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2 edition of Aberrant gene expression in acute myeloid leukemia. found in the catalog.

Aberrant gene expression in acute myeloid leukemia.

Ryan Peter Pinto

Aberrant gene expression in acute myeloid leukemia.

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Published .
Written in English


About the Edition

Acute myeloid leukemia (AML) is a rapidly progressing cancer characterized by an accumulation of myeloblasts in the bone marrow and peripheral blood. AMLs are a heterogeneous group of diseases, with individual cases displaying variability in presentation, treatment response and clinical outcome. These differences can most likely be accounted for by the underlying genetic heterogeneity in leukemic cells. Though there are a number of novel therapies with the potential for improving outcome, results from ongoing trials are modest at best. While chromosomal abnormalities and genetic mutations have been identified that may be used for prognosis and as possible targets for therapy, little is known about the genetic changes involved in the progression of disease in the majority of normal karyotype patients. Furthermore, since AML most likely represents a multi-hit disease, the nature of many of the secondary hits are also unknown. It is evident that the entire list of genetic lesions in AML is far from complete. Identifying aberrantly expressed genes that contribute to the transformed nature of the hematopoietic cell will broaden our understanding of the development and progression of the disease as well as identify novel potential targets for therapy. Representational difference analysis (RDA) is a cDNA subtractive hybridization screen that I used to identify aberrantly expressed genes in AML, from which over thirty potential candidates were identified. I have chosen seven of these genes for further examination by analyzing their expression in AML cell lines and primary patient samples. The role of aberrant angiotensin expression in AML, one of the genes identified through the screen, was also investigated using a known inhibitor of its pathway in AML cells. LMO1, another gene identified from the screen, was assayed as a marker of minimal residual disease (MRD) in AML along with a panel of other MRD markers in a group of patient samples obtained at diagnosis, remission and relapse. The knowledge gained from these research studies provides the basis for further investigation involving the molecular detection of residual disease and the development of targeted therapies in AML.

The Physical Object
Pagination139 leaves.
Number of Pages139
ID Numbers
Open LibraryOL21549430M
ISBN 109780494219256

Title: Single Autosomal Trisomy in Acute Myeloid Leukemia and Myelodysplastic Syndrome VOLUME: 1 ISSUE: 2 Author(s):S. K. Ma and T. S.K. Wan Affiliation:Hematology Section, The University of Hong Kong, Hong Kong China Keywords:Single Autosomal Trisomy, Acute Myeloid Leukemia, Myelodysplastic Syndrome, Aberrant CD7 expression, Myeloid Leukemia AML, Fluorescence in situ hybridization, MLL Gene Cited by: 2. Marcucci G, Yan P, Maharry K, et al. Epigenetics meets genetics in acute myeloid leukemia: clinical impact of a novel seven-gene score. J Clin Oncol ; Cheung N, Fung TK, Zeisig BB, et al. Targeting Aberrant Epigenetic Networks Mediated by PRMT1 and KDM4C in Acute Myeloid Leukemia.


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Aberrant gene expression in acute myeloid leukemia. by Ryan Peter Pinto Download PDF EPUB FB2

Acute myeloid leukemia (AML) is a heterogeneous disease that is characterized by distinct cytogenetic or genetic abnormalities.

Recent discoveries in cancer epigenetics demonstrated a critical role of epigenetic dysregulation in AML : Xianwen Yang, Molly Pui Man Wong, Ray Kit Ng. Acute myeloid leukemia (AML) is a heterogeneous disease that is characterized by distinct cytogenetic or genetic abnormalities.

Recent discoveries in cancer epigenetics demonstrated a critical role of Author: Xianwen Yang, Molly Pui Man Wong, Ray Kit Ng. Acute myeloid leukemia (AML) is a heterogeneous disease that remains challenging to treat because of patient factors (age and coexisting diseases) and intrinsic biologic factors.

Acute myeloid leukemia (AML) patients with high level of EVI1 are associated with unfavorable overall survival, which was aggravated by simultaneous high expression of ATG7 in these patients.

Aberrant methylation of the RIZ1 gene in myelodysplastic syndrome and acute myeloid leukemia Author links open overlay panel Naoki Mori a Kentaro Yoshinaga a Kaori Tomita a Mari Ohwashi a Toshiaki Cited by:   Double CEBPA mutations, but not single CEBPA mutations, define a subgroup of acute myeloid leukemia with a distinctive gene expression profile that is uniquely associated with Cited by: Acute Myeloid Leukemia (AML), 15 cases were Acute Lymphocytic Leukemia (ALL) and 2 cases were Mixed Phenotypic Acute Leukemia (MPAL).

29/50 cases (%) had conventional phenotypes while 21/50 cases (%) showed aberrant expression. Aberrant myeloid marker expression in precursor B-cell and T-cell leukemias. The World Health Organization (WHO) characterization of the immunophenotype of precursor B-cell acute lymphoblastic leukemia (pre-B ALL) includes the possible expression of myeloid cluster of differentiation.

Aberrant Expression of CD Markers in Acute Leukemia Naghmana Mazhar et al. Ann. Pak. Inst. Med. Sci. ; 9(3): In 10 patients lymphoid lineage associated antigens were present on acute myeloid leukemia cases while 9 cases showed myeloid associated antigens expression on acute lymphoid leukemia File Size: KB.

Acute myeloid leukemia (AML) with a complex aberrant karyotype is a distinct biological entity. It is characterized by: (1) a sharp increase in incidence above age 50; (2) a characteristic pattern of chromosomal gain and, especially, loss, that is, of 5q14q33, 7q32q35, and 17p13, translating into reduced expression of genes in these regions; (3) a unique gene expression Cited by: Bullinger L, Dohner K, Bair, E, et al.

Use of gene-expression profiling to identify prognostic subclasses in adult acute myeloid leukemia. N Engl J Med ;– PubMed CrossRef Google ScholarAuthor: Alan D. Friedman. The MLL gene, located at 11q23, is frequently involved in cytogenetic abnormalities in both AML and acute lymphoblastic leukemia (ALL), occurring in 5–6% of patients with AML, 7–10% of Cited by: miRNAs regulate gene expression, and thus play an important role in critical cellular processes.

Aberrant miRNA expression patterns have been found in various types of cancer. So far, information about the expression of miRNAs in pediatric acute myeloid leukemia Cited by: Acute myeloid leukemia in adults is a highly heterogeneous disease. Gene expression profiling performed using unsupervised algorithms can be used to distinguish specific groups of patients within a large patient cohort.

The identified gene expression signatures can offer insights into underlying physiological mechanisms of disease by: 4. Acute myeloid leukemia (AML) is the most prevalent acute leukemia in adults. It is an aggressive hematologic malignancy that results in the disruption of normal self-renewal, differentiation, and hematopoietic stem and progenitor cell expansion, leading to increased proliferation and accumulation of immature nonfunctioning myeloid progenitors Cited by: 1.

Epigenetics describes modifications of gene expression without alteration of DNA sequences. 5,6 Aberrant DNA methylation is among the best characterized and therapeutically targetable of the epigenetic changes occurring in leukemia.

5,6 However, most studies of aberrant Cited by: Epigenetic Perturbations by ArgMutated DNMT3A Potentiate Aberrant Stem Cell Gene-Expression Program and Acute Leukemia Development Rui Lu,1,2 Ping Wang,3 Trevor Parton,1 Yang Zhou,4.

Abstract Acute myeloid leukemia (AML) is a group of diseases that are very heterogeneous with regard to cytogenetic aberrations, gene mutations, and changes in expression of numerous genes.

A new class of genes known as microRNAs recently was found to be involved in myeloid by: Extended data figures. ion of ENL impairs the growth of AML. is required for AML growth in vivo.

ion of ENL deregulates core cellular processes and oncogenic pathways that are required for AML maintenance. depletion decreases the occupancies of total Pol II and Pol II S2P on ENL-bound by: The development of acute leukemias is associated with MLL gene alterations in about 10% of all leukemia cases of acute lymphoblastic leukemia and acute myeloid leukemia).

MLL alterations correlate with specific disease subtypes (acute myeloid and acute lymphocytic leukemias), a specific gene expression Cited by: 1. Aberrant DNA methylation is a feature of cancer including acute myeloid leukemia (AML). It was first established that global DNA hypomethylation combined with hypermethylation of specific gene Author: Ying Qu.

Expression of ETS2 is observed in a variety of cell types. During murine development, it is highly expressed in newly forming cartilage including skull precursor cells, and vertebral primordia [74]. Sumarsono, et al. created transgenic mice. Aberrant DNA methylation is frequently found in human malignancies including acute myeloid leukemia (AML).

While most studies focus on later disease stages, the onset of aberrant DNA methylation events and their dynamics during leukemic progression are largely unknown. We screened genome-wide for aberrant Cited by: Acute myeloid leukemia (AML) is a heterogeneous disease and the pathogenesis of most types of AML is unknown.

The combination of results from studies of primary tumors, in vitro cultures, and mechanistic molecular experiments will contribute to the understanding of the role of aberrant. Homeobox (HOX) proteins and the receptor tyrosine kinase FLT3 are frequently highly expressed and mutated in acute myeloid leukemia (AML).

Aberrant HOX expression is found in nearly all AMLs that harbor a mutation in the Nucleophosmin (NPM1) gene, and FLT3 is concomitantly mutated in approximately 60% of these cases. Little is known about how mutant NPM1 (NPM1 mut) cells maintain aberrant Cited by: Lu et al. establish that Argmutated DNMT3A contributes to acute myeloid leukemia (AML) pathogenesis through epigenetic activation of leukemia-related genes.

Inhibition of Dot1l reverses mutant DNMT3A-induced gene expression Cited by: The expression of microRNAs (miRNAs) is deregulated in acute myeloid leukemia (AML), but the corresponding functional miRNA‐controlled pathways are poorly understood.

Integration of messenger RNA (mRNA) and miRNA expression. Ectopic expression of miRa in mouse HSC/progenitors results in acquisition of self-renewal capacity by myeloid progenitors, biased myeloid differentiation, and the development of a myeloproliferative disorder that progresses to acute myeloid leukemia Cited by:   NUP98 gene rearrangements have been reported in acute myeloid leukemia, giving rise to fusion proteins that seem to function as aberrant transcription factors, and are thought to be associated with poor prognosis.

A patient with treatment-related acute myeloid leukemia Cited by: Recent advances in our understanding of the pathogenesis of AML have involved elucidation of the role of aberrant chromosomal rearrangement, amplifications, deletions, and point mutations, and aberrant Author: Kim L.

Rice, Monica Buzzai, Jessica K Altman, Jonathan D. Licht. Purpose The Microarray Innovations in Leukemia study assessed the clinical utility of gene expression profiling as a single test to subtype leukemias into conventional categories of myeloid and lymphoid Cited by: Acute myeloid leukemia (AML) is a clonal hematopoietic disease caused by both inherited and acquired genetic alterations.

Current AML classification and prognostic systems incorporate genetic Cited by:   Acute myeloid leukemia with t(8;21)(q22;q22); RUNX1-RUNX1T1 [AML with t(8;21)] accounts for approximately 5% of all AMLs.

It results from a translocation from the RUNX1 gene (also Cited by: 4. Still, it is unclear how CTCF binding is perturbed in leukemia or in cancer in general. We studied CTCF binding by ChIP-Seq in cells from patients with acute myeloid leukemia (AML) and in normal bone.

Acute myeloid leukemia (AML) is the most common acute leukemia in adults. also suggests a potential role of aberrant patterns of set of AML samples. The gene-expression predictor defined Cited by: Acute myeloid leukemia (AML) is a genetically heterogeneous clonal malignancy characterized by recurrent gene mutations.

Genomic heterogeneity, patients’ individual variability, and recurrent gene Author: Jifeng Yu. Mori N, Yoshinaga K, Tomita K, Ohwashi M, Kondoh T, Shimura H, et al. Aberrant methylation of the RIZ1 gene in myelodysplastic syndrome and acute myeloid leukemia.

Leuk Res. The advent of next-generation sequencing technologies has unveiled a new window into the heterogeneity of acute myeloid leukemia (AML).

In particular, recurrent mutations in spliceosome machinery and genome-wide aberrant Cited by:   In hematologic malignancies, aberrant DNA hypermethylation is thought to have relevance to leukemogenesis For example, during the progression of chronic myelogenous leukemia (CML), theABL1 promoter of the BCR-ABL fusion gene becomes significantly hypermethylated,18 Also, aberrant hypermethylation of the p15 INAK4B tumor suppressor gene Cited by: Treatment of Myelodysplastic Syndrome and Acute Myeloid Leukemia by Immunomodulatory and Epigenetic Drugs.

By Ota Fuchs. Submitted: Acute myeloid leukemia (AML) is associated with poor prognosis in elderly patients. (DCK mutations or aberrant gene expression Author: Ota Fuchs.

Cytogenetic analysis of metaphase cells is a key component to the evaluation of all patients with newly diagnosed or suspected acute myeloid leukemia (AML). The malignant cells in most patients with .During the onset and progression of hematological malignancies, many changes occur in cellular epigenome, such as hypo- or hypermethylation of CpG islands in promoter regions.

DNA methylation is an epigenetic modification that regulates gene expression Cited by: 4.Figure 2: Bone marrow smear, gene expression, immunophenotypic features of T-ALL with t() fusion.(A) Bone marrow smear from the patient under study, increase in lymphoblasts and absence of Author: Kave Jasseb, Maria Kavianpour, Javad Mohammadi Asl, Zahra Shahpouri Arani, Vahid Fallah Azad, Mansou.