Relevant bibliographies by topics / Cell fusion in neoplasma

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Academic literature on the topic 'Cell fusion in neoplasma'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Cell fusion in neoplasma"

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Cheah, Chan Y., Kate Burbury, Jane F. Apperley, Francoise Huguet, Vincenzo Pitini, Martine Gardembas, David M. Ross, et al. "Patients with myeloid malignancies bearing PDGFRB fusion genes achieve durable long-term remissions with imatinib." Blood 123, no. 23 (June 5, 2014): 3574–77. http://dx.doi.org/10.1182/blood-2014-02-555607.

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Key Points Imatinib achieves deep and durable remissions in patients with myeloid neoplasms bearing PDGFRB. Allogeneic stem cell transplantation is no longer indicated for patients with chronic myeloproliferative neoplasm bearing PDGFRB who respond to imatinib.
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Schischlik, Fiorella, Jelena D. Milosevic Feenstra, Elisa Rumi, Daniela Pietra, Bettina Gisslinger, Martin Schalling, Edith Bogner, Heinz Gisslinger, Mario Cazzola, and Robert Kralovics. "Fusion Gene Detection Using Whole Transcriptome Analysis in Patients with Chronic Myeloproliferative Neoplasms and Secondary Acute Myeloid Leukemia." Blood 126, no. 23 (December 3, 2015): 4093. http://dx.doi.org/10.1182/blood.v126.23.4093.4093.

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Abstract Fusion oncogenes resulting from chromosomal aberrations are common disease drivers in myeloid malignancies. The most prominent example is BCR-ABL1 fusion present in chronic myeloid leukemia, which together with essential thromobocythemia (ET), primary myelofibrosis (PMF) and polycythemia vera (PV) belongs to the classic myeloproliferative neoplasms (MPN). The BCR-ABL1 negative MPNs are driven by somatic mutations in JAK2, MPL and CALR. MPN patients can progress to acute myeloid leukemia (AML) but the transformation process is not well understood. Studies using standard karyotyping and SNP microarrays have shown that disease progression is characterized by an increase in karyotype complexity. We aimed to identify novel fusion oncogenes in patients with BCR-ABL1 negative MPN during chronic phase and disease progression in high-throughput and cost-efficient manner using RNA-seq technology. In addition this approach enabled us to perform RNA-seq variant calling for identification of gene mutations on the same cohort of patients. Whole transcriptome sequencing was performed on 121 patients (112 chronic phase MPN and 9 secondary AML samples) and 23 healthy controls in a 100 base pair paired-end manner. The cohort consisted of 44% PMF, 22% ET, 12% PV and 6% secondary AML patients. The output of three fusion detection tools (Defuse, Tophat-fusion and SOAPfuse) was combined in order to increase sensitivity. Extensive filtering steps were applied in order to enrich for cancer specific fusion events, including filtering for fusions appearing in healthy individuals, filtering for read-throughs and false positives with external databases and manual inspection of sequencing reads. The outcome of analysis for Defuse, Tophat-fusion and SOAPfuse resulted in the total of 52, 54 and 38 candidate fusions, respectively. Candidate fusions were Sanger-sequenced and for Tophat-fusion and Defuse the validation rate was 60%, while for SOAPfuse only 20% could be validated. Approximately 70% of the fusion candidates were not shared among the 3 tools which underlines the importance of selecting the union of all calls from each tool rather than the intersect. We did not observe clustering of breakpoints along the genome. Most fusion candidates could be detected in PMF which corresponds to the disease entity that was most represented in the cohort (44% of patients). No enrichment for fusions was found in 7 triple negative (no JAK2, CALR, MPL mutations) cases. 42% of chromosomal aberrations were translocations, followed by duplication (31%), inversion (14%) and deletion events (11%). Among the intragenic fusions, approximately half had genomic breakpoints less than 1 Mb apart. 70% of validated fusions were out of frame, while 28% were in frame. In the leukemic samples a higher abundance of fusions was found (4/9). Typical fusions for de novo AML were not detected within secondary AML (sAML) samples. We did not detect a recurrent fusion oncogene in our patient cohort. In a PMF patient with JAK2-V617F mutation we identified a BCR-ABL1 fusion, indicating a clonal exchange which was consistent with patient's phenotype. Another PMF patient exhibited an inversion event involving the first exon of CUX1, causing a CUX1 loss of function. Other fusions in chronic MPN patients affected genes involved in histone modifications (SMYD3-AHCTF1, KDM4B-CYHR1). In post-MPN AML patients we identified a somatic in frame-fusion involving INO80D and GPR1 and a fusion truncating the first 3 exons of RUNX2 (XPO5-RUNX2). The high quality of RNA sequencing data, allowed us to set up a variant detection workflow that will be compared with matched samples that have been exome sequenced. Preliminary results could demonstrate that mutations in the JAK2 gene in a cohort of 96 patients were all correctly recalled, emphasizing its sensitivity. Fusion events among patients in chronic phase MPN are rare and the majority of these events imply loss of function of both fusion gene partners. This approach adds valuable information on the true frequency of inactivation of genes such as CUX1 in patients, as small inversions like the one described above would not be detectable by other methods. Detection of a subclone with BCR-ABL1 fusion underlines the strength of the fusion detection workflow for diagnostic purposes. Typical de novo AML fusions were not found in sAML and further suggests that de novo AML and sAML are distinct disease entities on a genetic level. Disclosures Gisslinger: Janssen Cilag: Honoraria, Speakers Bureau; Sanofi Aventis: Consultancy; AOP ORPHAN: Consultancy, Honoraria, Research Funding, Speakers Bureau; Celgene: Consultancy, Honoraria, Research Funding, Speakers Bureau; Novartis: Honoraria, Research Funding, Speakers Bureau; Geron: Consultancy. Kralovics:AOP Orphan: Research Funding; Qiagen: Membership on an entity's Board of Directors or advisory committees.
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Seeber, Andreas, Lea Holzer, Andrew Elliott, Dietmer Dammerer, Vaia Florou, Roman Groisberg, Benjamin Henninger, et al. "Deciphering the molecular landscape and the tumor microenvironment of perivascular epitheloid cell neoplasma (PEComa)." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): 11539. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.11539.

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11539 Background: PEComa is a rare mesenchymal neoplasm composed of perivascular epithelioid cells. Due to its rarity, diagnosis is challenging and no standardized treatment guidelines have been established. A subgroup of PEComas are characterized by a loss of function mutation in TSC1/2 that activates the PIK3-Akt-mTOR pathway. In the majority of patients, however, the molecular landscape and the composition of the tumor microenvironment (TME) remain largely unclear. Thus, we conducted this study to elucidate the genetic landscape of PEComas. A comparative analysis was performed with melanoma as a representative immunogenic tumor type. Methods: Thirty-five PEComa specimens were centrally analysed at the Caris Life Sciences laboratory. NextGen DNA sequencing (NextSeq, 592 gene panel or NovaSeq, whole-exome-sequencing), whole-transcriptome RNA sequencing (NovaSeq) and immunohistochemistry (Caris Life Sciences, Phoenix, AZ) were performed. Gene expression profiling (GEP) was performed by unsupervised hierarchical clustering. RNA deconvolution analysis was performed using the Microenvironment Cell Populations (MCP)-counter method to quantify immune cell populations (Becht 2016, Genome Biology). Results: The most common mutations detected in this cohort were TP53 (47%), ATRX (32%), TSC1/2 (11%/29%) and MSH3 (17%). Interestingly, TP53 mutations occurred less frequently (25 vs 60%, p = 0.055) in TSC1/2-mutated ( TSC1/2-mt) compared to TSC1/2-wildtype ( TSC1/2-wt) tumors, whereas MSH3 (25%, n = 1/4) and ERCC2 (14%, n = 2/14) mutations were exclusively observed in TSC1/2-mt cases. TSC1/2 mutations and other mTOR signalling pathway alterations, including two TFE gene fusion transcripts, were mutually exclusive. Of note, we found that 33.3% (n = 2) of TSC2-mt tumors were associated with high PIK3-Akt-mTOR pathway expression, while 100% (n = 3) of TSC1-mt tumors demonstrated lower expression. Deficient mismatch repair/microsatellite instability-high and high tumor mutational burden were rare (2.9%, n = 1 each) and observed concurrently in absence of PD-L1 expression. Overall, PD-L1 expression was observed in 21.9% (n = 7) of patients. An exploratory comparison with melanoma revealed that PEComa TMEs were characterized by a significant increase of NK cells and fibroblasts, as well as a relevant decrease of CD8+ T cells and B cells. Conclusions: Within this study we discovered a heterogeneous molecular landscape with a high prevalence of TSC1/2 mutations that were in part associated with transcriptional up-regulation of the PIK3-Akt-mTOR pathway. Furthermore, the relatively immune-cold TME compared to melanoma suggests increased lymphocyte infiltration may be required to increase the efficacy of immune checkpoint inhibitors for PEComa.
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Imperial, Sandy L., and Jagmohan S. Sidhu. "Nonseminomatous Germ Cell Tumor Arising in Splenogonadal Fusion." Archives of Pathology & Laboratory Medicine 126, no. 10 (October 1, 2002): 1222–25. http://dx.doi.org/10.5858/2002-126-1222-ngctai.

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Abstract Splenogonadal fusion is a rare congenital malformation in which the spleen is abnormally connected to the gonads or to the mesonephric derivatives. A few more than 150 cases have been described in the world literature. We report an additional case of splenogonadal fusion. A nonseminomatous germ cell tumor was found in the testicle involved in this splenogonadal fusion. To our knowledge, this is the third reported case of a testicular neoplasm associated with splenogonadal fusion and the first reported case of intra-abdominal nonseminomatous germ cell testicular tumor arising in this rare anomaly. The literature pertaining to splenogonadal fusion and the testicular tumor arising in this anomaly is briefly reviewed.
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Haferlach, Claudia, Wencke Walter, Manja Meggendorfer, Constance Baer, Anna Stengel, Stephan Hutter, Niroshan Nadarajah, Wolfgang Kern, and Torsten Haferlach. "The Diverse Landscape of Fusion Transcripts in 25 Different Hematological Entities." Blood 136, Supplement 1 (November 5, 2020): 16–17. http://dx.doi.org/10.1182/blood-2020-137518.

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Background: Genomic alterations are a hallmark of hematological malignancies and comprise small nucleotide variants, copy number alterations and structural variants (SV). SV lead to the co-localization of remote genomic material resulting in 2 different scenarios: 1. breakpoints are located within 2 genes leading to a chimeric fusion gene and a fusion transcript, 2. breakpoints are located outside of genes, frequently placing one nearby gene under the influence of the regulatory sequences of the partner, leading to a deregulated - usually increased - transcription. Aim: The frequency of fusion transcripts was determined across hematological entities in order to 1) identify recurrent partner genes across entities, 2) evaluate the specificity of fusion transcripts and genes involved in fusions for distinct entities. Cohort and Methods: Whole transcriptome sequencing (WTS) was performed in 3,549 patients in 25 different hematological entities (table). 101 bp paired-end reads were produced on a NovaSeq 6000 system (Illumina, San Diego, CA) with a yield between 35 and 125 million paired reads per sample. Potential fusions were called using 3 different callers (Arriba, STAR-Fusion, Manta), only fusions called by at least 2 callers, validated by whole genome sequencing (data available for all cases) and with at least one protein coding partner were kept for further analyses. Reciprocal fusion transcripts were counted as one fusion event. Results: In total 1,309 fusion transcripts were identified in 932 of 3,549 (26.3%) patients. 221 patients showed > 1 fusion (2 fusions: 150, 3: 36, >3: 35). 806 distinct fusion transcripts were divided into recurrent fusions (n=50) and unique fusions, i.e. found only in 1 case (n=756). Out of 932 patients with at least 1 fusion, 541 (58%) patients harbored a minimum of one recurrent fusion. The proportion of patients harboring any or a recurrent fusion varied substantially between different entities with high frequencies for both in CML (96.5%/96.5%), B-lineage ALL (53.1%/41.3%), AML (42.8%/31.2%), and T-lineage ALL (35.3%/12.6%). In several myeloid entities low fusion frequencies were observed (e.g. PMF, MDS/MPN-U, MDS, figure A). No fusion transcripts were detected in ET. Strikingly, fusions were detected in a substantial proportion of cases with lymphoid neoplasms but only very few occurred recurrently (e.g. T-PLL: 47.8%/4.3%, FL: 39.3%/4.9%, figure A). With regard to age, only patients with AML and T-ALL harboring recurrent fusions were significantly younger than corresponding cases without recurrent fusions (59 vs 71 yrs, p<0.0001; 35 vs 38 yrs, p=0.02). Only in AML patients with unique fusions were older (70 vs 66 yrs, p=0.02), while no age differences were observed between cases with and without unique fusions in other entities. 23/50 (46%) of the recurrent fusions were specific for one entity (12 in myeloid, 11 in lymphatic entities), while the other 54% (27/50) were observed in 2 to 7 different entities. Of these 27 recurrent fusions, only 16 fusions were shared between myeloid and lymphatic entities, while 10 were restricted to myeloid and one fusion to lymphatic entities (figure B). In total 1,270 different genes were involved in the 806 distinct fusions, indicating a broad spectrum of potential functional impact. 54 genes were involved only in recurrent fusions, 27 genes in both recurrent and unique fusions, while 1,189 genes were solely involved in unique fusions. Four genes involved in recurrent fusions and 32 genes involved in unique fusions are FDA approved drug targets (Human Protein Atlas). Only 16% (199/1270) of the genes were involved in more than one fusion: 3 genes (ETV6, KMT2A, RUNX1) in 14 fusions, 2 genes (ABL1, BCR) in 11 fusions, 16 genes in 4 to 10 fusions, 38 genes in 3 fusions, 140 in 2 fusions. Several genes frequently involved in fusions in hematological malignancies (e.g. ABL1, ETV6, KMT2A) and 78/1189 genes only involved in unique fusions were also reported to be partners in fusions in non-hematological malignancies. Conclusions: As known, in CML and acute several leukemias a high proportion of patients harbor fusions of which many occur recurrently, suggesting a substantial pathogenic impact and, thus, requiring detection in a diagnostic work-up. In BCR-ABL1 negative chronic myeloid malignancies few fusions were observed while lymphoma patients carry frequently non-recurrent fusions with so far unknown impact on pathogenesis and prognosis. Disclosures No relevant conflicts of interest to declare.
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Aldera, Alessandro Pietro, and Komala Pillay. "Clear Cell Sarcoma of the Kidney." Archives of Pathology & Laboratory Medicine 144, no. 1 (March 27, 2019): 119–23. http://dx.doi.org/10.5858/arpa.2018-0353-rs.

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Clear cell sarcoma of the kidney is an uncommon malignant pediatric renal neoplasm that typically presents in the 2- to 3-year age group and has a propensity for aggressive behavior and late relapses. Histologically, this tumor exhibits a great diversity of morphologic patterns that can mimic most other pediatric renal neoplasms, often leading to confusion and misdiagnosis. Until recently, adjunct immunohistochemical and molecular genetic tests to support the diagnosis were lacking. The presence of internal tandem duplications in BCL-6 coreceptor (BCOR) and a translocation t(10;17) creating the fusion gene YWHAE-NUTM2B/E have now been well accepted. Immunohistochemistry for BCOR has also been shown to be a sensitive and specific marker for clear cell sarcoma of the kidney in the context of pediatric renal tumors. Improved intensive chemotherapy regimens have influenced the clinical course of the disease, with late relapses now being less frequent and the brain having overtaken bone as the most common site of relapse.
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Taylor, Justin, Christina Marcelus, Dean Pavlick, Ryma Benayed, Akihide Yoshimi, Emiliano Cocco, Benjamin H. Durham, et al. "Characterization of Ntrk fusions and Therapeutic Response to Ntrk Inhibition in Hematologic Malignancies." Blood 130, Suppl_1 (December 7, 2017): 794. http://dx.doi.org/10.1182/blood.v130.suppl_1.794.794.

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Abstract Chromosomal rearrangements involving the neurotrophic receptor tyrosine kinases NTRK1-3 produce oncogenic fusions in a wide variety of adult and pediatric cancers. Although the frequency of NTRK fusions in most cancers is <5%, efficacy in solid tumors harboring these fusions is striking with a 76% durable response rate recently reported with the highly selective pan-TRK inhibitor larotrectinib (LOXO-101) in a cohort comprised of 17 unique tumor types. By contrast, the frequency of NTRK fusions is not well appreciated in hematologic malignancies and targeting of NTRK fusions has not been clinically tested. Herein, we describe the occurrence of NTRK fusions across >7,000 patients with hematologic malignancies and characterize their signal transduction, transforming properties, and response to larotrectinib in vitro and in an AML patient and corresponding patient-derived xenograft (PDX) in vivo . We performed targeted RNA sequencing using the Foundation One Heme sequencing panel across 7,311 cases of hematologic malignancies and discovered 8 patients (0.11%) harboring NTRK fusions. Fusions occurred in patients with histiocytic (LMNA-NTRK1, TFG-NTRK1) and dendritic cell (TPR-NTRK1) neoplasms (n=2/78), ALL (ETV6-NTRK3; n=1/659) as well as two with AML (n=2/1201). While previous case reports have reported ETV6-NTRK3 fusions in ALL and AML, our cohort also included an ETV6-NTRK2 fusion previously unreported in AML. In addition, we detected two multiple myeloma patients with NTRK3 fusions (UBE2R2-NTRK3 and HNRNPA2B1-NTRK3; n=2/1859) which represent the first description of NTRK fusions in myeloma. The fusion breakpoints are predicted to create in-frame fusions containing the tyrosine kinase domain of each of the NTRK genes and Sanger sequencing of RT-PCR on available tissues confirmed this. We next cloned 4 of these fusions and tested their transforming capacity in cytokine-dependent murine hematopoietic cells (Ba/F3 cells), which do not express endogenous Trk proteins. Despite equivalent levels of Trk expression, the transforming properties and auto-phosphorylation of each TRK fusion was distinct (A). The LMNA-NTRK1 and ETV6-NTRK2 fusions caused robust cytokine-independent growth. In contrast, additional NTRK fusions in which the 5' partner lacked classic oligomerization domains resulted in slower transformation (UBE2R2-NTRK3 fusion)or no transformation (HNRNPA2/B1-NTRK3). Consistent with these different growth properties, each fusion activated PI3K-AKT signaling to differing degrees after cytokine withdrawal (B) . Finally, the cells that gained cytokine-independence were exquisitely sensitive to treatment with larotrectinib. In contrast, Ba/F3 cells transformed by BRAF V600E mutation were unresponsive to Trk inhibition (C). The course of the above studies identified a patient with an ETV6-NTRK2 fusion AML. Using a PDX generated from this patient, we initiated treatment with larotrectinib (200mg/kg/day) after 8 weeks of transplantation when human myeloid leukemia engraftment reached a median of 15%. Larotrectinib treatment reduced human chimerism compared with mice receiving vehicle (although human myeloid leukemia cells persisted even with larotrectinib treatment- D). Consistent with the response of the AML PDX to Trk inhibition, treatment of the same patient with larotrectinib initiated under the FDA expanded access program resulted in clinical partial remission. This was due to eradication of the ETV6-NTRK2 mutant clone, which was sustained until outgrowth of a treatment refractory ETV6-MECOM clone resulted in progressive disease. FACS sorting and analysis of the AML revealed that each ETV6 fusion occurred in a distinct AML clone. Serial targeted RNA-seq analysis of bulk cells identified reduction of expression of the ETV6-NTRK2 fusion throughout the period of LOXO-101 treatment with concomitant increased expression of the ETV6-MECOM fusion (E). We herein describe that NTRK fusions occur across patients with a wide variety of hematologic malignancies and are amenable to Trk inhibition. Further studies to evaluate the clonality of NTRK fusions across cancers and whether this is predictive of therapeutic response to Trk inhibition will be critical based on the case here. Nonetheless, the clinical response here in a refractory patient argues for the need for systematic evaluation of NTRK fusions despite their rarity across hematologic neoplasms. Figure Figure. Disclosures Pavlick: Foundation Medicine: Employment. Watts: Jazz Pharmaceuticals: Consultancy, Speakers Bureau. Albacker: Foundation Medicine Inc.: Employment, Equity Ownership. Mughal: Foundation Medicine, Inc: Employment, Other: Stock. Ebata: LOXO Oncology: Employment. Tuch: LOXO Oncology: Employment. Ku: LOXO Oncology: Employment. Arcila: Archer: Honoraria; Raindance Tecnologies: Honoraria; Invivoscribe: Honoraria. Ali: Foundation Medicine, Inc: Employment, Other: Stock. Park: Amgen: Consultancy.
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Xie, Zhongqiu, Mihaela Babiceanu, Shailesh Kumar, Yuemeng Jia, Fujun Qin, Frederic G. Barr, and Hui Li. "Fusion transcriptome profiling provides insights into alveolar rhabdomyosarcoma." Proceedings of the National Academy of Sciences 113, no. 46 (October 31, 2016): 13126–31. http://dx.doi.org/10.1073/pnas.1612734113.

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Gene fusions and fusion products were thought to be unique features of neoplasia. However, more and more studies have identified fusion RNAs in normal physiology. Through RNA sequencing of 27 human noncancer tissues, a large number of fusion RNAs were found. By analyzing fusion transcriptome, we observed close clusterings between samples of same or similar tissues, supporting the feasibility of using fusion RNA profiling to reveal connections between biological samples. To put the concept into use, we selected alveolar rhabdomyosarcoma (ARMS), a myogenic pediatric cancer whose exact cell of origin is not clear. PAX3–FOXO1 (paired box gene 3 fused with forkhead box O1) fusion RNA, which is considered a hallmark of ARMS, was recently found during normal muscle cell differentiation. We performed and analyzed RNA sequencing from various time points during myogenesis and uncovered many chimeric fusion RNAs. Interestingly, we found that the fusion RNA profile of RH30, an ARMS cell line, is most similar to the myogenesis time point when PAX3–FOXO1 is expressed. In contrast, full transcriptome clustering analysis failed to uncover this connection. Strikingly, all of the 18 chimeric RNAs in RH30 cells could be detected at the same myogenic time point(s). In addition, the seven chimeric RNAs that follow the exact transient expression pattern as PAX3–FOXO1 are specific to rhabdomyosarcoma cells. Further testing with clinical samples also confirmed their specificity to rhabdomyosarcoma. These results provide further support for the link between at least some ARMSs and the PAX3–FOXO1-expressing myogenic cells and demonstrate that fusion RNA profiling can be used to investigate the etiology of fusion-gene-associated cancers.
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Lim, Ha Jin, Jun Hyung Lee, Ju-Hyeon Shin, Seung Yeob Lee, Hyun-Woo Choi, Hyun Jung Choi, Seung Jung Kee, Jong Hee Shin, and Myung-Geun Shin. "Diagnostic Validation of a Clinical Laboratory-Oriented Targeted RNA Sequencing System As a Comprehensive Assay for Hematologic Malignancies." Blood 136, Supplement 1 (November 5, 2020): 38–39. http://dx.doi.org/10.1182/blood-2020-142264.

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Introduction Targeted RNA sequencing (RNA-seq) is a highly accurate method for sequencing transcripts of interest and can overcome limitations regarding resolution, throughput, and multistep workflow. However, RNA-seq has not been widely performed in clinical molecular laboratories due to the complexity of data processing and interpretation. We developed a customized targeted RNA-seq panel with a data processing protocol and validated its analytical performance for gene fusion detection using a subset of samples with different hematologic malignancies. Additionally, we investigated its applicability for identifying transcript variants and expression analysis using the targeted panel. Methods The target panel and customized oligonucleotide probes were designed to capture 84 genes associated with hematologic malignancies. Libraries were prepared from 800 to 1,500 ng of total RNA using GeneMediKit NGS-Leukemia-RNA kit (GeneMedica, Gwangju, Korea) and sequenced using Miseq reagent kit v3 (300 cycles) and MiseqDx (Illumina, San Diego, CA, USA). The diagnostic samples included one reference DNA (NA12878), one reference RNA (Cat no. 740000, Agilent Technologies), 14 normal peripheral blood (PB) samples, four validation bone marrow (BM) samples with known gene fusions, and 30 clinical BM or PB samples from seven categories of hematologic malignancies. The clinical samples included 27 BM aspirates and three PB samples composed of six acute myeloid leukemia, nine B-lymphoblastic leukemia/lymphoma, four T-lymphoblastic leukemia/lymphoma, three mature B-cell neoplasms, six MPN, one myelodysplastic/myeloproliferative neoplasm, and one myeloid/lymphoid neoplasm with eosinophilia and gene rearrangement. For the analytical validation of fusion detection, target gene coverage, between-run and within-run repeatability, and dilution tests (1:2 to 1:8 dilution) were performed. For the comparative analysis of fusion detection, the RNA-seq data were analyzed by STAR-Fusion and FusionCatcher and processed with stepwise filtering and prioritization strategy (Figure 1), and the result was compared to those of multiplex RT-PCR (HemaVision kit; DNA Technology, Aarhus, Denmark) or FISH (MetaSystems Gmbh, Althusseim, Germany) using 30 clinical samples. The RNA-seq data from clinical samples were additionally analyzed by FreeBayes for variant detection and by StringTie for expression profiling (Figure 1). Results First, the analytical validation showed reliable results in target gene coverage, between-run and within-run repeatability, and linearity tests. The uniformity of coverage (% of base pairs higher than 0.2 × total average depth) was calculated to be 99.8%, which revealed even coverage for the target genes in the panel using the reference DNA. Both in the within-run and between-run tests, the read counts and FFPM (fusion fragments per million) of all replicates showed reliable repeatability (r2 = 0.9655 and 0.9874, respectively). The FFPM of the diluted analytical samples including BCR-ABL1 and PML-RARA showed linear log2-fold-changes (r2 = 0.9852 and 0.9447, respectively). Second, compared to multiplex RT-PCR and FISH using 30 clinical samples, targeted RNA-seq combined with filtering and prioritization strategies detected all 13 known fusions and newly detected 17 fusions. Finally, 16 disease- and drug resistance-associated variants on the expressed transcripts of ABL1, GATA2, IKZF1, JAK2, RUNX1, and WT1 were simultaneously designated and expression analysis showed distinct four clusters of clinical samples according to the cancer subtypes and lineages. Conclusions Our customized targeted RNA-seq system provided a stable analytical performance and a more sensitive identification of gene fusions than conventional molecular methods in various clinical samples. In addition, clinically significant variants in the transcripts and expression profiling could be simultaneously identified directly from the RNA-seq data without the need for additional parallel testing. Our study identified the advantages of the clinical laboratory-oriented targeted RNA-seq system to enhance the diagnostic yield for gene fusion detection and to simplify the diagnostic steps as providing a comprehensive tool for analyzing hematologic malignancies in the clinical laboratory. Figure 1 Disclosures Lee: National Research Foundation of Korea: Research Funding.
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Kasbekar, Monica, Valentina Nardi, Paola Dal Cin, Andrew M. Brunner, Yi-Bin Chen, Christine Connolly, Amir T. Fathi, et al. "Targeted FGFR Inhibition Results in Hematologic and Cytogenetic Remission in a Myeloid Neoplasm Driven By a Novel PCM1-FGFR1 Fusion: Data from an Expanded Access Program." Blood 134, Supplement_1 (November 13, 2019): 5371. http://dx.doi.org/10.1182/blood-2019-124100.

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Introduction In 2008, the World Health Organization defined a new classification of myeloid and lymphoid neoplasms with eosinophilia that result from gene rearrangements of PDGFRA, PDGFRB, and FGFR1. While rearrangements involving PDGFRA and PDGFRB generally respond well to imatinib, those associated with FGFR1 are typically aggressive and require treatment with allogeneic hematopoietic stem cell transplantation (SCT). Here we present the case of a patient with a previously unreported fusion of PCM1-FGFR1. The patient was treated with an Oral, potent, selective, and irreversible small-molecule inhibitor of FGFR 1- 4 (futibatinib (TAS-120)) under an expanded access program, resulting in the first reported instance of complete hematologic and cytogenetic remission using futibatinib in an FGFR-driven myeloid neoplasm. Results A 55-year-old male presented with dyspnea and fatigue and was found to have peripheral eosinophilia (3,660/microliter) and thrombocytopenia (46,000/microliter). Diagnostic bone marrow biopsy was notable for a hypercellular (cellularity >95%), erythroid dominant marrow with increased eosinophilic forms and increased pronormoblasts. Break-apart fluorescence in situ hybridization (FISH) studies revealed an FGFR1 gene rearrangement in 11.3% of nuclei (normal < 5.7%). The nature of the rearrangement was shown to be a paracentric inversion of chromosome 8p based on the distinct gap between the 5'FGFR1 and 3'FGFR1 probes in metaphase FISH (Figure 1). A validated, targeted next generation sequencing assay for fusion transcript detection (heme fusion assay) revealed a previously unreported PCM1-FGFR1 fusion transcript (40 unique fusion reads), with an in-frame fusion of PCM1 (exons 1-36) to FGFR1 (exons 11-18). No additional clonal markers were identified. The patient was not considered an SCT candidate due to medical comorbidities and was enrolled on a single-patient protocol expanded access program for futibatinib. He was initially treated with prednisone for control of his eosinophilia, and then started on oral therapy with futibatinib (20 mg daily). Within 1 month of initiation of futibatinib, prednisone was tapered without recurrence of eosinophilia and with improvement in platelet count (169,000/microliter). After 6 months, repeat bone marrow biopsy showed a moderately hypocellular marrow with maturing trilineage hematopoiesis. Additionally, the paracentric inversion of chromosome 8p was no longer observed in metaphase FISH, consistent with cytogenetic remission. Furthermore, the PCM1-FGFR1 fusion transcript was no longer detectable by heme fusion assay. The patient has experienced grade 2 skin rash requiring brief dose interruption (7 days) followed by dose reduction to 16 mg daily, on which he remains. He has also experienced grade 2 hyperphosphatemia, a known side effect of futibatinib, which is adequately controlled with sevelamer. The patient continues on futibatinib, with ongoing evidence of hematologic and cytogenetic remission after 11 months of therapy. Conclusions To our knowledge, this case represents the first report of a PCM1-FGFR1 fusion driving a myeloid neoplasm with eosinophilia. Treatment with futibatinib has resulted in hematologic and cytogenetic remission, with treatment successfully ongoing after 11 months. Our findings support further exploration of FGFR inhibitors as a therapeutic strategy for myeloid/lymphoid neoplasms driven by FGFR1 rearrangement, particularly in individuals who are not candidates for SCT. A phase 2 study of futibatinib in patients with FGFR1 driven myeloid/lymphoid neoplasms is planned. Disclosures Brunner: Astra Zeneca: Research Funding; Celgene: Membership on an entity's Board of Directors or advisory committees, Research Funding; Forty Seven Inc: Membership on an entity's Board of Directors or advisory committees; Jazz Pharma: Membership on an entity's Board of Directors or advisory committees; Novartis: Research Funding. Chen:Magenta: Consultancy; Takeda: Consultancy; Kiadis: Consultancy; Incyte: Consultancy; Abbvie: Consultancy. Fathi:Amphivena, Kite, Jazz, NewLink Genetics,: Honoraria; Agios, Astellas, Celgene, Daiichi Sankyo, Novartis, Takeda, Amphivena, Kite, Forty Seven,Trovagene, NewLink genetics, Jazz, Abbvie, and PTC Therapeutics: Consultancy. Narayan:Genentech: Other: Equity ownership (spouse); Merck: Other: Equity ownership (spouse); Takeda: Other: Employment (spouse). Benhadji:Taiho Oncology: Employment. Hobbs:Incyte: Consultancy, Research Funding; Merck: Research Funding; Jazz pharmaceuticals: Consultancy; Celgene: Consultancy; Bayer: Research Funding; Agios: Consultancy.
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Dissertations / Theses on the topic "Cell fusion in neoplasma"

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Copeman, M. C. "Alterations to the extracellular matrix in neoplasia : a study in suppressed and tumorigenic hybrid cells." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233450.

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Hess, Patricia M. "Role of c-Jun NH-terminal Kinase in Bcr/Abl Induced Cell Transformation: a dissertation." eScholarship@UMMS, 2003. https://escholarship.umassmed.edu/gsbs_diss/88.

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The c-Jun NH2-terminal kinase (JNK) group of kinases include ten members that are created by alternative splicing of transcripts derived from Jnk1, Jnk2 and Jnk3 genes. The JNK1 and JNK2 protein kinases are ubiquitously expressed while JNK3 is expressed in a limited number of tissues. The JNK signaling pathway is implicated in multiple physiological processes including cell transformation. There is growing evidence that JNK signaling is involved in oncogenesis. Nevertheless, the role that JNK plays in malignant transformation is still unclear. The aim of this thesis is to examine the role of JNK in malignant transformation. For this purpose, I used the Bcr/Abl oncogene as a transforming agent. Bcr/Abl is a leukemogenic oncogene that is created by reciprocal translocation between chromosome 9 and 22. The translocation breakpoint is variable and several different Bcr/Abl isoforms have been identified such as Bcr/AblP185 and Bcr/AblP210, whose expression is associated with different types of leukemia. Bcr/Abl activates the JNK signaling pathway in hematopoietic cells and increases AP-1 transcription activity. Furthermore, dominant negative approaches demonstrate that inhibition of c-Jun or JNK prevents Bcr/ Abl-induced cell transformation in vitro. These data implicate the JNK signaling pathway in Bcr/Abl transformation although the role that JNK might have in this process is unclear. Thus, I examined the importance of JNK signaling in Bcr/Abl-induced lymphoid or myeloid transformation. For this purpose I compared Bcr/AblP185- and Bcr/AblP210- induced transformation of wild-type and JNK1-deficient cells using three approaches: in vitro, in vivo and ex vivo. The results obtained with the in vitro approach suggest that both Bcr/AblP185 and Bcr/AblP210 require JNK activity to induce lymphoid transformation. While JNK1-deficiency inhibits Bcr/AblP210 oncogenic potential in lymphoid cells both in vitro and in vivo, pharmacological inhibition of JNK activity (JNK1 and/or JNK2) blocked Bcr/AblP185 induced malignant proliferation in vitro. The differential requirement for JNK observed in the two Bcr/Abl isoforms can be ascribed to the presence in Bcr/AblP210 of the Dbl domain which can activate the JNK pathway in vitro. In the case of Bcr/AblP210, JNK1 is critical for the survival of the ex vivo derived transformed lymphoblasts upon growth factor removal. This result correlates with the fact that mice reconstituted with Bcr/AblP210 transformed Jnk1-l- bone marrow showed normal malignant lymphoid expansion in the bone marrow yet they had reduced numbers of lymphoblast in the bloodstream and lacked peripheral organ infiltration. Thus JNK1 is essential for the survival of the transformed lymphoblast outside the bone marrow microenvironment in Bcr/AblP210induced lymphoid leukemia. Interestingly, while JNK1 is essential for lymphoid transformation, it is dispensable for the proliferation of transformed myeloblasts. Taken together these results indicate that the JNK signaling pathway plays an essential role in the survival of Bcr/AblP210 lymphoblasts and that JNK-deficiency decreases the leukomogenic potential of Bcr/AblP210 in vivo. Thus, cell survival mediated by JNK may contribute to the pathogenesis of proliferative diseases.
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CHAMBI, ROSA M. C. "Proteínas de fusão endostatina-peptídeos com atividade apoptótica: expressão e estudo de atividade antiangiogênica." reponame:Repositório Institucional do IPEN, 2009. http://repositorio.ipen.br:8080/xmlui/handle/123456789/10166.

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Tese (Doutoramento)
IPEN/T
Instituto de Pesquisas Energeticas e Nucleares - IPEN-CNEN/SP
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Bardsley, David William. "Electroacoustic cell fusion." Thesis, Cardiff University, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305186.

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Heilman, Susan Ann. "Cooperative Oncogenesis and Polyploidization in Human Cancers: A Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/327.

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A common phenotype observed in most cancers is chromosomal instability. This includes both structural and numerical chromosomal aberrations, which can promote carcinogenesis. The fusion gene CBFB/MYH11 is created by the structural chromosomal inversion(16)(p13.1q22), resulting in the fusion protein CBFβ-SMMHC, which blocks differentiation in hematopoietic progenitor cells. This mutation alone, however, is not sufficient for transformation, and at least one additional cooperating mutation is necessary. The role of wildtype Cbfb in modulating the oncogenic function of the fusion protein Cbfβ-SMMHC in mice was examined. Transgenic mice expressing the fusion protein, but lacking a wild-type copy of Cbfb, were created to model the effects of these combined mutations. It was found that wild-type Cbfb is necessary for maintaining normal hematopoietic differentiation. Consequently, complete loss of wild-type Cbfb accelerates leukemogenesis in Cbfb/MYH11 mice compared to mice expressing both the fusion and wild-type proteins. While there is no evidence in human patient samples that loss of wild-type Cbfb expression cooperates with the fusion protein to cause transformation, it is apparent from these experiments that wild-type Cbfβ does play a role in maintaining genomic integrity in the presence of Cbfβ-SMMHC. Experiments have also shown that loss of Cbfb leads to accumulation of hematopoietic progenitor cells, which may acquire additional cooperating mutations. Not unlike CBFB/MYH11, the human papillomavirus (HPV) E6 and E7 proteins are not sufficient for cellular transformation. Instead, high risk HPV E7 causes numerical chromosomal aberrations, which can lead to accumulation of additional cooperating mutations. Expression of HPV-16 E7 and subsequent downregulation of the retinoblastoma protein (Rb) has been shown to induce polyploidy in human keratinocytes. Polyploidy predisposes cells to aneuploidy and can eventually lead to transformation in HPV positive cells. There are several possible mechanisms through which E7 may lead to polyploidization, including abrogation of the spindle assembly checkpoint, cleavage failure, abrogation of the postmitotic checkpoint, and re-replication. Rb-defective mouse and human cells were found to undergo normal mitosis and complete cytokinesis. Furthermore, DNA re-replication was not found to be a major mechanism to polyploidization in HPV-E7 cells upon microtubule disruption. Interestingly, upon prolonged mitotic arrest, cells were found to adapt to the spindle assembly checkpoint and halt in a G1-like state with 4C DNA content. This post-mitotic checkpoint is abrogated by E7-induced Rb-downregulation leading to S-phase induction and polyploidy. This dissertation explores two examples of the multi-step pathway in human cancers. While certain genes or genetic mutations are often characteristic of specific cancers, those mutations are often not sufficient for transformation. The genetic or chromosomal abnormalities that they produce often stimulate the additional mutations necessary for oncogenesis. The studies with Cbfb/MYH11 and HPV E7 further exemplify the significance of numerical and structural chromosomal aberrations in multi-step carcinogenesis.
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Lichius, Alexander. "Cell fusion in Neurospora crassa." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/7561.

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The primary research aims of this thesis were the identification of novel cell fusion mutants of Neurospora crassa and the subsequent functional characterization of selected candidate proteins during conidial anastomosis tube (CAT)-mediated cell fusion by means of genetic, molecular, biochemical and live-cell imaging analysis. Chapter 1 provides a general introduction of the model organism and the cell fusion processes studied during different stages of the fungal lifecycle. Chapter 2 summarizes the materials and methods used. Chapter 3 introduces the comparative genomics screen conducted between appressorium-mediated plant infection by the rice blast fungus Magnaporthe oryzae and hyphal fusion in Neurospora crassa. Novel cell fusion mutants were identified in MAP kinase signalling, redox-signalling and Rho-type GTPase signalling pathways, whereas no functional overlap in the cAMP response pathway between both species could be found. Chapter 4 demonstrates how newly developed fluorescent reporters for F-actin and activated Rho GTPases in filamentous fungi lead to novel insights into the dynamic rearrangement of the F-actin cytoskeleton and cortical activation of Rho GTPases during cell symmetry breaking, polarized tip growth and cell fusion. Chapter 5 focuses on the role of the cell wall integrity (CWI) MAP kinase pathway during cell fusion, and in particular, on the function of the terminal MAP kinase MAK-1 during CAT homing and fusion pore formation. Inhibitor studies indicated that MAK-1 kinase activity is required for its own recruitment to the fusion site already during homing and for cell wall remodelling during fusion pore enlargement between interacting cells. Chapter 6 presents ultrastructural scanning electron microscope (SEM) studies which indicate that defects in hyphal attachment, extracellular matrix deposition and cell wall remodelling prematurely abort morphogenesis of the female fruitbody. These findings are put into context with defects observed in mutants of components acting in related signalling pathways which appear to regulate non-self fusion events at later stages of sexual development leading to fertilization in N. crassa. Chapter 7 provides the first evidence for a role of NADPH-oxidase (NOX)-generated reactive oxygen species (ROS) in the regulation of morphogenetic changes required for CAT-mediated cell fusion. Redox-modification of signalling proteins might be involved in cell-cell chemoattraction. Chapter 8 provides a summary of the key findings and discusses future directions.
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Manson, Graham. "Electrofusion of cells : development of a fusion apparatus and a protocol for cell fusion." Thesis, University of Aberdeen, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297646.

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Design and construction of an apparatus to provide signal sources for electrofusion of cells is described. Experiments were performed with the apparatus on mammalian human cells and plant protoplasts to derive the best protocols to achieve alignment and fusion. Four versions of the apparatus were constructed with modifications being determined by both the results of the cell experiments and electronic experiments on circuit design. The protocols to be followed to achieve fusion of cells in different media were confirmed by experiment, and the signal on the cell was mathematically analysed. Using the results of this analysis, an improved protocol was produced for achievement of cell fusion in binary or multiple cell clusters in various suspension media, by manipulation of electrical signals. Suggestions are made for circuit construction using new integrated circuit elements and microcontrollers, with machine operation and information logging being directed by a personal computer.
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Côté, Marceline. "Fusion and cell entry by oncogenic sheep retroviruses." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66893.

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Jaagsiekte sheep retrovirus (JSRV) and enzootic nasal tumour virus (ENTV) are two highly related oncogenic retroviruses that induce a contagious cancer in sheep and goats respectively. Both JSRV and ENTV use hyaluronidase-2 (Hyal2) as a cell entry receptor, yet JSRV induces lung tumours and ENTV causes tumours in the nasal epithelium. Unlike most acutely transforming retroviruses, the genomes of JSRV and ENTV do not contain an oncogene derived from the host cell; instead, the viral envelope protein (Env) functions as an active oncogene in addition of mediating cell entry. JSRV and ENTV Env are first synthesized as precursors that are cleaved by a cellular protease into two functional subunits: the surface (SU) subunit that contains the receptor binding domain and the transmembrane (TM) subunit that mediates membrane fusion. While most of previous studies have focused on the oncogenic properties of these proteins, little was known about how they mediate membrane fusion and viral entry. The goal of my Ph.D study was to investigate the mechanisms of fusion and cell entry by JSRV and ENTV Env as well as their regulations. We found that, although most retroviruses are believed to use a pH-independent pathway for entry, JSRV requires an acidic pH for entry and fusion and that its fusogenicity was negatively regulated by its cytoplasmic tail. Unexpectedly, ENTV Env requires an unusually low pH (<4.5) for fusion activation. While an irreversible inhibitor, Bafilomycin A1, which prevents acidification in the endosomes and lysosomes inhibited entry of JSRV and ENTV, ENTV Env-mediated infection was considerably enhanced in the presence of lysosomotropic agents or leupeptin, suggesting that JSRV and ENTV likely fuse in distinct cellular compartments. Importantly, we found that SU also modulates the fusion activity of JSRV and ENTV Env, despite that TM dictates the differential pH requirements between JSRV and ENTV.
Le virus JSRV (Jaagsiekte sheep retrovirus) et ENTV (enzootic nasal tumor virus) sont deux rétrovirus oncogéniques apparentés qui induisent un cancer contagieux chez le mouton et la chèvre respectivement. Le récepteur utilisé lors de l'entrée de JSRV et d'ENTV dans la cellule cible est la protéine cellulaire hyaluronidase-2 (Hyal2). Cependant, alors qu'ils reconnaissent le même récepteur à la surface de la cellule, JSRV cause la formation de tumeurs au poumon tandis qu'ENTV induit l'apparition de tumeurs nasales. À l'opposé de la plupart des rétrovirus oncogéniques causant rapidement la formation de tumeurs, les génomes du JSRV et d'ENTV ne contiennent pas d'oncogène dérivé de la cellule hôte. Étonnamment, la protéine virale d'envelope (Env) joue un rôle d'oncogène actif en plus d'assurer ses fonctions durant l'entrée virale. Les Envs du JSRV et d'ENTV sont d'abord synthétisées sous forme de précurseurs qui seront éventuellement clivés dans l'appareil de golgi par une protéase cellulaire en ses deux sous-unités fonctionnelles : la sous-unité de surface (SU), qui contient le domaine de liaison au récepteur, et la sous-unité transmembranaire (TM) qui possède l'activité fusogénique. Alors que la plupart des études sur le JSRV et l'ENTV se concentrent sur les propriétés oncogéniques d'Env, les mécanismes par lesquels Env accomplit l'entrée virale et provoque la fusion de la membrane virale et la membrane cellulaire demeurent inconnus. Le but de ce projet de doctorat était d'étudier les mécanismes d'activation de la fusion ainsi que de mieux comprendre leur régulation. Alors qu'en principe la majorité des rétrovirus entrent dans la cellule via la fusion à la surface de la cellule à pH neutre, notre étude démontre que JSRV requiert un pH acide pour l'entrée et la fusion virale. De plus, l'activité fusogénique d'Env est régulée négativement par sa queu
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Wong, Wing-sze, and 黃詠詩. "Fusion genes in non-small cell lung cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43781378.

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Paterson, David Archibald. "Human cytomegalovirus glycoprotein H complex and cell fusion." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271225.

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Books on the topic "Cell fusion in neoplasma"

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S, Zänker Kurt, and SpringerLink (Online service), eds. Cell Fusion in Health and Disease: I: Cell Fusion in Health. Dordrecht: Springer Science+Business Media B.V., 2011.

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Gogichadze, G. K. Karyogamic theory of cancer cell formation from the view of the XXI century. Hauppauge, N.Y: Nova Science Publishers, 2009.

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T, Gogichadze, ed. Karyogamic theory of cancer cell formation from the view of the XXI century. New York: Nova Biomedical Books, 2010.

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Sowers, Arthur E., ed. Cell Fusion. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-9598-1.

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Chen, Elizabeth H., ed. Cell Fusion. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-250-2.

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Pfannkuche, Kurt, ed. Cell Fusion. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2703-6.

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Dittmar, Thomas. Cell Fusion in Health and Disease: II: Cell Fusion in Disease. Dordrecht: Springer Science+Business Media B.V., 2011.

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Dittmar, Thomas, and Kurt S. Zänker, eds. Cell Fusion in Health and Disease. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0763-4.

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Dittmar, Thomas, and Kurt S. Zänker, eds. Cell Fusion in Health and Disease. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0782-5.

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Bos, Evelyne Catharina Wilhelmina. Coronavirus spike protein: Role in entry and cell-to-cell fusion. [Leiden: University of Leiden, 1998.

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Book chapters on the topic "Cell fusion in neoplasma"

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De Baetselier, Patrick, Ed Roos, Hendrik Verschueren, Steven Verhaegen, Daniel Dekegel, Lea Brys, and Michael Feldman. "Acquisition of Metastatic Properties via Somatic Cell Fusion: Implications for Tumor Progression in Vivo." In New Experimental Modalities in the Control of Neoplasia, 41–55. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5242-6_3.

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Mitsuhashi, Jun. "Cell Fusion." In Invertebrate Tissue Culture Methods, 369–77. Tokyo: Springer Japan, 2002. http://dx.doi.org/10.1007/978-4-431-67875-5_40.

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Stumm, Markus, and Rolf-Dieter Wegner. "Cell Fusion." In Diagnostic Cytogenetics, 282–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59918-7_16.

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Anné, Jozef. "Cell Fusion." In Biotechnology, 93–139. Weinheim, Germany: Wiley-VCH Verlag GmbH, 2008. http://dx.doi.org/10.1002/9783527620838.ch4.

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Vignery, Agnès. "Macrophage Fusion." In Cell Fusion, 149–61. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-250-2_9.

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Ydenberg, Casey A., and Mark D. Rose. "Yeast Mating." In Cell Fusion, 3–20. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-250-2_1.

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Vignery, Agnès. "Methods to Fuse Macrophages In Vitro." In Cell Fusion, 383–95. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-250-2_22.

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Spear, Patricia G. "Virus-Induced Cell Fusion." In Cell Fusion, 3–32. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-9598-1_1.

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Szoka, Francis C. "Lipid Vesicles." In Cell Fusion, 209–40. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-9598-1_10.

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Düzgüneş, Nejat, Keelung Hong, Patricia A. Baldwin, Joe Bentz, Shlomo Nir, and Demetrios Papahadjopoulos. "Fusion of Phospholipid Vesicles Induced by Divalent Cations and Protons." In Cell Fusion, 241–67. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-9598-1_11.

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Conference papers on the topic "Cell fusion in neoplasma"

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Aranda, S., and H. Aranda-Espinoza. "Virus—Cell—Fusion." In MEDICAL PHYSICS. ASCE, 1998. http://dx.doi.org/10.1063/1.56373.

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Mishchenko, A., R. Hatzky, A. Könies, Olivier Sauter, Xavier Garbet, and Elio Sindoni. "Global particle-in-cell simulations of Alfvénic modes." In THEORY OF FUSION PLASMAS. AIP, 2008. http://dx.doi.org/10.1063/1.3033718.

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Hossain, Mohammed I., Amirali K. Gostar, Alireza Bab-Hadiashar, and Reza Hoseinnezhad. "Visual Mitosis Detection and Cell Tracking Using Labeled Multi-Bernoulli Filter." In 2018 21st International Conference on Information Fusion (FUSION 2018). IEEE, 2018. http://dx.doi.org/10.23919/icif.2018.8455486.

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MOON, DAVID D. "THE NUCLEOVOLTAIC CELL." In Proceedings of the 11th International Conference on Cold Fusion. WORLD SCIENTIFIC, 2006. http://dx.doi.org/10.1142/9789812774354_0071.

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Cheng, Eric Dahai, Subhash Challa, and Rajib Chakravorty. "Microscopic Cell Detection Based on Multiple Cell Image Segmentations and Fusion Algorithms." In 2009 2nd International Conference on Biomedical Engineering and Informatics. IEEE, 2009. http://dx.doi.org/10.1109/bmei.2009.5305006.

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Chen, Shuxun, Xiaolin Wang, Jinping Cheng, Chi-wing Kong, Shuk Han Cheng, Ronald A. Li, and Dong Sun. "Artificially induced cell fusion by optical tweezers manipulation." In 2013 IEEE 13th International Conference on Nanotechnology (IEEE-NANO). IEEE, 2013. http://dx.doi.org/10.1109/nano.2013.6720868.

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Mizuta, Y., H. Takuya, T. D. Nguyen, and K. Taguchi. "Cell Fusion and Distinction between Viable Cell and Non-Viable Cell Using Dielectrophoresis and Optical Tweezers." In 2015 International Conference on Electrical, Automation and Mechanical Engineering. Paris, France: Atlantis Press, 2015. http://dx.doi.org/10.2991/eame-15.2015.16.

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Barkat, Mourad, and Pramod Varshney. "On distributed cell-averaging CFAR detection with data fusion." In 26th IEEE Conference on Decision and Control. IEEE, 1987. http://dx.doi.org/10.1109/cdc.1987.272808.

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Botelho, Silvia, Celina da Rocha, Monica Figueiredo, Paulo Drews, and Gabriel Oliveira. "Growing Cell Structures Applied to Sensor Fusion and SLAM." In 2010 Latin American Robotics Symposium and Intelligent Robotic Meeting (LARS). IEEE, 2010. http://dx.doi.org/10.1109/lars.2010.17.

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Dahai Cheng, Eric, Subhash Challa, Rajib Chakravorty, and John Markham. "Microscopic cell segmentation by parallel detection and fusion algorithm." In 2008 IEEE 10th Workshop on Multimedia Signal Processing (MMSP). IEEE, 2008. http://dx.doi.org/10.1109/mmsp.2008.4665055.

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Reports on the topic "Cell fusion in neoplasma"

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Olmsted-Davis, Elizabeth A., Alan R. Davis, Michael Heggeness, Francis Gannon, Mary Dickinson, John Hipp, and Jennifer West. Cell Therapy to Obtain Spinal Fusion. Fort Belvoir, VA: Defense Technical Information Center, July 2008. http://dx.doi.org/10.21236/ada488580.

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Henry, Michael. Cell Fusion and Breast Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, September 2008. http://dx.doi.org/10.21236/ada495341.

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Olmstead-Davis, Elizabeth A. Cell Therapy to Obtain Spinal Fusion. Fort Belvoir, VA: Defense Technical Information Center, February 2006. http://dx.doi.org/10.21236/ada448465.

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Rago, Constantino, and Peter Willett. Data-Fusion: Performance Enhancement Via Resolution Cell Processing. Fort Belvoir, VA: Defense Technical Information Center, November 1995. http://dx.doi.org/10.21236/ada304817.

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Lazebnik, Yuri. Cell Fusion as a Cause of Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, January 2008. http://dx.doi.org/10.21236/ada501720.

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Lazebnik, Yuri. Cell Fusion as a Cause of Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, March 2009. http://dx.doi.org/10.21236/ada502565.

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Lazebnik, Yuri. Cell Fusion as a Cause of Prostate Cancer Metastases. Fort Belvoir, VA: Defense Technical Information Center, April 2011. http://dx.doi.org/10.21236/ada562123.

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Lazebnik, Yuri. Cell Fusion as a Cofactor in Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, January 2010. http://dx.doi.org/10.21236/ada554548.

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Sisemore, James D. Does the SBCT Intelligence Structure Need a Dedicated ACE/Fusion Cell? Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada429468.

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Gong, Jianlin. Prevention and Treatment of Spontaneous Mammary Carcinoma With Dendritic Tumor Fusion Cell Vaccine. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada395983.

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