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Academic literature on the topic 'T-MDS'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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Journal articles on the topic "T-MDS"

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Yoshimi, Akihide, and Omar Abdel-Wahab. "Splicing factor mutations in MDS RARS and MDS/MPN-RS-T." International Journal of Hematology 105, no. 6 (May 2, 2017): 720–31. http://dx.doi.org/10.1007/s12185-017-2242-0.

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Alvares, Caroline, Sue Ashley, Radovan Saso, Gita Patel, Amrana Qureshi, Michael Potter, Mark Ethell, Jennifer Treleaven, Claire Dearden, and Gareth Morgan. "A Comparative Analysis of Outcomes in Primary Myelodysplastic Syndrome (MDS) and Therapy-Related MDS Reveals Two Subgroups with Differing Risk Profiles: Implications for the Application of a Prognostic Classification." Blood 106, no. 11 (November 16, 2005): 2532. http://dx.doi.org/10.1182/blood.v106.11.2532.2532.

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Abstract Myelodysplastic syndrome is a heterogenous clonal disorder stemming from an insult at the progenitor cell level. The development of an International Prognostic Scoring System (IPSS) based on bone marrow blast percentage, degree of cytopenia and karyotype has allowed the widespread application of the IPSS to guide therapy in patients with MDS. To date, there are no reports distinguishing primary MDS from therapy related MDS (t-MDS) in terms of outcomes within a treatment algorithm. We performed a comparative analysis of patients with primary MDS and t-MDS, to ascertain whether both groups have similar risk profiles and outcomes within a defined treatment protocol. Between 1995 and 2005, 95 patients were diagnosed with MDS at our centre with an average follow-up of 6 years. In total, 50 patients presented in a de novo setting of which 41 received intensive therapy and 9 patients received non-intensive treatment. Of the 45 patients diagnosed with t-MDS, 25 received intensive treatment and 20 patients were managed non-intensively. Therapeutic decisions were based on ECOG performance status and cytogenetic risk group. Demographic analysis of primary and t-MDS patients showed no significant differences when comparing age, sex, degree of presentation cytopenia, or median IPSS score (IPSS 2.0 for primary MDS and 1.5 for t-MDS, p=0.4). In the primary MDS group, 32 patients had an IPSS of ≥1.5 (INT-2/high risk MDS) compared to 27 patients in the t-MDS group. There were 18 patients with primary MDS and 18 patients with t-MDS in the INT-1/low risk category (IPSS ≤1.0). Cytogenetic analysis of primary MDS and t-MDS patients showed a greater frequency of complex karyotypes and chromosome 7 abnormalities in t-MDS patients. A normal karyotype was commoner in the primary group (19:6 patients respectively). The median overall survival (OS) was 25 months for primary MDS patients and 16 months for the t-MDS group (p=0.1). On multivariate analysis, WBC and blast percentage were independent predictors of OS in primary MDS patients (p<0.001, p=0.02). Using a WBC cut-off of 4.0, the median survival was 46 months if WBC <4.0 and 11 months if WBC ≥ 4.0 (p=0.003). IPSS score was not a significant prognostic parameter for this group. In t-MDS patients, Hb, platelets and IPSS score were all independent predictors of OS (p=0.05, p=0.04, p=0.009). WBC was not significant. This group had a median survival of 21 months if IPSS ≤1.0 and 10 months if IPSS >1.0, p=0.02). Remission rates were higher in primary MDS (86%) compared to t-MDS patients (68%) within the intensively treated arm (81% versus 39% for whole group, respectively). However, this did not translate into a better relapse free survival for primary MDS patients (p=0.9). Univariate analysis using binary logistic regression did not identify any factors that predicted response in the primary group. Age was a significant predictive factor for likelihood of response in the t-MDS group (p=0.008). These findings suggest that prognostic systems may need to be refined in MDS for patients presenting with de novo or therapy related disease. Adjustment for performance status may additionally contribute to risk based therapeutic protocols. According to our results, primary MDS may be more chemosensitive than t-MDS but if responses are obtained in t-MDS patients, they are maintained at a similar rate to primary MDS.

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Volpe, Virginia Olivia, Najla Al Ali, Onyee Chan, Eric Padron, David A. Sallman, and Rami S. Komrokji. "SF3B1 Splicing Mutation in the Context of Therapy Related MDS." Blood 136, Supplement 1 (November 5, 2020): 31–32. http://dx.doi.org/10.1182/blood-2020-138833.

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Background: Therapy related myelodysplastic syndromes (t-MDS) account for 10-20% of all myelodysplastic syndromes (MDS). They are associated with poor outcome namely driven by high occurrence of poor risk cytogenetics and TP53 mutations. Acquired SF3B1 splicing mutation is the sole somatic mutation (SM) associated with favorable outcome in de novo MDS and is described among 80% of patients with ring sideroblasts (RS) subytpe. The prognostic value of SF3B1 SM in the context of t-MDS has not been reported. We aimed to compare the outcomes of patients with SF3B1 mutation (mut) between t-MDS and de novo MDS, and the outcome among t-MDS patients harboring SF3B1 mut to those with SF3B1 wild type t-MDS. Patients and Methods: Patients with myelodysplastic syndrome seen at Moffitt Cancer Center between 2013 and 2019 were evaluated and included for analysis. SF3B1 mutational status was assessed via next generation sequencing. We included patients with known SF3B1 status. These patients were further stratified into de novo MDS and those with t-MDS. Further, outcomes of t-MDS patients were evaluated based on SF3B1-mut vs SF3B1-WT. Baseline characteristics were compared by chi square (categorical variables) and t- test (continuous variables). Survival estimates were calculated using the Kaplan-Meier method from date of diagnosis and groups were compared using log-rank test. Multivariate survival analysis performed by means of Cox proportional hazards regression. Results: In a large cohort of patients with myelodysplastic syndrome, 320 patients were identified with SF3B1 SM who were classified as de novo MDS (n=289) and t-MDS (n=31). Baseline characteristics were similar among both groups with t-MDS patients being slightly older and harboring high risk cytogenetics. Mutational distribution was also similar except for CBL which was more observed in t-MDS compared to de novo (10% vs 1%, p-value =.002). AML, transformation rate was 12.5% vs 12.9% for de novo MDS and t-MDS respectively, p-value .943. Median overall survival (OS) in those with de novo MDS SF3B1-mut vs t-MDS SF3B1-mut was 103 months vs 59 months, p-value .001. t-MDS patients were then stratified by wild type SF3B1 (SF3B1-WT) and SF3B1-mut. Of the 272 t-MDS in our database with known SF3B1 status, 31 were SF3B1-mut (11%). Of those with SF3B1-mut, 60% were classified as MDS-RS compared to 4.1% of those SF3B1-wt with t-MDS. Complex cytogenetics were seen in 37.4% vs 10.3% of patients with SF3B1-WT vs SF3B1-mut, p-value .009. TP53 mutation was seen in 36.1% SF3B1-WT vs 10% SF3B1-mut, p-value .004. AML transformation rate was 34.4% in SF3B1-WT compared to 12.9% SF3B1-mut, p-value .016. Median overall survival was17 months in SF3B1-WT vs 43 months in SF3B1-mut, p-value .004. Conclusion: In our study, SF3B1 mutations are more commonly seen in de novo than in therapy related MDS. De novo MDS SF3B1-mut had better outcomes compared to t-MDS SF3B1-mut although rate of AML transformation was similar. In patients with therapy related MDS, those with SF3B1-mut had better outcomes than those with SF3B1-WT. Additionally complex cytogenetics, TP53 mutation, and transformation to AML occurred more with SF3B1-WT than with SF3B1-mut. In the absence of SF3B1 mut, t-MDS with ring sideroblasts has been reported to have higher rate of TP53 mut compared to de novo MDS-RS. To our knowledge, our data is first to suggest that among t-MDS patients, SF3B1-mut may portend a better prognosis. Disclosures Padron: BMS: Research Funding; Novartis: Honoraria; Kura: Research Funding; Incyte: Research Funding. Sallman:Celgene, Jazz Pharma: Research Funding; Agios, Bristol Myers Squibb, Celyad Oncology, Incyte, Intellia Therapeutics, Kite Pharma, Novartis, Syndax: Consultancy. Komrokji:Acceleron: Honoraria; Geron: Honoraria; Agios: Honoraria, Speakers Bureau; AbbVie: Honoraria; JAZZ: Honoraria, Speakers Bureau; Incyte: Honoraria; Novartis: Honoraria; BMS: Honoraria, Speakers Bureau.

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Chakraborty, Sujata, Can-Lan Sun, Liton Francisco, Melanie Sabado, Liang Li, Karen L. Chang, Stephen Forman, Smita Bhatia, and Ravi Bhatia. "Accelerated Telomere Shortening Precedes Development of Therapy-Related Myelodysplasia or Acute Myelogenous Leukemia After Autologous Transplantation for Lymphoma." Journal of Clinical Oncology 27, no. 5 (February 10, 2009): 791–98. http://dx.doi.org/10.1200/jco.2008.17.1033.

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Purpose Therapy-related myelodysplasia or acute myelogenous leukemia (t-MDS/AML) is a lethal complication of autologous hematopoietic stem-cell transplantation (aHCT) for Hodgkin's lymphoma (HL) and non-Hodgkin's lymphoma (NHL). Here, we investigated the hypothesis that accelerated telomere shortening after aHCT could contribute to the development of t-MDS/AML. Patients and Methods A prospective longitudinal cohort was constructed to investigate the sequence of cellular and molecular abnormalities leading to development of t-MDS/AML after aHCT for HL/NHL. This cohort formed the sampling frame for a nested case-control study to compare changes in telomere length in serial blood samples from patients who developed t-MDS/AML with matched controls who did not develop t-MDS/AML. Results An initial increase in telomere length at day 100 after aHCT was followed by an accelerated telomere shortening in t-MDS/AML patients when compared with controls. These telomere alterations preceded the onset of t-MDS and were independent of other known risk factors associated with development of t-MDS/AML on multivariate analysis. Additionally, we observed reduced generation of committed progenitors in patients who developed t-MDS/AML, indicating that these telomere alterations were associated with reduced regenerative capacity of hematopoietic stem cells. Conclusion The development of t-MDS/AML after aHCT is associated with and preceded by markedly altered telomere dynamics in hematopoietic cells. Accelerated telomere loss in patients developing t-MDS/AML may reflect increased clonal proliferation and/or altered telomere regulation in premalignant cells. Genetic instability associated with shortened telomeres may contribute to leukemic transformation in t-MDS/AML.

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A., Arathi C., Puttaraj K. R., and Shobha S. N. "An Association Between Hypoplastic Myelodysplastic Syndrome and T-Prolymphocytic Leukaemia." Journal of Laboratory Physicians 3, no. 01 (January 2011): 049–51. http://dx.doi.org/10.4103/0974-2727.78568.

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ABSTRACTMyelodysplastic syndrome (MDS) represents one of the most challenging health-related problems in the elderly, characterized by dysplastic morphology in the bone marrow in association with ineffective hematopoiesis. Hypoplastic MDS (h-MDS) accounts for 12-17% of all patients with MDS and has yet to be shown to alter the disease course or prognosis. The concept that T-cell-mediated autoimmunity contributes to bone marrow failure in MDS has been widely accepted due to hematologic improvement after immunosuppressive therapy. T-cell expansion is known to occur in these patients, but development of chronic T-cell disorders, especially T-prolymphocytic leukemia (PLL) in a hypocellular MDS is extremely rare, which has an aggressive course. The possible explanation for the association between the two disorders is that T-PLL might arise from a clonally arranged MDS stem cell. We report a unique case of h-MDS with non-progressive pancytopenia and severe hypocellular marrow for 2 years, followed by T-PLL within few months.

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Yucel, Orhan Kemal, Rima M. Saliba, Gabriela Rondon, Sairah Ahmed, Amin M. Alousi, Borje S. Andersson, Qaiser Bashir, et al. "Comparable Outcomes of Therapy-Related and De Novo Myelodysplastic Syndrome after Allogeneic Hematopoietic Stem Cell Transplantation." Blood 128, no. 22 (December 2, 2016): 2276. http://dx.doi.org/10.1182/blood.v128.22.2276.2276.

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Abstract Therapy-related myelodysplastic syndrome (t-MDS) is a well-known complication of conventional chemoradiotherapy used to treat a variety of hematologic malignancies as well as solid tumors. Because of poor prognosis of t-MDS when treated with conventional therapy, allogeneic hematopoietic stem cell transplantation (HSCT) is usually recommended with encouraging results reported. Herein, we retrospectively analyzed outcomes in of 309 adult patients with t-MDS (n =101) and de novo MDS (n=208) receiving allogeneic HSCT from 2005 to 2015 at MD Anderson Cancer Center and compared their outcomes adjusted for disease characteristics. The study cohort had median age of 59 (range, 18-77) at HSCT. Histological subtype at diagnosis was RAEB-1 and -2 in 120 (39%) and CMML in 30 (10%) patients. When cytogenetics were classified by monosomal karyotype (MK) defined by Breems et al., 87 patients (27%) had MK-positive (MKpos), 99 patients (32%) MK-negative (MKneg) and 100 patients (32%) good risk cytogenetics (including normal karyotype (n=88) and del(5q), del(12p), del(20q) (n=12)). Donors were matched related donor (MRD, n=177), matched unrelated donor (MUD, n=114) or haploidentical donor (n=18). Most patients received a myeloablative conditioning regimen (n=181, 59%). Hematopoietic stem cell comorbidity index (HCT-CI) was ≥3 in 144 (47%) patients. Among t-MDS and de novo MDS; median age, donor type and conditioning intensity were not different (Table 1). Compared with de novo MDS, t-MDS patients had more MKpos (20% vs. 46%, p<0.001) less good risk cytogenetics (38% vs. 10%, p<0.001) and more HCT-CI ≥3 (31% vs. 79%, p<0.001). The median time from diagnosis to HSCT was shorter in t-MDS (6 mo. vs. 9 mo., p<0.001). The median follow up of 139 survivors was 37 (range, 3-125) months. Outcome analyses were stratified for t-MDS and de novo MDS patients due to different disease characteristics observed. Univariate analyses showed that MKpos was associated with a poor prognosis for the cumulative incidence of progression both in t-MDS and de novo MDS compared with good cytogenetics (HR=4.3, p=0.05, HR=6.9, p<0.001, respectively) (Figure 1). BM blast count ≥3% at HSCT was also associated with increased incidence of progression in both groups (HR=1.5, p=0.2, HR=1.9, p=0.02, respectively). This enabled us to analyze t-MDS and de novo MDS together for multivariate regressions which revealed that MKpos patients with BM blast count ≥3% had the highest risk for disease progression compared with patients without MKpos and with BM blast count <3% (HR=5.8) (Table 2). Patients with MKpos but with BM blast count <3% also had higher incidence of progression (HR=3.9). The outcomes by risk groups for progression was comparable for t-MDS and de novo MDS (Data not presented). For progression free survival (PFS), univariate analyses revealed that MKpos had poor prognosis for both in t-MDS and de novo MDS compared with good-risk cytogenetics (HR=2.9, p=0.025 and HR=8.4, p<0.001, respectively). MKneg were also associated with inferior PFS compared with good-risk cytogenetics in both t-MDS and de novo MDS (HR=2.1, p=0.1 and HR=2.3, p=0.001, respectively). BM blast count ≥3% also decreased PFS both in t-MDS and de novo MDS for PFS (HR=1.6, p=0.07 and HR=1.8, p=0.004, respectively). When t-MDS and de novo MDS were analyzed together for multivariate regressions, we found that MKpos patients with BM blast count ≥3% had lowest PFS while patients good risk cytogenetics had the best outcomes independent of their BM blast count (Table 2). There was no impact of t-MDS on PFS and similar to progression, the outcomes were not inferior in t-MDS (Data not presented). In conclusion, although t-MDS has been felt to have a relatively poor prognosis after HSCT, our results suggest that t-MDS has comparable outcomes with de novo MDS after allogeneic HSCT when adjusted for disease characteristics. Patients with MKpos in t-MDS and de novo MDS have very high incidence of disease progression and low PFS and represent a target population for innovative transplant strategies. Disclosures Ciurea: Cyto-Sen Therapeutics: Equity Ownership; Spectrum Pharmaceuticals: Other: Advisory Board.

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Singhal, Deepak, L. Amilia Wee, Wendy T. Parker, Sarah Moore, Milena Babic, Jinghua Feng, Andreas W. Schreiber, et al. "The Frequency of Genetic Mutations in T-MN Is High and Comparable to Primary MDS but the Spectrum Is Different." Blood 128, no. 22 (December 2, 2016): 3157. http://dx.doi.org/10.1182/blood.v128.22.3157.3157.

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Abstract Introduction: Therapy-related myeloid neoplasms (T-MN; inclusive of T-MDS and T-AML) are aggressive neoplasms occurring after exposure to chemo (CT) and/or radiotherapy (RT) and are characterized by poor prognosis. Unlike primaryMDS and AML, the mutational architecture of T-MN has not been well elucidated. Most published studies in T-MN are small in size with a restricted panel of genes tested. Here we compare the cytogenetic and mutation profile of T-MN and primary MDS patients from the South Australian Myelodysplastic Syndrome (SA-MDS) registry. Methods: Demographic, clinical and laboratory data including cytogenetic profile of 147 T-MN and 744 primary MDS patients were analysed. Targeted Massively Parallel Sequencing of a custom panel of 27 myeloid genes (all coding regions) was performed on bone marrow samples from 60 T-MN and 142primary MDS patient samples. Results: Median age of T-MN and primary MDS was 71 (20-91) and 73 years (19-98), respectively. In T-MN patients the most frequent primary neoplasms were lymphoproliferative neoplasms (n=56, 38%) and prostate cancer (n=22, 15%). Sixty-three (43%) patients had received CT only, 34 (23%) patients RT only, and 48 (33%) patients had received both CT and RT. The T-MN group consisted of 104 T-MDS (71%) and 43 T-AML (29%). Poor risk cytogenetics were more frequent in T-MN cases following CT than after RT alone, and more frequent than in primary MDS cases (52% vs 25% vs 13%; P<0.0001 Fig 1A). Overall survival (OS) of T-MN cases was shorter than in primary MDS (P=0.001; Fig 1B). Within the T-MN group, T-AML cases had shorter OS than T-MDS cases (14.7 vs 5.0 months, P<0.0001; Fig 1C). Within each International Prognostic Scoring System (IPSS) cytogenetic risk group the T-MN patients had shorter OS than primary MDS patients (Fig 1D). Mutation profiling detected at least one mutation in 117/142(82%) of primary MDS cases (total 324 mutations), similar to previous reports. Contrary to the published literature (42-58%; Shih et al, Haematologica 2013 & Ok CY et al, Leuk Res 2015), a high proportion of T-MN (54/60; 90%) patients showed at least 1 mutation. Notably, 14/15 (93%) of normal karyotype T-MN cases harbored at least one mutation. Although frequency of mutation was similar between T-MN and primary MDS cases, mutation burden and pattern were different (Fig 2). Multiple mutations were detected in 75% of primary MDS compared to 48% of T-MN cases. Mutations in spliceosome complex genes were detected in 44% of primary MDS cases, with SF3B1 being most common, while only 7% of T-MN cases (4/60) harboured these mutations. Mutations in TET2, ASXL1, NOTCH1, and RUNX1 were less frequent in T-MN compared to primary MDS (Fig 2). Mutations in TP53 were detected in 17/60 T-MN cases (28%), were associated with del7q/complex/monosomal karyotypes (15/17; 88%) and with prior CT±RT exposure. We then compared mutation frequency between T-AML and T-MDS cases. The proportion of patients with at least one mutation (89% vs 93%) and the mean number of mutations per case (1.84 vs 1.57) were similar. The genes in which mutations occurred were different: DNMT3A was more frequent in T-AML (36% vs 15%), while NOTCH1 (17%), SF3B1 (7%), and EZH2 (11%) mutations were seen only in T-MDS. Multiple somatic mutations in the same gene were detected in 30% (42/142) and 18% (11/60) of primary MDS and T-MN cases, respectively; most often in TET2, ASXL1, KRAS, NRAS, and TP53. In 41% (13/32) primary MDS and 28% (2/7) of T-MN cases harboring multiple somatic TET2 mutations, the variant allele frequency was similar (40-50%) suggesting biallelic clonal origin. Conclusions: Contrary to published literature, mutation frequency in our study is higher in T-MN and is similar to primary MDS. Though frequency of mutation is similar in T-MN and primary MDS, mutation pattern was different. Unlike primary MDS, mutations in the spliceosome complex were rare in T-MN while TP53 mutations were detected in 28% of T-MN cases. Multiple somatic mutations in the same gene were detected in 30% primary MDS and 18% T-MN cases. In summary, this study highlights differences in cytogenetic and mutation profiling between primary MDS and T-MN, and provides insight into molecular pathogenesis of T-MN. Disclosures Ross: BMS: Honoraria; Novartis Pharmaceuticals: Honoraria, Research Funding.

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Xicoy, Blanca, María-José Jimenez, Olga García, Marisa Calabuig, Rosa Coll, Elisa Orna, María Teresa Cedena, et al. "Comparison of Clinical Characteristics and Prognosis of a Series of Patients from the Spanish Registry of MDS Diagnosed with Myelodysplastic/Myeloproliferative Neoplasms According to the 2016 Reviewed Classification of the World Health Organization." Blood 132, Supplement 1 (November 29, 2018): 3048. http://dx.doi.org/10.1182/blood-2018-99-111883.

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Abstract Background: The 2016 reviewed classification of the World Health Organisation (WHO) defines a group of myelodysplastic/myeloproliferative neoplasms (MDS/MPN) including the chronic myelomonocytic leukemia (CMML), the myelodyplastic syndrome with ring sideroblasts and thrombocytosis (MDS-RS-T) and the MDS/MPN unclassifiable (MDS/MPN-U). The presence of typical clinical characteristics of MDS and MPN hinders the diagnosis and the prognosis of MDS/MPN-U. Aim: The objective of this study was to compare the clinical characteristics and the prognosis of a series of patients with MDS/MPN such as CMML, MDS-RS-T and MDS/NPM-U from the Spanish registry of MDS. Method: We analized 107 patients diagnosed with MDS/MPN (MDS-RS-T, MDS/NPM-U and CMML) according to the 2016 WHO classification. A comparison of the clinical characteristics, overall survival (OS) and cumulative incidence of progression (CIP) was performed. Results: Median (range) age was 74 (23-93) years and 68/107 (64%) were males. The number of patients in each group was: MDS-RS-T (n=45), MDS/MPN-U (n=29) and CMML (n=33). The main clinical characteristics of the three groups are described in Table 1. There were significant statistical differences in hemoglobin and lactate dehydrogenase levels and leukocyte, monocyte and platelet counts between the three groups. With a median (range) of follow-up of 3.1 (0.3-19.3), 3.7(0.7-10.4) and 4 (1.8-8.5) years for MDS-RS-T, MDS/MPN-U, and CMML, respectively, the OS (95%CI) at 5 years was significantly better in patients with MDS-RS-T (61% [42%; 80%]) compared to MDS/MPN-U and CMML patients (21% [1%; 41%] and 19% [3%; 35%], p=0.002) (Figure 1). The CIP (95%CI) at 5 years between the three groups was significantly different: MDS/MPN-U and CMML (40% [18%; 61%] and 32% (14%-52%, respectively) vs. MDS/RS-T 8% [0.4%; 30%]) (p=0.005) (Figure 2). Conclusions: 1) In this series of patients with MDS/MPN (MDS-RS-T, MDS/MPN-U and CMML) according to the 2016 WHO classification clinical characteristics were similar except for hemoglobin and lactate dehydrogenase levels and leukocyte, monocyte and platelet counts. 2) Patients with MDS-RS-T had longer OS and less CIP than those with MDS/MPN-U and CMML; 3) The prognosis of MDS/MPN-U and CMML were similar. Supported by grants from: AGAUR 9015-470120/2015, 2017-SGR288 (GRC), CERCA Program from Generalitat de Catalunya, and "La Caixa" Foundation. Disclosures No relevant conflicts of interest to declare.

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Ayanlar-Batuman, O., J. Shevitz, UC Traub, S. Murphy, and D. Sajewski. "Lymphocyte interleukin 2 production and responsiveness are altered in patients with primary myelodysplastic syndrome." Blood 70, no. 2 (August 1, 1987): 494–500. http://dx.doi.org/10.1182/blood.v70.2.494.494.

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Abstract Immunoregulatory T and B cell functions in 15 patients with primary myelodysplastic syndrome (MDS) were studied by measuring the proliferative and the stimulatory capacity of T and B cells, respectively, in autologous (auto) and allogeneic (allo) mixed lymphocyte reaction (MLR). T cell proliferation in the auto MLR was 25% of the control (P less than .02), whereas proliferation in the allo MLR was normal. When control T cells were stimulated by MDS B cells, their proliferative response was only 57% of the control (P less than .01). The mechanism responsible for these abnormalities was studied by determining the capacity of MDS and normal T cells to produce interleukin 2 (IL 2) and to generate IL 2 receptors (IL 2R) following stimulation with control and MDS B cells. In the auto MLR of MDS patients, only 3% +/- 2% of T cells developed IL 2R positivity, whereas in control cultures 12% +/- 2% of T cells were positive, as determined by immunofluorescence, using a monoclonal antibody (MoAb) directed against the IL 2R, and FACS analysis. When MDS T cells were stimulated by control B cells, IL 2R generation and the production of IL 2 were within normal limits. In contrast, when control T cells were stimulated by MDS B cells or control B cells, the MDS B cells induced production of only 26% of IL 2 as compared with control B cells. In parallel experiments, IL 2R generation in control T cells stimulated by either MDS or control B cells was similar. We conclude that in the primary MDS, T and B cell interactions are impaired. Although MDS T cells develop normal quantities of IL 2R and produce normal amounts of IL 2 when stimulated by control B cells, they are markedly impaired when stimulated by self B cells. Similarly, MDS B cells can induce IL 2R generation in control T cells but not in MDS T cells. Myelodysplastic B cells are also defective in inducing IL 2 production by normal T cells in an allo MLR. These in vitro abnormalities strongly suggest that generation of lymphocytes with immunoregulatory functions is impaired in patients with MDS.

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Ayanlar-Batuman, O., J. Shevitz, UC Traub, S. Murphy, and D. Sajewski. "Lymphocyte interleukin 2 production and responsiveness are altered in patients with primary myelodysplastic syndrome." Blood 70, no. 2 (August 1, 1987): 494–500. http://dx.doi.org/10.1182/blood.v70.2.494.bloodjournal702494.

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Immunoregulatory T and B cell functions in 15 patients with primary myelodysplastic syndrome (MDS) were studied by measuring the proliferative and the stimulatory capacity of T and B cells, respectively, in autologous (auto) and allogeneic (allo) mixed lymphocyte reaction (MLR). T cell proliferation in the auto MLR was 25% of the control (P less than .02), whereas proliferation in the allo MLR was normal. When control T cells were stimulated by MDS B cells, their proliferative response was only 57% of the control (P less than .01). The mechanism responsible for these abnormalities was studied by determining the capacity of MDS and normal T cells to produce interleukin 2 (IL 2) and to generate IL 2 receptors (IL 2R) following stimulation with control and MDS B cells. In the auto MLR of MDS patients, only 3% +/- 2% of T cells developed IL 2R positivity, whereas in control cultures 12% +/- 2% of T cells were positive, as determined by immunofluorescence, using a monoclonal antibody (MoAb) directed against the IL 2R, and FACS analysis. When MDS T cells were stimulated by control B cells, IL 2R generation and the production of IL 2 were within normal limits. In contrast, when control T cells were stimulated by MDS B cells or control B cells, the MDS B cells induced production of only 26% of IL 2 as compared with control B cells. In parallel experiments, IL 2R generation in control T cells stimulated by either MDS or control B cells was similar. We conclude that in the primary MDS, T and B cell interactions are impaired. Although MDS T cells develop normal quantities of IL 2R and produce normal amounts of IL 2 when stimulated by control B cells, they are markedly impaired when stimulated by self B cells. Similarly, MDS B cells can induce IL 2R generation in control T cells but not in MDS T cells. Myelodysplastic B cells are also defective in inducing IL 2 production by normal T cells in an allo MLR. These in vitro abnormalities strongly suggest that generation of lymphocytes with immunoregulatory functions is impaired in patients with MDS.

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Dissertations / Theses on the topic "T-MDS"

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Schaab, Roxana Magdalena [Verfasser], Detlef T. [Akademischer Betreuer] Haase, Silke J. [Gutachter] Pauli, and Margarete [Gutachter] Schön. "Zusammenhänge zwischen TP53-Mutationsstatus, genetischer Instabilität und Prognose bei MDS und sekundärer AML mit komplex aberrantem Karyotyp / Roxana Magdalena Schaab ; Gutachter: Silke J. Pauli, Margarete Schön ; Betreuer: Detlef T. Haase." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2020. http://d-nb.info/1207153478/34.

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Michl, Zbyněk. "T-Mobile MDA II v Linuxu." Master's thesis, Vysoké učení technické v Brně. Fakulta informačních technologií, 2009. http://www.nusl.cz/ntk/nusl-236630.

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MSc. thesis deals with mobile digital assistant T-Mobile MDA II running Linux operating system. The first part presents device identification and parameters' specification of the MDA II. The second part focuses on selection of GNU distribution with Linux bootloader and Linux kernel support comparison. The subject of the last part is MDA II component code implementation and its merging into Linux kernel.

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Qian, Zheng. "Functional analysis of Meq, a Marek's disease virus (MDV)bZIP protein associated with T cell transformation." Case Western Reserve University School of Graduate Studies / OhioLINK, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=case1057671034.

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Eng, Kevin T. "Non-Natural Nucleotides as Modulators of ATPases." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1270568112.

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Centuori, Sara Mozelle. "NEGATIVE REGULATION OF REGULATORY T CELLS BY MYELOID-DERIVED SUPPRESSOR CELLS IN CANCER." Diss., The University of Arizona, 2011. http://hdl.handle.net/10150/145099.

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Myeloid-derived suppressor cells (MDSC) and regulatory T cells (Treg) play an essential role in the immunosuppressive networks that contribute to tumor immune evasion. The mechanisms by which tumors promote the expansion and/or function of these suppressive cells and the cross-regulation between MDSC and Treg remain incompletely defined. The current work evaluates the influence of MDSC, expanded in two mouse cancer models, on immunosuppressive Treg. We demonstrate that tumor-induced MDSC endowed with the potential of suppressing conventional T lymphocytes surprisingly impair TGF-β1-mediated generation of induced Treg (iTreg) from naïve CD4⁺ T lymphocytes. Suppression of iTreg generation by MDSC occurs early in the differentiation process, and is cell contact dependent. This inhibition of FoxP3-expressing T lymphocyte differentiation by MDSC does not depend on arginase 1, cystine/cysteine depletion, iNOS/NO, or PD-1/PD-L1 signaling. These findings therefore indicate that MDSC from tumor-bearing hosts have the heretofore unreported ability to restrict some immunosuppressive Treg subpopulations.

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Basu, Debasmita. "EX VIVO EXPANSION OF TUMOR-SPECIFIC T CELLS WITH SEQUENTIAL COMMON GAMMA CHAIN CYTOKINES RENDER THEM REFRACTORY TO MDSC UPON ADOPTIVE IMMUNOTHERAPY." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2198.

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Myeloid derived suppressor cells (MDSCs) are heterogeneous population of immature cells at various stages of differentiation, characterized by the presence of CD11b and Gr1 in mice. They are major contributors of the tumor-induced immune suppression against the tumors. So far, various strategies have been introduced to overcome the endogenous MDSCs. Most of these approaches rely on the elimination of MDSCs and it is not clear whether tumor-reactive T cells may be differentiated towards phenotypes that are refractory to MDSCc. Our laboratory has previously shown that high affinity T cells derived from tumor-sensitized wild-type FVB mice and expanded ex vivo with the alternating common gamma chain cytokine formulation (initiation of culture with IL-7 + IL-15 followed by one day pulse with IL-2 and continuation of culture with IL-7 + IL-15) can successfully induce tumor regression in FVBN202 transgenic mouse model of breast carcinoma upon adoptive immunotherapy (AIT), only when combined with the depletion of endogenous MDSCs. In this study we have introduced a novel formulation of the sequential common gamma chain cytokines (initiation of culture with IL-7 + IL-15 followed by the expansion with IL-2 until 6 days) for the ex vivo expansion of the autologous and tumor-sensitized low affinity T cells derived from FVBN202 mice and further used for AIT. This novel formulation induced differentiation of tumor-reactive CD8+ T cells mainly towards effector and effector/memory phenotypes that were refractory to MDSCs in vitro and in vivo. AIT by using these T cells induced rejection of primary neu positive tumors and generated long-term memory responses against the recall tumor challenge. Importantly, these T cells also resulted in the inhibition of neu antigen negative relapsed tumor cells. Our findings in the present study provide a platform for AIT of breast cancer patients. .

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Ortiz, Myrna Lillian. "Immature Myeloid Cells Promote Tumor Formation Via Non-Suppressive Mechanism." Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5089.

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ABSTRACT Although there is ample evidence linking chronic inflammation with cancer, the cellular mechanisms involved in early events leading to tumor development remain unclear. Myeloid cells are an intricate part of inflammation. They consist of mature cells represented by macrophages, dendritic cells and granulocytes and a population of Immature Myeloid Cells (IMC), which in healthy individuals are cells in transition to mature cells. There is a substantial expansion of IMC in cancer and many other pathological conditions which is associated with pathologic activation of these cells. As a result, these cells acquire the ability to suppress immune responses and are termed Myeloid-derived Suppressor Cells (MDSCs). Although the role of MDSC in immune suppression in cancer and tumor progression is well established, their contribution to tumor development is still uncertain. The fact that cells with MDSC phenotype and function are observed in chronic inflammation raised the possibility that these cells can contribute to initial stages of tumor development. To address this question, we used an experimental system where the number of IMC was regulated by the expression of S100A9 protein. In this project, we used two different models of chronic inflammation in S100A9 transgenic (S100A9tg) and S100A9 knock-out (S100A9KO) mice. In the first model, we created the conditions for topical accumulation of these cells in the skin in the absence of infection or tissue damage using S100A9tg mice. Accumulation of IMC in the skin resulted in a dramatic increase in the formation of skin tumors during epidermal carcinogenesis. Conversely, lack of myeloid cell accumulation in S100A9KO mice substantially reduced the formation of skin papillomas. The effect of IMC was not associated with immune suppression but with the recruitment of CD4+ T cells mediated by CCL4 chemokine released by activated IMC. Elimination of CD4+ T cells or blockade of CCL4 abrogated the increase in tumor formation caused by myeloid cells. Thus, this study implicates the accumulation of IMC as an initial step in facilitating of tumor formation, which can mediate the recruitment of CD4+ T cells via the release of CCL4 chemokine. In the second model, we used inflammation-associated lung cancer caused by the chemical lung carcinogen urethane in combination with exposure to cigarette smoke referred to throughout as CS. Exposure of mice to CS alone resulted in a significant accumulation of cells with typical MDSC phenotype in different organs; however, these cells lacked immune suppressive activity and could not be defined as bona fide MDSC. When CS was combined with the single dose of urethane, it led to the accumulation of immune suppressive cells. The expansion of MDSC followed the onset of lung tumors development. This suggests that MDSC in this model is not the preceding factor but rather a consequence of tumor formation. Further studies are necessary to determine the relevance of targeting these cells for cancer treatment and prevention.

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Darr, Timothy, Ronald Fernandes, John Hamilton, and Charles Jones. "Verification, Validation and Completeness Support for Metadata Traceability." International Foundation for Telemetering, 2010. http://hdl.handle.net/10150/605983.

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ITC/USA 2010 Conference Proceedings / The Forty-Sixth Annual International Telemetering Conference and Technical Exhibition / October 25-28, 2010 / Town and Country Resort & Convention Center, San Diego, California
The complexity of modern test and evaluation (T&E) processes has resulted in an explosion of the quantity and diversity of metadata used to describe end-to-end T&E processes. Ideally, it would be possible to integrate metadata in such a way that disparate systems can seamlessly access the metadata and easily interoperate with other systems. Unfortunately, there are several barriers to achieving this goal: metadata is often designed for use with specific tools or specific purposes; metadata exists in a variety of formats (legacy, non-legacy, structured and unstructured metadata); and the same information is represented in multiple ways across different metadata formats.

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Lau, Alan. "Molecular cloning of human T-cell leukaemia virus type I (HTLV-I) proteins and the role of HTLV-I infection in multiple drug resistance (MDR)." Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/29746.

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To facilitate the structural and functional analysis of Human T-cell leukaemia virus type-I (HTLV-I) a recombinant proviral expression system was to be employed in which viral protein expression is uncoupled from the inefficient process of infection. Several molecular genomic HTLV-I proviral clones were isolated and used to express viral proteins. However, none of these molecular HTLV-I proviral clones were found to be fully competent for virus expression and did not allow the further development of the expression system. HTLV-I is etiologically linked to a rapidly progressing T-cell malignancy known as adult T-cell leukaemia (ATL) and a degenerative neurological disorder called HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). These diseases are noted for their poor response and high resistance to chemotherapy. Clinical drug resistance has been associated with the overexpression of the mdr-1 gene and its protein product P-glycoprotein (PGP). The presence of multiple drug resistant (MDR) cell phenotypes in peripheral blood mononuclear cells (PMBC) from HTLV-I infected patients was assessed and enchanced mdr-1 mRNA expression and PGP drug efflux activity was observed. MDR phenotypes were found in nine out of ten HTLV-I infected subjects tested. Development of MDR was independent of disease type or status with significant MDR activity being found in ATL, lymphoma type ATL, TSP/HAM and asymptomatic individuals. Furthermore the demonstration of stimulation and trans-activation of the mdr-1 gene suggests potential molecular mechanisms for the development of drug resistant cell phenotypes induced by HTLV-I infection.

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Bondu, Sabrina. "Conséquences fonctionnelles des mutations du gène SF3B1 dans les syndromes myélodysplasiques avec sidéroblastes en couronne A variant erythroferrone induced by clonal erythropoiesis disrupts iron homeostasis in SF3B1-mutated myelodysplastic syndrome High speed of fork progression induces DNA replication stress in SF3B1-mutated erythroblasts." Thesis, Sorbonne Paris Cité, 2019. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2405&f=17384.

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Les syndromes myélodysplasiques (SMD) avec sidéroblastes en couronne (SMD-SC) sont des pathologies clonales de la cellule souche hématopoïétique caractérisées par une érythropoïèse inefficace et une surcharge mitochondriale et systémique en fer. Le gène SF3B1 est muté chez 90% des patients porteurs d’un SMD-SC. Il code pour un facteur d’épissage appartenant au complexe U2 du spliceosome. L’interaction de SF3B1 avec l’intron au niveau du site de branchement permet le recrutement d’U2. SF3B1 s’associe aussi avec la chromatine et sa dynamique de distribution dans le noyau est sous le contrôle de diverses protéines de réparation de l’ADN, telles FANCD2, FANCI, et BRCA1. Les conséquences fonctionnelles des mutations du gène SF3B1 (SF3B1MUT) dans les SMD-SC sont mal connues. Lors de ma thèse, je me suis intéressée aux anomalies d’épissage générées en aval des mutations de SF3B1 dans les cellules des patients porteurs d’un SMD. En accord avec les précédentes analyses de séquençage de l’ARN dans les pathologies SF3B1MUT, les mutations de SF3B1 sont associées à une utilisation préférentielle de sites accepteurs alternatifs dans les cellules mononucléées (CMN) de SMD. Nous avons identifié la surexpression d’un transcrit alternatif de l’érythroferrone (ERFE) dans les CMN et érythroblastes en culture SF3B1MUT. ERFE est une hormone sécrétée par les érythroblastes qui régule l’expression hépatique de l’hepcidine, cette dernière limitant la biodisponibilité du fer dans le plasma. Le transcrit alternatif d’ERFE (ERFE+12) n’est retrouvé que dans les cellules érythroïdes SF3B1MUT et son expression reflète l’érythropoïèse clonale induite par les mutations de SF3B1. ERFE+12 est traduit en un variant protéique fonctionnel. L’augmentation des concentrations des protéines ERFE canonique et alternative dans le plasma des patients SMD SF3B1MUT est corrélée à la diminution des taux d’hepcidine, et explique le développement précoce d’une surcharge systémique en fer. J’ai ensuite caractérisé les processus de réplication et de réparation de l’ADN dans les érythroblastes primaires humains SF3B1MUT et dans la lignée érythroïde murine G1E-ER4 CRISPR-Cas9 Sf3b1K700E. Nos expériences démontrent que les mutations de SF3B1 confèrent un avantage de prolifération aux précurseurs érythroïdes immatures en augmentant leur dynamique de réplication de l’ADN, via l’accélération de la progression des fourches. L’augmentation de la vitesse des fourches de réplication s’accompagne d’une exposition d’ADN simple-brin recouvert par la protéine p-RPA32, mais ne conduit pas à la formation de cassures double-brin de l’ADN. Les mutations de SF3B1 contribuent donc à accroître de façon inadéquate le compartiment des cellules érythroïdes immatures dans la moelle osseuse des patients SMD-SC. Nos prochains travaux viseront à déterminer par quels mécanismes les fourches de réplication sont accélérées, notamment avec l’exploration des intermédiaires de transcription R-loops
Myelodysplastic syndromes with ring sideroblasts (MDS-RS) are clonal hematopoietic stem cell (HSC) disorders characterized by anemia, bone marrow (BM) erythroid dysplasia and systemic iron accumulation. Mitochondrial iron accumulation and apoptosis of mature erythroblasts cause ineffective erythropoiesis. Splicing factor gene SF3B1 is mutated in ~90% of MDS-RS. SF3B1 mediates U2 snRNP recruitment to the branch point (BP) by interacting with the intronic RNA on both sides of the BP. SF3B1 also interacts with nucleosomes located at exonic positions. The nuclear dynamics of SF3B1 is under the control of Fanconi anemia FANCD2 and FANCI proteins, suggesting coordination between DNA repair pathway and cotranscriptional splicing during S phase. In response to DNA damage, the BRCA1/SF3B1 complex facilitates the splicing of DNA repair genes. Functional consequences of SF3B1 mutations in MDS-RS are still unknown. We first assessed the consequences of SF3B1 gene mutations on gene expression and splicing by sequencing the transcriptome of the BM mononuclear cells (MNC). SF3B1 hotspot mutations induce cryptic 3’ splice site selection through use of a different BP, as previous studies in MDS and other SF3B1-driven cancers have already shown. We identified an alternative transcript of erythroferrone (ERFE) in MNC of MDS patients with SF3B1 mutation. ERFE has recently been described as a major erythroid regulator of hepcidin, a key hormone that is involved in the control of iron homeostasis in the body. The expression of the variant ERFE transcript was restricted to SF3B1-mutated erythroblasts and allows the monitoring of clonal erythropoiesis. ERFE neo-isoform (ERFE+12) accounts for an overall increase of ERFE expression in SF3B1MUT MDS. ERFE+12 is translated into a functional variant protein in SF3B1MUT erythroblasts. Plasma concentrations of both canonical and aberrant ERFE proteins are significantly more elevated in SF3B1MUT MDS compared to SF3B1WT MDS and inversely correlated to hepcidin/ferritin ratio. Thus, we identified a SF3B1-dependent and erythroid cell intrinsic mechanism of hyperferritinemia in MDS-RS. We next analysed the DNA replication and DNA repair processes in human SF3B1MUT primary erythroblasts and in murine CRISPR-Cas9 Sf3b1K700E G1E-ER4 proerythroblastic cell line. We confirmed that SF3B1MUT erythroblasts have an increased proliferation rate, but they enter into terminal erythroid differentiation more rapidly than healthy controls or SF3B1WT MDS. We reported an increased DNA replication dynamics, since the rate of DNA fiber elongation is accelerated in Sf3b1K700E G1E-ER4 cells. It has recently been suggested that high speed of fork progression induces DNA replication stress. Consistently, we observed the spontaneous accumulation of single-stranded DNA covered by replication protein A in actively dividing SF3B1MUT proerythroblast and basophilic erythroblasts. No DNA-double strand break and no fork collapse were observed in SF3B1MUT cells. Thus, SF3B1 mutations induce a replication stress without stalling forks and contribute to the development of a clonal erythropoiesis. Mechanistically, we hypothesize that replication forks encounter less obstacles in SF3B1-mutated compared to SF3B1-wildtype erythroblasts. To address this point, we will investigate the presence of R-loops at the promoter regions of selected genes

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Books on the topic "T-MDS"

1

Sarah (Sally) Mary Friend, Robinson T. Savage Jr. and their descendants of Sang Run, MD. Frederick, MD: Emma Gus Press, 2014.

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Carton, James. Haematopathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0015.

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This chapter discusses haematopathology, including iron deficiency anaemia, anaemia of chronic disease, megaloblastic anaemias, hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, thalassaemias, sickle-cell disorders, idiopathic thrombocytopenic purpura (ITP), thrombotic thrombocytopenic purpura (TTP), von Willebrand disease, haemophilia, thrombophilia, acute B-lymphoblastic leukaemia, acute myeloid leukaemias, chronic lymphocytic leukaemia (CLL), chronic myelogenous leukaemia, polycythaemia vera (PV), essential thrombocythaemia (ET), primary myelofibrosis (PMF), myelodysplastic syndromes (MDS), follicular lymphoma, diffuse large B-cell lymphoma, Burkitt’s lymphoma (BL), extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), mantle cell lymphoma, classical Hodgkin’s lymphoma (cHL), lymphoplasmacytic lymphoma (LPL), plasma cell myeloma, primary amyloidosis, and mature T-cell non-Hodgkin’s lymphomas.

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Jaza, Mylia Tiye Mal, and Mary M. Jefferson. The Old Negro and The New Negro by T. LeRoy Jefferson, MD. Xlibris Corporation, 2006.

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Jaza, Mylia Tiye Mal, and Mary M. Jefferson. The Old Negro and The New Negro by T. LeRoy Jefferson, MD. Xlibris Corporation, 2006.

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The Making of a Rescuer: The Inspiring Life of Otto T. Trott, MD, Rescue Doctor & Mountaineer. Victoria, British Columbia, Canada: Trafford Publishing, 2008.

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Breitbart, William, Phyllis Butow, Paul Jacobsen, Wendy Lam, Mark Lazenby, and Matthew Loscalzo, eds. Psycho-Oncology. 4th ed. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190097653.001.0001.

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Psycho-Oncology, 4th edition, follows the publication of Psycho-Oncology, 3rd edition in 2015. This is the latest in the series of textbooks which have defined the field of psycho-oncology. William Breitbart, MD, serves as the new senior editor along with associate editors Phyllis N. Butow, PhD, MPH, of the University of Sydney; Paul B. Jacobsen, PhD, of the U.S. National Cancer Institute; Wendy W. T. Lam, RN, PhD, of the University of Hong Kong; Mark Lazenby, APRN, PhD, of the University of Connecticut School of Nursing; and Matthew J. Loscalzo, MSW, of the City of Hope. In this 4th edition of Psycho-Oncology, we feel we have accomplished the delicate task of having this “Official Textbook of our Field” serve both as the source textbook providing the broadest and most multidisciplinary essential science and practice of the field of psycho-oncology, as well as the newest and latest innovations and cutting-edge research and clinical practice that would equip our readers with the knowledge and resources to participate in the “new frontiers of psycho-oncology.” Several new sections and areas of update include: 1. Evidence-Based Interventions; 2. Digital Health Intervention; 3. Biobehavioral Psycho-Oncology; 4. Geriatric Oncology; 5. Pediatric Psycho-Oncology; 6. Survivorship; 7. Palliative Care and Advanced Planning; 8. Diversities in the Experience of Cancer; 9. Behavioral and Psychological Factors in Cancer Risk; Screening for Cancer in Normal and At-Risk Populations; 10. Screening and Testing for Germ Line and Somatic Mutations; 11. Screening and Assessment in Psychosocial Oncology; 12. Building Supportive Care Teams; 13. Psycho-Oncology in Health Policy.

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International Harvester: Super and Non-Series A, B, C, Mta, H, M, Md, Cub (Prior 1957), Mtad, 4, 6, D6, W6Ta, W6Tad, 9, D9 (I & T Shop Service Manuals). Primedia Business Directories & Books, 1989.

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Edition, Mon Carnet Des Mots de Passe. Mon Carnet de Codes Secrets: Carnet de Mots de Passe - Carnet Pour Conserver Vos Mots de Passe et Identifiants, Email, Questions Secr�tes etc. . + Conseils Pour Votre Mdp - Format A5 15 X 22 Cm X 120 Pages - Cadeau Id�al Pour une T�te en L'air ! Independently Published, 2020.

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Mon Carnet Des Mots de Passe Edition. Carnet de Mots de Passe: Carnet de Mots de Passe - Carnet Pour Conserver Vos Mots de Passe et Identifiants, Email, Questions Secr�tes etc. . + Conseils Pour Votre Mdp - Format A5 15 X 22 Cm X 120 Pages - Cadeau Id�al Pour une T�te en L'air ! Independently Published, 2020.

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Mon Carnet Des Mots de Passe Edition. Putain J'ai Encore Oubli� Mon Mot de Passe: Carnet de Mots de Passe - Carnet Pour Conserver Vos Mots de Passe et Identifiants, Email, Questions Secr�tes etc + Conseils Pour Votre Mdp - Format A5 15x22cm X 120 Pages - Cadeau Id�al Pour une T�te en L'air ! Independently Published, 2020.

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Book chapters on the topic "T-MDS"

1

Mukherjee, Saikat, Soubhik Ghosh, and Arindam Bhattacharyya. "Regulation of T-reg/Th-17 Balance: One Step Closer Towards Immunotherapy Against Malaria Infection." In Plasmodium Species and Drug Resistance [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97045.

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According to World Malaria Report 2020, the rate of decline in malaria case incidence and deaths caused by malaria has ceased in latter half of the past decade. Though Artemisinin Combination Therapy (ACT) is still the major therapeutic approach globally to treat malaria patients, increased resistance of Plasmodium sp. to artemisinin can be looked upon as a major factor responsible for the rate of decline. In the present world, immunotherapeutic approaches are in the limelight to treat several infections, autoimmune disorders, cancers but application of such therapeutic measures in case of malaria are yet not available. Among different immune cells, T-regulatory cells (T-reg) and Th-17 cells and the balance between them, helps in determining the outcome of the immune response in host during both lethal and non-lethal malaria. TGFβ and IL-6 are two major cytokines that play important role in fine tuning the Treg/Th-17 balance by modulating dendritic cell responses, specially by regulating the ratio between myeloid DC and plasmacytoid DC (mDC/pDC). Studies in rodent malaria models have revealed that neutralization of IL-6 by using anti IL-6 monoclonal antibodies in-vivo has been found effective in declining the parasitemia, malaria induced deaths and also in reverting back the altered T-reg/Th-17 balance to normal levels. Apart from these, autophagy is one of the major factors which also contributes to regulate the T-reg/Th-17 balance. In malaria infected mice, autophagy induction has been found to normalise the dysregulated T-reg/Th-17 ratio and promote anti-inflammatory Th-2 pathway by supressing pro-inflammatory Th-1 pathway. So, Treg/Th-17 balance and its associated regulators can be important immunotherapeutic targets for malaria prevention in near future.

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Bruger, Annika M., Christophe Vanhaver, Kirsten Bruderek, Giada Amodio, Ece Tavukçuoğlu, Günes Esendagli, Silvia Gregori, Sven Brandau, and Pierre van der Bruggen. "Protocol to assess the suppression of T-cell proliferation by human MDSC." In Methods in Enzymology, 155–92. Elsevier, 2020. http://dx.doi.org/10.1016/bs.mie.2019.05.046.

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Sutter, DMD, Ben A. "Complex Medical Diagnoses With an Underlying Dental Etiology." In Advances in Medical Technologies and Clinical Practice, 1243–315. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-5225-9254-9.ch018.

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The aim of this chapter is to present a series of chronic pain clinical cases that were originally diagnosed by non-dental healthcare professionals, as being something other than temporomandibular disorders (TMD). Specifically, the individual patient diagnoses were Phantom Bite Syndrome (PB), Meniere's Disease (MD), Cervical Dystonia (CD), and Trigeminal Neuralgia (TN), where the prior treatments rendered to each patient that were based upon these diagnoses, were all unsuccessful. Each patient was then re-evaluated with a series of biometric occlusal measurement technologies, which included the T-Scan 9/BioEMG III synchronization module. This two-function synchronized system was utilized in the re-diagnosis of each patient, as well as during their rendered occlusal treatment, in evaluating the accuracy of the treatment results, and during each patient's post-treatment maintenance. The four patients were treated with disclusion time reduction (DTR), after which each patient's symptoms either greatly improved, or resolved completely. The observations made in this chapter are highly suggestive that TMD can present as one of these alternative diagnoses, or that TMD was their original problem condition that was misdiagnosed, absent the objective occlusal force and timing data offered by the T-Scan 9 system.

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Rene, Eldon R., Shishir Kumar Behera, and Hung Suck Park. "Predicting Adsorption Behavior in Engineered Floodplain Filtration System Using Backpropagation Neural Networks." In Machine Learning Algorithms for Problem Solving in Computational Applications, 179–94. IGI Global, 2012. http://dx.doi.org/10.4018/978-1-4666-1833-6.ch011.

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Engineered floodplain filtration (EFF) system is an eco-friendly low-cost water treatment process wherein water contaminants can be removed, by adsorption and-or degraded by microorganisms, as the infiltrating water moves from the wastewater treatment plants to the rivers. An artificial neural network (ANN) based approach was used in this study to approximate and interpret the complex input/output relationships, essentially to understand the breakthrough times in EFF. The input parameters to the ANN model were inlet concentration of a pharmaceutical, ibuprofen (ppm) and flow rate (md– 1), and the output parameters were six concentration-time pairs (C, t). These C, t pairs were the times in the breakthrough profile, when 1%, 5%, 25%, 50%, 75%, and 95% of the pollutant was present at the outlet of the system. The most dependable condition for the network was selected by a trial and error approach and by estimating the determination coefficient (R2) value (>0.99) achieved during prediction of the testing set. The proposed ANN model for EFF operation could be used as a potential alternative for knowledge-based models through proper training and testing of variables.

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Marongwe, Ngonidzashe, and Peter Makaye. "Violence and the Politics of the Movement for Democratic Change-Tsvangirai’s (MDC-T) Mobilisation and Continued Survival, 1999-2014." In Myths of Peace and Democracy? Towards Building Pillars of Hope, Unity and Transformation in Africa, 167–94. Langaa RPCIG, 2016. http://dx.doi.org/10.2307/j.ctvk3gm8z.8.

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"Introduction." In Psycho-Oncology, edited by William S. Breitbart, 1–4. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190097653.003.0001.

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Psycho-Oncology, 4th edition, is the first edition of this series of textbooks, which have defined the field of psycho-oncology, to be edited without Jimmie C. Holland as the senior editor. Hence, those of us who have taken on the both sacred and significant responsibility of editing this 4th edition of Psycho-Oncology have done so with a sense of both sadness and honor. William Breitbart, MD, serves as the new senior editor along with associate editors Phyllis N. Butow, PhD, MPH, of the University of Sydney; Paul B. Jacobsen, PhD, of the U.S. National Cancer Institute; Wendy W. T. Lam, RN, PhD, of the University of Hong Kong; Mark Lazenby, APRN, PhD, of the University of Connecticut School of Nursing; and Matthew J. Loscalzo, MSW, of the City of Hope. In this 4th edition of Psycho-Oncology, we feel we have accomplished the delicate but critical task of balancing the tasks of having this ‘Official Textbook of our Field” to serve both as the source textbook that provided the broadest and most multidisciplinary and essential science and practice of the field of psycho-oncology, as well as the newest and latest innovations and cutting-edge research and clinical practice that would equip our readers with the knowledge and resources to participate in the “new frontiers of psycho-oncology.”

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Chirisa, Innocent, Elmond Bandauko, Gladys Mandisvika, Aaron Maphosa, and Liaison Mukarwi. "Whose City Is It Anyway?" In Advances in Hospitality, Tourism, and the Services Industry, 182–98. IGI Global, 2017. http://dx.doi.org/10.4018/978-1-5225-0576-1.ch009.

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The purpose of this chapter is describe why and how a multiplicity of especially diverging forces, ‘voices' and rationalities can work against effective place branding. Specifically, it aims to demonstrate by the case of Harare, the capital city of Zimbabwe, that economic hardships are the major place shaper rather than the wishes and marketing strategies that may be put in place by the state. An ailing economy will naturally see the terrain and fabric of a place, in this case, a city deteriorating both in terms of its service performance and in terms of outlook. This is in contrast with the main urban planning philosophies of order, amenity, functionality, aesthetics and convenience. The post-colonial Harare has suffered major blows of trying to retain its vividness and functionality due to a number of forces including state control and interference, the consistently perturbed political economy that explains rising retrenchments, unemployment and underemployment, which has seen the ushering in of rampant informality. Both the state and the non-state actors, including politicians and households have laid claim on the affairs of the city without approaching the same with a sense of place stewardship. Proper city branding presupposes shared visioning and moving on an agreed path and trajectory. However, characteristic of Harare is disparate and fragmented efforts, most of which work against the cause of city branding. Street vending, of late, is the major cancer haemorrhaging the city fabric and outlook. Even the politicians, who have assumed a major seat in the decision-making of the affairs of the city, seem not to agree on the way forward. Although, the city is under the leadership of the opposition – MDC-T councilors, their role has not been subsumed, within the council chambers as one that matters. The councilors have largely been silenced, if not technically, co-opted. The role of physical planning, on the other side of the story, has become increasingly nullified. Some real estate investors are considering reducing their portfolios. The dramatis personæ and the effects it is inflicting on the ground needs adequate scholarly interrogation hence the line of the argument in this paper: Whose city is it anyway? Unless, the city is seen as a collective responsibility), efforts to brand will simply prove futile and a waste of time. Overall, there is an economy that needs first to be fixed and players that need aligning their inspirations, aspirations and actions for achieving a branded city. Planning has to be given its place because it provides a solid foundation upon which actions are built.

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"h it Drought igohccausrsw in el v is i rt a normal l as ulao ll wya ra ll i , re ncfla im curring featur ll a a ti rcearse . g I im t e is s . e I of climate; severity levels) and the vulnerability of society to the aberration, atteom cc puorrsariyniesveanrt. esTuh lt e o na fttuhrealoecvceunrtre (i n .e c . e , m of etpeeorrsoilso te g n ic tallad rg ro e-usgch al t e ) m rai annfe al nltafreeaatsu in r contr . Meaonfythpe ast to eocp li lmeaatseara id nid ty , i s which is sociate th re estorc ic ctuerdtao per disruptions in the global circulation pattern of the dr rence lo owftah tm er oesp is helrie td . e E , xipfoasnuy re th tiongd , ro th uagthtwvearc ie asnsd pa o t ia to ll yaa lt nedrm Pl oaoiurngs ht wedo if f f ic N ith most of Auo lt rythv is A ua m li esri ic f a ri , caa , nIdn ng droug d A ia u , s C tra h l ina, ht in So ia u ; th tthheey Great drought occurrence. Vulnerability, on the other hand, B east A ha si vae , d is e m de otgerrampihniecd ch bayrascotceira is l ti fcasc , to treschsnuoclhogays , ppoop li u cy la , ti aonnd , rTerhgaizo il, wes is nfsacpt erc tern Euro em e p iv heads is beyspme, anoyrttohehae both the vaes te arsn Uni region uarlplauns te odfS tates, social behaviour. These factors change over time, and nature of d re w la attievre . r th es upsonvsue ln teoratbhielsie ty c h is a n li gkeesl . yStuobs increase or decrease in cussed in mdo ro re ugdh et t a , il a la cthearriancttehriisstc ic hatph te art . will be dis isdaemne ti c re agl io in n w in il tlenhsaiv ty e , did ff uerraetn io tneefqfu ec etnst , d ev ro eungihfttshe in ytahree in D th reouagm ht oiusn th teocfonpsreeqcu ip ein ta cteioonfarencae tu iv readl re odvuecrt io anntcehra is ntg ic esd , because societal char , acatned ri st sipcas tia w l il c l ha hraavce leexntg en th d , e d al tpheoru io gdhoofth ti emrec , li u m su a a ti l c ly faacs to erasso ( nsuocrhm as orheigihnvdu is lcnuesrsab . th ilHe it ow sye to ev ac derro , umg uch can be d tions fhrto , m an mdasnuybs one reeqgue to ntlecshsaepnt societal te ional and edrisscw ip il l w ar mepoefr te a n tures, high winds, and low relative humidity) linary perspectives. th oerledv and a c ss aoncisaitgendi fi w ca it nht ly it aigngrm av aantyertehgeiosnesveo ri f ty thoeftphre in criapeanlt. Dr iny sseeaassoonugohfto is c als on, occu c r ur o re rneclea , teddeltaoysthienttihmeinsg ta r ( t i. e o ., f Because drought affects so many economic and social p th ri encriapianlsc ( rio . p e. , grroaw in tfh al lstraegnecse ) aonf rains in relation to intensity d , n the effectiveness of a se vca to ri rest , yscoofreds is coifpld in ef eisn . it Iinonasdhda it vieonb , ebeencaduesveeldorpoeudgbhyte cl viemna ts ti ) c . T ch haursa , c te eraicsh ti cs d ro aungdhtimypeaacruimsbuenr iq oufe ra iinn fa it lsltohcecug rs lo w be it , h in vaa ry l ing frequency in nearly all regions of Magalhaes ts. For example, developed and ltdyepvees lo opfinegc on coomuinctrs ie yss tem al s i , kea , ndth in e y cl eiam rs attihcadt if ofeetreanl. c e ( s19b8e8 tw ) eheanvef iv v e iv c id olnysp ec o u in ti tveeddoruotug th heta id peporlooagcihceasltdaik ff eenretnoce define it also reflect regional and and ccurred in northe s (Wilhite 1992). Impacts also timin 1g9o8f3r , ai nno fa ti lnlg an d th iemcpraic ti tcsaalstliB nk ra azgielsb . ebtew tw ee enen19t7h9esdo if cfieert al spcaotn ia tlelxytaonfdd ro te umgphot. raA ll y u , ni dveep rs eanldd in e g fi ni o ti nonthoef dur D at riooung , hitntseenvse it r y it , y a is nddegpeeongdreanpthin ca olto ex nl t y en tonof the dGrloaung tz h t ( 1i9s 85 an ) cuonnrcelau listic expectation. Wilhite and specific dro a should reflect a regio dneadltbhia as tdse in fi cnei ti w on at serofsudp ro p u ly g h is twmaatdeerbsyuphpu li m ug ahnt ac etp iv is i o ti d es e , anbdutveag ls e o ta t o io nntohneadreem gi aonnd ’ s s larg D el eyfianiftu io nncst io onfdorfocu li gmhat ti ccan re gbiemcea . tegorised broadly wi es. The soc th ie ty it , s ec f o ar n -o re mayc , hianngcdhiaem ra pca te crtiss , t ic msao ke fdirtos ug ef hfte , ctaslo nviron onngaGs la enittzh er 19c8o5n ). c ep Ctoun al c ep otruaol pe dreaftiinoin ti aolns ( W ar i e lh it oefatnhde not M im an pyo ss piebo le p , letociodn en si t d if eyradnrdomq ent uugahntt if dty if o . ficult, though dictionary t be largely atdheesccro ip ntc io enptyopfe , d generally defining of th ro e ug p h he t, naonmdetnhouns . the boundarie a F re orgeenxearm ic pilne , thseo ir frneaatlu it rya , l or the compone dnrpohu ysical t. Tghhet ri h ev as e nt b . oFtihg ur ae1n .3 atiu ll ruasl tra atn es d th saotc , iianlE 19 n 9 cy 6 c ) lo dpeefd in ia e sk associated wsodfroCulg im ht a te as a ‘a nndeW xt eeantdheedrp (S e c ri hondei -d er atrh eg e io enveinsta ( p i. reo ., dupc ro tboafbb il o it tyho th feoc re i g th iodnr ’ osuegxhptos fo urrean to yrseelaasto iv n e , taoytehaer , stoar ti sste ic vaelramluyletairysea -r omfedaenfifcoirenatre ra giinofn all currence at various These types of definitions are useful for furthering ’." In Droughts, 38–39. Routledge, 2016. http://dx.doi.org/10.4324/9781315830896-27.

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Conference papers on the topic "T-MDS"

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Xu, Jingke, Yaqian Zhang, and Zhifang Zhang. "A Capacity-Achieving T-PIR Scheme Based On MDS Array Codes." In 2019 IEEE International Symposium on Information Theory (ISIT). IEEE, 2019. http://dx.doi.org/10.1109/isit.2019.8849312.

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Sakib, Shadman, Md Abu Bakr Siddique, and Md Abdur Rahman. "Performance Evaluation of t-SNE and MDS Dimensionality Reduction Techniques with KNN, ENN and SVM Classifiers." In 2020 IEEE Region 10 Symposium (TENSYMP). IEEE, 2020. http://dx.doi.org/10.1109/tensymp50017.2020.9230983.

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Mousazadeh, Saman, and Mahmood Karimi. "Parameter Estimation for Student-t ARCH Model using MDL Criterion." In 2007 IEEE International Conference on Signal Processing and Communications. IEEE, 2007. http://dx.doi.org/10.1109/icspc.2007.4728379.

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Reguant, Victor Domingo, Francesc Enrich Prats, Ramon Martin de Pozuelo, Francesc Pinyol Margalef, and Gabriel Fernandez Ubiergo. "Delivery of H264 SVC/MDC streams over wimax and DVB-T networks." In 2008 IEEE International Symposium on Consumer Electronics - (ISCE 2008). IEEE, 2008. http://dx.doi.org/10.1109/isce.2008.4559440.

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Raber, Patrick, Rosa A. Sierra, Shuzhong Zhang, Paul Thevenot, and Paulo C. Rodriguez. "Abstract LB-077: T cells conditioned with MDSC show an increased anti-tumor activity after adoptive T cell based immunotherapy." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-lb-077.

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Zeng, Qi, Jesse R. Qualliotine, Lee Blosser, Drew Pardoll, and Young J. Kim. "Abstract 3250: Caspase-1 from MDSC promote MyD88 dependent carcinogenesis that is T-cell independent." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3250.

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Park, Cheon Ho, Sang Soon Byun, Jin Yong An, Sun Hyung Ha, Hye Rim Han, Nu Ri Kang, Beom Yong Park, et al. "Abstract 1626: PMC309, a highly selective anti-VISTA antibody enhances T cell activation through blocking the interaction of T cells and myeloid derived suppressor cells (MDSC)." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1626.

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Eckard, Sterling, Aurelien Sarde, Li Mei, Curtis Ruegg, Patrick Chun, and Victoria Smith. "Abstract 528: MDSC suppress the T cell repertoire and contribute to a pathologic cytokine milieu in cancer patients." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-528.

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Retseck, Janet, Amanda Gillespie-Twardy, Alexis Nasr, Hui-Min Lin, Yan Lin, John Kirkwood, Lisa H. Butterfield, Haris Zahoor, Cindy Sander, and Ahmad A. Tarhini. "Abstract 4302: Long term monitoring of circulating regulatory T cells (Treg), myeloid derived suppressor cella (MDSC) and type I effector T cells in melanoma patients treated with neoadjuvant ipilimumab." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4302.

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Ulutin, O. N., G. Cizmeci, U. Cornelli, and J. Fareed. "CLINICAL AND LABORATORY STUDIES ON THE EFFECTIVENESS OF DEFIBROTIDE IN PERIPHERAL VASCULAR DISEASE OF ATHEROSCLEROTIC ORIGIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643148.

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Defibrotide is a derivative of polydeoxyribonucleotide extracted from bovine lung which has been found to produce profound activation of endothelial cells as evidenced by the increase of tissue plasminogen activator (t-PA) and prostacyclin levels in animal models. Administration of a 600 mg dose daily for six weeks to patients with peripheral obliterative diseases resulted in significant clinical improvements in post-treatment exercise tests and radionuclide arteriography. Results were consistent with improvements in the circulation. Ex vivo blood analysis showed marked increases in the production of t-PA and prostacyclin levels. Other laboratory tests were also suggestive of activated endothelial states. Platelet C-AMP levels were increased, whereas MDA and TXB2 levels were reduced. No systemic anticoagulation was observed in terms of alterations of the global coagulant tests (PT, APTT, etc.). These studies suggest that Defibrotide mainly acts via the modulation of the endothelial function and acts in a novel fashion in contrast to other drugs used in this area.

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Reports on the topic "T-MDS"

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Johnson, S. Single Manager Responsibility for Joint Service Military Diving Technology and Training (MDT&T),. Fort Belvoir, VA: Defense Technical Information Center, July 1996. http://dx.doi.org/10.21236/ada316548.

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