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ETV6 protein, human

Q: How can PubCompare.ai help researchers study the ETV6 protein more effectively?

PubCompare.ai is a powerful AI-driven platform that can assist researchers in optimizing their studies of the ETV6 protein. The platform allows you to quickly screen protocol literature more efficiently, leveraging AI to pinpoint critical insights that can help you identify the most effective protocols related to the ETV6 protein for your specific research goals. The platform's AI-driven analysis can highlight key differences in protocol effectiveness, enabling you to choose the best option for reproducibility and accuracy in your ETV6 protein research.

Q: Are there different variations or types of the ETV6 protein that researchers should be aware of?

Yes, there are different isoforms and variations of the ETV6 protein that researchers should be familiar with. The ETV6 gene can undergo alternative splicing, resulting in multiple protein isoforms with slightly different structures and functions. Additionally, genetic mutations or rearrangements involving the ETV6 gene have been associated with certain types of cancer, such as acute lymphoblastic leukemia and myelodysplastic syndrome. Understanding these variations is crucial for designing targeted studies and therapies related to the ETV6 protein.

Q: What are some specific applications of the ETV6 protein in research and clinical settings?

The ETV6 protein has a variety of applications in both research and clinical settings. In research, the ETV6 protein is a commonly used model to study transcription regulation, hematopoiesis, and the molecular pathways involved in cancer development. Clinically, the ETV6 protein and its associated genetic alterations are used as biomarkers for the diagnosis and prognostic assessment of certain types of leukemia and lymphoma. Additionally, therapies targeting the ETV6 protein or its downstream effectors are being investigated as potential treatments for ETV6-related cancers.

Q: Are there any common challenges or considerations researchers should be aware of when working with the ETV6 protein?

One common challenge when working with the ETV6 protein is the complexity of its regulatory networks and the plethora of interacting partners it has. The ETV6 protein is involved in a wide range of cellular processes, and understanding its specific roles in different contexts can be challenging. Additionally, the genetic alterations and mutations associated with the ETV6 gene can be diverse, requiring careful study and analysis. Researchers should also be mindful of the potential off-target effects of any interventions targeting the ETV6 protein, as it is a key regulator of important cellular functions.

The ETV6 (Ets Variant 6) protein is a transcription factor that plays a key role in regulating gene expression during cellular processes.
It is involved in hematopoiesis, the development and differentiation of blood cells, and has been implicated in various types of cancer, including leukemias and lymphomas.
Researchers can explore the ETV6 protein using PubCompare.ai, a powerful AI-driven platform that helps optimize research protocols.
PubCompare.ai allows users to quickly locate relevant protocols from literature, preprints, and patents, and use AI-comparisons to identify the best protocols and products for their specific research needs.
This streamlines the research process and provides valuable insights to advance the understanding of the ETV6 protein and its biological functions.

Most cited protocols related to «ETV6 protein, human»

Risk-Stratification Approach in Pediatric ALL

Cited 34 times

Risk classification was based on presenting features and treatment response. B-cell precursor cases with age between 1 and 10 years and leukocyte count <50 × 10⁹/L, DNA index ≥ 1.16, or t(12;21)[ETV6-RUNX1] were provisionally classified as low-risk ALL. Cases with t(9;22)[BCR-ABL1] were considered to have high-risk ALL, while the remaining cases were provisionally classified as standard (intermediate)-risk ALL. The final risk status was determined by MRD levels. Any patient with ≥ 1% bone marrow MRD on day 19 of remission induction, or 0.1% to 0.99% MRD after completion of 6-week induction therapy was considered to have standard-risk ALL. MRD ≥ 1% after completion of induction therapy denoted high-risk ALL.

Pui C.H., Campana D., Pei D., Bowman W.P., Sandlund J.T., Kaste S.C., Ribeiro R.C., Rubnitz J.E., Raimondi S.C., Onciu M., Coustan-Smith E., Kun L.E., Jeha S., Cheng C., Howard S.C., Simmons V., Bayles A., Metzger M.L., Boyett J.M., Leung W., Handgretinger R., Downing J.R., Evans W.E, & Relling M.V. (2009). Treatment of Childhood Acute Lymphoblastic Leukemia Without Prophylactic Cranial Irradiation. The New England journal of medicine, 360(26), 2730-2741.

Publication 2009

Bone Marrow ETV6 protein, human Leukocyte Count Neoadjuvant Therapy Patients Pre-B Lymphocytes Remission Induction RUNX1 protein, human

High-risk ALL Protocol for Children

Cited 7 times

The National Cancer Institute and institutional review boards of all participating POG institutions approved this study. Written informed consent was obtained from guardians or parents according to the guidelines of the National Institutes of Health. Patients with B precursor ALL aged 1 to 21.99 years first enrolled on the COG P9900 classification/induction study, and received Induction chemotherapy according to NCI risk group. All patients ultimately enrolled in this study received a 4 drug (prednisone, vincristine, asparaginase, daunorubicin) Induction. Patients with an M2 (5–25% blasts) marrow at end Induction (day 29) received 2 additional weeks of therapy with the same agents. Patients who had <5% marrow blasts at day 29 or day 43 were eligible to participate in post-Induction trials for low (P9904), standard (P9905) or high risk ALL (P9906). Patients eligible for the study reported herein (P9906) either met the Shuster age/sex/WBC criteria for higher risk[20 ,23 (link)] (Supplementary Table 1), or they had CNS3 leukemia (5 or more WBC/microliter with blasts present on initial cerebrospinal fluid examination), testicular leukemia, or an MLL translocation. Patients with a Philadelphia chromosome or hypodiploidy (DNA index <0.81 or <45 chromosomes) were not eligible. Patients with the favorable genetic features of ETV6-RUNX1 (formerly TEL-AML1) fusion or trisomies of both chromosomes 4 and 10 were not eligible unless they had CNS3 or testicular leukemia. Diagnostic immunophenotyping, cytogenetic and molecular genetic studies needed to determine information required for eligibility for P9906 were performed at reference laboratories as described previously. [23 (link)]

Bowman W.P., Larsen E.L., Devidas M., Linda S.B., Blach L., Carroll A.J., Carroll W.L., Pullen D.J., Shuster J., Willman C.L., Winick N., Camitta B.M., Hunger S.P, & Borowitz M.J. (2011). Augmented Therapy Improves Outcome For Pediatric High Risk Acute Lymphocytic Leukemia: Results Of Children’s Oncology Group Trial P9906. Pediatric blood & cancer, 57(4), 569-577.

Publication 2011

Asparaginase Cerebrospinal Fluid Chromosomes Chromosomes, Human, Pair 4 Daunorubicin Diagnosis Eligibility Determination Ethics Committees, Research ETV6 protein, human Induction Chemotherapy Legal Guardians Leukemia Marrow Parent Patients Pharmaceutical Preparations Philadelphia Chromosome Population at Risk Prednisone RUNX1 protein, human TEL-AML1 fusion protein Testis Therapeutics Translocation, Chromosomal Trisomy Vincristine

Prognostic Risk Classification in Pediatric ALL

Cited 6 times

From October 29, 2007 to March 26, 2017, 598 eligible patients aged between 0.12 to 18.9 years (median, 6.04) with newly diagnosed ALL were enrolled in Total Therapy Study 16 (ClinicalTrials.gov, number NCT00549848) at St. Jude Children’s Research Hospital (14 ). The trial protocol was approved by the institutional review board and is available in the Supplementary information. The study was conducted in accordance with the Declaration of Helsinki, and written informed consent was obtained from the parents or guardians and assent from the patients, as appropriate.
The diagnosis of ALL was based on the immunophenotypic and genetic characteristics of the leukemic cells (14 ). Genomic classification was based on cytogenetics, FISH for ETV6-RUNX1, TCF3-PBX1, BCR-ABL1 and KMT2A-rearrangement, and transcriptome sequencing (RNA-seq) where available (n=502) (13 (link)). Details for genomic classification are provided in Supplementary Figs. S2–4. MRD levels were determined by flow cytometry (14 , 34 (link)) in blood samples on day 8 and in bone marrow samples on day 15 and day 42 (the end of remission induction); a negative MRD was defined as a level <0.01%.
Patients with B-ALL between 1 and 10 years, with a blood leukocyte count at presentation < 50 x 10³/µL, DNA index ≥1.16 (high-hyperdiploidy) or ETV6-RUNX1 fusion were provisionally classified as having low-risk ALL. Those with MRD≥1% on day 15 of induction or 0.01% to <1% on day 42 were classified to have standard (intermediate)-risk ALL. Patients with the BCR-ABL1 or ETP ALL, infants with KMT2A rearrangement, and any patients with day-42 MRD≥1% (regardless of provisional classification) or persistent MRD during the consolidation phase were classified to have high-risk ALL. The remaining patients, including those with TCF3-PBX1, hypodiploidy with less than 44 chromosomes, T-ALL, testicular leukemia or a CNS-3 status (≥5 leukocytes/µL of cerebrospinal fluid with blasts or cranial palsy) at diagnosis were considered to have standard-risk ALL.

Jeha S., Choi J., Roberts K.G., Pei D., Coustan-Smith E., Inaba H., Rubnitz J.E., Ribeiro R.C., Gruber T.A., Raimondi S.C., Karol S.E., Qu C., Brady S.W., Gu Z., Yang J.J., Cheng C., Downing J.R., Evans W.E., Relling M.V., Campana D., Mullighan C.G, & Pui C.H. (2021). Clinical Significance of Novel Subtypes of Acute Lymphoblastic Leukemia in the Context of Minimal Residual Disease–Directed Therapy. Blood Cancer Discovery, 2(4), 326-337.

Publication 2021

BLOOD Bone Marrow Cerebrospinal Fluid Chromosomes Cranium Diagnosis Ethics Committees, Research ETV6 protein, human Figs Fishes Flow Cytometry Genome Germ Cells Immunophenotyping Infant Legal Guardians Leukemia Leukocyte Count Leukocytes MLL protein, human Parent Patients pbx1 protein, human Polyploidy Remission Induction RNA-Seq RUNX1 protein, human T-Cell Leukemia-Lymphomas, Adult TCF3 protein, human Testis Therapeutics

Targeted Sequencing of Myeloid Neoplasms

Cited 6 times

Mononuclear cells were enriched through Ficoll-Hypaque gradient centrifugation and cryopreserved until use. Genomic DNA was extracted using the DNeasy Blood and Tissue Kit (QIAGEN, Hilden, Germany). The mutational status of 79 protein coding genes was determined centrally at The Ohio State University by targeted amplicon sequencing using the MiSeq platform (Illumina, San Diego, CA). In brief, DNA library preparations were performed according to the manufacturer’s directions. Samples were pooled and run on the MiSeq machine using the Illumina MiSeq Reagent Kit v3. Sequenced reads were aligned to the hg19 genome build using the Illumina Isis Banded Smith-Waterman aligner. Single nucleotide variant and indel calling were performed using, respectively, MuTect and VarScan.^{27 (link),28 (link)} All called variants underwent visual inspection of the aligned reads using the Integrative Genomics Viewer (Broad Institute, Cambridge, MA).^{29 (link)} Variant filtering was done using the MuCor algorithm.^{30 (link)} The variant allele fraction (VAF) cut-off was set to 0.10 for inclusion into the analyses. To distinguish between driver and passenger mutations, the analysis was repeated with a VAF cut-off of 0.30 (Supplementary Figure S1). Variants (missense, nonsense or frameshift) were considered to be mutations if they were not reported in the 1000 Genome database, dbSNP137, or dbSNP142. In the instances when less than 15 reads were present, the gene mutation status was determined not to be evaluable. Testing for the presence or absence of FLT3 internal tandem duplication (FLT3-ITD) was performed using the Pindel algorithm on the targeted sequencing data. In addition to the 79 gene sequencing panel, testing for CEBPA mutations was performed with Sanger sequencing methods as previously described,^{7 (link)} thus resulting in a total of 80 genes whose mutational status was assessed in our study. In accordance with the revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia,^{31 (link)} only patients with biallelic CEBPA mutations were considered as CEBPA mutated. Gene mutations were assigned to nine previously described^{2 (link)} functional groups: 1) chromatin remodeling (ASXL1, BCOR, BCORL1, EZH2 and SMARCA2); 2) cohesin complex (RAD21, SMC1A, SMC3 and STAG2); 3) kinases {AXL, FLT3 [both FLT3-ITD and tyrosine kinase domain mutations (FLT3-TKD)], KIT and TYK2}; 4) methylation-related (DNMT3A, IDH1, IDH2, and TET2); 5) NPM1 (NPM1); 6) RAS pathway (CBL, KRAS, NRAS and PTPN11); 7) spliceosome (SF3B1, SRSF2, U2AF1 and ZRSR2); 8) transcription factors (CEBPA, ETV6, IKZF1, GATA2, NOTCH1 and RUNX1); and 9) tumor suppressors (PHF6, TP53 and WT1).

Eisfeld A.K., Mrózek K., Kohlschmidt J., Nicolet D., Orwick S., Walker C.J., Kroll K.W., Blachly J.S., Carroll A.J., Kolitz J.E., Powell B.L., Wang E.S., Stone R.M., de la Chapelle A., Byrd J.C, & Bloomfield C.D. (2017). The mutational oncoprint of recurrent cytogenetic abnormalities in adult patients with de novo acute myeloid leukemia. Leukemia, 31(10), 2211-2218.

Publication 2017

Alleles BCORL1 protein, human BLOOD CEBPA protein, human Cells Centrifugation cohesins DNA Library ETV6 protein, human EZH2 protein, human Ficoll FLT3 protein, human Frameshift Mutation GATA2 protein, human Gene Products, Protein Genes Genome Hypaque IDH2, human INDEL Mutation K-ras Genes Leukemia Methylation Mucor Mutation Mutation, Nonsense Neoplasms NPM1 protein, human NRAS protein, human Nucleotides Patients Phosphotransferases Protein Tyrosine Kinase PTPN11 protein, human RUNX1 protein, human SMARCA2 protein, human SMC3 protein, human Spliceosomes Strains Tissues TP53 protein, human Transcription Factor Tumor Suppressor Genes TYK2 Kinase ZRSR2 protein, human

Myeloid Gene Panel Sequencing for Variant Detection

Cited 5 times

All patients were analyzed via a myeloid gene panel containing ASXL1, BCOR, BRAF, CSNK1A1, CBL, DNMT3A, ETV6, EZH2, FLT3-TKD, GATA1, GATA2, IDH1, IDH2, JAK2, KIT, NRAS, KRAS, MPL, NPM1, PHF6, RUNX1, SF3B1, SRSF2, TET2, TP53, U2AF1 and WT1. The library of 26 genes was generated with the ThunderStorm (RainDance Technologies, Billerica, MA, USA), and CSNK1A1 with the Access Array System (Fluidigm, San Francisco, CA, USA). Both libraries were sequenced and demultiplexed on a MiSeq instrument (Illumina, San Diego, CA, USA) as described previously.^{20 (link)} The FASTQ files were further processed using the Sequence Pilot software version 4.1.1 Build 510 (JSI Medical Systems, Ettenheim, Germany) for alignment and variant calling. Analysis parameters were set according to the manufacturer’s default recommendation. The validity of the somatic mutations was checked against the publicly accessible Catalogue Of Somatic Mutations In Cancer (COSMIC) v69 database, and functional interpretation was performed using SIFT 1.03, PolyPhen 2.0 and MutationTaster 1.0 algorithms.^{21 (link)} Additionally, TP53 variants were verified using the International Agency for Research on Cancer (IARC) repository.^{22 (link)} Single-nucleotide polymorphisms (SNP) were annotated according to the National Center for Biotechnology Information Single Nucleotide Polymorphism Database (NCBI dbSNP). The detection limit for small nuclear variants was 3% variant allele frequency (VAF). Variants (n=9) not yet described in any public database were excluded from statistical analyses.

Meggendorfer M., Haferlach C., Kern W, & Haferlach T. (2017). Molecular analysis of myelodysplastic syndrome with isolated deletion of the long arm of chromosome 5 reveals a specific spectrum of molecular mutations with prognostic impact: a study on 123 patients and 27 genes. Haematologica, 102(9), 1502-1510.

Publication 2017

BRAF protein, human Cosmic composite resin CSNK1A1 protein, human Diploid Cell ETV6 protein, human EZH2 protein, human FLT3 protein, human GATA1 protein, human GATA2 protein, human Gene Library Genes IDH2, human JAK2 protein, human K-ras Genes Malignant Neoplasms Mutation NPM1 protein, human NRAS protein, human Patients RUNX1 protein, human Single Nucleotide Polymorphism TP53 protein, human

Most recents protocols related to «ETV6 protein, human»

Myeloid Panel Amplicon Sequencing

Next generation sequencing was performed using the Illumina Ampliseq Myeloid panel including 40 genes (ABL1, ASXL1, BCOR, BRAF, CALR, CBL, CEBPA, CSF3R, DNMT3A, ETV6, EZH2, FLT3, GATA2, HRAS, IDH1, IDH2, IKZF1, JAK2, KIT, KRAS, MPL, MYD88, NF1, NPM1, NRAS, PHF6, PRPF8, PTPN11, RB1, RUNX1, SETBP1, SF3B1, SH2B3, SRSF2, STAG2, TET2, TP53, U2AF1, ZRSR2, WT1). Genomic DNA was purified from peripheral blood at baseline and 9 months after the first vaccination. Libraries were prepared using the Ampliseq for Illumina Myeloid Panel protocol, and 2 × 150 bp paired-end sequencing was done on the NextSeq 500 platform (Illumina^® Inc, San Diego, CA, USA). The Illumina Sequencing Analysis Viewer (SAV) software was used for quality control of the sequencing runs. Alignment of sequencing data to the human reference genome (GRCh37/hg19) and variant calling of mapped reads were performed in CLC Genomics Workbench software v.22. The VarSeq™ software v.2.2.4 (Golden Helix, Inc., Bozeman, MT, USA) was applied for annotation and filtering of variants. Variants with coverage <100x, a variant allele frequency (VAF) <1%, and germline, introns, and SNPs with minor allele frequency >1% (ExAC variant frequencies, Broad Institute, MA, USA) were excluded from further analysis.

Grauslund J.H., Holmström M.O., Martinenaite E., Lisle T.L., Glöckner H.J., El Fassi D., Klausen U., Mortensen R.E., Jørgensen N., Kjær L., Skov V., Svane I.M., Hasselbalch H.C, & Andersen M.H. (2023). An arginase1- and PD-L1-derived peptide-based vaccine for myeloproliferative neoplasms: A first-in-man clinical trial. Frontiers in Immunology, 14, 1117466.

Publication 2023

BLOOD BRAF protein, human calreticulin, human CEBPA protein, human CSF3R protein, human ETV6 protein, human EZH2 protein, human FLT3 protein, human GATA2 protein, human Genes Genome Genome, Human Germ Line Helix (Snails) IDH2, human Introns JAK2 protein, human K-ras Genes NPM1 protein, human NRAS protein, human PTPN11 protein, human Renal Adysplasia RUNX1 protein, human Sequence Alignment SETBP1 protein, human SH2B3 protein, human Single Nucleotide Polymorphism Strains TP53 protein, human Vaccination ZRSR2 protein, human

BCP-ALL Cytogenetic Profiling Protocol

Bone marrow and/or peripheral blood samples were collected from children with BCP-ALL at time of diagnosis. In accordance with the declaration of Helsinki, and as approved by the Medical Ethics Committee of the Erasmus Medical Center, Rotterdam, The Netherlands, written informed consent to use excess diagnostic material for research purposes was obtained from parents or guardians. Children with newly diagnosed ALL in three consecutive Dutch Childhood Oncology Group trials (DCOG ALL-8, ALL-9, and ALL-10) (18 (link)), and two German Cooperative ALL trials (COALL 06-97 and 07-03) (19 (link)) were included in this study. The major known cytogenetic subtypes of BCP-ALL, BCR-ABL1, ETV6-RUNX1, KMT2A/MLL-rearranged, TCF3-PBX1, as well as ploidy status (high hyperdiploidy; 51-65 chromosomes, near tetraploidy; >65 chromosomes, and low hypodiploidy; <39 chromosomes) were determined using karyotyping, fluorescence in situ hybridization (FISH) and RT-PCR by reference laboratories. Mononuclear cells were obtained from bone marrow and/or peripheral blood samples by Lymphoprep density gradient centrifugation and blast percentage was determined based on morphology using May-Grunwald-Giemsa staining (20 (link)). If necessary, samples were enriched to >90% leukemic blasts using negative beads enrichment. RNA and DNA were routinely isolated from samples using TRIzol reagents.

Hormann F.M., Hoogkamer A.Q., Boeree A., Sonneveld E., Escherich G., den Boer M.L, & Boer J.M. (2023). Integrating copy number data of 64 iAMP21 BCP-ALL patients narrows the common region of amplification to 1.57 Mb. Frontiers in Oncology, 13, 1128560.

Publication 2023

BLOOD Bone Marrow Cells Centrifugation, Density Gradient Child Chromosomes Ethics Committees ETV6 protein, human Fluorescent in Situ Hybridization Legal Guardians lymphoprep May-Grunwald Giemsa stain MLL protein, human Neoplasms Parent pbx1 protein, human Polyploidy Reverse Transcriptase Polymerase Chain Reaction RUNX1 protein, human TCF3 protein, human Tetraploidy trizol

Differential Gene Expression Analysis of iAMP21 Pediatric ALL

Gene expression microarrays (Affymetrix U133 Plus 2) from a previously described population-based paediatric ALL cohort were used (25 (link), 26 (link)). In short, expression data was normalized using vsnrma (27 (link)), and batch effects were removed using the empirical Bayes method (28 (link)). Differential gene expression between 12 iAMP21 and 143 B-other cases was determined using Limma with false discovery rate (FDR) multiple testing correction (29 ). Gene expression data are available at GEO under accession number GSE87070 (see Supplementary Table S1 for used samples). As a validation cohort, RNA sequencing gene expression data from the Pediatric Cancer (PeCan) database (https://pecan.stjude.cloud/) were used. Gene expression in fragments per kilobase per million mapped reads (FPKM) of selected genes was extracted. BCP-ALL samples annotated as BCR-ABL1, ETV6-RUNX1, TCF3-PBX1, high hyperdiploidy, low hypodiploidy, and infant ALL were excluded from analysis, resulting in a validation cohort of 17 iAMP21 samples and 174 B-other samples. Differential gene expression of target genes was determined using the Mann Whitney U test with Bonferroni multiple testing correction.

Publication 2023

ETV6 protein, human Gene Expression Genes Infant Malignant Neoplasms Microarray Analysis pbx1 protein, human Pecans Polyploidy RUNX1 protein, human TCF3 protein, human

Cytogenetic, FISH, and MLPA Analysis

Cytogenetics, FISH and Multiplex Ligation-dependent Probe Amplification (MLPA) (MRC Holland, The Netherlands) were performed, as previously described [23 (link)–25 (link)]. Abnormalities detected by these methods are provided in Supplementary Table 2. Copy number data for nine genes/regions targeted in the SALSA MLPA P335 (CDKN2A/B, PAX5, IKZF1, BTG1, EBF1, RB1, ETV6, PAR1 region) and P327 (ERG) kits were included. Detection of risk-stratifying genetic abnormalities by WGS required these key features: (1) ploidy and focal CNA required CNA and/or SV information and (2) gene fusion required evidence of a SV [26 (link), 27 (link)].

Ryan S.L., Peden J.F., Kingsbury Z., Schwab C.J., James T., Polonen P., Mijuskovic M., Becq J., Yim R., Cranston R.E., Hedges D.J., Roberts K.G., Mullighan C.G., Vora A., Russell L.J., Bain R., Moorman A.V., Bentley D.R., Harrison C.J, & Ross M.T. (2023). Whole genome sequencing provides comprehensive genetic testing in childhood B-cell acute lymphoblastic leukaemia. Leukemia, 37(3), 518-528.

Publication 2023

B Cell-Specific Transcription Factor CDKN2A Gene Congenital Abnormality ETV6 protein, human Fishes Gene Fusion Genes Multiplex Ligation-Dependent Probe Amplification Reproduction

Pediatric B-ALL Treatment Protocol

All pediatric B-ALL patients were treated according to the COALL 08–09 study protocol (v. 01.10.2010). The total number of B-ALL patients analyzed was 36, 69% of them being diagnosed with common-ALL and 28% with pre-B-ALL, one patient with pro-B-ALL. The majority of patients (~31%) featured the hyperdiploidy subtype, ~22% were of the molecular subtype ETV6-RUNX1 (Table S1). Patients of the control group were hospitalized due to a non-hematologic malignancy. Bone marrow or peripheral blood was obtained as surplus material during standard diagnostic procedures. Subsequent analysis was performed with the consent of the patients or patient’s parents in agreement with the ethics committee of Rhineland-Palatinate (no. 2018–13713). Samples were handled in accordance with the current (2013) version of the Declaration of Helsinki. Remission was defined as <5% blast cells.

Ziegler N., Cortés-López M., Alt F., Sprang M., Ustjanzew A., Lehmann N., El Malki K., Wingerter A., Russo A., Beck O., Attig S., Roth L., König J., Paret C, & Faber J. (2023). Analysis of RBP expression and binding sites identifies PTBP1 as a regulator of CD19 expression in B-ALL. Oncoimmunology, 12(1), 2184143.

Publication 2023

BLOOD Bone Marrow Ethics Committees ETV6 protein, human Hematologic Neoplasms Parent Patients Polyploidy Precursor B-Cell Lymphoblastic Leukemia-Lymphoma RUNX1 protein, human Stem Cells Tests, Diagnostic

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Salsa mlpa kit p335 by MRC-Holland

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What is the ETV6 protein and what is its role in the human body?

How can PubCompare.ai help researchers study the ETV6 protein more effectively?

PubCompare.ai is a powerful AI-driven platform that can assist researchers in optimizing their studies of the ETV6 protein. The platform allows you to quickly screen protocol literature more efficiently, leveraging AI to pinpoint critical insights that can help you identify the most effective protocols related to the ETV6 protein for your specific research goals. The platform's AI-driven analysis can highlight key differences in protocol effectiveness, enabling you to choose the best option for reproducibility and accuracy in your ETV6 protein research.

Are there different variations or types of the ETV6 protein that researchers should be aware of?

Yes, there are different isoforms and variations of the ETV6 protein that researchers should be familiar with. The ETV6 gene can undergo alternative splicing, resulting in multiple protein isoforms with slightly different structures and functions. Additionally, genetic mutations or rearrangements involving the ETV6 gene have been associated with certain types of cancer, such as acute lymphoblastic leukemia and myelodysplastic syndrome. Understanding these variations is crucial for designing targeted studies and therapies related to the ETV6 protein.

What are some specific applications of the ETV6 protein in research and clinical settings?

The ETV6 protein has a variety of applications in both research and clinical settings. In research, the ETV6 protein is a commonly used model to study transcription regulation, hematopoiesis, and the molecular pathways involved in cancer development. Clinically, the ETV6 protein and its associated genetic alterations are used as biomarkers for the diagnosis and prognostic assessment of certain types of leukemia and lymphoma. Additionally, therapies targeting the ETV6 protein or its downstream effectors are being investigated as potential treatments for ETV6-related cancers.

Are there any common challenges or considerations researchers should be aware of when working with the ETV6 protein?

One common challenge when working with the ETV6 protein is the complexity of its regulatory networks and the plethora of interacting partners it has. The ETV6 protein is involved in a wide range of cellular processes, and understanding its specific roles in different contexts can be challenging. Additionally, the genetic alterations and mutations associated with the ETV6 gene can be diverse, requiring careful study and analysis. Researchers should also be mindful of the potential off-target effects of any interventions targeting the ETV6 protein, as it is a key regulator of important cellular functions.

More about "ETV6 protein, human"

The ETV6 (Ets Variant 6) gene, also known as the TEL gene, encodes a critical transcription factor that plays a pivotal role in regulating gene expression during crucial cellular processes.
This protein is heavily involved in hematopoiesis, the development and differentiation of blood cells, and has been strongly implicated in various types of cancer, including leukemias and lymphomas.
Researchers can leverage the power of PubCompare.ai, an innovative AI-driven platform, to optimize their investigations of the ETV6 protein.
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This streamlines the research process and provides invaluable insights to advance the understanding of the ETV6 protein and its diverse biological functions.
The MiSeq system, a powerful next-generation sequencing (NGS) platform from Illumina, can be employed to study the ETV6 gene and its expression patterns.
The SALSA MLPA kit P335 is a useful tool for the detection of chromosomal aberrations involving the ETV6 gene.
The MiSeq platform and MiSeq instrument offer high-throughput sequencing capabilities that can be leveraged to investigate the genomic landscape of ETV6-related malignancies.
Furthermore, the HiSeq 2000 and HiSeq 4000 sequencing systems from Illumina provide additional NGS solutions for in-depth analysis of the ETV6 gene and its involvement in disease processes.
Fetal bovine serum (FBS) is a common cell culture supplement that can be utilized in experiments studying the ETV6 protein and its role in cellular differentiation and proliferation.
The High-Capacity cDNA Reverse Transcription Kit from Applied Biosystems, a division of Life Technologies, is a useful tool for generating complementary DNA (cDNA) from RNA samples, enabling the study of ETV6 gene expression.
Additionally, the Life Technologies 3,500 Genetic Analyzer offers capillary electrophoresis-based sequencing capabilities that can be employed to characterize the ETV6 gene and its variants.
Finally, TaqMan probes, a powerful qPCR technology, can be utilized to quantify the expression levels of the ETV6 gene in various biological systems and clinical samples, providing valuable insights into its regulatory mechanisms and potential as a biomarker or therapeutic target.