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Journal articles on the topic 'The CMR'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 February 2022

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1

Reiter, Andreas, Gunay Ahmadova, Mohamad Jawhar, Andres Virchis, Tim Somervaille, Mark Williams, Bernd Schönberger, et al. "Clinical Characteristics and Treatment with Various Tyrosine Kinase Inhibitors in Patients with ETV6-ABL1 positive Eosinophilia-Associated Myeloproliferative Neoplasms." Blood 128, no. 22 (December 2, 2016): 3114. http://dx.doi.org/10.1182/blood.v128.22.3114.3114.

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Abstract The ETV6-ABL1 fusion gene, as consequence of a t(9;12)(q34;p13), is a rare but recurrent genetic aberration found in chronic or blast phase of eosinophilia-associated myeloproliferative neoplasms (MPN-eo) and de novo acute B-cell lymphoblastic leukemias (B-ALL) or lymphoblastic T-cell lymphomas (T-LBL). Here, we sought to evaluate a) relevant clinical characteristics, b) treatment options and c) survival in 7 ETV6-ABL1 positive patients (male, n=4; median age 46 years; range 20-61). Cytogenetic analyses revealed a conventional reciprocal translocation t(9;12)(q34;p13) in 3 cases, an ins(12;9)(p13;q34q22) and a normal karyotype in one patient each, and a complex karyotype in 2 patients. In all cases, ETV6-ABL1 was confirmed by FISH analysis and/or RT-PCR. Histopathological diagnoses of the hypercellular bone marrow (BM) included atypical chronic myeloid leukemia (n=3), MPN-eo (n=3, concomitant T-LBL in one patient) or chronic myelomonocytic leukemia (n=1). In peripheral blood, all patients presented with left shifted leukocytosis (median 84 x 109/l, range 21-143) and significant (>1.5 x 109/l) eosinophilia (median 6.1 x 109/l, range 2.0-7.1) but without increased blast cells. Splenomegaly was present in 60% of patients. After a median of 3 months (range 0-6) from diagnosis, all patients were treated with a TKI (imatinib, n=5; dasatinib, n=1; nilotinib, n=1) at standard doses. On dasatinib (#2) or nilotinib (#3), 2 patients achieved a complete hematologic remission (CHR) within 3 months and complete cytogenetic remission (CCR) after 5 months (#3) or complete molecular remission (CMR) after 18 months (#2), respectively (Figure). On imatinib (n=5), 2 of 5 patients (#4 and #5) achieved a CHR within 3 months with loss of CHR after 9 (#4) and 5 months (#5), respectively. Patient #4 developed a myeloid sarcoma. After local radiation, he received an allogeneic stem cell transplant (SCT) but died 8 months later due to GvHD while in CMR. Patient #5 switched to nilotinib and achieved a CCR and CMR after 3 and 10 months, respectively. Patient #1 has not achieved a significant response after 4 months on imatinib. Patient #6 showed progressive disease within 2 months on imatinib, but achieved a rapid CHR and durable CCR and CMR on dasatinib after 13 and 14 months, respectively. Patient #7 presented with a classical myeloid/lymphoid (T-LBL) neoplasm with eosinophilia (MLN-eo) according to the WHO classification. On imatinib, a regression of lymphadenopathy, but persistence of leukocytosis and eosinophilia was observed. With increasing leukocytosis and reappearance of lymphadenopathy, the patient was switched to dasatinib (9 months), followed by nilotinib (2 months). The responses were only partial and transient and the patient died 23 months after diagnosis with myeloid blast phase (secondary acute myeloid leukemia). Overall, after a median treatment time of 22 months (range, 3-58), 4 patients are in CCR (n=1, patient #3) or CMR (n=3; patients #2, #5, #6) while on a second generation TKI and two patients (#4, #7) have died. On imatinib, none of 5 patients achieved a CCR or CMR. We conclude that a) cytogenetic analysis is an important tool for the identification of potential TK fusion genes such as ETV6-ABL1, b) ETV6-ABL1 is a candidate for incorporation into the WHO-defined subcategory ´MLN-eo´, c) patients with MPN-eo can achieve durable CHR, CCR or CMR on TKI with second generation TKI being more effective than imatinib d) close monitoring by cytogenetics, FISH and RT-PCR is recommended for early identification of inadequate response or resistance. Figure (A) responses and (B) overall survival in 7 patients with ETV6-ABL1 positive MPN-eo treated with various tyrosine kinase inhibitors.Abbreviation, CHR:complete hematologic response; CCR: complete cytogenetic response; CMR: complete molecular response; CP: chronic phase; BP: blast phase; allo SCT: allogeneic stem cell transplantation. Figure. (A) responses and (B) overall survival in 7 patients with ETV6-ABL1 positive MPN-eo treated with various tyrosine kinase inhibitors.Abbreviation, CHR:complete hematologic response; CCR: complete cytogenetic response; CMR: complete molecular response; CP: chronic phase; BP: blast phase; allo SCT: allogeneic stem cell transplantation. Disclosures Somervaille: Novartis: Consultancy, Honoraria; Imago Biosciences: Consultancy. Haferlach:MLL Munich Leukemia Laboratory: Employment, Equity Ownership.
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2

Proszkowiec-Weglarz, Monika, and Tom E. Porter. "Functional characterization of chicken glucocorticoid and mineralocorticoid receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 5 (May 2010): R1257—R1268. http://dx.doi.org/10.1152/ajpregu.00805.2009.

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Glucocorticoid (GR) and mineralocorticoid (MR) receptors are ligand-activated transcription factors that belong to the nuclear hormone receptor superfamily. Little is known about the function of GR and MR in avian species. Recently, the chicken homologue of the GR (cGR) gene was cloned, and its tissue-specific expression was characterized, whereas the full-length sequence of the chicken MR (cMR) gene remains unknown. Therefore, the aims of this project were to clone the full-length cMR and to functionally characterize both chicken receptors. Cos-7 cells were transiently transfected with cGR or cMR expression vectors along with a glucocorticoid response element-luciferase (GRE-Luc) reporter construct. Transfected cells were then treated with increasing doses of corticosterone (CORT) or aldosterone (ALDO) alone and with GR or MR antagonists (ZK98299 and spironolactone, respectively). Transactivation of cGR or cMR was evaluated by luciferase assay. CORT and ALDO induced cGR- and cMR-driven transcriptional activity in a dose-dependent manner. Each receptor responded to both steroids, but cMR transcriptional activity was induced by lower levels of CORT and ALDO than cGR. Coexpression of both chicken corticosteroid receptors in Cos-7 cells had no synergistic or additive effect on CORT- or ALDO-induced transcriptional activity. Corticosteroid-dependent transactivation of cGR and cMR was partially blocked by antagonists. ZK98299 showed high specificity to cGR, while spironolactone had agonist properties toward both receptors. Immunocytochemistry was used to assess the cellular localization of both receptors. Corticosteroids induced translocation of both receptors into the nucleus. The functional properties of cGR and cMR determined in this study will be helpful in defining the physiological roles of GR and MR in avian species.
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3

Abdelaziz, Hanaa MM, Ahmed M. Tawfik, Ayman A. Abd-Elsamad, Sherif A. Sakr, and Abdulsalam M. Algamal. "Cardiac magnetic resonance imaging for assessment of mitral stenosis before and after percutaneous balloon valvuloplasty in comparison to two- and three-dimensional echocardiography." Acta Radiologica 61, no. 9 (January 14, 2020): 1176–85. http://dx.doi.org/10.1177/0284185119897368.

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Background The experience with cardiac magnetic resonance (CMR) in mitral stenosis (MS) is limited in contrast to mitral regurgitation. Purpose To compare CMR versus 2D and 3D transthoracic (TTE) and 3D transesophgeal (TEE) echocardiography in assessment of rheumatic MS before and after percutaneous balloon mitral valvuloplasty (PBMV). Material and Methods Twenty consecutive symptomatic patients with MS were evaluated prospectively and independently by CMR, TTE, and TEE pre-PBMV, and by CMR and TTE post-PBMV. Mitral valve area (MVA) was assessed by CMR planimetry, TTE and TEE planimetry, and pressure half time (PHT). Further assessment included trans-mitral velocity, mitral regurgitation (MR), and left atrial (LA) volume. Results PBMV was successful in 18 patients and failed in two patients (one with MVA <1.5 cm2, one developed severe MR). Pre-PBMV and MVA by CMR, 2D TTE, biplane, 3D TTE, 3D TEE, and PHT were 1.16, 1.16, 1.10, 1.02, 1.05, and 0.99 cm2, respectively. Post-PBMV, a significant increase in MVA was observed (2.15, 2.06, 2.07, 2.04, and 2.03 cm2, respectively). High agreement was observed between CMR and echocardiography before and after PBMV, except for PHT method. CMR significantly underestimated trans-mitral velocity and gradients compared to echocardiography (P<0.001). Before PBMV, mild MR was observed in 11, 12, and 19 patients by 2D TTE, 3D TTE, and CMR. After PBMV, MR was observed in all patients (19 mild, one severe) by all modalities. Echocardiography significantly underestimated LA volume compared to CMR (P<0.001). LA volume decreased significantly after PBMV (P<0.001). Conclusion CMR provides comprehensive assessment of several parameters in MS patients before and after intervention. Agreement with echocardiography is acceptable.
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Chiaretti, Sabina, Antonella Vitale, Loredana Elia, Anna Lucia Fedullo, Silvana Albino, Alfonso Piciocchi, Paola Fazi, et al. "Multicenter Total Therapy Gimema LAL 1509 Protocol for De Novo Adult Ph+ Acute Lymphoblastic Leukemia (ALL) Patients. Updated Results and Refined Genetic-Based Prognostic Stratification." Blood 126, no. 23 (December 3, 2015): 81. http://dx.doi.org/10.1182/blood.v126.23.81.81.

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Abstract Introduction: Management of Ph+ ALL has changed since the introduction of tyrosine kinase inhibitors (TKI). We previously reported the preliminary findings of the GIMEMA LAL 1509 total therapy protocol, based on dasatinib plus steroids administration as induction therapy (Chiaretti et al, ASH 2014). The updated results on overall survival (OS), disease-free survival (DFS) and the impact of a genetic-based prognostic stratification are hereby provided. Methods: Steroids were administered from day -6 to day 31. Dasatinib (140 mg/day) was given between days 1 and 84. Patients reaching a complete molecular response (CMR, i.e. BCR/ABL1 to ABL1 ratio=0) at the end of induction (day 85) continued Dasatinib. Patients in complete hematologic remission (CHR), but not in CMR, underwent chemotherapy (clofarabine-cyclophosphamide) and/or an allogeneic transplant (HSCT), according to eligibility and donor availability. Dasatinib was administered until disease progression. Molecular testing was used to identify the presence of the BCR/ABL1 transcript on bone marrow samples, to define the fusion protein and to quantify BCR/ABL1 levels at baseline and follow-up (FU). Mutational screening was performed in relapsed cases, based on material availability. SNP array analysis was carried out using the Cytoscan HD arrays (Affymetrix, Santa Clara, CA) to identify genomic aberrations. Results: 60/63 enrolled patients were eligible. Median age was 41.9 years (range 18.7-59.1), 34 were males and 26 females; median WBC count was 12.5 x 109/l (range 1.4-178.0); the p190 fusion product was detected in 33 patients, p210 in 18 and p190/p210 in 9. Median FU is 28.4 months (range 4.2-43.7). After the steroid pre-phase, 38 patients (63%) had a blast reduction ≥75%. At day 85, 58 patients were in CHR (97%), while 2, in CHR at day 57, lost it: both harbored the p210 fusion transcript. They both returned into CHR following chemotherapy. A sustained CMR was obtained in 11 patients (18.6%): 72% had a p190 fusion transcript. No deaths in induction occurred. Among the CMR patients, only 1 experienced a hematologic relapse, which carried a T315I mutation. Of the 46 non-CMR cases, 14 relapses occurred, 8 of which in p210+ patients. Overall, there have been 12 deaths in CHR. OS is 58.3% (95%CI: 44.4-76.3) at 36 months and DFS at 30 months is 48.9% (95%CI: 36.8.0-64.9). A better DFS was observed in patients who obtained a CMR compared to cases with minimal residual disease (MRD) at day 85 (75% vs 44%, p=0.06), and in p190+ vs p210+ patients (57.1% vs 39.6%, p=ns). Mutational screening, performed in 7/15 cases at hematologic relapse detected mutations in 5: 3 T315I and 2 V299L, of which 1 with a concomitant F317I and F317L. SNP array analysis, performed in 39 cases with available DNA, showed that the most frequent aberrations were deletions of IKZF1 (85%), PAX5 (38%), CDKN2A/B (33%), MLLT3 (33%), RB1 (28%) and JAK2 (28%). While IKZF1 deletions alone did not impact on CHR or CMRachievement and DFS, a significantly worse DFS (p=0.01) and increased cumulative incidence of relapse (CIR, p=0.024) were observed in cases harboring deletions of IKZF1 plus CDKN2A/B and PAX5 (DFS: 40% vs 65% at 18 months; CIR: 40% vs 14% at 18 months (Fig. 1A and B). The relevance of this finding was further refined by stratifying patients according to the fusion protein: the impact of IKZF1 plus CDKN2A/B and PAX5 deletions is prognostically relevant in p190+, but not in p210+ patients, possibly because of the worse outcome of the latter group (Fig. 2). Finally, this analysis identified a set of genes specifically deleted in CMR cases; investigations are ongoing on additional cases to validate their potential role in predicting response to TKI. Conclusions: In this updated analysis of the GIMEMA 1509 trial, we confirm the effectiveness of a chemo-free induction in inducing CHR in almost all adult Ph+ ALL patients (97%) and CMR in a subgroup of cases (18.6%). OS and DFS at 36 months and 30 months, approaching 60% and 50%, are encouraging. More importantly, CMR achievement at day 85 is associated with extremely promising results, being 75% at 30 months, underlying that CMR should be regarded as a primary endpoint in Ph+ ALL. We confirm that p210+ patients may require an intensified approach, given the lower rate of CMR achievement and the higher relapse rate. Finally, we provide evidence that a broader genetic characterization at diagnosis allows a more refined prognostic stratification of Ph+ ALL patients. Disclosures Martinelli: Pfizer: Consultancy; Ariad: Consultancy; AMGEN: Consultancy; BMS: Consultancy, Speakers Bureau; ROCHE: Consultancy; MSD: Consultancy; Novartis: Consultancy, Speakers Bureau. Foà:Roche: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Speakers Bureau.
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5

George, Sarah, Laura Horvath, Robert Molokie, John Berry, Damiano Rondelli, and Ronald Hoffman. "Response to Therapy with Imatinib Mesylate in Patients with CML Is Poor in Non-Caucasian Patients." Blood 104, no. 11 (November 16, 2004): 2937. http://dx.doi.org/10.1182/blood.v104.11.2937.2937.

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Abstract Imatinib mesylate is a targeted therapy for chronic myeloid leukemia (CML). All phases of CML are susceptible to imatinib, with more durable responses occurring in patients in chronic phase. Studies in patients with chronic phase CML who have been treated with imatinib have shown a complete hematologic remission (CHR) rate of 97%, a complete cytogenetic remission (CCR) rate of 70%, and a complete molecular remission (CMR) rate of 10%. Racial and ethnic differences have not been extensively studied in relation to cancer outcomes, and no studies to date have demonstrated a difference in outcomes based upon race or ethnicity of patients with CML treated with imatinib. Methods : A retrospective chart review of patients with CML who have been treated with imatinib at the University of Illinois, the Westside VA, and MacNeal hospitals over the past 3 years was performed. Primary endpoints were rates of CHR, CCR, and CMR in Caucasian (C) and non-Caucasian (NC) patients with CML on treatment with imatinib. A secondary endpoint was the correlation of Sokal scores at initiation of imatinib with rates of CHR, CCR, and CMR. Results: 26 charts were reviewed of 7 C and 19 NC patients ( 12 African American, 5 Latino, 1 Indian, 1 Lebanese) in chronic phase CML. For C patients at the initiation of imatinib, mean age was 46 (45 for NC) and mean Sokal score was 0.79 (0.75 for NC). 32% (8/25) of patients had cytogenetic abnormalities in addition to the Philadelphia chromosome, all of whom were NC (50% were pretreated; 29% obtained CCR). Mean duration from diagnosis to treatment with imatinib was 5 months for C and 9 months for NC. Mean length of follow up while on imatinib was 28 months for C and 14 months for NC, with early termination due to lack of follow up, progression of disease, and death. 31% (8/26) of patients (25% C, 75% NC) had received prior treatments with agents such as IFN, AraC, busulfan, anagrelide, homoharrington, and allogeneic SCT. 100% of pretreated C had CCR (vs 33% of pretreated NC). CHR rate was 100% in C (4/4) vs. 87.5% (14/16) in NC. CCR was obtained in 100% of C (6/6) but only 14% (2/14) of NC. CMR rate was noted to be 33% (1/3) in Caucasians compared to 8.3% (1/12) in NC. Low risk Sokal scores were associated with CHR rate of 100% in C (3/3) and 75% (6/8) in NC, as well as CCR rate of 100% in C (5/5) and only 25% (2/8) in NC. Conclusions: NC patients have a poorer response to treatment with imatinib for CML. The discrepancy between complete response rates (most notably the CCR rate) between C and NC patients could be accounted for by differences in the genetic characteristics of the disease, metabolism, or adherence rates. NC patients with low risk Sokal scores also had poorer complete response rates than C patients with the same risk scores. Prospective studies are needed to further evaluate these differences and discern their etiology. Given poor CCR rates, NC patients should be HLA typed soon after diagnosis and considered for transplant if a matched donor is available.
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Hanson, Laura B., James B. Grand, Michael S. Mitchell, D. Buck Jolley, Bill D. Sparklin, and Stephen S. Ditchkoff. "Change-in-ratio density estimator for feral pigs is less biased than closed mark - recapture estimates." Wildlife Research 35, no. 7 (2008): 695. http://dx.doi.org/10.1071/wr08076.

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Closed-population capture–mark–recapture (CMR) methods can produce biased density estimates for species with low or heterogeneous detection probabilities. In an attempt to address such biases, we developed a density-estimation method based on the change in ratio (CIR) of survival between two populations where survival, calculated using an open-population CMR model, is known to differ. We used our method to estimate density for a feral pig (Sus scrofa) population on Fort Benning, Georgia, USA. To assess its validity, we compared it to an estimate of the minimum density of pigs known to be alive and two estimates based on closed-population CMR models. Comparison of the density estimates revealed that the CIR estimator produced a density estimate with low precision that was reasonable with respect to minimum known density. By contrast, density point estimates using the closed-population CMR models were less than the minimum known density, consistent with biases created by low and heterogeneous capture probabilities for species like feral pigs that may occur in low density or are difficult to capture. Our CIR density estimator may be useful for tracking broad-scale, long-term changes in species, such as large cats, for which closed CMR models are unlikely to work.
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El Ghannudi, Soraya, Philippe Germain, Gerlinde Averous, Afshin Gangi, Thomas H. Schindler, and Alessio Imperiale. "PET/CMR." JACC: Cardiovascular Imaging 13, no. 5 (May 2020): 1270–75. http://dx.doi.org/10.1016/j.jcmg.2019.09.002.

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8

Hehlmann, Rüdiger, Michael Lauseker, Benjamin Hanfstein, Martin C. Müller, Annette Schreiber, Ulrike Proetel, Markus Pfirrmann, et al. "Complete Molecular Remission (CMR 4.5) of CML Is Induced Faster by Dose – Optimized Imatinib and Predicts Better Survival - Results From the Randomized CML-Study IV." Blood 120, no. 21 (November 16, 2012): 67. http://dx.doi.org/10.1182/blood.v120.21.67.67.

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Abstract Abstract 67 Dose optimized imatinib (IM) at doses of 400– 800mg has been shown to induce faster and deeper cytogenetic and molecular – responses than standard IM (400mg/day). Since complete molecular remission (CMR 4.5) identifies a subgroup of patients who may stay in remission even after discontinuation of treatment, it was of interest to analyse whether CMR 4.5 is reached faster with dose optimized IM and whether CMR 4.5 correlates with survival. CMR 4 and CMR 4.5 are defined as ≤ 0.01% BCR-ABL IS or ≥ 4. log reduction and ≤ 0.0032% BCR-ABL IS or ≥ 4.5 log reduction, respectively, from IRIS baseline as determined by real-time PCR. CML-Study IV is a five arm randomized study of IM 400 mg vs IM 400 mg + IFN vs. IM 400 mg + Ara C vs. IM after IFN failure vs. IM 800 mg. In the IM 800 arm, a 6 weeks run in period at IM 400 mg was followed by a dose increase to 800 mg and then by a dose reduction according to tolerability. Grade 3 or 4 adverse effects (AE) were to be avoided. From July 2002 to March 2012 a total of 1551 patients with newly diagnosed chronic phase CML were randomized of whom 1525 were evaluable. Median age was 52 years, 88% were EUTOS low risk, 12% high risk, 36% were Euro score low risk, 52% intermediate and 12% high risk, 38% were Sokal low risk, 38% intermediate and 24% high risk. 113 patients were transplanted, 246 received 2nd generation TKI. 152 patients have died, 90 of CML or unknown reasons, 62 of not directly CML-related causes. After a median observation time of 67,5 months 6 years OS was 88.2% and PFS 85.6%. CCR, MMR, CMR 4 and CMR 4,5 were achieved significantly faster with dose optimized IM (400 – 800 mg). No significant differences in remission rates were observed between IM 400 mg and the combination arms IM 400 mg + IFN and IM 400 mg + Ara C, whereas IM after IFN failure thus far yielded significantly slower response rates. After 4 years CCR rates were for IM 400, IM 400 + IFN, IM 400 + Ara C, IM 400 after IFN, and IM 800, 80%, 75%, 73%, 59% and 80%, respectively, MMR rates 84%, 77%, 82%, 61% and 88%, CMR 4 rates 57%, 55%, 55%, 40% and 65%, and CMR 4.5 rates 40%,42%, 42%, 28% and 52%, respectively. CMR 4 was reached after a median of 27 months with IM 800 and 41.5 months with IM 400. CMR 4.5 was reached after a median of 41.5 months with IM 800 and 63 months with IM 400. EUTOS low risk patients reached all remissions faster than EUTOS high risk patients. The differences of CMR 4 rates between IM 800 and IM 400 at 3 years were 13% and at 4 years 8%, and of CMR 4.5 rates at 3 years 10% and at 4 years 13%. Grade 3 and 4 AE were not different between IM 400 and dose optimized IM 800. Independent of treatment approach, CMR 4 and more clearly CMR 4.5 at 3 years predicted better OS and PFS, if compared with patients without CMR 4 or CMR 4.5, respectively. CMR 4 and 4.5 were stable. After a median duration of CMR 4 of 3.7 years only 4 of 792 patients with CMR 4 have progressed. Life expectancy with CMR 4 and 4.5 was identical to that of the age matched population. We conclude that dose optimized IM induces CMR 4.5 faster than IM 400 and that CMR 4 and CMR 4.5 at 3 years are associated with a survival advantage. Dose optimized IM may provide an improved therapeutic basis for unmaintained treatment discontinuation in patients with CML. Disclosures: Hehlmann: Novartis: Research Funding. Müller:Novartis, BMS: Consultancy, Honoraria, Research Funding. Haferlach:MLL Munich Leukemia Laboratory: Equity Ownership. Schnittger:MLL Munich Leukemia Laboratory: Equity Ownership. Hochhaus:Novartis, BMS, MSD, Ariad, Pfizer: Consultancy Other, Honoraria, Research Funding.
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Lamure, Sylvain, François Van Laethem, Delphine De Verbizier, Claire Lozano, Eve Gehlkopf, Jean-Jacques Tudesq, Chris Serrand, et al. "Clinical and Product Features Associated with Outcome of DLBCL Patients to CD19-Targeted CAR T-Cell Therapy." Cancers 13, no. 17 (August 25, 2021): 4279. http://dx.doi.org/10.3390/cancers13174279.

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CD19-directed CAR T-cells have been remarkably successful in treating patients with relapsed/refractory (R/R) diffuse large B-cell lymphoma (DLBCL) and transformed follicular lymphoma (t-FL). In this cohort study, we treated 60 patients with axicabtagene ciloleucel or tisagenlecleucel. Complete and partial metabolic responses (CMR/PMR) were obtained in 40% and 23% of patients, respectively. After 6.9 months of median follow-up, median progression-free survival (mPFS) and overall survival (mOS) were estimated at 3.1 and 12.3 months, respectively. Statistical analyses revealed that CMR, PFS, and OS were all significantly associated with age-adjusted international prognostic index (aaIPI, p < 0.05). T-cell subset phenotypes in the apheresis product tended to correlate with PFS. Within the final product, increased percentages of both CD4 and CD8 CAR+ effector memory cells (p = 0.02 and 0.01) were significantly associated with CMR. Furthermore, higher CMR/PMR rates were observed in patients with a higher maximal in vivo expansion of CAR T-cells (p = 0.05) and lower expression of the LAG3 and Tim3 markers of exhaustion phenotype (p = 0.01 and p = 0.04). Thus, we find that aaIPI at the time of infusion, phenotype of the CAR T product, in vivo CAR T-cell expansion, and low levels of LAG3/Tim3 are associated with the efficacy of CAR T-cell therapy in DLBCL patients.
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Karim, Md Robiul, Rongjun Wang, Haiju Dong, Longxian Zhang, Jian Li, Sumei Zhang, Farzana Islam Rume, et al. "Genetic Polymorphism and Zoonotic Potential ofEnterocytozoon bieneusifrom Nonhuman Primates in China." Applied and Environmental Microbiology 80, no. 6 (January 10, 2014): 1893–98. http://dx.doi.org/10.1128/aem.03845-13.

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ABSTRACTEnterocytozoon bieneusiis an important zoonotic pathogen. To assess the human-infective potential ofE. bieneusiin nonhuman primates (NHPs), we examined the prevalence and genotype distribution ofE. bieneusiin 23 NHP species by PCR and sequence analysis of the ribosomal internal transcribed spacer (ITS). A total of 1,386 fecal specimens from NHPs from five provinces in China were examined, andE. bieneusiwas detected in 158 (11.4%) specimens from five NHP species, including cynomolgus monkey (67.7%), rhesus macaque (8.8%), Japanese macaque (33.3%), white-headed langur (13.6%), and golden snub-nosed monkey (3.5%) (P< 0.0001). The infection rates were 70.2%, 21.5%, 8.5%, 7.5%, and 5.6% in Guangdong, Yunnan, Guangxi, Henan, and Sichuan Provinces, respectively (P< 0.0001). The prevalence was significantly higher in captive (13.7%) than in free-range (5.0%) animals (P< 0.0001). Altogether, 16 ITS genotypes were observed, including nine known genotypes (IV, D, Henan V, Peru8, PigEBITS7, EbpC, Peru11, BEB6, and I) and seven new genotypes (CM1 to CM7). The common genotypes included CM1, IV, and D, which were detected in 43, 31, and 30 specimens, respectively. Phylogenetic analysis revealed that seven known genotypes (but not BEB6 and I) and four new genotypes (CM1, CM2, CM3, and CM6) belonged to the previously described group 1 with zoonotic potential. Genotypes CM5 and CM7 clustered with group 2, whereas genotype CM4 did not belong to any of the previously proposed groups. It was concluded that humans and NHPs residing in the same geographical location shared the sameE. bieneusigenotypes, indicating a potential role of these animals in the zoonotic transmission ofE. bieneusi.
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Sinusas, Albert J., and Dana C. Peters. "Diffusion Tensor CMR." JACC: Basic to Translational Science 3, no. 1 (February 2018): 110–13. http://dx.doi.org/10.1016/j.jacbts.2018.01.008.

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12

Nagel, Eike, and Y. Chandrashekhar. "Stress-Only CMR." JACC: Cardiovascular Imaging 13, no. 5 (May 2020): 1296–98. http://dx.doi.org/10.1016/j.jcmg.2020.04.001.

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Mewton, Nathan, Franck Thuny, and Pierre Croisille. "T2-Weighted CMR." JACC: Cardiovascular Imaging 5, no. 2 (February 2012): 233–34. http://dx.doi.org/10.1016/j.jcmg.2011.11.010.

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14

Holmvang, Godtfred, and G. William Dec. "CMR in Myocarditis." JACC: Cardiovascular Imaging 5, no. 5 (May 2012): 525–27. http://dx.doi.org/10.1016/j.jcmg.2012.01.014.

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15

Kadletz, A. "Geneva Conv. 1956 (CMR) - Austria/Conv. Geneve 1956 (CMR) - Autriche." Uniform Law Review - Revue de droit uniforme 6, no. 2 (April 1, 2001): 424–25. http://dx.doi.org/10.1093/ulr/6.2.424.

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Kadletz, A. "Geneva Conv. 1956 (CMR) - Germany/Conv. Geneve 1956 (CMR) - Allemagne." Uniform Law Review - Revue de droit uniforme 6, no. 2 (April 1, 2001): 426–27. http://dx.doi.org/10.1093/ulr/6.2.426.

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Kadletz, A. "Geneva Conv. 1956 (CMR) - Germany/Conv. Geneve 1956 (CMR) - Allemagne." Uniform Law Review - Revue de droit uniforme 6, no. 2 (April 1, 2001): 426–29. http://dx.doi.org/10.1093/ulr/6.2.426-a.

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Kadletz, A. "Geneva Conv. 1956 (CMR) - Germany/Conv. Geneve 1956 (CMR) - Allemagne." Uniform Law Review - Revue de droit uniforme 6, no. 2 (April 1, 2001): 428–29. http://dx.doi.org/10.1093/ulr/6.2.428.

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Kadletz, A. "Geneva Conv. 1956 (CMR) - Germany/Conv. Geneve 1956 (CMR) - Allemagne." Uniform Law Review - Revue de droit uniforme 6, no. 2 (April 1, 2001): 430–31. http://dx.doi.org/10.1093/ulr/6.2.430.

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Kadletz, A. "Geneva Conv. 1956 (CMR) - Germany/Conv. Geneve 1956 (CMR) - Allemagne." Uniform Law Review - Revue de droit uniforme 6, no. 2 (April 1, 2001): 430–33. http://dx.doi.org/10.1093/ulr/6.2.430-a.

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Kadletz, A. "Geneva Conv. 1956 (CMR) - Germany/Conv. Geneve 1956 (CMR) - Allemagne." Uniform Law Review - Revue de droit uniforme 6, no. 2 (April 1, 2001): 432–33. http://dx.doi.org/10.1093/ulr/6.2.432.

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Kadletz, A. "Geneva Conv. 1956 (CMR) - Germany/Conv. Geneve 1956 (CMR) - Allemagne." Uniform Law Review - Revue de droit uniforme 6, no. 3 (December 1, 2001): 680–81. http://dx.doi.org/10.1093/ulr/6.3.680-a.

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Siehr, K. "Geneva Conv. 1956 (CMR) - Germany/Conv. Geneve 1956 (CMR) - Allemagne." Uniform Law Review - Revue de droit uniforme 6, no. 3 (December 1, 2001): 682–83. http://dx.doi.org/10.1093/ulr/6.3.682.

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Siehr, K. "Geneva Conv. 1956 (CMR) - Switzerland/Conv. Geneve 1956 (CMR) - Suisse." Uniform Law Review - Revue de droit uniforme 6, no. 3 (December 1, 2001): 682–85. http://dx.doi.org/10.1093/ulr/6.3.682-a.

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Siehr, K. "Geneva Conv. 1956 (CMR) - Switzerland/Conv. Geneve 1956 (CMR) - Suisse." Uniform Law Review - Revue de droit uniforme 6, no. 3 (December 1, 2001): 684–85. http://dx.doi.org/10.1093/ulr/6.3.684.

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NEGUSSIE, E., I. STRANDÉN, and E. MÄNTYSAARI. "Genetic analysis of clinical mastitis during different risk periods in Finnish Ayrshire." Agricultural and Food Science 16, no. 2 (December 4, 2008): 115. http://dx.doi.org/10.2137/145960607782219373.

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Clinical mastitis (CM) records from first-lactation Finnish Ayrshire were analysed by linear and threshold models to assess the effects trait definition on estimates of genetic parameters and sire evaluation. The studied CM traits were defined by dividing lactation into six lactation stages (risk periods) by days (d) after calving: CM1 (-7 to 150 d), CM2 (-30 to 30 d), CM3 (-30 to 150 d), CM4 (31 to 150 d), CM5 (150 to 300 d), CM6 (-30 to 300 d). In addition, two data sets were prepared to assess the effect of excluding (Data I) or including (Data II) records of culled cows on estimates of genetic parameters. Sire variances and heritabilities were larger using Data II. When data from longer intervals was used heritabilities of CM were slightly higher than shorter intervals indicating that longer intervals tend to obscure genetic variation between animals. Of all CM traits, heritability of liability to CM with threshold-liability model was highest for CM2 (h2=0.083) implying that most of the genetic information on CM is in early lactation. In sire evaluation, a multitrait index calculated by combining CM2, CM4 and CM5 had the highest correlation with all other univariate CM trait evaluations. This and the magnitude (less than 1.0) of genetic correlations between CM traits suggest that a multitrait model considering CM from the different risk periods would be appropriate for CM sire evaluation.;
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Putzeys, J. "Geneva Conv. 1956 (CMR) - Netherlands/Conv. Geneve 1956 (CMR) - Pays-Bas." Uniform Law Review - Revue de droit uniforme 6, no. 2 (April 1, 2001): 434–37. http://dx.doi.org/10.1093/ulr/6.2.434.

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Roca-Luque, Ivo, Ana Van Breukelen, Francisco Alarcon, Paz Garre, Jose M. Tolosana, Roger Borras, Paula Sanchez, et al. "Ventricular scar channel entrances identified by new wideband cardiac magnetic resonance sequence to guide ventricular tachycardia ablation in patients with cardiac defibrillators." EP Europace 22, no. 4 (February 26, 2020): 598–606. http://dx.doi.org/10.1093/europace/euaa021.

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Abstract Aims Ventricular tachycardia (VT) substrate-based ablation has become a standard procedure. Electroanatomical mapping (EAM) detects scar tissue heterogeneity and define conduction channels (CCs) that are the ablation target. Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) is able to depict CCs and increase ablation success. Most patients undergoing VT ablation have an implantable cardioverter-defibrillator (ICD) that can cause image artefacts in LGE-CMR. Recently wideband (WB) LGE-CMR sequence has demonstrated to decrease these artefacts. The aim of this study is to analyse accuracy of WB-LGE-CMR in identifying the CC entrances. Methods and results Thirteen consecutive ICD-patients who underwent VT ablation after WB-LGE-CMR were included. Number and location of CC entrances in three-dimensional EAM and in WB-LGE-CMR reconstruction were compared. Concordance was compared with a historical cohort matched by cardiomyopathy, scar location, and age (26 patients) with LGE-CMR prior to ICD and VT ablation. In WB-CMR group, 101 and 93 CC entrances were identified in EAM and WB-LGE-CMR, respectively. In historical cohort, 179 CC entrances were identified in both EAM and LGE-CMR. The EAM/CMR concordance was 85.1% and 92.2% in the WB and historical group, respectively (P = 0.66). There were no differences in false-positive rate (CC entrances detected in CMR and absent in EAM: 7.5% vs 7.8% in WB vs. conventional CMR, P = 0.92) nor in false-negative rate (CC entrances present in EAM not detected in CMR: 14.9% vs.7.8% in WB vs. conventional CMR, P = 0.23). Epicardial CCs was predictor of poor CMR/EAM concordance (OR 2.15, P = 0.031). Conclusion Use of WB-LGE-CMR sequence in ICD-patients allows adequate VT substrate characterization to guide VT ablation with similar accuracy than conventional LGE-CMR in patients without an ICD.
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Sado, Daniel M., Jonathan M. Hasleton, Anna S. Herrey, and James C. Moon. "CMR in Heart Failure." Cardiology Research and Practice 2011 (2011): 1–11. http://dx.doi.org/10.4061/2011/739157.

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Fontaine, B., P. Frimat, and P. Boitte. "Éthique et décret « CMR »." Éthique & Santé 2, no. 2 (May 2005): 61–66. http://dx.doi.org/10.1016/s1765-4629(05)80514-8.

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Hall, Joseph W., John H. Grose, and Mark P. Haggard. "CMR for complex signals." Journal of the Acoustical Society of America 81, S1 (May 1987): S54. http://dx.doi.org/10.1121/1.2024287.

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Hall, J. W., J. H. Grose, and D. R. Hatch. "Gating effects in CMR." Journal of the Acoustical Society of America 97, no. 5 (May 1995): 3273–74. http://dx.doi.org/10.1121/1.411617.

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Fischer, F., and A. Stuttgart. "Select Bibliography on CMR." Uniform Law Review - Revue de droit uniforme 1, no. 3 (August 1, 1996): 609–16. http://dx.doi.org/10.1093/ulr/1.3.609.

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Keenan, Niall G., and Dudley J. Pennell. "CMR of Ventricular Function." Echocardiography 24, no. 2 (February 2007): 185–93. http://dx.doi.org/10.1111/j.1540-8175.2007.00375.x.

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Connelly, Kim A., Andrew T. Yan, Eitan Amir, and Paaladinesh Thavendiranathan. "CMR and Tissue Characterization." Journal of the American College of Cardiology 73, no. 25 (July 2019): 3359. http://dx.doi.org/10.1016/j.jacc.2019.03.521.

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Shaw, Peter W., and Christopher M. Kramer. "The case for CMR." Journal of Nuclear Cardiology 22, no. 5 (July 8, 2015): 968–70. http://dx.doi.org/10.1007/s12350-015-0147-y.

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Bahadur, D., and D. Das. "Properties of CMR composites." Journal of Chemical Sciences 115, no. 5-6 (October 2003): 587–606. http://dx.doi.org/10.1007/bf02708250.

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Hombach, V., S. Kelle, R. Gebker, E. Nagel, H. Thiele, J. Schulz-Menger, O. Bruder, E. Fleck, and H. A. Katus. "Curriculum Kardiale Magnetresonanztomographie (CMR)." Der Kardiologe 8, no. 6 (December 2014): 451–61. http://dx.doi.org/10.1007/s12181-014-0623-7.

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Leyva, Franciscxo. "CMR for CRT implantation?" International Journal of Cardiology 270 (November 2018): 353–54. http://dx.doi.org/10.1016/j.ijcard.2018.07.095.

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40

Petersen, Steffen E. "CMR and LV Noncompaction." JACC: Cardiovascular Imaging 6, no. 9 (September 2013): 941–43. http://dx.doi.org/10.1016/j.jcmg.2013.03.007.

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Kwong, Raymond Y., and Michael Jerosch-Herold. "CMR and Amyloid Cardiomyopathy." JACC: Cardiovascular Imaging 7, no. 2 (February 2014): 166–68. http://dx.doi.org/10.1016/j.jcmg.2013.12.002.

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Salerno, Michael. "Feature Tracking by CMR." JACC: Cardiovascular Imaging 11, no. 2 (February 2018): 206–8. http://dx.doi.org/10.1016/j.jcmg.2017.01.024.

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Ferreira, Vanessa M. "CMR Mapping for Myocarditis." JACC: Cardiovascular Imaging 11, no. 11 (November 2018): 1591–93. http://dx.doi.org/10.1016/j.jcmg.2018.01.002.

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Kramer, Christopher M., and Y. Chandrashekhar. "Quantitative Myocardial Perfusion CMR." JACC: Cardiovascular Imaging 11, no. 5 (May 2018): 784–86. http://dx.doi.org/10.1016/j.jcmg.2018.04.001.

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Kwong, Raymond Y., Christopher M. Kramer, and Y. Chandrashekhar. "CMR Global Longitudinal Strain." JACC: Cardiovascular Imaging 11, no. 10 (October 2018): 1554–55. http://dx.doi.org/10.1016/j.jcmg.2018.09.002.

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Kramer, Christopher M., and Y. Chandrashekhar. "Multiparametric CMR in Cardiomyopathies." JACC: Cardiovascular Imaging 12, no. 8 (August 2019): 1712–14. http://dx.doi.org/10.1016/j.jcmg.2019.07.003.

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Yang, Dongguang, Ri Zhang, Yunfeng Shen, Xuhui Zhang, and De Pei Wu. "Comparison of Combination Therapy of Imatinib with Trisenox Versus Imatinib Monotherapy for Chronic Myeloid Leukemia Patients in Chronic Phase." Blood 108, no. 11 (November 1, 2006): 2159. http://dx.doi.org/10.1182/blood.v108.11.2159.2159.

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Abstract Targeted therapy with the Bcr-Abl tyrosine kinase inhibitor Imatinib Mesylate can induce high response rates in chronic myelogenous leukemia (CML) patients. However, evidences that discontinuation of imatinib mesylate inevitably exerts rapid loss of response and some patients with imatinib mesylate monotherapy virtually occur potential relapse suggest that the modification of treatment strategy is critical. We have previously demonstrated that the combination of trisenox (arsenic trioxide) with the tyrosine kinase inhibitor imatinib mesylate or genistein appears to induce markedly more cell apoptosis than imatinib mesylate alone through downregulating Bcl-XL and Bcr-Abl in Bcr-Abl gene transfected HL-60 cells. We here report the preliminary results of a pilot study comparing imatinib mesylate plus trisenox with imatinib mesylate alone for frontline treatment of CML patients. Up to date 56 patients were enrolled in this clinical trail. All patients (required to be 18 years or older with Bcr-Abl positive CML in chronic phase within three month of diagnosis) were divided into two groups, i.e., monotherapy group and combined therapy group. 42 patients entering monotherapy received imatinib mesylate 400mg daily and 14 patients entering combined therapy imatinib mesylate 400mg daily plus trisenox 10mg daily for one week and then twice a week. We compared treatment results of both groups including complete hematologic response(CHR), major/complete cytogenetic response(MCR/CCR),--defined as 1–35% Ph+ and 0% Ph+ metaphases respectively and major/complete molecular response(MMR/CMR),--defined as ≥ 3 log reduction and negative expression in Bcr-Abl transcript numbers assayed by RQ-PCR respectively. The median follow-up for patients in both groups lasted 36 months. In the combined therapy group, the median age of patients is 42 years old (range, 22–61), the CHR, MCR, CCR, MMR and CMR is 92.8%, 64.3%, 42.9%, 35.7% and 21.4%, respectively. While in the imatinib mesylate monotherapy group, the median age of patients is 46 years old (range, 23–65), the CHR, MCR, CCR, MMR and CMR is 85.7%, 59.5%, 40.5%, 33.3% and 19%, respectively. Although combination therapy of imatinib with trisenox is not significantly superior to imatinib mesylate monotherapy in efficacy, no resistance case happens in the combination therapy group, in the imatinib mesylate monotherapy group, imatinib resistance occurs in 4 patients. In addition, the safety and tolerability of a combination of imatinib mesylate and trisenox is good. This result indicates that the combination of imatinib and trisenox to treat chronic myeloid leukemia may be promising in avoiding the occur of imatinib resistance.
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Baublys, Arvydas, and Nijolė Batarlienė. "THE POSSIBILITIES OF INSTALLING ELECTRONIC CMR WAYBILL IN ROAD TRANSPORT SECTOR / ELEKTRONINIO CMR VAŽTARAŠČIO DIEGIMO GALIMYBĖS KELIŲ TRANSPORTO SEKTORIUJE." Mokslas – Lietuvos ateitis 7, no. 5 (February 3, 2016): 583–88. http://dx.doi.org/10.3846/mla.2015.821.

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In the article opportunities of changing paper CMR waybill into electronic are analysed, whereas the paper CMR waybill does not guarantee operational information exchange between participants of logistics chain components in road transport. Due to this reason use ofelectronic CMR waybill becomes more and more important. According to researches done by article authors, the article submitted the limitations of paper CMR waybill, benefits of electronic CMR waybill, concept model of implementing electronic CMR waybill and application possibilities of supply chain components. Straipsnyje nagrinėjamos popierinio CMR važtaraščio galimybės keisti jį į elektroninį CMR važtaraštį, nes popierinis jau nebeužtikrina operatyvių informacijos mainų tarp vežimo dalyvių kelių transporte. Naudoti elektroninį važtaraštį tampa vis aktualiau. Remiantis atliktų tyrimų rezultatais straipsnyje pateikiami pagrindiniai popierinio CMR važtaraščio trūkumai, įvardijami elektroninio važtaraščio privalumai, elektroninio CMR važtaraščio realizavimo koncepcinis modelis ir jo taikymo galimybės visiems vežimo dalyviams.
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Dziechciarz, Mateusz. "The use of electronic consigment note e-CMR." Europa Regionum 35 (2018): 21–32. http://dx.doi.org/10.18276/er.2018.35-02.

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Clarke, M. "Geneva Conv. 1956 (CMR) - United Kingdom/Conv. Geneve 1956 (CMR) - Royaume-Uni." Uniform Law Review - Revue de droit uniforme 6, no. 2 (April 1, 2001): 436–37. http://dx.doi.org/10.1093/ulr/6.2.436.

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