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Relevant bibliographies by topics / Lymphoblasts

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Academic literature on the topic 'Lymphoblasts'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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Journal articles on the topic "Lymphoblasts"

1

Whitehead, VM, DS Rosenblatt, MJ Vuchich, JJ Shuster, A. Witte, and D. Beaulieu. "Accumulation of methotrexate and methotrexate polyglutamates in lymphoblasts at diagnosis of childhood acute lymphoblastic leukemia: a pilot prognostic factor analysis." Blood 76, no. 1 (July 1, 1990): 44–49. http://dx.doi.org/10.1182/blood.v76.1.44.44.

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Abstract Lymphoblasts in bone marrow samples, obtained from 43 children with acute lymphoblastic leukemia at diagnosis, were incubated with 1.0 mumols/L [3H] methotrexate for 24 hours in vitro. Nonexchangeable methotrexate and methotrexate polyglutamates were separated and quantitated. Event-free survival at 5 years was 38% +/- 9% for all 43 patients (27 failures), and 44% +/- 10% for the 35 with non-T, non-B- cell acute lymphoblastic leukemia (20 failures). Of these 35 children, those whose lymphoblasts accumulated more than 100 pmol methotrexate and 500 pmol methotrexate polyglutamates per billion cells experienced better 5-year event-free survival than those whose lymphoblasts did not (65% +/- 12% v 22% +/- 9%, P = .010). This difference characterized “good-risk” patients who were female (P = .014), less than age 7 at diagnosis (P = .005), or had low initial white blood cell counts (less than 20 X 10(9)/L, P = .018). Findings were similar for the 43 children with acute lymphoblastic leukemia and for the “good-risk” children in this total group. Thus, the ability of lymphoblasts to accumulate methotrexate and form methotrexate polyglutamates may be important to the curative properties of current therapy of acute lymphoblastic leukemia in children, particularly for “good-risk” patients. In such patients, inherent rather than acquired drug resistance may be the initial event leading to treatment failure.

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Whitehead, VM, DS Rosenblatt, MJ Vuchich, JJ Shuster, A. Witte, and D. Beaulieu. "Accumulation of methotrexate and methotrexate polyglutamates in lymphoblasts at diagnosis of childhood acute lymphoblastic leukemia: a pilot prognostic factor analysis." Blood 76, no. 1 (July 1, 1990): 44–49. http://dx.doi.org/10.1182/blood.v76.1.44.bloodjournal76144.

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Lymphoblasts in bone marrow samples, obtained from 43 children with acute lymphoblastic leukemia at diagnosis, were incubated with 1.0 mumols/L [3H] methotrexate for 24 hours in vitro. Nonexchangeable methotrexate and methotrexate polyglutamates were separated and quantitated. Event-free survival at 5 years was 38% +/- 9% for all 43 patients (27 failures), and 44% +/- 10% for the 35 with non-T, non-B- cell acute lymphoblastic leukemia (20 failures). Of these 35 children, those whose lymphoblasts accumulated more than 100 pmol methotrexate and 500 pmol methotrexate polyglutamates per billion cells experienced better 5-year event-free survival than those whose lymphoblasts did not (65% +/- 12% v 22% +/- 9%, P = .010). This difference characterized “good-risk” patients who were female (P = .014), less than age 7 at diagnosis (P = .005), or had low initial white blood cell counts (less than 20 X 10(9)/L, P = .018). Findings were similar for the 43 children with acute lymphoblastic leukemia and for the “good-risk” children in this total group. Thus, the ability of lymphoblasts to accumulate methotrexate and form methotrexate polyglutamates may be important to the curative properties of current therapy of acute lymphoblastic leukemia in children, particularly for “good-risk” patients. In such patients, inherent rather than acquired drug resistance may be the initial event leading to treatment failure.

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Little, L., M. Alcouloumre, A. M. Drotar, S. Herman, R. Robertson, R. Y. Yeh, and A. L. Miller. "Properties of N-acetylglucosamine 1-phosphotransferase from human lymphoblasts." Biochemical Journal 248, no. 1 (November 15, 1987): 151–59. http://dx.doi.org/10.1042/bj2480151.

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Human lymphoblast and fibroblast cell lines from a patient with I-cell disease and normal individuals were characterized with respect to certain properties of UDP-N-acetylglucosamine:lysosomal enzyme precursor N-acetylglucosamine phosphotransferase. The enzyme isolated from normal lymphoblast and fibroblast cell lines expressed similar kinetic properties, substrate specificities and subcellular localizations. Coincident with the severe reduction of N-acetylglucosamine phosphotransferase activity in both I-cell fibroblast and lymphoblast cell lines, there was an increased secretion of several lysosomal enzymes compared to normal controls. Subsequent examination of N-acetyl-beta-D-hexosaminidase secreted by the I-cell lymphoblasts demonstrated a significant increase in adsorption of the I-cell enzyme to Ricinus communis agglutinin, a galactose-specific lectin. However, the I-cell lymphoblasts did not exhibit the significant decrease in intracellular lysosomal activities seen in I-cell fibroblasts. Our results suggest that lymphoblasts not only represent an excellent source for the purification of N-acetylglucosamine phosphotransferase, but in addition, represent a unique system for studying alternate mechanisms involved in the targeting of lysosomal enzymes.

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Prokop, Aram, Banu Bagci, Guenaelle Lingfeld, Lucia Badiali, Karin Garbrecht, Ulrike Mietzsch, Thomas Wieder, Peter T. Daniel, and Günter Henze. "Sensitivity of Childhood Acute Lymphoblastic Leukemia (ALL) to Idarubicin Is Significantly Higher Than to Daunorubicin Treatment Based on Ex Vivo Apoptosis Induction." Blood 104, no. 11 (November 16, 2004): 4495. http://dx.doi.org/10.1182/blood.v104.11.4495.4495.

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Abstract Anthracyclines, especially daunorubicin, play a very important role in the treatment of acute lymphoblastic leukemia (ALL) and the relapsed ALL in childhood. In the present study, primary lymphoblasts isolated from 65 children with de novo ALL (median: 5.8 years; range: 1.9 – 16.9 years) and relapsed ALL (median: 12.7 years; range: 1.3 – 17.9 years) were treated with daunorubicin (10 mmol/l) or idarubicin (2 mmol/l) in vitro. We could show that both anthracylines induce apoptosis, as evidenced by measurement of genomic DNA fragmentation. Interestingly, daunorubicin only induced modest apoptosis, whereas idarubicin displayed a significantly stronger apoptosis inducing effect. Furthermore the treatment of daunorubicin-resistant lymphoblasts with idarubicin resulted in good response in most of the resistant cell populations. Out of the 65 patients analysed in this study 23 were female (13 de novo ALL, 10 relapsed ALL) and 42 were male (29 de novo ALL, 13 relapsed ALL). Primary lymphoblasts were obtained by bone marrow aspiration and separated by centrifugation over Ficoll. Within these cell populations following immunologic subgroups were found: 35 c-ALL, 10 pre-B-ALL, 7 pro-B-ALL, 10 T-ALL and 3 pre-T-ALL. Daunorubicin induced apoptosis in 33 out of 65 lymphoblast populations (response rate 50.8 %). Nevertheless, a far higher response rate was observed for idarubicin with 59/65 (90,8 %) (p < 0.008), if response is defined as apoptosis induction higher than 1 %. Daunorubicin-resistance was found in 32/65 (49,2 %), resistance to both was observed in 6/65 (9,2 %). Treatment of daunorubicin-resistant lymphoblasts with idarubicin resulted in significant apoptosis induction in 26 out of 32 cell populations (81,3 %). We clearly demonstrated here that the in vitro treatment of lymphoblasts from children with de novo or relapsed ALL with idarubicin induces significantly higher response rates than daunorubicin treatment. The ex vivo sensitivity of daunorubicin-resistant lymphoblasts of childhood ALL to idarubicin treatment reflects the better potency of idarubicin to induce apoptosis and to overcome daunorubicin resistance. These data prompted us to study the clinical relevance of idarubicin in ongoing clinical trials to improve existing therapeutic regiments. First clinical data point to a good tolerability of idarubicin in the treatment of relapsed ALL in childhood.

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Katik, Banu, Anja Selig, Janna Velder, Elvira E. Shults, Thomas Wieder, Guenter Henze, Hans-Guenther Schmalz, and Aram Prokop. "New Pinostilbene Analogues Overcome Anthracycline Resistance in Acute Lymphoplastic Leukemia Ex Vivo." Blood 108, no. 11 (November 16, 2006): 4403. http://dx.doi.org/10.1182/blood.v108.11.4403.4403.

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Abstract Anthracylines play a very important role in the treatment of acute lymphoblastic leukemia (ALL) and relapsed ALL in childhood, however resistance to anthracyclines leads to a poor prognosis. In the present study, we have synthesized two new pinostilbene analogues, i.e. trans-3,4′-dihydroxy-5-methoxystilbene and (E)-resveratrol 4′-O-ß-D-glucopyranoside, which are able to overcome anthracycline resistance in childhood acute lymphoblastic leukemia (ALL) ex vivo and induce apoptosis in established leukemia cell lines via mitochondrial pathway. Apoptosis induction has been investigated by flowcytometric measurement of DNA-fragmentation [LC 50: 10 μM for (1) and (2)], mitochondrial membrane potential reduction and phosphatedylserin-staining on cell membrane surface. Cell death by necrosis could be excluded by a lactatdehydrogenase-release assay. For the first time we analysed the antileukemic and chemopreventive potentials of the pinostilbene analogues (1) and (2) ex vivo in a significant number of primary lymphoblasts of patients suffering from childhood ALL. Patients: Primary lymphoblasts isolated from 22 children with de novo ALL (median: 6.8 years; range 0,6–16.9 years) and relapsed ALL (median:7.2 years) were tested for ex vivo drug response with the anthracyclines daunorubicin (10 μmol/l) and doxorubicin (10 μmol/l) and two new pinostilbene analogues (1) and (2) (10μmol/l), according to their LC50 values in established cell lines. We could demonstrate in these primary cells that the pinostilbenes (1) and (2) were even more effective as compared with the anthracyclines. Out of 22 patients 14 were female (14 de novo ALL) and 8 were male (6 de novo ALL, 2 relapsed ALL). Within these cell populations following immunologic subgroups were found: c-ALL, pre-B-ALL, pro-B-ALL, T-ALL and pre-T-ALL. Results: Daunorubicin induced apoptosis in 6 out of 22 lymphoblast populations (response rate 27,3 %). A similar response rate was observed after treatment with doxorubicin: only 5 of 22 lymphoblast populations responded (22,7%). Nevertheless, far higher response rates were observed for (1) with 11/15 (73,3 %; p<0.005) and for (2) with 15/17 (88,2%; p<0.0002, all p-values by t-test). Interestingly, treatment of daunorubicin-resistant lymphoblasts resulted in significant apoptosis induction in 6 out of 10 cell populations after treatment with compound (1) (response rate 60 %) and in 6/6 after treatment with compound (2) (response rate 100%). Furthermore, pinostilbene (2) showed significant synergistic activity with daunorubicin in 2 of 3 lymphoblast populations. We clearly demonstrated that the ex vivo treatment of lymphoblasts from children with de novo and relapsed ALL with the new pinostilbenes (1) and (2) induced significantly higher response rates than daunorubicin or doxorubicin treatment. In conclusion, the high ex vivo sensitivity of anthracycline resistant leukemia cells to pinostilbene treatment reveals the great proapoptotic and chemopreventive potential of this new class of antileukemic agents.

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Maslak, P. "Lymphoblasts." ASH Image Bank 2004, no. 0202 (February 2, 2004): 100992. http://dx.doi.org/10.1182/ashimagebank-2004-100992.

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Whitehead, VM, MJ Vuchich, SJ Lauer, D. Mahoney, AJ Carroll, JJ Shuster, DW Esseltine, C. Payment, AT Look, and J. Akabutu. "Accumulation of high levels of methotrexate polyglutamates in lymphoblasts from children with hyperdiploid (greater than 50 chromosomes) B-lineage acute lymphoblastic leukemia: a Pediatric Oncology Group study." Blood 80, no. 5 (September 1, 1992): 1316–23. http://dx.doi.org/10.1182/blood.v80.5.1316.bloodjournal8051316.

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Hyperdiploidy (greater than 50 chromosomes, or a DNA index greater than 1.16) confers a favorable prognosis in B-lineage acute lymphoblastic leukemia of childhood. Children with B-lineage acute lymphoblastic leukemia whose lymphoblasts at diagnosis accumulate high levels of methotrexate (MTX) and MTX polyglutamates (MTXPGs) in vitro experience a better event-free survival than those whose lymphoblasts do not (Blood 76:44, 1990). Lymphoblasts from 13 children with hyperdiploidy (greater than 50 chromosomes) accumulated high levels of MTX-PGs (1,095 and 571 to 2,346 pmol/10(9) cells [median and 25% to 75% intraquartile range]). These levels were higher than those in B-lineage lymphoblasts from 19 children with other aneuploidy (326 and 159 to 775 pmol/10(9) cells) and 15 children with diploidy (393 and 204 to 571 pmol/10(9) cells) (P = .0015). Chromosomal trisomies in hyperdiploid cases were highly nonrandom. Chromosome 9 was not one of the chromosomes involved in trisomies, even though this chromosome contains the gene for folate polyglutamate synthetase, which is the enzyme required for MTXPG synthesis. The correlation between MTXPG level and percentage of S- phase cells was weak, suggesting that increased levels of MTXPGs could not be attributed to elevated proportions of cells in active DNA synthesis. The ability of hyperdiploid lymphoblasts to accumulate high levels of MTXPGs may increase their sensitivity to MTX cytotoxicity, accounting in part for the improved outlook for hyperdiploid patients treated with regimens that emphasize MTX as a primary component of continuation therapy.

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Schwartz, C. L., C. P. Minniti, P. Harwood, S. Na, M. L. Banquerigo, L. C. Strauss, J. Kurtzberg, S. D. Smith, and C. I. Civin. "Elimination of clonogenic malignant human T cells using monoclonal antibodies in combination with 2'-deoxycoformycin." Journal of Clinical Oncology 5, no. 12 (December 1987): 1900–1911. http://dx.doi.org/10.1200/jco.1987.5.12.1900.

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2'Deoxycoformycin (dCF) specifically inhibits adenosine deaminase (ADA) and causes selective cytotoxicity of normal and malignant T cells. In clinical trials, dCF caused rapid lysis of malignant T lymphoblasts. Although dCF has been associated with dose-limiting nonhematopoietic toxicities, myelosuppression has not been observed. Since dCF is relatively nontoxic to hematopoietic stem cells, we tested dCF for utility in the ex vivo purging of malignant T lymphoblasts from remission leukemic bone marrow for autologous bone marrow transplantation. We found that T lymphoblast cell lines were sensitive to dCF (plus deoxyadenosine [dAdo]) under conditions that did not ablate human hematopoietic colony-forming cells. Moreover, combined pharmacologic (dCF plus dAdo) and immunologic (anti-T cell monoclonal antibodies [McAb] plus complement) purging resulted in additive reduction in clonogenic T lymphoblasts. These results provide the basis for a clinical trial of bone marrow transplantation using combined pharmacologic/immunologic purging of T lymphoblasts from patients' harvested autologous marrow.

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Sandlund, John T., Patricia L. Harrison, Gaston Rivera, Frederick G. Behm, David Head, James Boyett, Jeffrey E. Rubnitz, et al. "Persistence of lymphoblasts in bone marrow on day 15 and days 22 to 25 of remission induction predicts a dismal treatment outcome in children with acute lymphoblastic leukemia." Blood 100, no. 1 (July 1, 2002): 43–47. http://dx.doi.org/10.1182/blood.v100.1.43.

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Abstract We determined the prognostic importance of morphologically identifiable persistent disease at day 15 and days 22 to 25 of remission induction in childhood acute lymphoblastic leukemia (ALL). Among 546 patients entered on 2 consecutive protocols, 397 patients had evaluable bone marrow (BM) examinations on day 15 (± 1 day) and 218 on days 22 to 25 (± 1 day). Fifty-seven patients (14%) had persistent lymphoblasts (≥ 1%) in the BM on day 15 and 27 patients (5.5%) had persistent lymphoblasts on days 22 to 25. The 5-year event-free survival (EFS) was significantly worse for patients with lymphoblasts on day 15 (40% ± 6%) or on days 22 to 25 (4% ± 3%) as compared to those without lymphoblasts on these dates (78% ± 2% and 76% ± 2%, respectively, P < .001 for both comparisons). A worse prognosis was observed even for patients with a low percentage of lymphoblasts (ie, 1%-4%) at either day 15 (5-year EFS = 56% ± 8%) or days 22 to 25 (5-year EFS = 0%) compared to those without morphologically identifiable persistent lymphoblasts at these times (P < .001 for both comparisons). The prognostic impact of persistent lymphoblasts on both dates remained significant after adjusting for other known risk factors, including treatment protocol, age, white blood cell count, DNA index, cell lineage, and central nervous system status, and National Cancer Institute/Rome criteria simultaneously. Hence, persistence of lymphoblasts (even 1%-4%) on day 15 of remission induction was associated with a poor prognosis and on days 22 to 25 signified a particularly dismal outcome; these very high-risk patients require novel or more intensive therapy to improve outcome.

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Homans, AC, EN Forman, and BE Barker. "Use of monoclonal antibodies to identify cerebrospinal fluid lymphoblasts in children with acute lymphoblastic leukemia." Blood 66, no. 6 (December 1, 1985): 1321–25. http://dx.doi.org/10.1182/blood.v66.6.1321.1321.

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Abstract The identification of small numbers of leukemic cells in the cerebrospinal fluid (CSF) presents a diagnostic problem in the treatment of children with acute lymphoblastic leukemia (ALL). We adapted a latex sphere rosetting technique to allow us to identify simultaneously cell surface markers and cell morphology in 199 CSF samples from 34 patients and 14 control subjects. In patients without leukemic meningitis, the majority of CSF lymphocytes (69%) were found to be mature T cells positive for OKT11. A much smaller number of cells (8%) were found to be B cells positive for la. In these children, only 3% of CSF lymphoid cells expressed the common acute lymphoblastic leukemia antigen (CALLA). Similar results were found in the control subjects. By contrast, 28 CSF samples from nine children with varying numbers of CSF lymphoblasts had much greater proportions of CALLA- and la-positive CSF cells (24% to 96%). Leukemic meningitis was present in one of these patients and later developed in four others. However, three patients with small numbers of lymphoblasts present but with low proportions of CALLA-positive CSF cells (less than 5%) subsequently had normal CSF examinations. We found the use of this rosetting technique valuable in providing information complementary to that obtained from cell morphology alone about the possible malignant nature of small numbers of lymphoblast-like CSF cells seen on cytocentrifuge preparations in children with ALL.

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Dissertations / Theses on the topic "Lymphoblasts"

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Murton, R. A. "Mechanisms associated with ethacrynic acid-induced Na'+, K'+ pump upregulation in Epstein-Barr virus-transformed lymphocytes." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244775.

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Wright, Adrienne M. P. "A role for nucleoside transport processes in the cytotoxicity of 2-chlorodeoxyadenosine in leukemic lymphoblasts from children with acute lymphoblastic leukemia." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23091.pdf.

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Antia, Irina J. "The turnover of sodium/potassium pumps in human lymphocytes during upregulation in response to lithium." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297074.

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Teyssou, Elisa. "Analyses génétiques et fonctionnelles de nouveaux gènes incriminés dans la Sclérose Latérale Amyotrophique (SLA) Genetic analysis of matrin 3 gene in French amyotrophic lateral sclerosis patients and frontotemporal lobar degeneration with amyotrophic lateral sclerosis patients Genetic analysis of CHCHD10 in French familial amyotrophic lateral sclerosis patients." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066738.

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La Sclérose Latérale Amyotrophique (SLA) est une maladie neurodégénérative fatale caractérisée par la dégénérescence des motoneurones centraux et périphériques. Elle est le plus souvent sporadique (SALS, 90% des cas), tandis que les formes familiales (FALS) représentent 10% des patients. Une vingtaine de gènes liés à la SLA ont été identifiés et sont responsables de 70% des FALS et 10% des SALS. Le but de ce projet était d’étudier la contribution de 6 gènes rares dans une large cohorte de patients français atteints de SLA et d’étudier les conséquences fonctionnelles de certains variants identifiés. La première partie de ce projet a consisté à réaliser l’analyse génétique des gènes MATR3, CHCHD10, SS18L1, SQSTM1, UBQLN2 et PFN1. Aucun variant causal ne fut identifié pour les 2 premiers gènes alors que 2 nouveaux variants possiblement pathogènes ont été identifiés dans le gène SS18L1, 4 mutations pour SQSTM1, 5 dans UBQLN2 et 2 mutations déjà répertoriées dans le gène PFN1. Cette analyse génétique a permis de souligner un chevauchement génétique entre SLA et maladie de Paget pour SQSTM1 et entre SLA et Paraplégie Spastique pour UBQLN2. La deuxième partie de ce projet a consisté en l’étude de la pathogénicité de certains variants que nous avons identifiés dans les gènes SQSTM1, UBQLN2 et PFN1, par l’analyse (i) des inclusions dans les tissus post mortem de patients, (ii) de l’expression et de la dégradation protéique dans des lymphoblastes issus de patients SLA et/ou (iii) des conséquences cellulaires après surexpression in vitro et in vivo. Ces analyses ont montré, concernant SQSTM1, qui est impliquée dans la formation des autophagosomes, que les mutations perturbaient l’agrégation protéique, que les mutations dans le gène UBQLN2 altéraient la dégradation lysosomale et la liaison de la protéine avec HSP70 et que celles dans PFN1 dérégulaient la voie de l’autophagie alternative et la mitophagie. Notre travail a permis (i) d’évaluer la contribution chez les patients français atteints de SLA de plusieurs gènes incriminés dans la SLA, (i) d’élargir le spectre génétique commun à la SLA et à d’autres pathologies et (iii) de mettre en avant la pertinence de l’implication des voies de dégradation protéique, notamment l’autophagie, dans la pathogénèse de la maladie
The fatal Amyotrophic Lateral Sclerosis (ALS) motor neuron disease is characterized by the degeneration of upper and lower motor neurons. Most ALS cases are sporadic (SALS) whereas ~10% are familial (FALS). A growing number of genes has been identified in ALS and represent 70% of FALS and 10% of SALS. The aims of this project were to analyze the contribution of 6 rare genes in a large population of French ALS patients and to study the pathogenic impact of some identified variants.The first part of this work was dedicated to the genetic analysis of MATR3, CHCHD10, SS18L1, SQSTM1, UBQLN2 and PFN1 genes. No causing variants were identified for MATR3 and CHCHD10 while 2 new variants, probably pathogenic, were identified for SS18L1, as well as 4 mutations for SQSTM1, 5 for UBQLN2 and 2 already reported mutations for PFN1. These analyses also highlighted a genetic overlap between ALS and other diseases: the Paget disease of bone for SQSTM1 and spastic paraplegia for UBQLN2. The second part of this work was to study the pathogenicity of some of the mutations identified in SQSTM1, UBQLN2 and PFN1 genes using analyses of (i) inclusions in ALS patient post-mortem tissue, (ii) protein expression and degradation pathways in patient lymphoblasts and/or (iii) cellular consequences after in vitro and in vivo overexpression. Our results showed prominent aggregation of mutant SQSTM1 (involved in autophagosomes formation), impaired lysosomal degradation and disrupted protein binding to HSP70 for mutant UBQLN2 and deregulated alternative autophagy and mitophagy pathways for mutant PFN1. Our results (i) precised the contribution of several genes in French ALS patients, (i) documented the genetic overlap between ALS and other diseases and (iii) highlighted the role of protein degradation pathways, especially autophagy, in the pathogenesis of ALS

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Zborovszky, Camila Carolina. "Mitochondrial complex I functionality and protein oxidative damage in lymphoblasts from lithium responsive patients with bipolar disorder, affected and unaffected relatives." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/33274.

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Background: Evidence has demonstrated that mitochondria underline the neurobiology of bipolar disorder (BD). Investigating complex I functionality in transformed lymphoblasts from lithium responsive patients with BD, its relation with increased oxidative damage, and the response to stress induced by low glucose treatment, will aid in the search for peripheral biomarkers for this debilitating disorder. Objective: Confirm the alterations in complex I activity as well as levels of its subunit, NDUFS7, in addition to oxidative damage to mitochondrial proteins, by increased levels of protein carbonyls and 3-nitrotyrosine content, in lymphoblasts . The response to low glucose stress will be evaluated by measuring complex I activity, NDUFS7 levels, and protein oxidative damage. Design: Complex I activity was measured by spectrophotometry and tyrosine-nitration induced damage was assessed using a competitive enzyme immunoassay. Immunoblotting was used to measure NDUFS7 levels and protein carbonyl levels. All assays were carried out in cell pellet fractions, except for complex I activity which was carried out in mitochondrial fractions. Patients: We studied lymphoblasts from patients (14 with BD, and 14 relatives of BD patients affected with a psychiatric illness) and from non-psychiatric comparison controls (N=15) as well as 16 relatives of BD patients unaffected by a psychiatric illness. Results: Our results showed that levels of complex I activity in lymphoblasts differed significantly between the groups, with the lowest values for control subjects, and highest in unaffected and affected relatives, under normal glucose conditions. We did not find significant differences between the groups in NDUFS7, protein carbonyl, and 3-nitrotyrosine levels, nor did we find any correlation between complex I activity and NDUFS7, protein carbonyl, and 3-nitrotyrosine levels, for both treatment conditions (normal and low glucose). Conclusions: These findings suggest an up-regulation of peripheral complex I activity in patients with BD and their relatives, as a potential compensatory mechanism preventing protein oxidative damage induced by complex I dysfunctionality . Future studies, evaluating the potential role of lithium in peripheral cells targeting sites such as complex I, are necessary in order to gain insight into the mechanisms in which cells can prevent the oxidative damage characteristic of the disorder.

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Kuchinskaya, Ekaterina. "Genetic studies of acute lymphoblastic leukemia /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-337-5/.

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Pettit, Andrew I. "Oxygen radical generation by lymphoblast NADPH oxidase in hypertension." Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/29519.

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Objectives. The aim of this thesis was to investigate increased reactive oxygen species production originating from NADPH oxidase in lymphoblasts from hypertensive subjects. Results. Combined intra and extracellular stimulated reactive oxygen species production was increased in hypertensive cell lines. The ROS production was abolished by Diphenyleneiodonium chloride but not by rotenone, indicating that a non-mitochondrial flavoprotein, such as NADPH oxidase, was involved. Analysis of NADPH oxidase subcomponents revealed an increase in p22phox in lymphoblasts from hypertensive subjects, accounting for some of the increased reactive oxygen species production. There was increased basal Tyr/Thr phosphorylation of p44/p42 MAPK in the hypertensive lymphoblasts, but the difference was lost on stimulation. The various kinase inhibitors had no effect on basal reactive oxygen species production. Tyrosine kinase inhibition produced up to 70% reduction in stimulated reactive oxygen species production in both cell lines. Inhibition of p44/p42 MAPK kinase, P13K, and PLA2 produced a small reduction in stimulated ROS production. There was no differential reduction in ROS production from the hypertensive group with these inhibitors, suggesting no role of these pathways in priming of NADPH oxidase. Conclusions. We have shown there is increased reactive oxygen species production in lymphoblasts from hypertensive subjects probably originating from NADPH oxidase. Increased expression of p22phox in hypertension lymphoblasts accounts for approximately a third of the increased reactive oxygen species production. We could not demonstrate tyrosine kinase, p38 MAPK, p44/p42 MAPK, P13K or PLA2 priming of reactive oxygen species production.

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Cartwright, Cher Suzanne. "Thiopurine Metabolism in Childhood Acute Lymphoblastic Leukaemia." Thesis, University of Sheffield, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500442.

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Lo, Tony Chung Tung. "Inactivation of SHIP1 in acute lymphoblastic leukemia." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1465620.

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Thesis (M.S.)--University of California, San Diego, 2009.
Title from first page of PDF file (viewed July 22, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 63-69).

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10

Kay, Gillian. "Characterisation of the lymphoblast β-adrenergic receptor in bipolar depression." Thesis, Imperial College London, 1991. http://hdl.handle.net/10044/1/46859.

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Books on the topic "Lymphoblasts"

1

Vora, Ajay, ed. Childhood Acute Lymphoblastic Leukemia. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-39708-5.

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Kato, Motohiro, ed. Pediatric Acute Lymphoblastic Leukemia. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-0548-5.

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3

Pullarkat, Vinod. Contemporary management of acute lymphoblastic leukemia. New Delhi, India: Jaypee Brothers Medical Publishers (P) Ltd, 2014.

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Vecchione, Severo. Acute lymphoblastic leukemia: Etiology, pathogenesis, and treatments. Hauppauge, N.Y: Nova Science Publishers, 2011.

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5

Secker-Walker, Lorna M. Chromosomes and genes in acute lymphoblastic leukemia. New York: Springer, 1997.

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Saha, Vaskar, and Pamela Kearns. New agents for the treatment of acute lymphoblastic leukemia. New York: Springer, 2011.

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Saha, Vaskar, and Pamela Kearns, eds. New Agents for the Treatment of Acute Lymphoblastic Leukemia. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-8459-3.

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Raybould, Simon. Spatial analysis of acute lymphoblastic leukaemia in Tyne and Wear. Newcastle upon Tyne: University of Newcastle upon Tyne Centre for Urban and Regional Development Studies, 1987.

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Raybould, Simon. Spatial analysis of acute lymphoblastic leukaemia in Tyne and Wear. Newcastle upon Tyne: University of Newcastle upon Tyne Centre for Urban and Regional Development Studies, 1987.

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Peter, Gale Robert, and Hoelzer Dieter, eds. Acute lymphoblastic leukemia: Proceedings of a Wyeth-Ayerst-UCLA Western Workshop--Acute Lymphoblastic Leukemia, held at Tapatio Springs, Texas, November 29-December 2, 1988. New York: Wiley-Liss, 1990.

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Book chapters on the topic "Lymphoblasts"

1

Carson, Dennis A., Carlos J. Carrera, Masaru Kubota, D. Bruce Wasson, and Taizo Iizasa. "Genetic Analysis of Deoxyadenosine Toxicity in Dividing Human Lymphoblasts." In Purine and Pyrimidine Metabolism in Man V, 207–11. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1248-2_31.

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Nuki, G., K. Astrini, D. Brenton, M. Cruikshank, J. Lever, and J. E. Seegmiller. "Purine and Pyrimidine Nucleotides in Some Mutant Human Lymphoblasts." In Ciba Foundation Symposium 48 - Purine and Pyrimidine Metabolism, 127–42. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720301.ch9.

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Schmitt-Gräff, Annette, and Giulio Gabbiani. "Cytoskeletal Organization of Normal and Leukemic Lymphocytes and Lymphoblasts." In Blood Cell Biochemistry, 73–98. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3796-0_3.

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Yamada, Yasukazu, Haruko Goto, and Nobuaki Ogasawara. "Phosphorylation of Purine Deoxynucleosides in Human T- and B-Lymphoblasts." In Purine and Pyrimidine Metabolism in Man V, 531–35. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5104-7_89.

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Vorwerk, P., J. Elsner, K. Mohnike, Y. Oh, R. G. Rosenfeld, and U. Mittler. "Expression of IGFBP-rP2 / CTGF is Specific for Malignant Lymphoblasts of Children with Acute Lymphoblastic Leucemia (ALL)." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 85–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-18156-6_15.

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Boss, Gerry R. "Cobalamin Inactivation Decreases Purine and Methionine Synthesis in Cultured Human Lymphoblasts." In Purine and Pyrimidine Metabolism in Man V, 639–41. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1248-2_99.

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Barankiewicz, J., R. Jimenez, J. Uyesaka, and H. E. Gruber. "Regulation of Adenosine Concentrations by Acadesine (Aica-Riboside) in Human B-Lymphoblasts." In Advances in Experimental Medicine and Biology, 275–78. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-2638-8_62.

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Zhao, Ke-Wei, and Arnold L. Miller. "Purification of the N-Acetylglucosamine-1-Phosphodiester α-N-Acetylglucosamindase from Human Lymphoblasts." In Molecular Mechanisms of Membrane Traffic, 371–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02928-2_76.

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Edwards, N. Lawrence, Annette M. Zaytoun, and Gail A. Renard. "Separate Mechanisms for Cellular uptake of Purine Nucleotides by B- and T-Lymphoblasts." In Purine and Pyrimidine Metabolism in Man V, 463–65. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1248-2_72.

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Pilz, Renate B., and Gerry R. Boss. "The Synthesis of Phosphoribosylpyrophosphate from Glucose Decreases During Amino Acid Starvation of Human Lymphoblasts." In Purine and Pyrimidine Metabolism in Man V, 611–14. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1248-2_95.

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Conference papers on the topic "Lymphoblasts"

1

Gupta, Lalit, Sanjay Jayavanth, and Aruna Ramaiah. "Identification of different types of lymphoblasts in acute lymphoblastic leukemia using relevance vector machines." In 2009 31st Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5334016.

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Gabler, C., T. Hieronymus, N. Blank, M. Schiller, JH Berden, S. Winkler, JR Kalden, and HM Lorenz. "OP0073 Histone release into the cytoplasm of human pbmcs and preapoptotic lymphoblasts." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.1237.

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Rocchi, Emmanuelle, Jean Vigo, Pierre M. Viallet, and Jean-Marie Salmon. "Multiparametric investigations for studying the time-dependence of the effect of Adriamycin on some human leukemic lymphoblasts using multiwavelength videomicrofluorometry." In BiOS Europe '96, edited by Irving J. Bigio, Warren S. Grundfest, Herbert Schneckenburger, Katarina Svanberg, and Pierre M. Viallet. SPIE, 1996. http://dx.doi.org/10.1117/12.260827.

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Leclerc, Gilles M., Guy J. Leclerc, Jeffim N. Kuznetsov, and Julio C. Barredo. "Abstract 2736: PIM2 is up-regulated in response to metformin-induced cell death triggered by ER stress/UPR in ALL lymphoblasts." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2736.

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Safuan, Syadia Nabilah Mohd, Mohd Razali Md Tomari, Wan Nurshazwani Wan Zakaria, Nurmiza Othman, and Nor Surayahani Suriani. "Computer Aided System (CAS) Of Lymphoblast Classification For Acute Lymphoblastic Leukemia (ALL) Detection Using Various Pre-Trained Models." In 2020 IEEE Student Conference on Research and Development (SCOReD). IEEE, 2020. http://dx.doi.org/10.1109/scored50371.2020.9251000.

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Tsomartova, Dibakhan Aslanbekovna, Nataliya Valentinovna Yaglova, and Sergey Stanislavovich Obernikhin. "ALTERED PROLIFERATION OF THYMIC LYMPHOCYTES IN PUBERTAL RATS EXPOSED TO LOW DOSES OF DDT." In International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.14.

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Low-dose developmental exposure to DDT alters proliferative activity of thymic lymphocytes of rats. Higher proliferation rate and low differentiated lymphoblast content are found in rat thymus during puberty.

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Suapang, Piyamas, Kathtaliya Pumjaroen, and Prasong Tosranon. "Segmentation of Acute Lymphoblastic Leukemia." In International Conference on Industrial Application Engineering 2020. The Institute of Industrial Applications Engineers, 2020. http://dx.doi.org/10.12792/iciae2020.021.

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Raasch, S., A. Bronsema, J. Müller, J. Strauss, M. Eschenburg, U. Zur Stadt, I. Vater, R. Siebert, and MA Horstmann. "FOXM1 haploinsufficiency in acute lymphoblastic leukemia." In 30. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch-onkologische Forschung. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1602194.

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Kassani, Sara Hosseinzadeh, Peyman Hosseinzadeh Kassani, Michal J. Wesolowski, Kevin A. Schneider, and Ralph Deters. "A Hybrid Deep Learning Architecture for Leukemic B-lymphoblast Classification." In 2019 International Conference on Information and Communication Technology Convergence (ICTC). IEEE, 2019. http://dx.doi.org/10.1109/ictc46691.2019.8939959.

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Thomas, Blessy, R. Harshitha, and A. Rafega Beham. "A Novel Approach to Detect Acute Lymphoblastic Leukemia." In 2018 3rd IEEE International Conference on Recent Trends in Electronics, Information & Communication Technology (RTEICT). IEEE, 2018. http://dx.doi.org/10.1109/rteict42901.2018.9012461.

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Reports on the topic "Lymphoblasts"

1

Shaw, Collin. Increased Glutathione Metabolic Defense Capabilities in Cultured Alzheimer's Diseased Lymphoblast Cell Lines. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1702.

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Ferrando, Adolfo A. Targeting Class I PI3Ks in the Treatment of T-cell Acute Lymphoblastic Leukemia. Fort Belvoir, VA: Defense Technical Information Center, August 2013. http://dx.doi.org/10.21236/ada591435.

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Brinker, C. Jeffrey, and Mekensey Buley. Identification and display of CRLF2 ligands for targeted nanoparticle delivery to acute lymphoblastic leukemia. Office of Scientific and Technical Information (OSTI), August 2012. http://dx.doi.org/10.2172/1051698.

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Xiang, Qi, and Yuping Zhang. The Influence of pegaspase on coagulation function and remission rate in adult patients with acute lymphoblastic leukemia. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0016.

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Ponvilawan, Ben, Pongthep Vittayawacharin, Pattaraporn Tunsing, and Weerapat Owattanapanich. Efficacy of Targeted Immunotherapy as Induction or Salvage Therapy in Acute Lymphoblastic Leukemia: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0011.

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