Academic literature on the topic 'Plasma Cell Leukemi'
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Journal articles on the topic "Plasma Cell Leukemi"
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Ishida, Yoji, Kazunori Murai, Kohei Yamaguchi, Takuo Miyagishima, Motohiro Shindo, Kazuei Ogawa, Takahiro Nagashima, et al. "Pharmacokinetic (PK) and Pharmacodynamic (PD) Study Of Dasatinib In Chronic Phase Of Newly Diagnosed Chronic Myeloid Leukemia (CML-CP)." Blood 122, no. 21 (November 15, 2013): 4031. http://dx.doi.org/10.1182/blood.v122.21.4031.4031.
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Abstract Purpose Dasatinib is a novel kinase inhibitor of BCR-ABL and SRC family kinases. Dasatinib has shown promising anti-leukemic activity in chronic myeloid leukemi (CML). Tounderstand how to administer dasatinib with best efficacy and less adverse events, the pharmacokinetic (PK) properties of dasatinib and the relationship of PK and pharmacodynamic (PD) characteristics were investigated in newly diagnosed CML-chronic phase (CP) patients. Methods and Materials The PK analysis of dasatinib: The plasma concentrations of dasatinib (1, 2, 4 hr after taking dasatinib post 28 days) were determined by Francia's method using high performance liquid chromatography with mass spectrometry. PK analysis was performed using Phoenixâ NLMEâ1.2. The maximum plasma concentration (Cmax) was determined by visually inspecting the profiles of plasma drug levels. PD analysis of dasatinib: Phospho-CrkL in CD 34 positive cells was analyzed by flow cytometry using anti-phospho-CrkL (Tyr207) antibody after incubation of bone marrow mononuclear cells in the presence of dasatinib for 2 hours. PK/PD analysis: Area under the curve (AUC) and time above IC50 were calculated using Phonix WinNonlin 6.3. Results Twenty-eight newly diagnosed CML-CP patients were included. The correlation between the efficacy and PK/PD parameters were analyzed using Peason's correlation coefficient test (Table1). The efficacy(expression of bcr/abl at 1 month) was not correlated with AUC, Cmax, AUC/IC50 and Cmax/IC50 but significantly correlated with TAIC50 (r=0.4763, p=0.0104). The reduction rate at 1 month was correlated significantly with only TAIC50(r=0.5136, p=0.0052)(Figure 2). Eight cases reached MMR at 3 month among 15, whose TAIC50s were more than 12 hrs(53.3%), while only 2 cases reached MMR among 13, whose those were less than 12 hrs(15.4%). Conclusion Dasatinib has anti-leukemic activity in a time dependent manner. Exposure more than 12 hrs at TAIC50 will get benefits of better prognosis. Disclosures: No relevant conflicts of interest to declare.
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I, Jamal. "Plasma Cell Leukemia: An Overview." Haematology International Journal 5, no. 1 (2021): 1–2. http://dx.doi.org/10.23880/hij-16000175.
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Sumeet, Bajaj Preeti, Kasture Jyoti Uttamrao, and Shah Balbir Singh. "Plasma Cell Leukemia: Clinicopathological Profile of Five Cases." Indian Journal of Forensic Medicine and Pathology 9, no. 3 (2016): 189–91. http://dx.doi.org/10.21088/ijfmp.0974.3383.9316.18.
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Hudák, Renáta, Ildikó Beke Debreceni, Ivett Deák, Gabriella Gál Szabó, Zsuzsanna Hevessy, Péter Antal-Szalmás, Bjarne Osterud, and János Kappelmayer. "Laboratory characterization of leukemic cell procoagulants." Clinical Chemistry and Laboratory Medicine (CCLM) 55, no. 8 (July 26, 2017): 1215–23. http://dx.doi.org/10.1515/cclm-2017-0021.
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Abstract Background: In acute myeloid leukemias, there is an increased chance to develop thrombotic disorders. We hypothesized that in addition to leukemic promyelocytes, monocytic leukemia cells may also have a higher procoagulant activity. Methods: Fibrin formation was assessed by a one-stage clotting assay using a magnetic coagulometer. The thrombin generation test (TGT) of magnetically isolated normal human monocytes, intact leukemic cells and their isolated microparticles was performed by a fluorimetric assay. Phosphatidylserine (PS) expression of leukemic cells and microparticle number determinations were carried out by flow cytometry. Results: All cell lines displayed a significant procoagulant potential compared to isolated normal human monocytes. In the TGT test, the mean of lagtime and the time to peak parameters were significantly shorter in leukemic cells (3.9–4.7 and 9.9–10.3 min) compared to monocytes (14.9 and 26.5 min). The mean of peak thrombin in various monocytic leukemia cell lines was 112.1–132.9 nM vs. 75.1 nM in monocytes; however, no significant difference was observed in the ETP parameter. Factor VII-deficient plasma abolished all procoagulant activity, whereas factor XII-deficient plasma did not affect the speed of fibrin formation and thrombin generation but modulated the amount of thrombin. Factor XI-deficient plasma affected the time to peak values in one leukemic cell line and also attenuated peak thrombin. Leukemia cell-derived microparticles from all three cell lines exerted a procoagulant effect by significantly shortening the lagtime in TGT; there was a nonsignificant difference in case of ETP parameter. Conclusions: All investigated monocytic leukemia cell lines exhibited significant thrombin generation. This phenomenon was achieved by the procoagulants on the surface of leukemic cells as well as by their microparticles.
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S, Nibhoria. "Plasma Cell Leukemia–A Case Report and Review of Literature." Cytology & Histology International Journal 5, no. 1 (2021): 1–4. http://dx.doi.org/10.23880/chij-16000133.
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Plasma cell leukaemia (PCL) is one of the most aggressive and rarest forms of plasma cell dyscrasia. As prognosis is very poor, it is very important to recognize this entity sufficiently early so that one can offer combination chemotherapy at the earliest which can prolong survival.
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Keita, Mohamed, Sokhna Aissatou Touré, Elimane Seydi Bousso, Alioune Badara Diallo, Nata Dieng, Serigne Mourtalla Gueye, Blaise Felix Faye, Moussa Seck, and Saliou Diop. "PLASMA CELL LEUKEMIA: AN AGGRESSIVE DISEASE, A CAUSE OF DIAGNOSTIC ERROR." International Journal of Medical Science and Dental Health 10, no. 04 (April 7, 2024): 15–20. http://dx.doi.org/10.55640/ijmsdh-10-04-23.
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Plasma cell leukemia (LP) is a rare and aggressive plasma cell tumor that manifests as significant clonal expansion of plasma cells in the bone marrow and peripheral blood. It is considered primary when it presents at initial diagnosis and secondary when it occurs in patients with pre-existing multiple myeloma (MM). Because of the high frequency of extramedullary injuries, plasma cell leukemia is a major source of diagnostic error that can lead to fatality. We report a case of plasma cell leukemia diagnosed at the clinical haematology department of the CNTS in Dakar (Senegal).
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Heumann, D., G. Losa, C. Barras, A. Morell, and V. von Fliedner. "Characterization of acute undifferentiated leukemia by combined analysis of plasma membrane-associated gamma-glutamyltranspeptidase and soluble terminal transferase." Blood 66, no. 2 (August 1, 1985): 255–58. http://dx.doi.org/10.1182/blood.v66.2.255.bloodjournal662255.
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gamma-Glutamyltranspeptidase (gamma-GT) is a plasma membrane-associated enzyme present in blasts of certain acute leukemias. We analyzed 90 cases of undifferentiated and differentiated acute leukemias for gamma- GT, using a colorimetric assay. Blasts of all patients with common acute lymphoblastic leukemia (ALL) and T-ALL were negative for gamma-GT (less than 5 units). In contrast, gamma-GT was significantly elevated in acute myeloblastic or monoblastic leukemia blasts (P less than .001). In 16 cases of acute undifferentiated leukemia (AUL) studied, the levels of gamma-GT ranged from 0 to 93 units; in eight cases, gamma- GT was positive (greater than 5 units), and six of these had 2% to 5% Sudan black-positive leukemic cells in the blast-enriched suspension. Combined gamma-GT/TdT analysis revealed that both enzyme markers were mutually exclusive in 75% of AUL cases, suggesting that gamma-GT+/TdT- blasts are of nonlymphoid origin, and gamma-GT-/TdT+ blasts are of lymphoid origin. Two cases were devoid of both enzyme activities and could represent truly undifferentiated leukemia. Thus, combined gamma- GT/TdT analysis underlines the heterogeneity of AUL and appears to be useful in defining the lineage commitment of undifferentiated leukemic blasts.
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Zhang, Ke, Hagop M. Kantarjian, Wanlong Ma, XI Zhang, Xiuqiang Wang, Zeev Estrov, Chen-Hsiung Yeh, et al. "Use of Ubiquitin-Proteasome System Profiling for Differentiating Between Various Leukemic Processes." Blood 114, no. 22 (November 20, 2009): 4712. http://dx.doi.org/10.1182/blood.v114.22.4712.4712.
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Abstract Abstract 4712 The ubiquitin-proteasome system (UPS) plays a major role in cell homeostasis in normal and neoplastic states. Expression and function of the UPS system vary with the specific characteristics of individual cell types, suggesting that determination of UPS “signatures” could be useful in identifying various cell populations. Since direct analysis of cancer cells is often problematic, even in hematologic diseases, we explored the potential of using UPS signatures in plasma to differentiate between various leukemias. We first analyzed plasma UPS profiles of patients with acute myeloid leukemia (AML; n=111), acute lymphoblastic leukemia (ALL; n=29), advanced myelodysplastic syndrome (MDS; n=20), chronic lymphocytic leukemia (CLL; n=118), or chronic myeloid leukemia (CML; n=128; 46 in accelerated/blast crisis [ACC/BL], 82 in chronic phase), and 85 healthy control subjects. Plasma levels of proteasome, ubiquitin (poly-ubiquitin), and the 3 proteasome enzymatic activities (chymotrypsin-like [Ch-L], caspase-like [Cas-L], trypsin-like [Tr-L]) were measured. Specific activities were calculated by normalizing each of the 3 enzyme activities to the levels of proteasome protein in plasma (Ch-L/p, Cas-L/p, and Tr-L/p). These 8 variables were used in multivariate logistic regression models to differentiate between leukemic processes. UPS signatures provided clear differentiation between patients with a leukemic process and normal controls (AUC=0.991), using 6 different variables (Tr-L/P, Ch-L, Ch-L/p, Cas-L, Cas-L/P, ubiquitin). Distinguishing between acute (AML, ALL, MDS) and chronic (CML, CLL) processes was less efficient (AUC=0.853 using Tr-L, Tr-L/P, Cas-L/P, Ch-L/P, proteasome, Ch-L), likely due to the high proportion (36%) of CML patients in ACC/BL phase. However, UPS signatures generally yielded powerful differentiation between individual leukemias (Table). MDS was not well differentiated from AML (AUC=0.791), reflecting the significant biological overlap of these diseases. These data support the potential usefulness of the UPS profile to aid in the differential diagnosis of various leukemias. Disclosures: No relevant conflicts of interest to declare.
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Heumann, D., G. Losa, C. Barras, A. Morell, and V. von Fliedner. "Characterization of acute undifferentiated leukemia by combined analysis of plasma membrane-associated gamma-glutamyltranspeptidase and soluble terminal transferase." Blood 66, no. 2 (August 1, 1985): 255–58. http://dx.doi.org/10.1182/blood.v66.2.255.255.
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Abstract gamma-Glutamyltranspeptidase (gamma-GT) is a plasma membrane-associated enzyme present in blasts of certain acute leukemias. We analyzed 90 cases of undifferentiated and differentiated acute leukemias for gamma- GT, using a colorimetric assay. Blasts of all patients with common acute lymphoblastic leukemia (ALL) and T-ALL were negative for gamma-GT (less than 5 units). In contrast, gamma-GT was significantly elevated in acute myeloblastic or monoblastic leukemia blasts (P less than .001). In 16 cases of acute undifferentiated leukemia (AUL) studied, the levels of gamma-GT ranged from 0 to 93 units; in eight cases, gamma- GT was positive (greater than 5 units), and six of these had 2% to 5% Sudan black-positive leukemic cells in the blast-enriched suspension. Combined gamma-GT/TdT analysis revealed that both enzyme markers were mutually exclusive in 75% of AUL cases, suggesting that gamma-GT+/TdT- blasts are of nonlymphoid origin, and gamma-GT-/TdT+ blasts are of lymphoid origin. Two cases were devoid of both enzyme activities and could represent truly undifferentiated leukemia. Thus, combined gamma- GT/TdT analysis underlines the heterogeneity of AUL and appears to be useful in defining the lineage commitment of undifferentiated leukemic blasts.
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SOEBORG-OHLSEN, A., and OLE P. NIELSEN. "Case of Leukemic Myelomatosis (Plasma Cell Leukemia)." Acta Medica Scandinavica 122, no. 3 (April 24, 2009): 271–79. http://dx.doi.org/10.1111/j.0954-6820.1945.tb04503.x.
Full textDissertations / Theses on the topic "Plasma Cell Leukemi"
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Champion, Ophélie. "Role of the mitochondrial channel VDAC2 in the regulation of apoptosis effector proteins BAK and BAX in Multiple Myeloma." Electronic Thesis or Diss., Nantes Université, 2024. http://www.theses.fr/2024NANU1030.
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Le Myélome Multiple (MM) est une hémopathie maligne rare où des plasmocytes tumoraux envahissent la moelle osseuse. Malgré les avancées thérapeutiques, les patients rechutent, notamment par échappement à l’apoptose. Ce travail vise à comprendre le mécanisme de mort cellulaire mis en place par VDAC2, qui appartient à la famille des canaux mitochondriaux voltage-dépendants avec VDAC1 et VDAC3. Les 3 VDACs sont exprimés de manière hétérogène dans le MM. Une faible expression de VDAC2 est associée à une survie globale défavorable dans 764 échantillons d’une cohorte de MM. De plus, l'expression de VDAC2 et de BAK est corrélée au niveau ARN et protéique. VDAC2 est crucial pour la stabilité protéique et la fonction de BAK, mais pas pour celle de BAX. Nous avons démontré que l’extinction de VDAC2 par CRISPR/Cas9 dans 2 lignées cellulaires de MM entraîne la dégradation de BAK par les voies du protéasome et du lysosome, ce qui abolit le priming mitochondrial. Inversement, l'inhibition transitoire de VDAC2, tout en maintenant les niveaux de protéine BAK, a augmenté le priming mitochondrial, a induit l'activation de BAK et a renforcé la mort cellulaire induite par des BH3-mimétiques ciblant MCL-1 (S63845) ou ciblant BCL-2 (vénétoclax) dans les cellules de MM. L’utilisation de l’Efsevin, un modulateur de VDAC2, synergise avec le S63845 et le vénétoclax dans les lignées et des échantillons primaires, représentant une cible thérapeutique potentielle. Enfin, la Leucémie à Plasmocytes secondaire (sPCL) est une forme rare de MM présentant peu d’options thérapeutiques. Nous avons démontré l’efficacité du DT2216, PROTAC ciblant la protéine BCL-XL sans induire de thrombocytopénie, dans des HMCLs et échantillons primaires dépendants de BCL-XL, qui active les effecteurs BAK et BAX et permet le relargage de cytochrome c, ce qui déclenche l'apoptoseMultiple Myeloma (MM) is a rare malignant hematological disorder where tumor plasma cells invade the bone marrow. Despite therapeutic advancements, patients experience relapses, particularly due to escape from apoptosis. This work aims to understand the mechanism of cell death mediated by VDAC2, which belongs to the family of voltage- dependent mitochondrial channels along with VDAC1 and VDAC3. The three VDACs are expressed heterogeneously in MM. Low expression of VDAC2 is associated with unfavorable overall survival in 764 samples from an MM cohort. Furthermore, the expression of VDAC2 and BAK is correlated at both RNA and protein levels. VDAC2 is crucial for protein stability and BAK function, but not for BAX. We demonstrated that the knockout of VDAC2 using CRISPR/Cas9 in two MM cell lines leads to the degradation of BAK via proteasomal and lysosomal pathways, abolishing mitochondrial priming. Conversely, transient inhibition of VDAC2, while maintaining BAK protein levels, increased mitochondrial priming, induced BAK activation, and enhanced cell death triggered by BH3 mimetics targeting MCL-1 (S63845) or BCL-2 (venetoclax) in MM cells. The use of Efsevin, a VDAC2 modulator, synergizes with S63845 and venetoclax in cell lines and primary samples, representing a potential therapeutic target. Lastly, secondary Plasma Cell Leukemia (sPCL) is a rare form of MM with limited treatment options. We have demonstrated the efficacy of DT2216, a PROTAC targeting BCL- XL protein without inducing thrombocytopenia, in BCL-XL-dependent HMCLs and primary samples, which activates BAK and BAX effectors and triggers apoptosis
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Manthri, Sukesh, Haroon Rehman, Rabia Zafar, and Kanishka Chakraborty. "A Rare Case of Non-Producing Primary Plasma Cell Leukemia." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/asrf/2019/schedule/89.
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Non-Secretory Multiple Myeloma (NSMM) is characterized by typical morphological and pathological multiple myeloma (MM) characteristics and the absence of an M-protein on immunofixation electrophoresis with estimated prevalence of 3%. Among the NSMM cases there is a subset in which no cytoplasmic Immunoglobulin synthesis is detected, and this entity is called ‘’Non-Producing’’ Multiple Myeloma (NPMM). Plasma cell leukemia (PCL) is an aggressive form of MM characterized by high levels of abnormal plasma cells circulating in the peripheral blood. We present a rare case of non-producing variant of PCL. 75-year-old male was admitted due to anemia and thrombocytopenia. His CBC revealed hemoglobin of 9.0 g/dl and platelets were 9 k/ul. CMP showed creatinine of 1.34 mg/dl, total protein of 6 g/dl, albumin 3.6 g/dl and corrected calcium was normal. LDH was 204 IU/L. Peripheral smear review showed 8% circulating atypical plasmacytoid cells, normochromic normocytic anemia and thrombocytopenia. SPEP showed no monoclonal protein. IgA was normal. IgG, IgM were low 315 mg/dl and 20 mg/dl respectively. Serum beta-2 microglobulin was high (5.5, 1.1 – 2.4 mg/dl). Serum free kappa light chain was low (0.15, 0.33-1.94 mg/dl), lambda light chain and ratio was normal. Skeletal survey showed possible lytic lesions in right femur neck and subtrochanteric left femur. Bone marrow biopsy showed plasma cell myeloma involving 90-95% of bone marrow cellularity. The plasma cells show morphologic heterogeneity with prominent immature, plasmablastic and pleomorphic morphology. Flow cytometry shows a dominant abnormal CD45-dim population with expression of CD38, CD138, CD56 and CD117 (partial). The abnormal cells are negative for cytoplasmic kappa and lambda immunoglobulin light chains and negative for myeloid and lymphoid markers (by flow cytometry and immunohistochemical stains). Complex chromosomal analysis. Plasma cell FISH studies was positive for t(11;14). Based on suggested revised diagnostic criteria for PCL from outcomes of patients at mayo clinic, our patient was diagnosed with plasma cell leukemia. Given aggressive biology of this disease, he was started on VD-PACE chemotherapy. Bone marrow biopsy after cycle 1 chemotherapy showed no morphologic, immunophenotypic or flow cytometric features of a plasma cell neoplasm. Given excellent treatment response and discussion with transplant center subsequent cycle 2 was changed to Velcade, Revlimid and low-dose dexamethasone. He is scheduled for stem cell transplant later this month. Primary plasma cell leukemia (pPCL) is the most aggressive form of the plasma cell dyscrasias. The outcome of pPCL has improved with the introduction of autologous stem cell transplantation and combination approaches with novel agents, including bortezomib and immunomodulatory drugs, such as lenalidomide. This case highlights the challenges in diagnosis of non-producer primary plasma cell leukemia.
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Lionetti, M. "BIOLOGICAL AND CLINICAL RELEVANCE OF MIRNA EXPRESSION SIGNATURES IN PRIMARY PLASMA CELL LEUKEMIA." Doctoral thesis, Università degli Studi di Milano, 2013. http://hdl.handle.net/2434/217172.
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Purpose: Plasma cell leukemia (PCL) is a very aggressive and rare hematological malignancy that can be distinguished into primary (pPCL), originating de novo, or secondary (sPCL), arising as a leukemic transformation of multiple myeloma (MM). Genomic and clinical differences between pPCL and MM have been demonstrated, mainly based on retrospective studies. This study was aimed at investigating the involvement of miRNAs in pPCL and their possible relationship with higher tumor aggressiveness.
Experimental design: MiRNA expression profiles were analyzed in highly-purified malignant plasma cells from 18 pPCL cases included in a prospective clinical trial. MiRNA expression patterns were evaluated in comparison with a representative series of multiple myeloma (MM) patients, in relation to the most recurrent chromosomal abnormalities (as assessed by fluorescence in situ hybridization and single nucleotide polymorphism-array analysis), and in association with clinical outcome. MiRNA expression was also integrated with gene expression profiles and computational prediction of miRNA target genes in pPCL and MM samples in order to identify putative target genes of deregulated miRNAs. The functional role of a few identified miRNAs in plasma cell dyscrasia pathogenesis was explored by transfection of synthetic pre/anti-miRNAs in multiple myeloma cell lines.
Results: We identified a series of deregulated miRNAs in pPCL (42 up- and 41 down-regulated) in comparison with MM. Some of them, based on their reported functions or putative target genes computed by integrative analysis, might have a role in the pathobiology of pPCL, such as miR-21, that was found to promote in vitro growth of MM cell lines. As regards chromosomal aberrations, the expression of some miRNAs mapped to hot-spot altered regions was associated with DNA copy number of the corresponding genomic loci; furthermore, TP53 deletion, a frequent cytogenetic lesion in our pPCL cohort, was found associated with a trend of down-regulation of miR-34a, whose tumor suppressor activity was demonstrated for the first time also in the context of MM. Finally, four miRNAs (miR-497, miR-106b, miR-181a* and miR-181b) were identified having expression levels correlated with treatment response, and four (miR-92a, miR-330-3p, miR-22, and miR-146a) with clinical outcome.
Conclusions: Overall, this study provides insights into the possible contribution of miRNAs in the pathogenesis of pPCL and suggests targets for future therapeutic investigations.
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Barbieri, M. "HIGH-THROUGHPUT SEQUENCING FOR THE IDENTIFICATION OF DIS3 MUTATIONS IN MULTIPLE MYELOMA." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/259303.
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Multiple myeloma (MM) is an incurable malignancy of mature plasma cells (PCs), and its pathogenesis is only partially understood. Recently, whole exome sequencing studies have identified mutations of DIS3, a catalytic subunit of the human exosome complex, in about 10% of MM patients. This study was aimed at investigating the spectrum of DIS3 mutations indifferent stages of plasma cell dyscrasia.
To analyze DIS3 mutations, we investigated by next generation sequencing (NGS) a retrospective cohort of 130 cases with MM at onset and 17 at relapse (of whom 15 were also tested at onset). Moreover, we examined 24 patients with primary PC leukemia (pPCL), 12 with secondary PCL and 20 multiple myeloma cell lines. Deep sequencing of the PIN (exons 1-4) and RNB (exons 10-18) DIS3 functional domains was performed by Roche 454 pyrosequencing on the Genome Sequencer Junior instrument. Mutations were validated by conventional Sanger sequencing or independent ultra-deep 454 pyrosequencing. All samples were characterized by fluorescence in situ hybridization (FISH) for the main genomic aberrations, such as IGH translocations, 13q and 17p deletions, hyperdiploidy, 1p33 (CDKN2C) loss and 1q21.3 (CKS1B) gain. In order to verify if the mutations detected on genomic DNA were expressed at transcriptomic level, DIS3 cDNA of mutated cases was subjected to deep sequencing. Global gene expression of MM patients was also profiled, looking for transcriptional patterns possibly related to DIS3 mutations. Additionally, to investigate DIS3 mutation status longitudinally, we analyzed 20 patients whose bone marrow specimens were collected at two different time points. Finally, the association of DIS3 mutations with clinical outcome was tested, comparing wild-type patients (n=12) with those characterized by mutations in PIN or RNB functional domains of DIS3 (n=4).
NGS analysis revealed the presence of 41 coding non-synonymous variants, with a mutant allele frequency ranging from 0.38% to 100% of total reads (median depth of coverage 245x, range: 64-1160). Among the 41 tumor-specific mutations, 30 (73%) were single nucleotide variations, and the remaining 11 (27%) were indels. Nine of these variants have been already reported by others, eight of which also specifically in MM patients, while 32 were novel. The great majority of mutations identified in our cohort of patients affected the RNB domain (30/41, 73.2%). The mutations affected 26 MM patients at diagnosis (26/130, 20%), four at relapse (4/17, 23.5%), six pPCL (6/24, 25%), four sPCL (4/12, 33.3%) cases, and three multiple myeloma cell lines (3/20, 15%). We observed a positive association of DIS3 mutations with the occurrence of translocations involving IGH@ locus, particularly with the t(11;14), and a negative association with hyperdiploid cases, but no association with 13q and 17p deletion, gain of chromosome 1q and loss of chromosome 1p. Additionally, we showed that mutant allele frequencies detected on genomic DNA and on retrotranscribed total RNA are linearly correlated. Moreover, in serially analyzed patients, we detected mutations at constant allele frequency at both time points, or acquired/increased variants in the late sample, consistent with the expected positive selection of mutated subclones. Furthermore, global gene expression profiling analysis revealed 119 differentially expressed genes (all up-regulated in mutated cases) between DIS3 mutated and wild-type cases. Finally, we tested the association of DIS3 mutations with clinical outcome in 16 pPCL patients for whom the follow-up was available, showing that mutational events did not show any impact neither on PFS nor OS.
Our data confirm DIS3 as frequently mutated in MM, and importantly, seem to indicate an even greater involvement of DIS3 alteration in more advanced stages of PC dyscrasias. Furthermore, these data, although requiring confirmation in independent patients’ series, support the hypothesis that DIS3 may play a role in development and progression of MM.
Further studies are required to elucidate the role of this gene in the pathogenesis of MM, as well as its potential use as a drug target.
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Adhinaveni, Ramesh. "Molecular analysis of different clinical presentations of chronic lymphocytic leukemia reveals novel molecular predictors and molecular heterogenety of different anatomical compartments." Doctoral thesis, Università del Piemonte Orientale, 2022. http://hdl.handle.net/11579/144065.
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Chronic lymphocytic leukemia (CLL) and Small lymphocytic lymphoma (SLL) are different manifestation of the same lymphoproliferative disease. Our study aims at evaluating molecular markers that predispose to chemorefractoriness in CLL and to identify molecular landscape of the different anatomical compartments of SLL. Fludarabine, cyclophosphamide, and rituximab (FCR) is the most effective chemoimmunotherapy regimen for young and fit CLL patients devoid of TP53 disruption. A cohort of 287 patients receiving first-line FCR was analyzed by next generation sequencing (NGS). By univariate analysis, BIRC3 mutations identify a poor prognostic subgroup of patients failing FCR (p<0.001) as cases harboring TP53 mutations (p<0.001). BIRC3 mutations maintained an independent association with an increased risk of progression (p=0.004) in multivariate analysis. By immunoblotting analysis, we showed that the non-canonical NF-KB pathway is active in BIRC3 mutated cell lines and in primary CLL samples. In vitro results indicate that BIRC3 mutated primary CLL cells are less sensitive to fludarabine. BIRC3 mutations may be used as a new molecular predictor to select high-risk patients for novel drugs. Regarding SLL, we investigated 12 SLL patients, provided with: cell free DNA (CfDNA) from plasma, genomic DNA (gDNA) from LNF biopsies, gDNA from CD19+ cells and from CD3+ cells, by using NGS. By comparing mutations identified, SLL genotyping on the cfDNA does not recapitulate SLL genetics and lacks 65.2% identified in the PB CD19+ cells and in the LNF. By considering the 44 mutations identified in the LNF and in the PB CD19+ cells, 20.4% of mutations were unique to the LNF biopsy, 36.4% were unique to the PB CD19+ cells and only 43.2% were shared. The analysis of the LNF only or of the PB CD19+ cell only may miss mutations with potential clinical relevance, suggesting that both these two compartments should be tested to have a comprehensive view of the SLL genetics relevance.
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Jouan, Alain. "Le complexe NADPH-oxydase producteur d'ions superoxyde des neutrophiles : étude immunochimique des facteurs cytosoliques d'activation." Université Joseph Fourier (Grenoble), 1995. http://www.theses.fr/1995GRE10154.
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Le complexe nadph-oxydase producteur d'ions superoxyde des neutrophiles est compose de sous-unites cytosoliques et membranaires qui s'assemblent au cours du processus d'activation de l'enzyme. La proteine g monomerique rac stimule considerablement l'activation. Nous avons produit des anticorps monoclonaux, polyclonaux et anti-peptides contre les constituants cytosoliques de ce complexe (facteurs cytosoliques), et contre le systeme des proteine g monomeriques associees au complexe. Les anticorps nous ont permis de mettre au point une technique elisa hypersensible de detection et de dosage des deux facteurs cytosoliques p47 et p67, applicable au suivi de ces facteurs au cours de leur purification. Un anticorps monoclonal anti-p67 nous a permis d'immunoprecipiter a partir du cytosol un complexe contenant p47 et p67, fonctionnel dans l'activation de l'oxydase. Nous avons montre que la proteine g monomerique rac n'est pas associee a ce complexe dans le cytosol ce qui suggere qu'elle joue un role au niveau membranaire. Nous avons enfin suivi l'apparition des differents constituants du complexe nadph-oxydase au cours de la differenciation de cellules hl60 de promyelocytes immatures en neutrophiles et correle cette apparition moleculaire a celle de l'activite oxydase. Les constituants qui apparaissent le plus tardivement sont les facteurs cytosoliques p47 et p67. Leur expression maximale est necessaire pour l'activite oxydase optimale
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Burianová, Ilona. "Inhibitory histondeacetyláz v léčbě plazmocelulární leukemie: vliv mikroprostředí kostní dřeně." Doctoral thesis, 2016. http://www.nusl.cz/ntk/nusl-351282.
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Multiple myeloma and its aggressive variant, plasma cell leukemia, are still considered to be incurable diseases despite the progressive treatment approaches comprising novel drugs. This can be attributed to the presence of the bone marrow microenvironment which plays an important role in drug resistance of myeloma cells. Hematopoietic cell lines derived from hematologic malignancies are suitable models for the study of etiopathogenesis of these malignant diseases and for testing new potential drugs. Establishment of these cell lines is still considered to be coincidental and rare event. The first part of the thesis is focused on establishment and characterization of the cell line UHKT-944 derived from a patient with primary plasma cell leukemia, and on completion of characterization of the cell line UHKT-893 derived from a patient with multiple myeloma. Additional analysis of UHKT-893 cell line were performed including sequence analysis of IgVH gene rearrangements and cytogenetic analysis which contributed to more detailed characterization of this cell line. During cultivation of UHKT-944 cells, we monitored the cell growth and confirmed dependence on interleukin-6 (IL-6). Immunophenotype analysis revealed the presence of surface markers characteristic of malignant plasma cells. UHKT-944 cells...
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CHAO, YA-LI, and 趙亞麗. "Identification of diabete-related plasma and liver protein markers by using post-translational proteomic approaches and a proteomic approach to decipher the growth inhibition and killing mechanism of nano-gold particles on human leukemia cells." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/09122331437848612324.
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碩士輔仁大學
生命科學系碩士班
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In this study, we utilized proteomic approaches to investigate the differentially expressed plasma protein related to diabetes. The streptozotocin (STZ) diabetic rats were utilized for investigation. Using high fat diet to induce the diabete-like phenotype, the STZ treated and the control rat were examined for the blood sugar level and regrouped for proteomic analysis. By employing our developed affinity chromatography, the total proteome as well as the phosphoproteome and glycoproteome from the rat plasma samples were purified and examined. Briefly, albumin, vitamin D-binding protein precursor, and transthyretin were down- regulated, phosphorylated- complement inhibitory factor H, serum albumin, and alpha-2-HS-glycoprotein were up- regulated, and glycosylated –fibrinogen B beta chain, carboxylesterase precursor, serine peptidase inhibitor were up-regulated in the plasma of diabeteic rats. The physiological significance of the identified proteins with diabetes was discussed. On the other hand, proteomic techniques were also utilized to inspect the mechanism of death elicited by Nanogold particles, which was found effectively inducing apoptosis in human chronic leukemia cells (K562). In conjunction with proteomic techniques and systems biology analysis, we suggest that endoplasmic reticulum (ER) stress response may be the major cellular event elicited by Nanogold particles and induce cell death if unmanageable.
Books on the topic "Plasma Cell Leukemi"
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Steensma, David P. Malignant Hematology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0296.
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The hematologic neoplasms include lymphoproliferative disorders (eg, chronic lymphocytic leukemia [CLL]/small lymphocytic lymphoma [SLL], large granular lymphocyte leukemia, hairy cell leukemia [HCL], Hodgkin lymphoma, non-Hodgkin lymphoma), plasma cell disorders (multiple myeloma, light chain amyloidosis, Waldenström macroglobulinemia, POEMS syndrome, heavy chain disease, plasmacytoma), chronic myeloid neoplasms (chronic myeloid leukemia, the BCR/ABL-negative myeloproliferative neoplasms, myelodysplastic syndromes), and acute leukemia (acute myeloid leukemia, acute lymphocytic leukemia). In addition, clonal but not overtly malignant conditions are common in the general population, including monoclonal gammopathy of undetermined significance (MGUS) and monoclonal B lymphocytosis (MBL).
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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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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, and Gareth Morris-Stiff. Bone and soft tissue malignancies. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199689842.003.0025.
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Haematological malignancies examines the epidemiology, genetics, clinical presentation and classification of these diseases, and presents current treatment approaches for each. First are the acute leukaemias, and the management of acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemia (AML). Chronic myeloid leukaemia, its genetics and sensitivity to tyrosine kinase inhibitors, is described. Myelodysplastic syndromes and their management, are followed by chronic lymphoid leukaemias, a large heterogeneous group of diseases, and their treatment. Hodgkin lymphoma, its pathology and presentation, staging and role of PET scanning, is described along with current treatment with chemotherapy and limited radiotherapy. Non-Hodgkin lymphoma is another heterogeneous group of diseases, divided into low-grade and high-grade pathology, and varying in their genetics, presentation, and management. Rituximab is a key component of chemotherapy regimens against B-cell lymphoma. Myeloma and other plasma cell dyscrasias are described, and treatment options reviewed. Myeloma remains incurable, but with appropriate management consistent with prolonged good quality life. Treatment includes chemotherapy, bisphosphonate therapy, analgesics and radiotherapy, Throughout this chapter is emphasised the importance of clinical trials in driving the rapid improvements in treatment of these diseases.
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Adam, Sheila, Sue Osborne, and John Welch. Haematological problems. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199696260.003.0012.
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This chapter discusses specific haematological disorders that require the patient to be admitted to the critical care unit. It describes the normal physiology of blood cells, clotting mechanisms, and fibrinolysis, and the management of related conditions such as thrombocytopenia, leukaemia, and clotting disorders such as disseminated intravascular coagulation. It also includes the management of the critical care patient with haematological malignancy. Specific therapies such as plasma exchange and anticoagulation therapy are discussed in detail and the monitoring of coagulation tests is explained. The chapter also describes the administration of blood and blood products, together with their associated hazards, and the effects of massive transfusions of blood.
Book chapters on the topic "Plasma Cell Leukemi"
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Joseph, Nisha S., Amarendra K. Neppalli, and Ajay K. Nooka. "Plasma Cell Leukemia." In Personalized Therapy for Multiple Myeloma, 121–29. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-61872-2_7.
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Hayman, Suzanne R. "Plasma Cell Leukemia." In Hematologic Malignancies: Multiple Myeloma and Related Plasma Cell Disorders, 119–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-08885-2_5.
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Joseph, Nisha S., and Sagar Lonial. "Plasma Cell Leukemia." In Neoplastic Diseases of the Blood, 639–44. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-64263-5_34.
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Gonsalves, Wilson I., and Shaji K. Kumar. "Plasma Cell Leukemia." In Biology and Management of Unusual Plasma Cell Dyscrasias, 1–16. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4419-6848-7_1.
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Eltorai, Ibrahim M. "Plasma Cell Leukemia (PCL)." In Rare Diseases and Syndromes of the Spinal Cord, 389–90. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45147-3_116.
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Gertz, Morie A., Laura Rosinol, and Joan Bladé. "Plasma Cell Leukemia and Extramedullary Plasmacytoma." In Hematologic Malignancies, 157–75. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-25586-6_9.
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Drappatz, Jan, and Kurt A. Jaeckle. "Neurological Complications of Plasma Cell Disorders." In Lymphoma and Leukemia of the Nervous System, 299–312. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7668-0_18.
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Hashmi, Shahrukh. "Hematological Malignancies in the UAE." In Cancer Care in the United Arab Emirates, 603–10. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-99-6794-0_38.
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AbstractHematologic malignancies make up a substantial portion of overall cancers, and unfortunately, the incidence of hematologic malignancies continues to grow in developed countries. These encompass both inherited and acquired cancers, though complicating the differentiation is the fact that some of the primary immunodeficiencies and bone marrow failure syndromes can lead to the development of leukemia and myelodysplastic syndrome as well, besides lymphomas. Plasma cell dyscrasias are also a complicated group of conditions that include, at one spectrum, AL amyloidosis, which can be rapidly fatal if untreated, and the monoclonal gammopathy of unknown significance, which can be a very slow-evolving condition. Many different classifications exist in the literature; however, in this chapter, we summarize the various classifications and then suggest the most standard classifications for the readers. The management aspects of hematologic malignancies are extremely complicated, as besides chemotherapies, immunotherapies, and radiation therapies, cellular therapies play a major role in curative therapy, including CAR-T cells and stem cell transplantation.
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Zegadlo, M., M. Matysiak, and M. Ochochka. "Plasma Cell Leukemia in a 7-month-old Infant." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 211–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-71960-8_25.
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Khojasteh, Ali. "Cardiac Disorders in Leukemias and Plasma-Cell Dyscrasias." In Cancer and the Heart, 175–84. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4898-9_15.
Full textConference papers on the topic "Plasma Cell Leukemi"
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Falang, A., G. M. Alessio, M. Donati, and T. A. Barbui. "DISSEMINATED INTRAVASCULAR COAGULATION (DIC) AND ACUTE LEUKEMIA:IDENTIFICATION OF A NEW CELLULAR PROCOAGULANT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643661.
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There is an enhanced incidence (>50%) of severe coagulopathy in association with several types of acute leukemias. Cell associated procoagulants are considered important in this context. So far only a Tissue Factor (TF)-type procoagulant has been described in leukemic cells. We have set up here the experimentalconditions to identify other possible cellular procoagulants in leukemia. We have tested blast cell extracts from 21 patients with 5 different cytological subtypes (from Ml to M5 of acute non lymphoid leukemia (ANLL), according to theFAB classification, in order to assay whether they express "cancer procoagulant" (CP), a F VH-independent FX activating cysteine proteinase (Falanga … Gordon, 1985; Donati, et al. 1986). All the samples shortened the recalcification time of normal human plasma, the effect being significantly greater (p<0.001) in the M3 group. The activity was 20% to 100% independent from the presence of FVII and was susceptible to 2 cysteine proteinase inhibitors (Iodoacetamide, 2 mM, and HgCl2 ,0.1 mM) in all of the extracts but the M5 type. In addition, M2 and M3 samples directly activated pure FX in a two stage clotting assay. Control cell extracts from 10 healthy donors did not show any procoagulant activity, under the same conditions. This study provides evidence for a new procoagulant expressed by cells of ANLL; the peculiar characteristics of this procoagulant (i.e. its confinement to the malignant phenotype, its shedding into the plasma, its possible modulation by vitamin K antagonists) make this observation of potential interest in the development of new diagnostic and therapeutic tools in ANLL.
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Thiyagarajan, Magesh. "Portable Plasma Biomedical Device for Cancer Treatment." In ASME 2011 6th Frontiers in Biomedical Devices Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/biomed2011-66030.
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This research study examined the effect of non-thermal portable atmospheric air plasma system on leukemia cancer cells. Acute monocytic leukemia cells (THP-1) were exposed to atmospheric pressure non-thermal plasma. To assess death caused by plasma exposure, cells were subjected to trypan blue exclusion assays and a kill-curve and assessment of death overtime were compiled using data from the assays. In addition to this, DNA was harvested from treated and untreated samples to determine if apoptotic ladders were present. Results have indicated that non-thermal plasma can cause cell death in THP-1 cells overtime, and the death that occurs corresponds directly to the amount of time that the cells were exposed to ionized plasma. Preliminary fluorescent imaging of the treated cells revealed that higher treatment doses are not only more likely to induce cellular death but are likely to induce necrotic death, while lower treatment doses that are capable of inducing death may induce apoptotic or programmed cellular death. Ideally the results obtained from these experiments will allow for further investigation of the effects of ionized non-thermal plasma on melanoma cell lines and will lead to an inexpensive method for treating early stage skin cancer and cancerous lesions.
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Gamba, G., L. Dezza, N. Montani, G. Gangale, G. Gangale, and E. Ascari. "EFFECT OF INTERFERON GAMMA ON PROCOAGULANT ACTIVITY FROM HUMAN PROMYELOCYTIC CELL LINE (HL 60)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643662.
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Interferon gamma (IFN), a lymphokine acting as biological response modifier, can induce morphological and phenotypic differentiation of some leukemic cell lines, specially along the monocytic pathway.Furthermore, myeloid leukemic cells and normal monocytes have been demonstrated to possess procoagulant activity (PCA).The aim of this study was to investigate the modulation of PCA induced by treatment with IFN on human promyelocytic cells from HL 60 cell line.Cells were cultured in suspension for 5days in RPMI 1640 medium supplemented with 10% fetal calf serum in the absence or in the presence of different concentrations of IFN (100-10.000 u/ml) at37°C and 5% CO2 Differentiation was assessed by morphological and cytochemical methods (MGG, ANAE, CAE, MPO) on cytospin preparations and surface marker analysis with monoclonal antibodies (0KMI, Mo2, MY9, MY7, MY4).PCA was measured as capacity to shortening ricalcification time of normal plasma and of factor VIII, VII and X deficient plasmas by the cells and the conditioned media.Untreated HL 60 cells exhibit high tissue factor-like PCA, related to the cellnumber. IFN treatment (1000 u/ml) induced at the same time, monocytic differentiation and significant increase in PCAboth in the cells and in the conditioned media.The PCA was not further affected by higher concentrations of IFN, unabletodetermine cell maturation.In conclusions the modulation by IFN seems to be dependent onmonocytic differentiation of HL 60 cells.
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Esumi, N., S. Todo, and S. Imashuku. "INTERACTION BETWEEN HEMOSTATIC COMPONENTS AND TUMOR CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643202.
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Involvement of platelets and coagulation systems in the hematogenous metastasis of tumor cells has been suggested from in vivo and in vitro studies, however, there is still controversy about the exact role of hemostasis in metastasis. To date, at least three types of platelet aggregating mechanisms and three types of tumor cell procoagulants have been reported in different tumor cells.We investigated platelet aggregating activity (PAA), procoagulant activity (PCA) and the relationship between these two activities, using eight human neuroblastoma cell lines, three human leukemia cell lines and human mature lymphocytes. PCA in tumor cells was measured by the single stage recalcification time and the assay with chromogenic substrate S2222. PAA was determined turbidometrically with an aggregometer by adding cell suspensions of tumor cells to platelet rich plasma (PRP). The effects of protease inhibitors, enzymes and thrombin inhibitors on PAA and PCA were also studied.Neuroblastoma cell suspensions showed high PCAs which were reduced in Factor VII deficient human plasma, indicating a tissue factor-like activity. NCG line possessing the highest PCA also showed a high PAA, which was inhibited by pretreatment of cell suspensions with phospholipase A2 and abolished in the presence of heparin, hirudin or MD805 in the assay system. Human leukemia cell lines and mature lymphocytes had weak to moderate PCAs without showing PAA, but became active to express PAA after being removed of cell surface sialic acid by neuraminidase. These results suggest that in neuroblastoma, PCA closely linked with PAA may play a role in the hematogenous metastasis. In hemopoietic cells, PAA expressed when cell surface sialic acid is removed does not correlate with PCA, and sialic acid in these cells possibly prevents direct interaction with platelets in the hemostatic homeostasis.
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Thiyagarajan, M., X. Gonzales, H. Anderson, and M. Norfolk. "Non-thermal plasma induction of preprogrammed cell death in monocytic leukemia cells." In 2012 IEEE 39th International Conference on Plasma Sciences (ICOPS). IEEE, 2012. http://dx.doi.org/10.1109/plasma.2012.6383688.
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Berthier, R., A. Duperray, O. Valiron, M. Prenant, I. Newton, and A. Schweitzer. "MEGAKARYOCYTIC DEVELOPMENT IN LIQUID CULTURES OF CRYOPRESERVED LEUKOCYTE STEM CELL CONCENTRATES FROM CHRONIC MYELOGENOUS LEUKEMIA PATIENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644622.
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The proliferation and differentiation of human megakaryocytes in liquid culture has been obtained using cryopreserved light density blood cell concentrates from chronic myelogenous leukemia (CML) patients. These cryopreserved leukocytes concentrates contain a large number of viable granulo-monocytic, erythroid and megakaryocytic committed stem cells. A high number of spontaneous megakaryocytic colonies was observed in semisolid cultures plated with the CML leukocytes concentrates. A liquid culture system using RPMI 1640 supplemented with 20% human plasma (HP) has been defined where maturing megakaryocytes make up 20 to 60% of the total cells after 14 days of incubation. The same cell suspension cultured in medium supplemented with 20% foetal calf serum (FCS) showed poor megakaryocytic cell development. The megakaryocytic nature of the cells produced in HP supplemented cultures was confirmed by cytological studies and indirect immunofluorescence labeling using monoclonal antibodies (MoAb) against membrane platelet GPIb and Ilbllla, and intracellular antigens like fibrinogen and von Willebrand factor.Ploidy of the cultured cells was studied after labeling with propidium iodide and the DNA fluorescence determined using the fluorescence activated cell sorter (FACSIV). Peaks of 8N, 16N and 32N cells were observed from HP supplemented cultures representing about 20% of the cells reacting with a GP11b111 a MoAb, while very few cells greater than 4N were observed in FCS supplemented cultures. The megakaryocytes produced in HP cultures could be further enriched by cell sorting on the FACSIV after labeling with an anti-IIbIIIa MoAb. Depending on the initial megakaryocytic concentration of the cells cultured, one to 2 é 106 megakaryocytes per hour could be harvested. Thus, cryopreserved CML blood stem cell concentrates seem to offer a reproducible source of human megakaryocytes which retain their capacity to proliferate and differentiate in liquid cultures supplemented with human plasma. These megakaryocytes can be used for the study of platelet glycoprotein biosynthesis as well as the regulation of megakaryocytopoiesis.
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Barekzi, N., and M. Laroussi. "Low temperature atmospheric pressure plasma kills leukemia cells." In 2012 IEEE 39th International Conference on Plasma Sciences (ICOPS). IEEE, 2012. http://dx.doi.org/10.1109/plasma.2012.6383691.
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Anderson, Heather, Xavier Gonzales, Samantha Valdez, and Magesh Thiyagarajan. "Activation of apoptotic cell death in human myeloid leukemia cells by RNS: A novel antitumor approach using resistive barrier plasma." In 2013 IEEE 40th International Conference on Plasma Sciences (ICOPS). IEEE, 2013. http://dx.doi.org/10.1109/plasma.2013.6634817.
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Paparo, Sabrina Marie, Rebeca Mendoza, Robert Chitren, Omar Al-Odat, Emily Nelson, Subash Jonnalagadda, Roger Strair, and Manoj Pandey. "Investigating the Therapeutic Potential of Soursop in Treating Hematologic Malignancies." In 28th Annual Rowan-Virtua Research Day. Rowan University Libraries, 2024. http://dx.doi.org/10.31986/issn.2689-0690_rdw.stratford_research_day.129_2024.
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Acute Myeloid Leukemia (AML) and Multiple Myeloma (MM) are hematologic malignancies that originate in the bone marrow and account for approximately 1.3% and 2% of cancer cases, respectively. AML is characterized by an accumulation of myeloblasts, or immature myeloid cells, that have the potential to spread to the peripheral blood. There is an uncontrolled proliferation of plasma cells in the bone marrow in MM. While the current treatment options for both AML and MM show promise in achieving initial remission, it is unfortunately common for patients to experience relapse and develop drug resistance. There is a theory that relapse and resistance could be attributed to the survival of progenitor cells with stem-cell-like properties in the protective niches of the bone marrow. Our research suggests that the plant, soursop, may have potential in combating hematologic cancers by triggering apoptosis and potentially preventing drug resistance and relapse. Soursop, scientifically known as Annona muricata, is a plant that thrives in tropical and subtropical regions. Every component of the plant, including the leaves, fruit, seeds, and bark, exhibit preventative properties against a wide range of diseases. Our study focuses on examining the effectiveness and mode of action of an extract obtained from soursop leaves. We aim to determine its potential in exhibiting anti-cancer properties, specifically against AML and MM cell lines. Our findings reveal that the extract from soursop leaves has the ability to trigger apoptosis and reduce cell viability in HL-60 and MM.1S cells. Through our research, we have discovered the inhibition or downregulation of the JAK/STAT pathway.
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Narahara, N., H. Sadakata, T. Uchiyama, K. Andoh, H. Tanaka, N. Kobayashi, and T. Maekawa. "MECHANISM OF ACTIVATION OF BLOOD COAGULATION BY LEUKOCYTE PROCOAGULANT ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643161.
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To investigate the process of activation mechanism of blood coagulation by leukocytes, binding of radiolabelled Factor X and the activation of Factor X on the cell surface of leukocytes were studied by using cultured leukemia cell line, Molt-4 cells. Cells were cultured in RPMI 1640 medium with 10% inactivated fetal, calf serum at a concentration of 1x106cells/ml. After 6 hours' stimulation with 1 ug/ml of endotoxin(LPS: Escherichia coli 026:B6), cells were separated by centrifugation, washed three times with Tris containing NaCl buffer(pH 7.5, TBS), and then suspended in TBS containing 0.5% bovine serum albumin(TBS-BSA) to the concentration of 5x106 cells/ml. Factors X, VII and IX were purified from fresh-frozen human plasma by the method of Bajaj in a modified version. Factor VIII was purified from cryoprecipitate as starting material. Factor X labelled with 1-125 by the method of McFarlane showed a single band on autoradiography. Specific radioactivity was 0.3 mCi/mg. For the study on binding of Factor X, TBS-BSA solution containing 4 mM of CaClp, various amounts of radiolabelled Factor X with/without purified Factors VII, VIII and IX were added to the LPS-stimulated washed cell suspension and mixed well. N-butyl-phtalate was layered over the reaction mixture after incubation at room temperature for various minutes. Total amount of bound Factor X was calculated from the radioactivity of the cell pellet separated by centrifugation of the reaction mixture. The Xa activity generated in the supernatants was assayed using S2222.Results: Factor X bound specifically to the LPS-stimulated Molt-4 cells. Amount of bound Factor X and the dissociation constant was 1.0 ng/5x10bcells (5.2x103sites/cell) and 5x106M, respectively. More amounts of Factor X bound when Factors VIII and IX were present in the reaction mixture than their absence. Five times more Factor Xa was generated when Factors VII, VIII and IX were present in the reaction mixture as compared with presence of Factor VII, alone. These results suggest that blood coagulation cascade proceeds on the LPS-stimulated leukocyte surface.