ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Regulation of gene expression of myeloperoxidase during myeloid differentiation (1988)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 136 (1988), S. 215-225 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Myeloperoxidase (MPO) is a major heme enzyme involved in inflammatory responses of polymorphonuclear leukocytes. Using cDNA and intron specific probes for MPO we studied the regulation of MPO expression during myeloid differentiation of the promyelocytic HL-60 leukemia cell line. Mature MPO mRNA species of 3.3, 2.8 and 1.6 kb and heterogenous nuclear (hn)RNA of 〉 8 and ∼4 kb were observed in wildtype HL-60 cells. Induction of differentiation of the cells towards either granulocytes or macrophages resulted in a profound decrease (〉 95%) in the concentration of MPO mRNA levels, showing that gene expression of MPO mRNA is closely linked to the stage of development of myeloid cells. Studies using normal and leukemic hematopoietic cells confirmed these findings and showed that myeloblasts and promyelocytes contain MPO mRNA. Rate of transcription of MPO was measured by a nuclear run-on assay in wild-type and day 3- and day -4 differentiated HL-60 cells and was nearly the same in all three. In contrast, rate of transcription of c-myc in the same nuclei became almost undetectable with induction of differentiation. Overall transcription decreased by 60% and 80% on day 3 and 4 of differentiation, respectively, compared to wild-type cells. Stability of mature MPO mRNA was also measured and found to be the same in wild-type and differentiated HL-60. Half-life of MPO hnRNA was ≤ 30 min in wild-type HL-60; nevertheless, this hnRNA was easily detectable 3 days after induction of differentiation of these cells. Taken together, the results show that decreased expression of MPO mRNA with differentiation occurs in part post-transcriptionally, possibly due to a failure in RNA processing. In addition, as overall transcription decreases during differentiation, MPO transcription is concomitantly reduced. This indicates that transcriptional and post-transcriptional mechanisms cooperate in the control of MPO gene expression.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041360203
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    facet.materialart.
    Unknown
    A Direct Measurement of Polarization Capacity and Phase Angle (1923)
    American Physical Society
    Details
    Publication Date: 1923-12-01
    Print ISSN: 0031-899X
    Electronic ISSN: 1536-6065
    Topics: Physics
    Published by American Physical Society
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    A Linear Photoelectric Densitometer (1935)
    American Institute of Physics
    Details
    Publication Date: 1935-04-01
    Print ISSN: 0034-6748
    Electronic ISSN: 1089-7623
    Topics: Electrical Engineering, Measurement and Control Technology , Physics
    Published by American Institute of Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    A CONSTANT FREQUENCY OSCILLATOR (1930)
    American Institute of Physics
    Details
    Publication Date: 1930-05-01
    Print ISSN: 0034-6748
    Electronic ISSN: 1089-7623
    Topics: Electrical Engineering, Measurement and Control Technology , Physics
    Published by American Institute of Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Genetic Profiling of Myeloproliferative Disorders by Single Nucleotide Polymorphism Oligonucleotide Microarray. (2006)
    American Society of Hematology
    Details
    Publication Date: 2006-11-16
    Description: Myeloproliferative disorders (MPD) are clonal hematopoietic diseases including polycythemia vera (PV), essential thrombocytosis (ET) and myelofibrosis with myeloid metaplasia (MMM). Single-nucleotide polymorphism DNA microarray (SNP-Chip) was used to analyze 43 MPDs. All five cases of PV having homozygous JAK2V617F had uniparental disomy (UPD), thus duplicating the allele with the mutated JAK2 and eliminateing the normal allele. Concerning MMM, either the Rb1 (13q14) or NF1 (17q11) gene was deleted in five of the 9 cases that had no Jak2 mutations. Two of these cases had UPD at 1p. Sequencing of the target genes within this region of UPD revealed a point mutation of the MPL gene (S240F or W515L). Each of these cases also had a deletion of Rb suggesting that the mutated MPL may co-operate with an aberrant Rb. The 9 cases of MMM with JAK2 mutations had only infrequent (2/9 cases) additional genomic alterations. Interestingly, No genomic alterations were noted in any of the cases (10) of ET having a normal Jak2. Two of 7 ET cases with JAK2 mutations had deletion of either 5q or trisomy 9. In summary, UPD is the predominant mechanism by which MPD develops homozygous JAK2 mutations. 1p UPD is a signpost that MPL is mutated in cases of MMM having wild-type JAK2; and these cells often have loss of Rb. ET cases with no JAK2 mutations are surprisingly free of genomic alterations.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    Hidden Abnormalities and Novel Classification of t(15;17) APL Based on Genomic Alterations. (2007)
    American Society of Hematology
    Details
    Publication Date: 2007-11-16
    Description: Acute promyelocytic leukemia (APL) is a hematopoietic malignant disease characterized by the chromosomal translocation t(15;17), resulting in the fusion of PML-RARA genes. We examined whether genomic alterations could be found other than t(15;17) using a sensitive technique in order to subcategorized this disease on the basis of genomic status. Thirty-three t(15;17) APL samples were analyzed with high-density single-nucleotide polymorphism microarray (50K SNP-chip) using the new algorithm AsCNAR (allele-specific copy-number analysis using anonymous references). Our analysis revealed that 10q (2 cases), 11p (3 cases) and 19q (1 case) regions were identified as loss of heterozygosity with normal copy number [we call this somatic uniparental disomy (UPD)] that could not be detected by karyotypic analysis. Nineteen samples (58%, Group A) did not have an obvious alteration. Fourteen samples (42%) showed either one or more genomic abnormalities: 6/14 of these samples (18%, Group B) had trisomy 8 either with or without duplication, deletion, and UPD; and 8/14 of these samples (24%, Group C) had abnormalities without trisomy 8. Interestingly, FLT3-ITD mutation (7/33 cases) was found only in Group A. These results suggest that the pathway of development of APL differs in each group; FLT3-ITD, trisomy 8 (probably c-Myc gene), and unknown factor(s) are involved in group A, B, and C, respectively. Here, we showed for the first time hidden abnormalities and novel disease-related genomic regions in t(15;17) APL. Our technique may become a routine, rapid, robust technique for subclassification of APL and to screen for novel therapeutic targets.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Rearrangement and Deletion of the PAX5 Gene in Pediatric Acute B-Cell Lineage Lymphoblastic Leukemia. (2007)
    American Society of Hematology
    Details
    Publication Date: 2007-11-16
    Description: Pediatric acute lymphoblastic leukemia (ALL) is the most common malignant disease in children. The disease results from accumulation of mutations of tumor suppressor genes and oncogenes. Recently, higher resolution SNP-chips (50,000–500,000 probes) have been developed allowing us to identify genes involved at the start sites of deletions/duplications. This permitted us both to identify unbalanced translocations involving t(1;19)(q23;p13) (TCF3/PBX1) and t(12;21)(p13;q11) (ETV6/RUNX1), as well as, to find novel fusion genes involving PAX5 in B-cell lineage ALL. PAX5 gene was rearranged to a variety of partner genes including ETV6, FOXP1, AUTS2 and C20orf112. In each case, tthe C-terminal end of the PAX5 gene was replaced by the partner gene. The PAX5 fusion gene products suppressed transcriptional activity of PAX5 in a dominant negative fashion. We also found a point mutation of PAX5 at codon 26 (Val 26 Gly); and this mutated PAX5 had attenuated transcriptional activity. Expression of PAX5/C20orf112 fusion gene in a B-cell line suppressed endgenous expression of PAX5 target genes including BLK1 and CD19. Furthermore, deletion of PAX5 was common in B-cell lineage ALL (34/339 cases). PAX5 gene is localized on chromosome 9p and concurrent deletion of PAX5 and INK4A genes were frequently detected in B-cell linage ALL. PAX5 gene may behave as a tumor suppressor gene during early development of B-cells and its alteration by either fusion to another gene, point mutation, or deletion may be associated with leukemogenesis of B-cell lineage ALL.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    Mutations in the gene encoding the transcription factor CCAAT/enhancer binding protein α in myelodysplastic syndromes and acute myeloid leukemias (2002)
    American Society of Hematology
    Details
    Publication Date: 2002-02-15
    Description: The CCAAT/enhancer binding protein α (C/EBPα) protein is essential for proper lung and liver function and granulocytic and adipose tissue differentation. It was hypothesized that abnormalties in C/EBPα function contribute to the development of malignancies in a variety of tissues. To test this, genomic DNA from 408 patient samples and 5 cell lines representing 11 different cancers was screened for mutations in the C/EBPα gene. Two silent polymorphisms termed P1 and P2 were present at frequencies of 13.5% and 2.2%, respectively. Of the12 mutations detected in 10 patients, silent changes were identified in one nonsmall cell lung cancer, one prostate cancer, and one acute myelogenous leukemia (AML) subtype M4. The 9 remaining mutations were detected in 1 of 92 (1.1%) myelodysplastic syndrome (MDS) samples and 6 of 78 (7.7%) AML (AML-M2 and AML-M4) samples. Some mutations truncated the predicted protein with loss of the DNA-binding (basic region) and dimerization (leucine zipper [ZIP]) domains by either deletions or nonsense codons. Also, inframe deletions or insertions in the fork region located between the leucine zipper and basic region, or within the leucine zipper, disrupted the α-helical phase of the bZIP domain. The inframe deletion and insertion mutations abrogated the transcriptional activation function of C/EBPα on the granulocyte colony-stimulating factor receptor promoter. These mutants localized properly to the nucleus, but were unable to bind to the C/EBP site in the promoter and did not possess dominant-negative activity. The mutations in the MDS patient and one AML-M2 patient were biallelic, indicating a loss of C/EBPα function. These results suggest that mutation of C/EBPα is involved in specific subtypes of AML and in MDS, but may occur rarely in other types of leukemias or nonhematologic malignancies.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    Genetic Profiling of Adult Acute Lymphoblastic Leukemia Cells by Single Nucleotide Polymorphism Oligonucleotide Microarray. (2007)
    American Society of Hematology
    Details
    Publication Date: 2007-11-16
    Description: Acute lymphoblastic leukemia (ALL) is a malignant disease of bone marrow cells, resulting from accumulation of genetic alterations of these cells. We analyzed 74 adult ALL samples by single-nucleotide polymorphism DNA microarray (SNP-Chip) using the new algorithm AsCNAR (allele-specific copy-number analysis using anonymous references). 71 samples (96%) showed genomic abnormalities in a mean 4.5 chromosomes including duplications, deletions and loss of heterozygosity with normal copy number [we call this uniparental disomy (UPD)]. About 25% of samples had a normal karyotype but each had genomic changes detectable by SNP-Chip. Importantly, 21 cases (28%) had UPD, and 29% of these had 9p UPD. Other genomic defects included deletions of p16INK4A in 18 cases (24%), deletions of ETV6 in 7 cases (9%), and hyperdiploidy (〉50 chromosomes) in 3 cases (4%). In contrast, we also analyzed 399 pediatric ALL samples and deletions occurred in p16INK4A (28%) and ETV6 (22%) and 29% cases had hyperdiploidy. Hyperdiploidy is associated with a good prognosis and occured much more frequency in pediatric ALL (29%) than adult ALL (4%) which may in part explain the better prognosis in pediatric ALL compared to adult ALL. Also, small copy number changes were detected in adult ALL including deletion of B-cell differentiation genes: EBF (4 cases, 5%), Pax5 (5 cases, 7%) and IKZF (Ikaros) (8 cases, 11%), as well as, deletion of miR-15a and miR-16-1 (2 cases, 3%), which is often found in CLL. Amplification of Rel and BCL11A occurred in one case and amplification of Akt2 occurred in another case. Moreover, we found PAX5/ETV6 fusion in one case (1%); in comparison, 14 of 399 pediatric ALL cases (4%) had PAX5 fusion genes. In summary, we discovered hidden abnormalities including small copy number change and UPD in adult ALL and identified differences between adult and pediatric ALLs. In the future, routine SNP-Chip analysis may provide novel subclassification criteria for ALL and identify unique therapeutic targets.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 10
    facet.materialart.
    Unknown
    Methylation Status and Polymorphism of Asparagine Synthetase Gene in Acute Lymphoblastic Leukemia Cells. (2005)
    American Society of Hematology
    Details
    Publication Date: 2005-11-16
    Description: Asparagine synthetase (ASY) is an enzyme expressed ubiquitously in mammalian cells. Expression of the gene, however, is repressed in acute lymphoblastic leukemia (ALL), and the cells are unable to synthesize sufficient asparagine. Depletion of asparagine by L-asparaginase leads to cell death in ALL; therefore, asparaginase has been used as treatment of ALL. Here, we show the methylation status of ASY gene in ALL clinical samples, and report a novel insertional polymorphism in the gene. The ASY gene has a CpG island located from −313 to +336 including 49 CpG sites. We analyzed the methylation status in the region by sodium bisulfite conversion of genomic DNA followed by PCR analysis. A total of 18 of 22 (82%) bone marrow samples of ALL at diagnosis were methylated in the CpG island. After chemotherapic induced-remission, all the bone marrow samples were unmethylated including the 18 patients whose ALL samples were methylated. Experiments by others using an ALL cell line showed that methylation of the ASY gene silenced the gene. In addition, we discovered either a 14 bp or 28 bp inserted sequence between +83 and +84 located in the 1st intron of the gene. Methylation status of the gene was independent of the insertion. To calculate the frequency of the insertion, 92 ALL samples were analyzed by PCR and sequencing. 69 samples (75%) did not contain the insertion in either allele, 22 samples (24%) contained the insertion in one allele, and only 1 sample (1%) contained the insertion in both alleles. To examine whether the insertion was specific for leukemic cells, we analyzed 71 non-ALL samples. 48 samples (68%) did not contain the insertion in either allele, 12 samples (27%) contained the insertion in one allele, and 4 samples (6%) contained the insertion in both allele. These results showed that the insertion is a germline polymorphism; we are exploring if this insertion changes expression of the gene. In summary, we found a novel insertional polymorphism in the ASY gene. Also, our data for the first time suggests that ALL cells cannot express ASY because the gene’s CpG island is methylated, thus explaining why ALL cells are sensitive to L-asparaginase. Notably, 18% of ALL samples were not methylated, and these patients might be expected to be resistant to L-asparaginase therapy suggesting that a simple test could be of therapeutic value.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...