Relevant bibliographies by topics / Leukaemia; Cytogenetic abnormalities

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  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Leukaemia; Cytogenetic abnormalities'

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

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Journal articles on the topic "Leukaemia; Cytogenetic abnormalities"

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Sarrou, Evgenia, Laura Richmond, Ruaidhrí J. Carmody, Brenda Gibson, and Karen Keeshan. "CRISPR Gene Editing of Murine Blood Stem and Progenitor Cells Induces MLL-AF9 Chromosomal Translocation and MLL-AF9 Leukaemogenesis." International Journal of Molecular Sciences 21, no. 12 (June 15, 2020): 4266. http://dx.doi.org/10.3390/ijms21124266.

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Chromosomal rearrangements of the mixed lineage leukaemia (MLL, also known as KMT2A) gene on chromosome 11q23 are amongst the most common genetic abnormalities observed in human acute leukaemias. MLL rearrangements (MLLr) are the most common cytogenetic abnormalities in infant and childhood acute myeloid leukaemia (AML) and acute lymphocytic leukaemia (ALL) and do not normally acquire secondary mutations compared to other leukaemias. To model these leukaemias, we have used clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 gene editing to induce MLL-AF9 (MA9) chromosomal rearrangements in murine hematopoietic stem and progenitor cell lines and primary cells. By utilizing a dual-single guide RNA (sgRNA) approach targeting the breakpoint cluster region of murine Mll and Af9 equivalent to that in human MA9 rearrangements, we show efficient de novo generation of MA9 fusion product at the DNA and RNA levels in the bulk population. The leukaemic features of MA9-induced disease were observed including increased clonogenicity, enrichment of c-Kit-positive leukaemic stem cells and increased MA9 target gene expression. This approach provided a rapid and reliable means of de novo generation of Mll-Af9 genetic rearrangements in murine haematopoietic stem and progenitor cells (HSPCs), using CRISPR/Cas9 technology to produce a cellular model of MA9 leukaemias which faithfully reproduces many features of the human disease in vitro.
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McCarthy, C. M. T., and S. M. Benson. "Cytogenetic abnormalities in acute myelomonocytic leukaemia." Mutation Research/Environmental Mutagenesis and Related Subjects 164, no. 3 (June 1986): 195–96. http://dx.doi.org/10.1016/0165-1161(86)90021-x.

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Farina, Mirko, Giuseppe Rossi, Daniella Bellotti, Eleonora Marchina, and Robert Peter Gale. "Is Having Clonal Cytogenetic Abnormalities the Same as Having Leukaemia?" Acta Haematologica 135, no. 1 (September 17, 2015): 39–42. http://dx.doi.org/10.1159/000437202.

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A finding of cytogenetic abnormalities, even when these are clonal and even when the abnormalities are typically associated with leukaemia, is not the same as a person having leukaemia. We describe a person who had acute myeloid leukaemia (AML) and achieved a complete haematological remission and who then had persistent and transient clonal cytogenetic abnormalities for 22 years but no recurrence of leukaemia. These data suggest that clones of myeloid cells with mutations and capable of expanding to levels detectable by routine cytogenetic analyses do not all eventuate in leukaemia, even after a prolonged observation interval. The possibility of incorrectly diagnosing a person as having leukaemia becomes even greater when employing more sensitive techniques to detect mutations such as by polymerase chain reaction and whole-exome or whole-genome sequencing. Caution is needed when interpreting clonal abnormalities in AML patients with normal blood and bone marrow parameters.
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Arruda, Walter Oleschko, María Belén Montú, Marcelo de Souza R. de Oliveira, and Ricardo Ramina. "Acute myeloid leukaemia induced by mitoxantrone: case report." Arquivos de Neuro-Psiquiatria 63, no. 2a (June 2005): 327–29. http://dx.doi.org/10.1590/s0004-282x2005000200024.

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Mitoxantrone (MX) is an immunosupressant drug used in secondarily progressive multiple sclerosis (SPMS) and in relapsing-remitting multiple sclerosis (RRMS). It has a leukemogenesis potential induced by cytogenetic abnormalities, though with a low incidence. Promyelocitic leukaemia (type M3) and other forms of acute myeloblastic leukaemias (M4 and M5) have been described in a few MS patients who received MX during their treatment. We describe a white female patient, 47 year-old, with SPMS (EDSS = 4) with 14 years of disease. She received MX during her disease and developed acute promyelocytic leukaemia (M3), with severe thrombocytopenia 30 months later. She ultimately died due to intracerebral hemorrhage. Other cases of treatment related to AML are reviewed and discussed.
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R., Senthilprabhu, Aruna R., and Ravichandran C. "Cytogenetic and molecular aberrations in childhood B lineage acute lymphoblastic leukaemia." International Journal of Contemporary Pediatrics 7, no. 3 (February 25, 2020): 511. http://dx.doi.org/10.18203/2349-3291.ijcp20200485.

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Background: Acute Lymphoblastic Leukemia (ALL) is a common hematological malignancy in children and is characterized by genetic changes such as mutations and chromosomal translocations. These cytogenetic and molecular abnormalities have got diagnostic and prognostic significance. Identification of these abnormalities helps in risk categorization and appropriate therapy. Aim of the study was to assess the cytogenetic/molecular abnormalities associated with B Lineage ALL in children.Methods: It was a hospital based retrospective observational study of 79 children diagnosed with B Lineage ALL by Bone marrow aspirate morphology and flow cytometry. Bone marrow samples or Peripheral blood were sent for cytogenetic/molecular analysis by Fluorescent in situ Hybridization technique. Descriptive data analysis was done using SPSS software.Results: Out of 199 cases 163(82%) were B Lineage ALL. 79(48%) undergone molecular analysis. Out of 79 cases of B lineage ALL, Translocation t(9;22) BCR-ABL1 was positive in 2(2.5%) cases , Translocation t(12;21) TEL/AML1 was positive 9(11%) cases and MLL (KMT2A) Gene Rearrangements was seen in 6(7.6%) children. Out of 79 cases of B lineage ALL, 6(7.6%) were Infantile ALL (Males 1(17%); Females 5(83%)). 4(67%) cases were positive for MLL (KMT2A) Gene Rearrangement, all of them were female children. Over all 17(22%) cases (Males 4(24%); Females 13(76%)) were positive for molecular abnormalities.Conclusions: Many children with ALL have got Cytogenetic and Molecular abnormalities. The highest percentage of cytogenetic and molecular genetic abnormalities was related to t(12;21)TEL/AML1 in B Lineage ALL children, if present confer favourable prognosis. MLL (KMT2A) Gene Rearrangement was the common molecular abnormality in Infantile B ALL, presence of it leads to high risk categorization and confer poor prognosis. The evaluation of cytogenetic and molecular genetic abnormalities in children is essential in estimating the prognosis in B Lineage ALL children, which will be a great contribution to offer appropriate therapeutic approaches.
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Young, Bryan D. "Cytogenetic and molecular analysis of chromosome 11q23 abnormalities in leukaemia." Baillière's Clinical Haematology 5, no. 4 (October 1992): 881–95. http://dx.doi.org/10.1016/s0950-3536(11)80050-8.

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Grimwade, David. "The clinical significance of cytogenetic abnormalities in acute myeloid leukaemia." Best Practice & Research Clinical Haematology 14, no. 3 (September 2001): 497–529. http://dx.doi.org/10.1053/beha.2001.0152.

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Manola, Kalliopi N. "Cytogenetic abnormalities in acute leukaemia of ambiguous lineage: an overview." British Journal of Haematology 163, no. 1 (July 25, 2013): 24–39. http://dx.doi.org/10.1111/bjh.12484.

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Harrison, Christine. "New genetics and diagnosis of childhood B-cell precursor acute lymphoblastic leukemia." Pediatric Reports 3, no. 2s (June 17, 2011): 4. http://dx.doi.org/10.4081/pr.2011.s2.e4.

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Over the last 50 years, while significant advances have been made in the successful treatment of childhood leukaemia, similar progress has been made in understanding the genetics of the disease. In childhood B-cell precursor acute lymphoblastic leukaemia (BCP-ALL), the incidences of individual chromosomal abnormalities are well established and cytogenetics provides a reliable tool for risk stratification for treatment. In spite of this role, a number of patients will relapse. Increasing numbers of additional genetic changes, including deletions and mutations, are being discovered. Their associations with established cytogenetic subgroups and with each other remain unclear. Whether they have a link to outcome is the most important factor in terms of refinement of risk factors in relation to clinical trials. For a number of newly identified abnormalities, appropriately modified therapy has significantly improved outcome. Alternatively, some of these aberrations are providing novel molecular markers for targeted therapy.
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Baqi, Saqi Md Abdul, Umme Kulsum Munmun, Md Rafiquzzaman Khan, Md Salahuddin Shah, Shafiqul Islam, Farzana Rahman, Md Abdul Aziz, and Masuda Begum. "Cytogenetic Pattern in Adult Patients with de novo Acute Myeloid Leukaemia: A Single Centre Study in Bangladesh." Haematology Journal of Bangladesh 4, no. 1 (June 20, 2020): 08–12. http://dx.doi.org/10.37545/haematoljbd202047.

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Background: Cytogenetic analysis performed at diagnosis is considered to be the most important prognostic factor in AML. Objective: The purpose of this study was to observe the pattern of cytogenetic abnormalities in adult patients with de novo AML. Method: Total fifty-two newly diagnosed de novo AML patients were selected for the study. Six cytogenetic abnormalities including t(8;21), t(15;17), inv(16), BCR-ABL1, FLT3-ITD & NPM1 mutations were detected by Real-Time PCR. Results: In this study, 36 (69.2%) patients showed different cytogenetic abnormalities. The t(15;17) was found to be the most common. t(15;17), t(8;21) and inv(16) were found only in M3, M2 and M4 FAB subtypes, respectively. Significant association was found with increasing age and cytogenetic risk groups. BCR-ABL1 mutation showed significant relation with increased age. FLT3-ITD mutation showed significant association with increased WBC count and inv16 was significantly associated with relatively less bone marrow blast percentage. Conclusion: Cytogenetic study should be performed routinely in all cases of AML for proper diagnosis, prediction of prognosis and implementation of effective therapeutic measures.
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Dissertations / Theses on the topic "Leukaemia; Cytogenetic abnormalities"

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Chase, Andrew John. "Cytogenetic and molecular characterisation of chromosome 13 abnormalities in leukaemia." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325910.

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Butler, Lisa H. "Chromosome translocations in haematopoietic neoplasms." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360209.

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Kempski, Helena Maria. "A molecular cytogenetic study of chromosome regions 11q23 and 21q22 in childhood leukaemia." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313659.

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Al-Shehhi, Halima. "A molecular cytogenetic investigation of secondary abnormalities and clonal evolution in ETV6-RUNX1 positive acute lymphoblastic leukaemia." Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/2807.

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The bacterial cell wall surrounds the cytoplasmic membrane and protects the cell against osmolysis in addition to providing shape. The cell wall is comprised of peptidoglycan, repeating units of N-acetly glucosamine and N-acetyl muramic acid form glycan strands and are crosslinked by short peptides that contain both L- and D-amino acids. Owing to the unique nature of peptidoglycan, and its absence in eukaryotic organisms, the cell wall has become an important target for many antibiotics, including the β-lactams and glycopeptides. Newly synthesised peptidoglycan contains pentapeptides, which extend from the lactyl moiety of the MurNAc sugar. These chains consist of L-alanine-D-γ- glutamate/glutamine-L-lysine/meso-diaminopimelic acid-D-alanine-D-alanine. The terminal D-alanine is often lost during cell wall maturation, either as a result of the crosslinking reaction, in which the penultimate D-alanine is attached to the side-chain of a neighbouring L-lysine or meso-diaminopimelic acid by an isopeptide bond, or as a consequence of the activities of DD-carboxypeptidases, and results in a tetrapeptide. The tetrapeptide can then be trimmed further to form a tripeptide by the action of LD-carboxypeptidases. Although many DD-carboxypeptidases have been well characterised, the majority of LD-carboxypeptidases that have been studied are active only against peptidoglycan fragments and so cannot be responsible for producing the tripeptides found in the cell wall. Of the LD-carboxypeptidases active against the mature cell wall, DacB (Streptococcus pneumoniae), Csd6 (Helicobacter pylori) and Pgp2 (Campylobacter jejuni), each has been shown to be essential in maintaining cell morphology. It should be noted, however, that neither Csd6 nor Pgp2 share any sequence similarity with DacB and belong to different peptidase families. This thesis concerns the structural and biochemical characterisation of DacB, herein renamed to LdcB (LD-carboxypeptidase B). The crystal structures of the apo form of LdcB from both S. pneumoniae and Bacillus subtilis were solved, revealing a single domain, globular protein with 2 sub-domains forming a V-shaped cleft in which the active site is located. LdcB binds one zinc ion per monomer, located at the bottom of the active site, and is a member of the LAS (lysostaphin, D-Ala-D-Ala peptidases, sonic hedgehog) family of metalloproteins. Additionally, the activity of LdcB as an LDcarboxypeptidase was confirmed and the crystal structure of LdcB from S. pneumoniae ii was solved in complex with a product mimic, M-Tri-Lys(D-Asn), revealing the molecular basis for peptidoglycan recognition in this family of enzymes. Finally, the affinity of LdcB for zinc and copper has been determined and it has been shown that catalysis is not inhibited by the substitution of zinc by copper or cobalt.
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Book chapters on the topic "Leukaemia; Cytogenetic abnormalities"

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Bendari, Mounia, Sofia Sraidi, and Nisrine Khoubila. "Haematological Malignancies: Overview of the Recent Progresses in Genetics." In Cytogenetics - Classical and Molecular Strategies for Analysing Heredity Material. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96913.

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Genetic defects play a major role in pathogenesis of the most of haematological malignancies, including cytogenetic abnormalities, gene mutations, and abnormal gene expression. Our knowledge about the genetics of haematological disorders has been dramatically improved during the past decade, due to revolution of sequencing technologies which have played a crucial role. In this chapter, we describe the techniques commonly employed for elucidating chromosomal aberrations, prognostic impact of recurrent chromosomal abnormalities, and recently updated risk stratification systems. We will summarise the chromosomal abnormalities recently identified on many of haematological diseases such acute myeloid leukaemia, acute lymphoid leukaemia, myelodysplasic syndrome, multiple myeloma, meyloproliferative disease and clarify their impacts on clinical phenotype and prognosis, as well as their role in the pathogenesis of these diseases. The aim of this chapter is to provide a brief overview of the recent progresses in haematological diseases genetics.
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Hilberink, Jacobien, and Gerwin Huls. "Treatment of AML in Older Patients." In Acute Leukemias. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.94979.

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Acute myeloid leukaemia (AML) is a disease mostly diagnosed in older adults. Treatment of older patients with AML remains challenging with higher rates of intrinsic chemotherapeutic resistance and decreased treatment tolerance. Indeed AML in older patients has different clinical and biologic characteristics compared to younger patients. Several treatment options are available for treatment of AML in older patients, namely conventional intensive chemotherapy (‘3 + 7’), low-dose cytarabine, and hypomethylating agents. Combinations with new drugs have been recently approved or are in advanced stages of clinical testing, namely venetoclax, midostaurin, glasdegib. Clinical decision making should take into account disease characteristics (e.g. cytogenetic and molecular abnormalities, white blood cell count), patient characteristics (e.g. performance, comorbidities, geriatric assessment) and patients’ preference when considering which treatment option is most suitable for the older patient. Allogeneic haematopoietic cell transplantation (HCT) as post-remission strategy should also be considered for older patients with AML. Allogeneic HCT following reduced-intensity conditioning or non-myeloablative conditioning has made this treatment option more suitable for older patients with a reduction in treatment-related mortality.
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