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Journal articles on the topic 'T (8;21)'

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Published: 4 June 2021
Last updated: 2 February 2022

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1

Maslak, P. "AML with t(8; 21)." ASH Image Bank 2004, no. 0524 (May 24, 2004): 101125. http://dx.doi.org/10.1182/ashimagebank-2004-101125.

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2

Maslak, P. "AML with t(8:21)." ASH Image Bank 2001, no. 1205 (December 5, 2001): 100215. http://dx.doi.org/10.1182/ashimagebank-2001-100215.

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3

Yang, Genyan, Waleed Khalaf, Louis van de Locht, Joop H. Jansen, Bert A. van der Reijden, Carsten Müller-Tidow, H. Ruud Delwel, Hubert Serve, D. Wade Clapp, and Scott W. Hiebert. "Epigenetic regulation of tumor suppressors in t(8:21)-containing AML." Annals of Hematology 83, no. 6 (March 30, 2004): 329–30. http://dx.doi.org/10.1007/s00277-003-0841-8.

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4

Somjee, Saika, Anupama Borker, Renee Gardner, and Maria C. Velez. "Multiple Granulocytic Sarcomas in Acute Myeloblastic Leukemia with Simultaneous Occurrence of t(8:21) and Trisomy 8." Leukemia & Lymphoma 42, no. 5 (January 2001): 1139–44. http://dx.doi.org/10.3109/10428190109097737.

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5

Gadage, VS, KS Galani, PS Kadam Amare, and N. Mittal. "Systemic mastocytosis with associated acute myeloid leukemia with t (8; 21) (q22; q22)." Indian Journal of Pathology and Microbiology 55, no. 3 (2012): 409. http://dx.doi.org/10.4103/0377-4929.101761.

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6

Gujral, Sumeet, Nikhil Rabade, Prashant Tembhare, Nikhil Patkar, Pratibha Amare, Brijesh Arora, and PG Subramanian. "'Childhood systemic mastocytosis associated with t (8; 21) (q22; q22) acute myeloid leukemia'." Indian Journal of Pathology and Microbiology 59, no. 3 (2016): 407. http://dx.doi.org/10.4103/0377-4929.188140.

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7

Zhang, Weina, Ying Lu, Tao Zhen, Xinjie Chen, Ming Zhang, Ping Liu, Xiangqin Weng, Bing Chen, and Yueying Wang. "Homoharringtonine synergy with oridonin in treatment of t(8; 21) acute myeloid leukemia." Frontiers of Medicine 13, no. 3 (June 2019): 388–97. http://dx.doi.org/10.1007/s11684-018-0624-1.

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8

Moghimi, Ali, Alan Mills, and Cathrine Mitchell. "21. Peripheral T-cell lymphoma with follicular pattern: a ‘real’ entity." Pathology 43 (2011): S95. http://dx.doi.org/10.1016/s0031-3025(16)33309-8.

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9

Tighe, Jane E., and Franco Calabi. "t(8;21) Breakpoints are Clustered between Alternatively Spliced Exons of MTG8." Clinical Science 89, no. 3 (September 1, 1995): 215–18. http://dx.doi.org/10.1042/cs0890215.

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1. The (8;21) translocation, which is consistently associated with a subgroup of acute myeloid leukaemia, involves two loci: runt on chromosome 21 and MTG8 on chromosome 8. 2. Breakpoints in runt fall within a single intron that is located immediately downstream of a phylogenetically conserved DNA-binding domain (the ‘runt box’). 3. We now show that most breakpoints on chromosome 8 fall within a region between two alternative 5′ MTG8 exons. Thus, we predict that chimaeric genes on both the derivative(8) and the derivative(21) chromosomes have the potential to be transcriptionally active.
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10

Sano, Hitoshi, Kentaro Ohki, Myoung-ja Park, Norio Shiba, Yusuke Hara, Manabu Sotomatsu, Daisuke Tomizawa, et al. "CSF3RandCALRmutations in paediatric myeloid disorders and the association ofCSF3Rmutations with translocations, including t(8; 21)." British Journal of Haematology 170, no. 3 (April 9, 2015): 391–97. http://dx.doi.org/10.1111/bjh.13439.

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11

Figura, N., M. Jain, A. Sim, E. Dean, Y. Balagurunathan, J. Chavez, B. Shah, et al. "OC-0559: Predictors of Failures following Chimeric Antigen Receptor T-cell (CAR T) Therapy." Radiotherapy and Oncology 152 (November 2020): S311—S312. http://dx.doi.org/10.1016/s0167-8140(21)00581-8.

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12

Erickson, P., J. Gao, KS Chang, T. Look, E. Whisenant, S. Raimondi, R. Lasher, J. Trujillo, J. Rowley, and H. Drabkin. "Identification of breakpoints in t(8;21) acute myelogenous leukemia and isolation of a fusion transcript, AML1/ETO, with similarity to Drosophila segmentation gene, runt." Blood 80, no. 7 (October 1, 1992): 1825–31. http://dx.doi.org/10.1182/blood.v80.7.1825.1825.

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Abstract We have developed a restriction map of the chromosome 21 breakpoint region involved in t(8;21)(q22;q22.3) acute myelogenous leukemia (AML) and have isolated a genomic junction clone containing chromosome 8 and 21 material. Using probes from these regions, rearrangements have been identified in each of nine cases of t(8;21) AML examined. In addition, we have isolated cDNA clones from a t(8;21) AML cDNA library that contain fused sequences from chromosome 8 and 21. The chromosome 8 component, referred to as ETO (for eight twenty-one), is encoded over a large genomic region, as suggested by the analysis of corresponding yeast artificial chromosomes (YACs). The DNA sequence of the chromosome 21 portion of the fusion transcript is derived from the normal AML1 gene. A striking similarity (67% identity over 387 bp, with a corresponding 69% amino acid identity) was detected between AML1 and the Drosophila segmentation gene, runt. The critical consequence of the translocation is the juxtaposition of 5′ sequences of AML1 to 3′ sequences of ETO, oriented telomere to centromere on the der(8) chromosome.
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13

Erickson, P., J. Gao, KS Chang, T. Look, E. Whisenant, S. Raimondi, R. Lasher, J. Trujillo, J. Rowley, and H. Drabkin. "Identification of breakpoints in t(8;21) acute myelogenous leukemia and isolation of a fusion transcript, AML1/ETO, with similarity to Drosophila segmentation gene, runt." Blood 80, no. 7 (October 1, 1992): 1825–31. http://dx.doi.org/10.1182/blood.v80.7.1825.bloodjournal8071825.

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We have developed a restriction map of the chromosome 21 breakpoint region involved in t(8;21)(q22;q22.3) acute myelogenous leukemia (AML) and have isolated a genomic junction clone containing chromosome 8 and 21 material. Using probes from these regions, rearrangements have been identified in each of nine cases of t(8;21) AML examined. In addition, we have isolated cDNA clones from a t(8;21) AML cDNA library that contain fused sequences from chromosome 8 and 21. The chromosome 8 component, referred to as ETO (for eight twenty-one), is encoded over a large genomic region, as suggested by the analysis of corresponding yeast artificial chromosomes (YACs). The DNA sequence of the chromosome 21 portion of the fusion transcript is derived from the normal AML1 gene. A striking similarity (67% identity over 387 bp, with a corresponding 69% amino acid identity) was detected between AML1 and the Drosophila segmentation gene, runt. The critical consequence of the translocation is the juxtaposition of 5′ sequences of AML1 to 3′ sequences of ETO, oriented telomere to centromere on the der(8) chromosome.
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14

Teachey, David T. "Novel Approaches to T-Cell ALL." Clinical Lymphoma Myeloma and Leukemia 21 (September 2021): S95—S98. http://dx.doi.org/10.1016/s2152-2650(21)01225-8.

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15

Yang, Deok-Hwan, Yeung-Chul Mun, Ho-Jin Shin, Yeo-Kyeoung Kim, Je-Jung Lee, Choi-Young Jin, Chu-Myong Seong, and Hyeoung-Joon Kim. "Predictable Prognostic Factor of CD56 Expression in Acute Myeloid Leukemia with t(8:21) Including Allogeneic Hematopoietic Stem Cell Transplantation." Blood 106, no. 11 (November 16, 2005): 3288. http://dx.doi.org/10.1182/blood.v106.11.3288.3288.

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Abstract CD56 expression in acute myeloid leukemia (AML) has been associated with extramedullary leukemia and multi-drug resistance, but the clinical and prognostic significances are not yet clearly defined. Recently, some investigators reported that AML patients with t(8;21) showed more frequent CD56 expression rate and the expression of CD56 antigen adversely affected disease-free survival (DFS). It could explain a diverse clinical outcome in AML patients with favorable cytogenetics. This study investigated CD56 expression in 37 adult de novo AML patients with t(8:21) between November 1996 and June 2005 at three institutions. Immunophenotyping was performed with flow cytometry (Coulter EPICS XL) and considered positive if at least 20% of blasts expressed. CD56 was expressed in 25 cases (67.6%). There was no statistically significant differences in age, sex, leukocyte count, the percentage of bone marrow blasts or the presence of additional cytogenetic abnormalities between the CD56+ and the CD56- group. The complete remission (CR) rate to standard dose cytarabine or N4-behenoyl-1-D-arabinofuranosylcytosine (BH-AC) and idarubicin was similar in both groups (91.7% v 88.7%; P=0.73), but the relapse rate to high-dose cytarabine or allogeneic hematopoietic stem cell transplantation (HST) was quite different (60% v 25%; P=0.08). Allogeneic HST was performed from siblings in 15 patients (40.5%) who achieved CR, 8 patients (32.0%) in CD56+ and 7 patients (58.3%) in CD56- group (P=0.16). The median durations of DFS were significantly shorter in CD56+ (median, 12.2 months) than in the CD56- group (median, not reached) (P =0.02). Also, the median durations of survival showed the same results in the CD56+ group (median, 14.9 months) compared with the CD56- group (median, not reached) (P=0.01). Within fifteen transplanted patients, the median durations of DFS in eight CD56+ patients was significantly shorter than seven CD56- patients (median, 24.4 months v not reached; P=0.02)(Fig.1 and 2).We concluded that CD56 expression was associated with reduced DFS and survival for AML patients with t(8:21) including transplanted patients. Although further larger studies are needed, we suggested that CD56 expression at diagnosis is a predictable prognostic factor in AML with t(8:21). Fig. 1 Disease-free survival (DFS) and Overall survival (OS) for patients with t(8:21) with CD56+ (n−25) and CD56− (n−12) group. Fig. 1. Disease-free survival (DFS) and Overall survival (OS) for patients with t(8:21) with CD56+ (n−25) and CD56− (n−12) group. Fig. 2 Within transplanted patients, decreases from survival (DFS) for patients with t(8:21) with and without CD56 expression. Fig. 2. Within transplanted patients, decreases from survival (DFS) for patients with t(8:21) with and without CD56 expression.
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16

Tighe, JE, A. Daga, and F. Calabi. "Translocation breakpoints are clustered on both chromosome 8 and chromosome 21 in the t(8;21) of acute myeloid leukemia." Blood 81, no. 3 (February 1, 1993): 592–96. http://dx.doi.org/10.1182/blood.v81.3.592.592.

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Abstract The t(8;21)(q22;q22) is consistently associated with acute myeloid leukemia (AML) M2. Recent data have suggested that breakpoints on chromosome 21 are clustered within a single intron of a novel gene, AML1, just downstream of a region of homology to the runt gene of D melanogaster. In this report, we confirm rearrangement at the same location in at least 12 of 18 patients with t(8;21). Furthermore, we have isolated recombinant clones spanning the breakpoint regions on both the der(8) and the der(21) from one patient. By using a chromosome 8 probe derived from these clones, we show that t(8;21) breakpoints are also clustered on chromosome 8.
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17

Tighe, JE, A. Daga, and F. Calabi. "Translocation breakpoints are clustered on both chromosome 8 and chromosome 21 in the t(8;21) of acute myeloid leukemia." Blood 81, no. 3 (February 1, 1993): 592–96. http://dx.doi.org/10.1182/blood.v81.3.592.bloodjournal813592.

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The t(8;21)(q22;q22) is consistently associated with acute myeloid leukemia (AML) M2. Recent data have suggested that breakpoints on chromosome 21 are clustered within a single intron of a novel gene, AML1, just downstream of a region of homology to the runt gene of D melanogaster. In this report, we confirm rearrangement at the same location in at least 12 of 18 patients with t(8;21). Furthermore, we have isolated recombinant clones spanning the breakpoint regions on both the der(8) and the der(21) from one patient. By using a chromosome 8 probe derived from these clones, we show that t(8;21) breakpoints are also clustered on chromosome 8.
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18

Grochowski, Jacek, Barbara Rys, Pawel Serda, and Ulrich Wagner. "Conformation in the solid state and in solution of (9R, 10R, 21R,-22R)-9, 10, 21, 22-Tetramethyl-9, 10, 21, 22-tetrahydro-7H, 12H,-19H, 24H-dinaphtho-[1, 8-f, g: 1′, 8′o, p][1.4.10.13]- tetraoxacyclooctadecin." Tetrahedron: Asymmetry 6, no. 8 (August 1995): 2059–66. http://dx.doi.org/10.1016/0957-4166(95)00268-t.

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19

Dicker, Frank, Claudia Haferlach, Wolfgang Kern, Torsten Haferlach, and Susanne Schnittger. "High Frequency of AML1/RUNX1 Mutations in Specific Cytogenetic Subgroups in De Novo Acute Myeloid Leukemia." Blood 110, no. 11 (November 16, 2007): 986. http://dx.doi.org/10.1182/blood.v110.11.986.986.

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Somatic mutations in the DNA-binding domain, the socalled Runt homology domain, of the AML1/RUNX1 gene have been identified to occur in acute myeloid leukaemia (AML) with the highest incidence in AML M0, in therapy-related myelodysplastic syndrome (t-MDS), in therapy-related AML (t-AML) and AML after MDS (s-AML). Cytogenetic aberrations that are associated with RUNX1 mutations (RUNX1mut) have been reported to be trisomy 13 in AML and trisomy 21 in myeloid malignancies, but also loss of chromosome 7q, mainly in t-MDS but rarely in t-AML. So far the majority of RUNX1mut have been described in secondary or therapy-related cases. Thus, we characterized a cohort of 119 patients (pts) with de novo AML and compared these results to 19 MDS and s-AML, 2 t-MDS (n=2) and 8 t-AML. The cohort was selected for specific cytogenetics with high reported frequencies of RUNX1mut: trisomy 13 (n=17), trisomy 21 (n=9), −7/7q- (n=34). In addition pts with normal karyotype (NK) (n=42), inv(3)/t(3;3) (n=12), trisomy 8 (n=11), complex karyotype (n=13) and 10 pts with various other cytogenetic aberrations (other) were analyzed. The incidence of RUNX1mut in the different cytogenetic subgroups was: 94% (16/17) in +13, 56% (5/9) in +21, 29% (10/34) in −7/7q-, 10% (4/42) in NK, 17% (2/12) in inv(3)/t(3;3), 18% (2/11) in +8, 0% (0/13) in complex karyotype and 20% (2/10) in other, respectively. Based on clinical history we observed RUNX1 mutations in: 6/19 (32%) in MDS/s-AML, 1/10 (10%) in t-MDS/t-AML and 34/119 (29%) in de novo AML. Of the 6 RUNXmut cases with MDS/s-AML the karyotypes were heterogeneous NK (n=1), −7 (n=2) +13 (n=1), +21 (n=1), and inv(3) (n=1). The only recurrent cytogenetic aberration in MDS/s-AML was −7, thus the frequency of RUNXmut in the MDS/s-AML group with −7 was 2/8 (25%). Also the only RUNX1mut case with t-AML revealed a −7. These data correspond to those reported in the literature. We further focussed on the analyses of RUNX1 in de novo AML which is rarely reported so far. In the de novo AML group only we detected RUNX1mut with the highest frequency in +13 (16/16; 100%) followed by +21 (4/8; 50%) −7 (7/21; 33%), + 8 (2/10, 20%), inv(3) (1/8; 12.5%), and NK (3/33; 9.1%). In addition, in the group with “other” aberration 2/8 were mutated. Interestingly, these 2 mutated cases displayed a high number of trisomies including +8 and +13. No RUNX1mut were detected in AML with complex karyotype (n=10). These data for the first time show that RUNX1mut are not strongly correlated to MDS, s-AML or t-AML. With almost the same frequency they can be observed in de novo AML if specific cytogenetic groups are considered. Thus the RUNXmut seem to be more related to these cytogenetic subgroups than to the MDS, s-AML or t-AML.
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Schnittger, Susanne, Frank Dicker, Wolfgang Kern, Torsten Haferlach, and Claudia Haferlach. "Cooperating Molecular Mutations in AML1/RUNX1 Mutated AML Differ Dependent on the Cytogenetic Subgroup." Blood 110, no. 11 (November 16, 2007): 365. http://dx.doi.org/10.1182/blood.v110.11.365.365.

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Abstract Certain mutations and chromosome aberrations have been shown to cooperate in AML leukemogenesis e.g. t(15;17) + FLT3 mutations, t(8;21) + KITD816 mutations, TP53 + complex aberrant karyotype. Previously AML1/RUNX1 mutations were associated with activating mutations e.g. in FLT3 and NRAS. We now performed a detailed analysis focused on distinct cytogenetic subgroups. A total of 120 selected AML with normal karyotype or recurrent aberrations were analyzed: normal karyotype (NK) (n=43); monosomy 7 (n=32), trisomy 8 (n=10), trisomy 13 (n=14), trisomy 21 (n=9), inv(3)/t(3;3) AML (n=12). Of these 105 were de novo, 7 had t-AML after previous chemotherapy (1 with NK, 4 with −7, 1 with +8, 1 inv(3)) and 8 had sAML after MDS (1 NK, 6 with −7, 1 with inv(3)). RUNX1 mutations were detected in cases with NK: 5/43 (11.6%); −7: 10/32 (31%); +8: 2/10 (20%); +13: 14/14 (100%); +21: 5/9 (55.6%), and inv(3)/t(3;3): 2/12 (12%). Thus, the subgroup with the highest RUNX1 mutation rate was +13 followed by +21. All cases were also analysed for FLT3-length mutations (FLT3-LM), FLT3-TKD mutations, MLL-PTD, NRAS, NPM1 and 38 in addition for CEBPA. NPM1mut and CEBPAmut were found to be nearly mutually exclusive of RUNX1mut. Further analysis was done for subgroups. NK subgroup: In 2 of 5 (40%) RUNX1mut AML with NK a FLT3-LM, in 2 a MLL-PTD, and 1 an NRAS mutation was detected. Thus within the 5 RUNXmut NK-AML a cooperating mutation was detected in all cases. −7 subgroup: No additional mutation was detected in the 10 RUNX1mut cases with −7. In contrast in RUNX1 unmutated cases (RUNX1wt) with −7 1/21 had FLT3-LM, 2/21 (9.5%) CEBPAmut, and 7/20 (35%) an NRASmut. + 8 subgroup: In 2 RUNXmut cases with +8 no further mutation was detected. In contrast 2 of the RUNXwt with +8 had an FLT3-LM, 3 a NPM1mut and 2 a NRASmut. +13 subgroup: All cases with +13 were RUNX1mut and 2/14 (14.3%) had a FLT3-LM and 1/14 (7.1%) a MLL-PTD. In this specific subgroup a 4-fold-elevated FLT3 expression was suggesting to be a specific cooperating event. +21 subgroup: All 5 RUNXmut with +21 had an additional aberration, 4 (80%) had FLT3-LM and 1 NPM1mut. Inv(3) subgroup: In both RUNX1mut inv(3) cases no additional mutation was found. In contrast 3/9 RUNX1wt cases with inv(3)/t(3;3) were NRAS mutated. Overall, additional mutations in RUNX1 mutated AML are very frequent in subgroups with NK and +21 (100%), unfrequent in +13 (21%) and absent in others (−7, +8, inv(3)/t(3;3)). In total (except +13, where no RUNX1wt cases were available), the frequency of additional mutations was higher in the RUNX1wtcases (41.6% vs. 87.8%) This is in contrast to previous reports that suggested that additional activating mutation in RUNX1mut AML are frequent. In contrast we found a high incidence of NRASmut in inv(3) (33%), −7 (35%), +8 (29%) and normal karyotype (14.3%) in cases with RUNX1wt. Monosomy 7 + RUNX1mut + NRASmut previously has been highly correlated to therapy related AML and AML after MDS. In our cohort with predominantely de novo AML we found a high correlation of RUNX1mut with −7 and a high correlation of −7 with NRAS, but no association of RUNX1mut with NRASmut. In addition, FLT3-LM has been highly correlated to AML1mut. We found this correlation only in cases with +21. In conclusion, FLT3-LM and NRAS mutations were detected as frequent cooperating mutations in RUNX1mut AML with NK and +21. No mutation cooperating with RUNXmut was detected in −7, +8, +13, and inv(3)/t(3;3). Here alternative mechanisms may drive leukemogenesis e.g. overexpression of FLT3 in +13 or dosage effects due to monosomies or trisomies.
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21

Maseki, N., H. Miyoshi, K. Shimizu, C. Homma, M. Ohki, M. Sakurai, and Y. Kaneko. "The 8;21 chromosome translocation in acute myeloid leukemia is always detectable by molecular analysis using AML1." Blood 81, no. 6 (March 15, 1993): 1573–79. http://dx.doi.org/10.1182/blood.v81.6.1573.1573.

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Abstract The AML1 gene was rearranged in leukemic cells with t(8;21)(q22;q22) or its variant, complex t(8;V;21) translocations from 33 acute myeloid leukemia (AML) patients. The AML1 rearrangement was also detected in three AML patients without t(8;21); two had a normal diploid karyotype, and one had a karyotype of 45,X, - X. The AML1 rearrangement in the t(8;21) breakpoint cluster region was not detected in leukemic cells with cytogenetic abnormalities other than t(8;21), or with normal diploidy obtained from 23 AML patients. Because leukemic cells of the five patients with complex t(8;V;21) translocations had a der(8)t(8;21) chromosome with a break in band 8q22 in common, the juxtaposition of the 5' side of AML1 to a predicted counterpart gene located in the breakpoint region of 8q22 may be an essential step in the leukemogenesis of AML with t(8;21). Our findings show that the 8;21 translocation, its variants, and the masked t(8;21) may all be detectable by the Southern hybridization method using the AML1 probes.
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Maseki, N., H. Miyoshi, K. Shimizu, C. Homma, M. Ohki, M. Sakurai, and Y. Kaneko. "The 8;21 chromosome translocation in acute myeloid leukemia is always detectable by molecular analysis using AML1." Blood 81, no. 6 (March 15, 1993): 1573–79. http://dx.doi.org/10.1182/blood.v81.6.1573.bloodjournal8161573.

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The AML1 gene was rearranged in leukemic cells with t(8;21)(q22;q22) or its variant, complex t(8;V;21) translocations from 33 acute myeloid leukemia (AML) patients. The AML1 rearrangement was also detected in three AML patients without t(8;21); two had a normal diploid karyotype, and one had a karyotype of 45,X, - X. The AML1 rearrangement in the t(8;21) breakpoint cluster region was not detected in leukemic cells with cytogenetic abnormalities other than t(8;21), or with normal diploidy obtained from 23 AML patients. Because leukemic cells of the five patients with complex t(8;V;21) translocations had a der(8)t(8;21) chromosome with a break in band 8q22 in common, the juxtaposition of the 5' side of AML1 to a predicted counterpart gene located in the breakpoint region of 8q22 may be an essential step in the leukemogenesis of AML with t(8;21). Our findings show that the 8;21 translocation, its variants, and the masked t(8;21) may all be detectable by the Southern hybridization method using the AML1 probes.
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23

Movafagh, A., N. Varma, and S. Varma. "Co-expression of two FAB-specific chromosome changes, t(15; 17) and t(8; 21), in a case of acute promyelocytic leukemia." Annals of Hematology 72, no. 6 (June 27, 1996): 375–77. http://dx.doi.org/10.1007/s002770050189.

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24

Singh, Pragya, Meetu Aggrawal, Leelawathi Dawson, and Amitabh Singh. "An unusual case of acute myeloid leukemia with t(8:21) presenting with hypereosinophilia showing dysplastic features." Indian Journal of Medical and Paediatric Oncology 41, no. 4 (2020): 612. http://dx.doi.org/10.4103/ijmpo.ijmpo_197_19.

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25

Baer, Maria R., Carleton C. Stewart, David Lawrence, Diane C. Arthur, John C. Byrd, Frederick R. Davey, Charles A. Schiffer, and Clara D. Bloomfield. "Expression of the Neural Cell Adhesion Molecule CD56 Is Associated With Short Remission Duration and Survival in Acute Myeloid Leukemia With t(8; 21)(q22; q22)." Blood 90, no. 4 (August 15, 1997): 1643–48. http://dx.doi.org/10.1182/blood.v90.4.1643.

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Abstract Although acute myeloid leukemia (AML) with t(8; 21) (q22; q22) is associated with a high complete remission (CR) rate and prolonged disease-free survival, treatment outcome is not universally favorable. Identifying factors that predict for treatment outcome might allow therapy to be optimized based on risk. AML with t(8; 21) has a distinctive immunophenotype, characterized by expression of the myeloid and stem cell antigens CD13, CD15, CD34, and HLADr, and frequent expression of the B-cell antigen CD19 and the neural cell adhesion molecule CD56, a natural killer cell/stem cell antigen. Because CD56 expression has been associated with both extramedullary leukemia and multidrug resistance, we sought to correlate CD56 expression with treatment outcome in AML with t(8; 21). Pretreatment leukemia cells from 29 adult de novo AML patients with t(8; 21) treated on Cancer and Leukemia Group B (CALGB) protocols were immunophenotyped by multiparameter flow cytometry as part of a prospective immunophenotyping study of adult AML (CALGB 8361). CD56 was expressed in 16 cases (55%). There was no correlation between CD56 expression and age, sex, white blood cell count, granulocyte count, the presence of additional cytogenetic abnormalities, or the presence of extramedullary disease at diagnosis. The CR rate to standard-dose cytarabine and daunorubicin was similar for cases with and without CD56 expression (88% v 92%; P = 1.0). Post-CR therapy included at least one course of high-dose cytarabine in 24 of 26 patients who achieved CR; numbers of courses administered were similar in cases with and without CD56 expression. Although post-CR therapy did not differ, CR duration was significantly shorter in cases with CD56 expression compared with those without (median, 8.7 months v not reached; P = .01), as was survival (median, 16.5 months v not reached; P = .008). We conclude that CD56 expression in AML with t(8; 21) is associated with significantly shorter CR duration and survival. Our results suggest that CD56 expression may be useful in stratifying therapy for this subtype of AML.
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26

Baer, Maria R., Carleton C. Stewart, David Lawrence, Diane C. Arthur, John C. Byrd, Frederick R. Davey, Charles A. Schiffer, and Clara D. Bloomfield. "Expression of the Neural Cell Adhesion Molecule CD56 Is Associated With Short Remission Duration and Survival in Acute Myeloid Leukemia With t(8; 21)(q22; q22)." Blood 90, no. 4 (August 15, 1997): 1643–48. http://dx.doi.org/10.1182/blood.v90.4.1643.1643_1643_1648.

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Although acute myeloid leukemia (AML) with t(8; 21) (q22; q22) is associated with a high complete remission (CR) rate and prolonged disease-free survival, treatment outcome is not universally favorable. Identifying factors that predict for treatment outcome might allow therapy to be optimized based on risk. AML with t(8; 21) has a distinctive immunophenotype, characterized by expression of the myeloid and stem cell antigens CD13, CD15, CD34, and HLADr, and frequent expression of the B-cell antigen CD19 and the neural cell adhesion molecule CD56, a natural killer cell/stem cell antigen. Because CD56 expression has been associated with both extramedullary leukemia and multidrug resistance, we sought to correlate CD56 expression with treatment outcome in AML with t(8; 21). Pretreatment leukemia cells from 29 adult de novo AML patients with t(8; 21) treated on Cancer and Leukemia Group B (CALGB) protocols were immunophenotyped by multiparameter flow cytometry as part of a prospective immunophenotyping study of adult AML (CALGB 8361). CD56 was expressed in 16 cases (55%). There was no correlation between CD56 expression and age, sex, white blood cell count, granulocyte count, the presence of additional cytogenetic abnormalities, or the presence of extramedullary disease at diagnosis. The CR rate to standard-dose cytarabine and daunorubicin was similar for cases with and without CD56 expression (88% v 92%; P = 1.0). Post-CR therapy included at least one course of high-dose cytarabine in 24 of 26 patients who achieved CR; numbers of courses administered were similar in cases with and without CD56 expression. Although post-CR therapy did not differ, CR duration was significantly shorter in cases with CD56 expression compared with those without (median, 8.7 months v not reached; P = .01), as was survival (median, 16.5 months v not reached; P = .008). We conclude that CD56 expression in AML with t(8; 21) is associated with significantly shorter CR duration and survival. Our results suggest that CD56 expression may be useful in stratifying therapy for this subtype of AML.
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Abdulateef, Nahla, Manar Ismail, Soha Elmorsy, Aziza ALswayyed, Essam Abdou, and Omima Elemam. "AML with Additional Cytogenetic Abnormalities to t(8: 21) has Poorer Survival than that with Isolated t(8;21): A Retrospective Multicenter Cohort Study." International Blood Research & Reviews 3, no. 1 (January 10, 2015): 36–46. http://dx.doi.org/10.9734/ibrr/2015/15529.

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28

Ruediger, Thomas, Bertrand Coiffier, Dennis D. Weisenburger, and Massimo Federico. "International T-Cell Lymphoma Classification Project: Angioimmunoblastic T-Cell Lymphoma." Blood 108, no. 11 (November 1, 2006): 2052. http://dx.doi.org/10.1182/blood.v108.11.2052.2052.

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Abstract Peripheral T-cell lymphomas are rare diseases: therefore, the International T-cell Lymphoma Project was undertaken to compare lymphomas at different sites throughout North America, Asia and Europe. Within this project, 243 angioimmunoblastic T-cell lymphomas (AILTs) were diagnosed which made up 21% of all peripheral T-cell lymphoma (PTCL). At presentation, generalized lymphadenopathy was noted in 76% of the patients. Interestingly, three patients presented with extranodal disease only. Among the skin symptoms, erythroderma was the most frequent (21% of patients). Hemolytic anemia was seen in 13% and dysproteinemia occurred in 50%, and among these monoclonal serum immunoglobulin was seen in 8% of the patients. Anemia, hypergammaglobulinemia and elevated LDH were significantly more frequent in AILT than in PTCL-unspecified. Similarly, patients with AILT had a significantly higher frequency of high stage disease (89% of the patients were stage 3 or 4), as well as worse prognostic indices. Despite this, their 5-year overall (33%) and failure-free survivals (18%) were similar to patients with PTCL-unspecified. Treatment was usually administered in combination with anthracycline. A few factors at presentation were prognostic for outcome, including the PIT (prognostic index for T-cell lymphoma; Gallamini et al.: Blood. 2004 Apr 1;103(7):2474–9), age, B-symptoms and performance status. The IPI, however, was not prognostic. Controlling for the PIT, a platelet count <150.000 μl was prognostic for overall survival whereas B-symptoms were prognostic for failure-free survival. In conclusion, AILT is an aggressive disease for which the optimum treatment has not yet been developed.
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29

Ferreira, Ricardo C., Henry Z. Simons, Whitney S. Thompson, Antony J. Cutler, Xaquin Castro Dopico, Deborah J. Smyth, Meghavi Mashar, et al. "IL-21 production by CD4+ effector T cells and frequency of circulating follicular helper T cells are increased in type 1 diabetes patients." Diabetologia 58, no. 4 (February 6, 2015): 781–90. http://dx.doi.org/10.1007/s00125-015-3509-8.

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30

Lai, Lilin, Nadine Rouphael, Yongxian Xu, Amy C. Sherman, Srilatha Edupuganti, Evan J. Anderson, Pamela Lankford-Turner, et al. "Baseline Levels of Influenza-Specific B Cells and T Cell Responses Modulate Human Immune Responses to Swine Variant Influenza A/H3N2 Vaccine." Vaccines 8, no. 1 (March 13, 2020): 126. http://dx.doi.org/10.3390/vaccines8010126.

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The cellular immune responses elicited by an investigational vaccine against an emergent variant of influenza (H3N2v) are not fully understood. Twenty-five subjects, enrolled in an investigational influenza A/H3N2v vaccine study, who received two doses of vaccine 21 days apart, were included in a sub-study of cellular immune responses. H3N2v-specific plasmablasts were determined by ELISpot 8 days after each vaccine dose and H3N2v specific CD4+ T cells were quantified by intracellular cytokine and CD154 (CD40 ligand) staining before vaccination, 8 and 21 days after each vaccine dose. Results: 95% (19/20) and 96% (24/25) subjects had pre-existing H3N2v specific memory B, and T cell responses, respectively. Plasmablast responses at Day 8 after the first vaccine administration were detected against contemporary H3N2 strains and correlated with hemagglutination inhibition HAI (IgG: p = 0.018; IgA: p < 0.001) and Neut (IgG: p = 0.038; IgA: p = 0.021) titers and with memory B cell frequency at baseline (IgA: r = 0.76, p < 0.001; IgG: r = 0.74, p = 0.0001). The CD4+ T cells at Days 8 and 21 expanded after prime vaccination and this expansion correlated strongly with early post-vaccination HAI and Neut titers (p ≤ 0.002). In an adult population, the rapid serological response observed after initial H3N2v vaccination correlates with post-vaccination plasmablasts and CD4+ T cell responses.
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31

Gauthier, Jordan, Cassie Chou, Alexandre V. Hirayama, Salvatore Fiorenza, Erik Kimble, Qian Wu, Jenna M. Voutsinas, et al. "IL-15 Serum Concentrations and CD19 CAR T-Cell Therapy: Impact on Clinical Outcomes and In Vivo CAR T Cell Kinetics." Transplantation and Cellular Therapy 27, no. 3 (March 2021): S196—S197. http://dx.doi.org/10.1016/s2666-6367(21)00243-8.

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32

Alpdogan, O., S. J. Muriglan, J. M. Eng, L. M. Willis, K. Tjoe, A. Kirovski, and M. R. Van Den Brink. "21 IL-15 administration after allogeneic HSCT enhances CD8+T (and NK/T) cell reconstitution through increased homeostatic proliferation without aggravating GVHD." Biology of Blood and Marrow Transplantation 9, no. 2 (February 2003): 69. http://dx.doi.org/10.1016/s1083-8791(03)80022-8.

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33

Mima, K., R. Nishihara, Z. R. Qian, H. Baba, and S. Ogino. "173PD MicroRNA MIR21, T cells, and PTGS2 expression in." Annals of Oncology 27 (December 2016): ix54. http://dx.doi.org/10.1016/s0923-7534(21)00331-8.

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34

Aslan, Vahap, O. Meltem Akay, Beyhan Durak, Sare Kabukcuoglu, and Zafer Gulbas. "Langerhans Cell Histiocytosis with Transformation to Acute Leukemia Showing 45, X, t (8; 21), 5 q -, - Y Karyotype." Leukemia & Lymphoma 43, no. 8 (January 2002): 1683–85. http://dx.doi.org/10.1080/1042819021000003036.

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35

Weisser, Martin, Susanne Schnittger, Wolfgang Kern, Wolfgang Hiddemann, Torsten Haferllach, and Claudia Schoch. "Prognostic Factors in CBFB-MYH11 Positive AML: Trisomy 21, AGE, and t(16;16) Are Associated with Inferior Outcome." Blood 106, no. 11 (November 16, 2005): 486. http://dx.doi.org/10.1182/blood.v106.11.486.486.

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Abstract The fusion transcript CBFB-MYH11 is the molecular correlate of inv(16)/t(16;16) and strictly associated with FAB subtype M4eo. This subgroup is associated with a favorable prognosis in AML. However, approximately 30% of the patients relapse. Our intention was to examine prognostic factors for the outcome within this subgroup. Therefore 153 CBFB-MYH11 positive AML patients were analyzed. The median age was 52 years (range 18–83), 80 patients were female, 73 were male. In 22 cases AML was therapy-related, in 131 cases a de novo AML was diagnosed. Inv(16) was detected in 138 and t(16;16) in 12 cases. In 3 cases neither inv(16) nor t(16;16) were detectable despite PCR and FISH positivity for CBFB-MYH11 suggesting cryptic rearrangements. The most frequent additional cytogenetic abnormalities were +8 (n=19), +9 (n=3), +21 (n=7), +22 (n=23). Cox regression analysis revealed that advanced age (OS: p=0.026; EFS: p=0.029) and increased CBFB-MYH11/ABL ratio at diagnosis (OS: 0.016, EFS: p=0.064) were associated with a worse prognosis. Using log rank test additional factors influencing survival were detected. These included: t(16;16) vs inv(16) (OS: n=8, censored 4, median 362 days vs n=118, censored 92, median not reached, p=0.018; EFS: n=8, censored 4, median 232 days vs n=118, censored 70, median 918 days, p=0.048) and trisomy 21 vs no additional aberrations (OS: n=6, censored 3, median 435 days vs n=74, censored 59, median not reached, p=0.024; EFS: n=6, censored 2, median 293 d vs n=74, censored 44, median 764 days, p=0.0047). Therapy related AML was associated with worse EFS than de novo AML (n=16, censored 6, median 371 days vs n=112, censored 70, median 1179 days, p=0.0167) and there was a trend towards worse OS (p=0.157 n=16, censored 10, median 764 days vs n=112, censored 88, median not reached). A multivariate analysis including t(16;16), age, CBFB-MYH11/ABL ratio, therapy related AML and +21 as covariates revealed t(16;16) and age as independent factor for OS (p=0.014 and p=0.015, respectively) and age, t(16;16), and +21 as independent factors for EFS (p=0.047, p=0.013, and p=0.016, respectively). There was no evidence that the additional aberrations +22 or +8 had an influence on survival. Taken together our data suggest that t(16;16) as compared to inv(16), trisomy 21 and age are associated with worse prognosis in patients with CBFB-MYH11 positive AML.
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36

Dufour, Carlo, Alberto Garaventa, Massimo Brisigotti, Cristina Rosanda, and Pier Giorgio Mori. "Massively Diffuse Multifocal Granulocytic Sarcoma in a Child with Acute Myeloid Leukemia." Tumori Journal 81, no. 3 (May 1995): 222–24. http://dx.doi.org/10.1177/030089169508100316.

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A case of granulocytic sarcoma in an 8-year-old boy with acute myeloid leukemia and t (8; 21) is reported. The case is of interest due to massive extension of the tumor, which may raise different diagnostic difficulties with other solid tumors such as lymphoma, Ewing sarcoma, and soft tissue sarcoma. Furthermore, the tumor was localized in some sites, such as the parotid region and peripheral nerves, which are not usually involved in granulocytic sarcoma. The case points out the diagnostic difficulties with this kind of tumor and appears to contribute to the identification of a subgroup of acute myeloid leukemia with peculiar features, such as M2 morphology with Auer rods, t (8; 21), granulocytic sarcoma and a poor prognosis.
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37

KARAPAZAR, ŞENAY. "SEIBERG–WITTEN EQUATIONS ON 8-DIMENSIONAL MANIFOLDS WITH SU(4)-STRUCTURE." International Journal of Geometric Methods in Modern Physics 10, no. 03 (January 10, 2013): 1220032. http://dx.doi.org/10.1142/s0219887812200320.

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Seiberg–Witten equations on 8-manifolds with Spin(7)-holonomy are introduced in [A. H. Bilge, T. Dereli and S. Koçak, Monopole equations on 8-manifolds with Spin(7) holonomy, Commun. Math. Phys.203(1) (1999) 21–30] and it is given a local solution for these equations. In this work, we write down similar Seiberg–Witten equations on 8-dimensional manifolds with SU(4)-structure and give a global solution for these equations.
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38

Kato, Keisuke, Ayako Tagusagawa, Chie Kobayashi, Kazutoshi Koike, and Masahiro Tsuchida. "Cytogenetic/Molecular Findings and Treatment Outcome of Childhood Acute Megakaryoblastic Leukemia. Possible Favorable Effect of High Dose Cytarabine and Stem Cell Transplantation." Blood 110, no. 11 (November 16, 2007): 4255. http://dx.doi.org/10.1182/blood.v110.11.4255.4255.

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Abstract Acute megakaryoblastic leukemia (AMKL) is a rare hematological malignancy. Childhood AMKL is classified into three categories including AMKL associated with Down syndrome (AMKL-DS), AMKL with t(1;22)(p13;q13)/RBM15-MKL1, and others. Previous studies have revealed AMKL with t(1;22)(p13;q13) occurs mainly in infant with poor prognosis, and patients with AMKL-DS generally show favorable course, mostly associated with GATA-1 mutation. Appropriate treatment strategy and the role of hematopoietic stem cell transplantation (SCT) remained controversial in childhood AMKL. Cases and Methods: Eleven cases with AMKL were analyzed and reviewed. Cytogenetic analysis was performed with G banding. Expression of RBM15-MKL1 was analyzed with RT-PCR method on seven cases with the material available. Results. The age at onset ranged from 6 months to 2 years and 6 months. Three were males and eight females. Five of 11 cases were AMKL-DS. Three were AMKL with t(1;22)(p13;q13), of which both two cases analyzed express RBM15-MKL1. Translocation at 11q23 was confirmed in two. Preceding MDS had been confirmed in one AMKL-DS and one AMKL with t(1;22)(p13;q13). The treatment differed among the cases; however, the regimens including high dose cytarabine (HD-CA) were utilized as first-line therapy in eight cases out of 11, resulting in long term remission in five. In particular, three AMKL with t(1;22)(p13;q13) attained long term remission with HD-CA containg regimen. Three cases underwent SCT on disease and two of three remain in remission for 7 years and 4 months, respectively. Two poor prognostic AMKL-DS cases had breakpoint at 22q13 where MKL1 resides and at 17p13 where TP53 is localized. Discussion. Childhood AMKL is heterogenous on cytogenetic/molecular aspects. HD-CA containing regimens might have favorable effect even on AMKL with t(1;22)(p13;q13) and the other poor prognostic AMKL. SCT might be effective even for refractory disease. patient characteristics case sex age at onset clinical feature karyotype RBM15-MKL1 treatment outcome abbreviations: M, male; F, female; y, year; mo, month; MDS, myelodysplastic syndrome; TMD, transient myeloproliferative disorder; NA, not available; CA, chemotherapeutic regimen containing normal dose of cytarabine; HD-CA, chemotherapeutic regimen containing high dose cytarabine; CR, complete remission; Rel, relapse; and DOD, died of disease 1 M 1y DS 53, XY, +6, +8, +10, +13, +14, +19, 21 NA CA 18y11mo CR 2 F 1y7mo 50, XX, +8, +19, +21, +22 − HD-CA 11y10mo CR 3 F 6mo preceding MDS 46, XX, t(1;22), t(11;14)(q23;q22) NA HD-CA 13y10mo CR 4 F 1y5mo 48, XX, t(1;22)(p13;q13), +2, +mar + HD-CA 12y10mo CR 5 F 2y6mo 46, XX, t(9;11;17)(p22;q23;q21) NA HD-CA, SCT 10y3mo CR 6 F 1y7mo DS 47, XX, +21 NA HD-CA 4y5mo CR 7 M 1y9mo 51, XY, t(1;22)(p13;q13), +6, +8, −17, +20, +21, +21, +mar + HD-CA 9y8mo CR 8 M 1y11mo DS 47, XY, der(5)t(1;5)(q21;q33), del(5)(q?), add(9)(q34), +21, add(22)(q13) − HD-CA, SCT induction failure, 7y8mo CR after SCT on disease 9 F 1y3mo DS, preceding TMD and MDS 48, XX, +8, +21 − CA 7y8mo CR 10 F 11mo DS 45, XX, add(3)(p25), −7, +11, add(11)(p11)X2, −13, der(17)t(13;17)(q12;p13) − CA, HD-CA, SCT 7mo Rel after CA, re-induction failure after HD-CA, SCT on disease, 1mo Rel, DOD 11 F 1y11mo 46, XX, inv(2)(p23;q37), der(5)t(5;15)(p15;q11)t(6;15)(p11;q26), der(6)t(6;15), del(15)(q11) − HD-CA, SCT 6mo Rel after HD-CA, SCT on disease, 4mo CR
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39

Yu, Jie, Bing Yu, Honglin Jiang, and Daiwen Chen. "Conjugated linoleic acid induces hepatic expression of fibroblast growth factor 21 through PPAR-α." British Journal of Nutrition 107, no. 4 (July 18, 2011): 461–65. http://dx.doi.org/10.1017/s0007114511003205.

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Fibroblast growth factor 21 (FGF21) is a PPAR-α-regulated metabolic regulator that plays critical roles in glucose homoeostasis, lipid metabolism, insulin sensitivity and obesity. Conjugated linoleic acids (CLA), especially trans-10 (t-10), cis-12 (c-12), have shown anti-obesity properties. In addition, CLA is reported as a high-affinity ligand and activator of PPAR-α. This raises the possibility that FGF21 might be involved in the anti-obesity effect of CLA. In the present study, we tested the hypothesis that FGF21 expression in the liver could be induced by t-10, c-12-CLA through PPAR-α. HepG2 cells were treated with 100 μm-bovine serum albumin, 10 μm-t-10, c-12-CLA or 100 μm-t-10, c-12-CLA for 8 h. A total of ten adult C57BL/6J mice were fed with the diets containing 1 % soya oil or t-10, c-12-CLA for 5 d. t-10, c-12-CLA stimulated hepatic FGF21 mRNA abundance as determined by real-time RT-PCR. t-10, c-12-CLA also increased serum FGF21 concentrations as measured by an ELISA. Co-transfection analysis indicated that reporter gene expression from the mouse FGF21 promoter was induced by t-10, c-12-CLA in a PPAR-α-dependent manner. Taken together, these results suggest that t-10, c-12-CLA induces hepatic FGF21 expression through PPAR-α. This FGF21 and PPAR-α linkage may provide another potential explanation for the anti-obesity effect of t-10, c-12-CLA.
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40

Ettinger, Ruth A., Eddie A. James, William W. Kwok, Arthur R. Thompson, and Kathleen P. Pratt. "Lineages of human T-cell clones, including T helper 17/T helper 1 cells, isolated at different stages of anti–factor VIII immune responses." Blood 114, no. 7 (August 13, 2009): 1423–28. http://dx.doi.org/10.1182/blood-2009-01-200725.

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AbstractThe development of neutralizing antibodies (inhibitors) after factor VIII (FVIII) infusions is a serious complication that affects approximately one-quarter of hemophilia A patients who have access to replacement therapy. To investigate the differentiation of naive T cells into FVIII-specific helper T cells that promote B-cell activation and antibody secretion, HLA-DRA-DRB1*0101-restricted T-cell clones that respond to a specific epitope in FVIII were isolated from a mild hemophilia A subject (the proband) 19 weeks and 21 months after his development of a high-titer inhibitor. Clones responding to the same epitope were also isolated from his multiply infused brother, who has not developed a clinically significant inhibitor. The 19-week proband clones were T helper (TH)17/TH1- or TH1/TH2-polarized, whereas all 8 clones isolated 21 months postinhibitor development were TH2-polarized cells. In contrast, all 6 clones from the brother who did not develop an inhibitor were TH1-polarized, indicating that tolerance to FVIII can be maintained even with circulating TH1-polarized cells that respond vigorously to in vitro FVIII stimulation. This is the first evidence that TH17/TH1-polarized cells play a role in hemophilic immune responses to FVIII. Furthermore, this is the first report of successful isolation and expansion of antigen-specific human TH17/TH1 clones using standard culture conditions.
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41

Varpula, M., P. Kiilholma, and P. Klemi. "CT and Ultra Low Field (0.02 T) MR Imaging of Uterine Cervical Carcinoma." Acta Radiologica 35, no. 4 (July 1994): 361–66. http://dx.doi.org/10.1177/028418519403500410.

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Nineteen pelvic MR and 21 CT examinations were performed in 21 patients with uterine cervical carcinoma. The results were compared with clinical (FIGO) staging in all patients, and with the histopathologic results after operation in 8. In the evaluation of local tumor growth CT agreed with clinical staging in 29%, MR imaging with clinical staging in 47% and CT with MR in 53%. The greatest discrepancy between the imaging methods and clinical examination was in the evaluation of parametrial extension. From 8 Stage I tumors with surgical confirmation the local tumor growth was overestimated with CT in 3 cases, with clinical examination in 2 and with MR imaging in 2 cases. CT and MR imaging at 0.02 T did not differ in the evaluation of parametrial tumor growth. Clinical examination overestimated parametrial growth but was relatively accurate in detecting vaginal wall involvement. MR imaging at 0.02 T is a convenient, inexpensive and accurate method for the local staging of early uterine cervical carcinoma.
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42

Zhu, Hong-Hu, Daihong Liu, Hao Jiang, Ya-Zhen Qin, Lan-Ping Xu, Qian Jiang, Xiao-Hui Zhang, et al. "KIT Mutation Versus MRD, Which Is More Important To Predict Relapse Of Acute Myeloid Leukemia With t (8; 21)?" Blood 122, no. 21 (November 15, 2013): 1309. http://dx.doi.org/10.1182/blood.v122.21.1309.1309.

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Abstract Background Although acute myeloid leukemia (AML) with t (8; 21) translocation generally belongs to the favorable-risk AML subtypes, relapse occurs in about 40% of cases and long-term (>5years) survival less than 50%. KIT-mutation (KIT+) and minimal residual disease (MRD) levels have been demonstrated as two most important risk factors in several retrospective studies. Until now, only two prospective studies (Our AML05 trial; French CBF-2006 trial) have assessed their respective prognostic values (Zhu HH, et al. Blood 2013; 121:4056; Jourdan E, et al. Blood 2013; 121:2213). We found both KIT+ and MRD were independent risk factors for relapse, but Joundan et al found only MRD rather than KIT+ was sole prognostic factor for relapse in multivariate anaysis. Both studies did not perform a comprehensive subgroup analysis combining the two factors, and risk-adopt postremission treatment might also affect this assessment. Therefore, we performed a subgroup analysis combining KIT mutation and MRD in a prospective protocol AML05 to answer which is more important to predict outcomes of t(8;21)AML. Methods From July, 2005, to Jan, 2013, 114 patients with t (8; 21) AML after achieving complete remission were included in this analysis. KIT mutations in exons 17 and 8 were screened using the direct sequencing method. MRD was detected using quantitative PCR to detect the RUNX1/RUNX1T1 transcript. MRD-positive (MRD+) was defined as < 3 log reduction of RUNX1/RUNX1T1 transcript from baseline after second consolidation therapy. Sixty-two patients received high-dose cytarabine-based consolidation chemotherapy (CT) or autologous hematopoietic stem-cell transplantation (auto-HSCT), and 52 patients received allogeneic HSCT (allo-HSCT). Results When receiving CT/auto-HSCT as postremission treatment, KIT+ patients (n=19) had a higher 3 year cumulative incidence of relapse (CIR) than KIT-patients (n=43) (94.4% vs. 38.2%, p<0.0001). Similar results also found in MRD+ (n=19) and MRD- (n=43) patients (CIR 92.9% vs. 46.6%, p<0.0001). Among KIT+ patients, a very high relapse rate was found in both MRD+ and MRD-patients (CIR, 100% vs.88.9%). However, among KIT-patients, MRD+ patients had a significant higher relapse rate than MRD-patients (CIR, 84.4% vs.26.3%, p=0.0006). When pooling KIT+ and or MRD+ into one group (KIT+/MRD+), this group had a significant higher relapse rate than KIT-MRD- group ( 94.4% vs. 26.3%, p<0.0001), However, the prognostic values of KIT and MRD was lost when patients received allo-HSCT (CIR of KIT+/MRD+ and KIT-MRD-, 23.8% vs. 15.6%, p=0.47). Similar results were also been found in disease-free survival (DFS) and overall-survival (OS). Multivariate analysis revealed that KIT+, MRD+, and treatment (allo-HSCT or CT/auto-HSCT) were three independent prognostic factors for relapse (all p<0.0001), DFS (all p<0.0001) and OS (p<0.0001, p<0.0001, p=0.007). Conclusions Both KIT status and MRD level were important to predict relapse of t (8;21) AML. KIT+ patients hold a very high relapse risk. Disclosures: No relevant conflicts of interest to declare.
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43

Krishnan, K., C. W. Ross, P. T. Adams, A. Pereira, and M. S. Roth. "Neural cell-adhesion molecule (CD 56)-positive, t(8; 21) acute myeloid leukemia (AML, M-2) and granulocytic sarcoma." Annals of Hematology 69, no. 6 (December 1994): 321–23. http://dx.doi.org/10.1007/bf01696563.

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44

Mehta, S., S. Singh, and Wang Ning Ling. "Study on the Relativity between Cytogenetics and Cytomorphology and its Prognosis Significance in Children with Acute Myelogenous Leukemia." Journal of Gandaki Medical College-Nepal 10, no. 2 (August 17, 2018): 35–41. http://dx.doi.org/10.3126/jgmcn.v10i2.20806.

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Objective: The main objective of this study was to retrospectively evaluate that the cytogenetic abnormalities is an important prognostic factor for the cure of acute myeloid leukemia (AML).Methods: This retrospective study enrolled newly diagnosed 70 cases (37 males and 33 females, aged 10.1 months to 14.5 years) of pediatric patients with AML during 2010 January - 2016 February from the Second Affiliated Hospital of Anhui Medical University. Excluding criteria were cases secondary to treatment-related MDS and AML. Samples were obtained from bone marrow cells in patients after treatment on the anterior superior iliac spine, blood diseases laboratory by direct culture or 24/48 hour short-term culture, G -banding technique for testing. Follow-up of 1 - 60 months, the analysis of treatment response rates of different karyotypes, distribution ratios in various subtypes, normal karyotype and abnormal karyotype. ISPSS17.0 software statistics was used for statistical analysis. Groups were compared using chi-square test; Survival rate was calculated by method of Kaplan Meier and survival difference between groups were compared with breslow test.Results: Among 70 cases, 42 cases were detected for chromosomal abnormalities (i.e. 60% of the total number of cases), M3 abnormal karyotype distortion rate of 78.5%, M2 abnormal karyotype aberrations 63.3%, M4 60.0%, M1 50%, M5 lowest 38.9 %, M7 nuclear aberrations highest rate was 100%. Total chromosomal aberration rate was 60%. Acute myeloid leukemia cases, t (8; 21) at most, there are 15 cases, and the presence of abnormal karyotype 86.7% in the original part of differentiated myeloid leukemia (M2); t (15; 17) has 11 cases, exists only in acute promyelocytic cell leukemia (M3). After treatment, the remission rate of t (8; 21) was 80%; the remission rate of t (15; 17) was 90%; the remission rate of other abnormal karyotype abnormalities was 50%; the remission rate of total abnormal karyotype was 71.4%. The event free survival rate was significantly different between normal karyotype, t (8; 21), t (15; 17) and other abnormal karyotype groups (P<0.05).Conclusions: Acute myeloid leukemia karyotype abnormalities among FAB subtypes are different; M3 is the highest rate of abnormal karyotype aberrations, M2, M4 medium, M5 minimum. t (15; 17) seen in acute promyelocytic leukemia (APL), prognosis is good; t (8; 21) is more common in M2, prognosis is good, also found in M4 and M5, worse prognosis; +8 Abnormalities found in AML M2, M3, M4, M5 and M6 subtypes, prognosis medium; inv (16) high white blood cells, low platelet poor prognosis, AML patients with normal karyotype prognosis medium. J-GMC-N | Volume 11 | Issue 01 | January-June 2018, Page: 35-41
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45

Nucifora, G., DJ Birn, P. Erickson, J. Gao, MM LeBeau, HA Drabkin, and JD Rowley. "Detection of DNA rearrangements in the AML1 and ETO loci and of an AML1/ETO fusion mRNA in patients with t(8;21) acute myeloid leukemia." Blood 81, no. 4 (February 15, 1993): 883–88. http://dx.doi.org/10.1182/blood.v81.4.883.883.

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Abstract The (8;21)(q22;q22) translocation is a frequent karyotypic abnormality seen in approximately 40% of patients with acute myeloid leukemia subtype M2 (AML-M2) and an abnormal karyotype. The translocation interrupts two genes, AML1 on chromosome 21 and ETO on chromosome 8, that are consequently fused in the der(8) chromosome to produce a novel chimeric gene and message. Selected genomic DNA probes from chromosome 21 and from chromosome 8 near the breakpoint junction detect rearrangements in the DNA of about 80% of the patients with the rearrangement at diagnosis and in relapse. We analyzed the DNA of 20 patients with t(8;21) AML by standard Southern blot with probes originating from chromosomes 21 and 8 near the breakpoint junction, and we identified rearranged bands in 17 of the 20 patients at diagnosis and in relapse. We also used the polymerase chain reaction (PCR) with appropriate primers from the AML1 and ETO genes to amplify the cDNAs from a cell line with the t(8;21) and from seven AML patients with the t(8;21). We detected a fused transcript in the cell line and in all of the patients analyzed, including three patients who did not show any rearrangement by Southern blot analysis and one patient in hematologic remission, who later relapsed. Combining the results from Southern blot and PCR analysis, we could detect the t(8;21) in all of the patients tested. These results indicate that, whereas several DNA probes used as genetic markers do detect the t(8;21) in most, but not all Southern blots of patients with AML, PCR amplification with primers from AML1 and ETO can be used as a more sensitive and accurate means for detecting this chromosomal abnormality, and for observing the patients' response to therapy.
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46

Nucifora, G., DJ Birn, P. Erickson, J. Gao, MM LeBeau, HA Drabkin, and JD Rowley. "Detection of DNA rearrangements in the AML1 and ETO loci and of an AML1/ETO fusion mRNA in patients with t(8;21) acute myeloid leukemia." Blood 81, no. 4 (February 15, 1993): 883–88. http://dx.doi.org/10.1182/blood.v81.4.883.bloodjournal814883.

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The (8;21)(q22;q22) translocation is a frequent karyotypic abnormality seen in approximately 40% of patients with acute myeloid leukemia subtype M2 (AML-M2) and an abnormal karyotype. The translocation interrupts two genes, AML1 on chromosome 21 and ETO on chromosome 8, that are consequently fused in the der(8) chromosome to produce a novel chimeric gene and message. Selected genomic DNA probes from chromosome 21 and from chromosome 8 near the breakpoint junction detect rearrangements in the DNA of about 80% of the patients with the rearrangement at diagnosis and in relapse. We analyzed the DNA of 20 patients with t(8;21) AML by standard Southern blot with probes originating from chromosomes 21 and 8 near the breakpoint junction, and we identified rearranged bands in 17 of the 20 patients at diagnosis and in relapse. We also used the polymerase chain reaction (PCR) with appropriate primers from the AML1 and ETO genes to amplify the cDNAs from a cell line with the t(8;21) and from seven AML patients with the t(8;21). We detected a fused transcript in the cell line and in all of the patients analyzed, including three patients who did not show any rearrangement by Southern blot analysis and one patient in hematologic remission, who later relapsed. Combining the results from Southern blot and PCR analysis, we could detect the t(8;21) in all of the patients tested. These results indicate that, whereas several DNA probes used as genetic markers do detect the t(8;21) in most, but not all Southern blots of patients with AML, PCR amplification with primers from AML1 and ETO can be used as a more sensitive and accurate means for detecting this chromosomal abnormality, and for observing the patients' response to therapy.
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47

Akamatsu, Norihiko, Hiroo Hasegawa, Yasuaki Yamada, Koki Makabe, Ryutaro Asano, Izumi Kumagai, Ken Murata, et al. "Selected IL-21R Expression and Apoptosis Induction by IL-21 in Follicular Lymphoma." Blood 104, no. 11 (November 16, 2004): 2284. http://dx.doi.org/10.1182/blood.v104.11.2284.2284.

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Abstract IL-21 receptor (IL-21R), a member of the common gamma receptor family, is expressed on many kind cells including T-cells, B-cells, and NK cells. IL-21 promotes the proliferation and maturation of NK cells and shows anti-tumor activities in animal systems. Although these results suggest its clinical use in the treatment of malignancies, it has also been shown that IL-21 may conversely accelerate the proliferation of IL-21R-expressing tumor cells. Considering the potential for therapeutic application of recombinant IL-21, we examined IL-21R expression and response to IL-21 in hematological malignancies. Using flow cytometry, we examined IL-21R expression in primary samples from AML, ALL, B-CLL, B-NHL and adult T-cell leukemia/lymphoma (ATLL) caused by a retrovirus, HTLV-1. Among 35 primary samples, only 5 samples from 16 patients with B-NHL and one sample from 8 patients with ATL were IL-21R positive. Of note, all the IL-21R positive NHL also expressed CD10, one of the marker molecules of follicular center cells. Indeed, two of the five patients were diagnosed follicular lymphoma with t(14;18)(q32;q21). Corresponding to these results, the follicular lymphoma cell line SUDHL-4 and most ATLL and HTLV-1-infected cell lines were IL-21R positive. Interestingly, IL21 showed dual effects on these cell lines; IL-21 stimulated the proliferation of ATLL cell lines but suppressed the proliferation of SUDHL-4. Annexin V and propidium iodide staining for detection of early and late apoptosis and mitochondrial membrane potential analysis indicated that the suppression was the result of apoptosis. Exposure of SUDHL-4 to IL-21 resulted in significant time-dependent induction of caspase-8 and caspase-3 activation. More importantly, IL-21 decreased Bcl-2 expression but drastically increased Bax expression. Thus, selected expression of IL-21R in follicular lymphoma cells and induction of apoptosis by IL-21 provide a strong background for IL-21 as an anti-neoplastic agent at least in a subset of follicular lymphoma.
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48

Araya, Paula, Katherine A. Waugh, Kelly D. Sullivan, Nicolás G. Núñez, Emiliano Roselli, Keith P. Smith, Ross E. Granrath, et al. "Trisomy 21 dysregulates T cell lineages toward an autoimmunity-prone state associated with interferon hyperactivity." Proceedings of the National Academy of Sciences 116, no. 48 (November 7, 2019): 24231–41. http://dx.doi.org/10.1073/pnas.1908129116.

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Trisomy 21 (T21) causes Down syndrome (DS), a condition characterized by high prevalence of autoimmune disorders. However, the molecular and cellular mechanisms driving this phenotype remain unclear. Building upon our previous finding that T cells from people with DS show increased expression of interferon (IFN)-stimulated genes, we have completed a comprehensive characterization of the peripheral T cell compartment in adults with DS with and without autoimmune conditions. CD8+ T cells from adults with DS are depleted of naïve subsets and enriched for differentiated subsets, express higher levels of markers of activation and senescence (e.g., IFN-γ, Granzyme B, PD-1, KLRG1), and overproduce cytokines tied to autoimmunity (e.g., TNF-α). Conventional CD4+ T cells display increased differentiation, polarization toward the Th1 and Th1/17 states, and overproduction of the autoimmunity-related cytokines IL-17A and IL-22. Plasma cytokine analysis confirms elevation of multiple autoimmunity-related cytokines (e.g., TNF-α, IL17A–D, IL-22) in people with DS, independent of diagnosis of autoimmunity. Although Tregs are more abundant in DS, functional assays show that CD8+ and CD4+ effector T cells with T21 are resistant to Treg-mediated suppression, regardless of Treg karyotype. Transcriptome analysis of white blood cells and T cells reveals strong signatures of T cell differentiation and activation that correlate positively with IFN hyperactivity. Finally, mass cytometry analysis of 8 IFN-inducible phosphoepitopes demonstrates that T cell subsets with T21 show elevated levels of basal IFN signaling and hypersensitivity to IFN-α stimulation. Therefore, these results point to T cell dysregulation associated with IFN hyperactivity as a contributor to autoimmunity in DS.
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49

Gupta, Shiphali, Judith Brody, Veena John, and Prasad Koduru. "Complex Translocation (8;16;21); a New Variant of t(8;21), with t(13;22) in Acute Myeloid Leukemia." Blood 106, no. 11 (November 16, 2005): 4342. http://dx.doi.org/10.1182/blood.v106.11.4342.4342.

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Abstract The translocation (8;21)(q22;q22) is a common recurrent chromosome aberration present in 10% to 15% of all acute myeloid leukemias. In approximately 3% of all cases with t(8;21), a variant of t(8;21) involving chromosomes 8,21 and other chromosomes is present. We report here a case of AML-M2 with a new complex translocation (8;16;21)(q22;p16.3;q22) associated with additional abnormality t(13;22)(q22;q13) not described before. Fluorescent in-situ hybridization analysis with probes for ETO and AML1 genes, and probes for the subtelomeric regions of chromosome 16 demonstrated an ETO-AML1 fusion signal on der(8). The 5′ region of ETO gene with chromosome arm distal to translocation breakpoint had moves to der(16) while region of AML1 probe proximal to translocation brealpoint stayed on der(21). The signal for the subtelomeric probe for 16p was present on der(21). Use of painting probe for chromosome 13 confirmed t(13;22). In a hematopoietic cell the expression of chimeric AML1- ETO protein resulting from t(8;21) plays a key role in leukemic transformation by targeting AML1-CBFB transcription factor complex, an essential regulator of genes required for normal hematopoietic cell development, by dominant negative effect on normal AML1 protein. However, the expression of AML1- ETO does not block normal differentiation of stem cells. Additional mutational events must occur in hematopoietic progenitor cell to block normal path of differentiation. Although clinical features of variant translocation is same as cases with conventional t(8;21), prognostic implications of variant (8;21) are yet to be established. Chromosome region 16p13 has been involved in clinically important translocations with poor prognosis such as t(8;16)(p11;p13) and t(11;16)(q23;p13) and may have similar implications. Translocation (8;21) is frequently accompanied by additional chromosome abnormalities i.e. loss of sex chromosome, trisomy 8 and structural abnormalities of 9q. Additional reports on secondary genetic alterations accompanying t(8;21) are needed to understand their cumulative effect. Chromosome region 16p13, 13q22 and 22q13 may harbor putative genes influencing normal path of differentiation.
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50

Stephens, Eddie, Ansh Mehta, Tanya Persoon, Shannon Baker, Remy David, Kavitha Nair, Yazan F. Madanat, et al. "Continuous Telemetry Monitoring in Chimeric Antigen Receptor (CAR) T-Cell Therapy Patients." Transplantation and Cellular Therapy 27, no. 3 (March 2021): S211—S212. http://dx.doi.org/10.1016/s2666-6367(21)00260-8.

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