u002Fjats:styled-content> patients with \u003Cjats:italic>\u003Cjats:styled-content style=\"fixed-case\">IDH\u003C\u002Fjats:styled-content>\u003C\u002Fjats:italic> mutations may benefit from allogeneic \u003Cjats:styled-content style=\"fixed-case\">SCT\u003C\u002Fjats:styled-content>.\u003C\u002Fjats:p>",{"EN":2162},"\u003Ci>\u003Cscp>IDH\u003C\u002Fscp>1\u003C\u002Fi> and 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 \u003Cjats:italic>Objective\u003C\u002Fjats:italic>: To assess cardiac status in a large group of patients with thalassemia major who had been treated in a standard way since their early infancy with intensive transfusions and deferoxamine chelation therapy and who had good compliance with this regimen. \u003Cjats:italic>Methods and Results\u003C\u002Fjats:italic>: We assessed clinically and echocardiographically 202 thalassemia major patients aged 27.3 ± 6.3 yr and 75 age and sex‐matched healthy controls. Overt cardiac disease was encountered in 14 patients (6.9%), including 5 (2.5%) with congestive heart failure, aged 26–37 yr, and 9 with systolic left ventricular (LV) dysfunction, aged 23–37 yr. Ten patients (5.0%) had a history of pericarditis. Left atrial and LV diameters, LV mass and cardiac output were significantly higher in patients than in controls, while peripheral resistance and LV afterload were significantly lower. Relative LV wall thickness did not differ between patients and controls, but it was significantly lower in patients with overt cardiac disease compared to those without (\u003Cjats:italic>P\u003C\u002Fjats:italic> < 0.05). Restrictive LV filling was observed in 37.6% of patients and was significantly more frequent in cases with overt cardiac disease (\u003Cjats:italic>P\u003C\u002Fjats:italic> < 0.01). Pulmonary hypertension was practically absent. Hematological parameters and pulmonary artery pressure levels were not independently associated with the presence of overt cardiac disease. \u003Cjats:italic>Conclusion\u003C\u002Fjats:italic>: Strict lifelong adherence to the standard transfusion and deferoxamine therapy reduces considerably the occurrence of heart failure, LV dysfunction and pericarditis, prevents early heart failure and pulmonary hypertension, but does not eliminate completely cardiac disease in patients with thalassemia major.\u003C\u002Fjats:p>","\u003Cjats:p>\u003Cjats:bold>Tóm tắt: \u003C\u002Fjats:bold> \u003Cjats:italic>Mục tiêu\u003C\u002Fjats:italic>: Đánh giá tình trạng tim mạch ở một nhóm lớn bệnh nhân thalassemia nặng đã được điều trị theo cách tiêu chuẩn từ khi còn nhỏ với liệu pháp truyền máu tích cực và chelat deferoxamine, những người có tuân thủ tốt phác đồ điều trị này. \u003Cjats:italic>Phương pháp và Kết quả\u003C\u002Fjats:italic>: Chúng tôi đã tiến hành đánh giá lâm sàng và siêu âm tim cho 202 bệnh nhân thalassemia nặng tuổi trung bình 27,3 ± 6,3 năm và 75 đối chứng khỏe mạnh cùng tuổi và giới tính. Bệnh tim mạch biểu hiện rõ đã được phát hiện ở 14 bệnh nhân (6,9%), trong đó có 5 bệnh nhân (2,5%) bị suy tim sung huyết, tuổi từ 26–37 năm, và 9 bệnh nhân bị rối loạn chức năng tâm thu thất trái (LV), tuổi từ 23–37 năm. Mười bệnh nhân (5,0%) có tiền sử viêm màng ngoài tim. Đường kính tâm nhĩ trái và LV, khối lượng LV và lưu lượng tim đều cao hơn đáng kể ở bệnh nhân so với các đối chứng, trong khi kháng lực ngoại vi và gánh nặng thất trái (afterload) thấp hơn đáng kể. Độ dày thành LV tương đối không khác nhau giữa bệnh nhân và đối chứng, nhưng giảm đáng kể ở các bệnh nhân có bệnh tim mạch biểu hiện rõ so với những người không có (\u003Cjats:italic>P\u003C\u002Fjats:italic> < 0,05). Sự lấp đầy LV có tính hạn chế được quan sát thấy ở 37,6% bệnh nhân và thường gặp hơn ở những trường hợp có bệnh tim mạch biểu hiện rõ (\u003Cjats:italic>P\u003C\u002Fjats:italic> < 0,01). Tăng huyết áp phổi hầu như không có. Các thông số huyết học và mức áp lực động mạch phổi không có liên quan độc lập với sự hiện diện của bệnh tim mạch biểu hiện rõ. \u003Cjats:italic>Kết luận\u003C\u002Fjats:italic>: Tuân thủ nghiêm ngặt phác đồ truyền máu và liệu pháp deferoxamine suốt đời đáng kể giúp giảm nguy cơ suy tim, rối loạn chức năng LV và viêm màng ngoài tim, ngăn ngừa suy tim sớm và tăng huyết áp phổi, nhưng không loại bỏ hoàn toàn bệnh tim mạch ở bệnh nhân thalassemia nặng.\u003C\u002Fjats:p>",{"EN":2486,"VI":2487},"Cardiac status in well‐treated patients with thalassemia major","Tình trạng tim mạch ở bệnh nhân thalassemia nặng được điều trị 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