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Dissertations / Theses on the topic 'Lymphoblastic'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 March 2023

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1

Paganin, Maddalena. ""High Risk" Acute Lymphoblastic Leukemia." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3427207.

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Acute lymphoblastic leukemia (ALL) is a neoplasia characterized by an abnormal, clonal and self-maintaining proliferation of lymphoid cells. In this three year of phd I tried to add some information to understand the complex molecular mechanisms underlying this disease. I performed my studies in the laboratory of "Oncoematologia Pediatrica, Dipartimento di Pediatria dell'Università degli studi di Padova" and for three months in the laboratory of Prof. A. A. Ferrando, Columbia University, Irving Cancer Center, New York. The recombination, insertion and deletion of immunoglobulin (Ig) and T

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2

Kuchinskaya, Ekaterina. "Genetic studies of acute lymphoblastic leukemia /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-337-5/.

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3

Cartwright, Cher Suzanne. "Thiopurine Metabolism in Childhood Acute Lymphoblastic Leukaemia." Thesis, University of Sheffield, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500442.

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4

Lo, Tony Chung Tung. "Inactivation of SHIP1 in acute lymphoblastic leukemia." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1465620.

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Thesis (M.S.)--University of California, San Diego, 2009.<br>Title from first page of PDF file (viewed July 22, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 63-69).

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5

Elmantaser, Musab Elmabrouk M. "Bone health in children with acute lymphoblastic leukaemia." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4447/.

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In chapter 1, bone structure, bone growth and development, osteoporosis in children and skeletal morbidities in children with acute lymphoblastic leukaemia (ALL) are discussed. After that, the mechanostat and the effect of whole body vibration (WBV) on bone health are considered. Finally, I examine diagnostic approaches to assess the musculoskeletal system. In chapter 2, the incidence and risk factors for skeletal morbidity in ALL children are determined. The medical records of all (n,186, male,110) children presenting with ALL between 1997 and 2007 and treated on UKALL97, UKALL97/01 or UKALL2

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6

Wilson, Kerrie Lauren. "Malignant stem cells in childhood acute lymphoblastic leukaemia." Thesis, University of Newcastle Upon Tyne, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.525030.

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7

Bomken, Simon Nicholas. "Investigating leukaemic propagation in childhood acute lymphoblastic leukaemia." Thesis, University of Newcastle Upon Tyne, 2013. http://hdl.handle.net/10443/1865.

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Childhood acute lymphoblastic leukaemia (ALL) does not possess a propagating cell hierarchy, at least as defined by B-cell precursor immunophenotype. Indeed, many, or even all, leukaemic blasts may have the potential to propagate the disease. This unusual characteristic mirrors the substantial capacity for clonal expansion demonstrated by fully differentiated normal lymphoid cells. This Fellowship aimed to investigate the genetic programmes underlying the propagation of acute lymphoblastic leukaemia. An initial candidate approach confirmed the expression of PIWIL2, a gene critical to the maint

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8

Sorour, Amani Fouad Abdel Halim. "Chromosome 6q16-21 deletions in acute lymphoblastic leukaemia." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399158.

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9

Mangolini, M. "Oncogenic signalling in t(12;21) Acute Lymphoblastic Leukaemia." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1415780/.

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The t(12;21)(p13;q22) translocation is present in up to 25% of children with pre-B cell Acute Lymphoblastic Leukaemia (ALL). This translocation involves two transcription factors, TEL (ETV6) and AML (RUNX1), both of which have crucial roles in regulating haematopoiesis. Clinically, TEL-AML1 positive patients have good prognoses. However, late relapses, additional genetic lesions affecting prognosis, and long-term side-effects of chemotherapy remain a cause for concern. In light of recent studies showing genetic and functional heterogeneities in cells responsible for cancer clone maintenance an

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10

Jackson, Rosanna Katherine. "Personalisation of dexamethasone in childhood acute lymphoblastic leukaemia." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3940.

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Dexamethasone (dex) is a key treatment for childhood acute lymphoblastic leukaemia (ALL), but is associated with significant variability in terms of toxicity and efficacy. In this project, the following variables were assessed to better understand how dex personalisation may be achieved: pharmacokinetics, intracellular dex accumulation, glucocorticoid receptor (GR) posttranslational modifications and B-cell maturation state. For pharmacokinetic studies, samples were collected from 154 patients randomised to short (10mg/m2 x 14 days) or standard (6mg/m2 x 28 days) dex induction therapy, as part

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11

Kanerva, Jukka. "Prognostic factors in childhood acute lymphoblastic leukemia (ALL)." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/kanerva/.

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12

Oliveira, Tiago M. "The importance of glycosylation in Acute Lymphoblastic Leukemia." Thesis, Griffith University, 2021. http://hdl.handle.net/10072/410463.

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Acute leukemias, such as acute lymphoblastic leukemia (ALL), are aggressive cancers characterized by the rapid proliferation of malignant hematopoietic cells. Throughout the last 60 years, childhood ALL’s long-term survival rates increased from less than 10% to more than 90%. Despite these improvements, certain subtypes remain hard to manage (e.g. mixed lineage leukemia, MLL-r), and even new therapies frequently fail. Therefore, identifying leukemia-cell restricted antigens in these ALL subtypes remains crucial in the quest to develop novel diagnostic tools and specific treatments. Traditional

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13

Oram, Sarah Helen. "Cis-regulation of LM02 in T-acute lymphoblastic leukaemia." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609663.

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14

Akers, Stephen Matthew. "Modeling central nervous system involvement in acute lymphoblastic leukemia." Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/11227.

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Thesis (Ph. D.)--West Virginia University, 2010.<br>Title from document title page. Document formatted into pages; contains x, 102 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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15

Thörn, Ingrid. "Minimal Residual Disease Assessment in Childhood Acute Lymphoblastic Leukemia." Doctoral thesis, Uppsala universitet, Institutionen för genetik och patologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-101028.

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Traditionally, response to treatment in hematological malignancies is evaluated by light microscopy of bone marrow (BM) smears, but due to more effective therapies more sensitive methods are needed. Today, detection of minimal residual disease (MRD) using immunological and molecular techniques can be 100 times more sensitive than morphology. The main aim of this thesis was to compare and evaluate three currently available MRD methods in childhood acute lymphoblastic leukemia (ALL): (i) real-time quantitative PCR (RQ-PCR) of rearranged antigen receptor genes, (ii) multicolor flow cytometry (FCM

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16

Nordlund, Jessica. "Gene Expression and DNA Methylation in Acute Lymphoblastic Leukemia." Doctoral thesis, Uppsala universitet, Molekylär medicin, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-179680.

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Pediatric acute lymphoblastic leukemia (ALL) is the most common malignancy in children, which results from the malignant transformation of progenitor cells in the bone marrow into leukemic cells. The precise mechanisms for this transformation are not well defined, however recent studies suggest that aberrant regulation of gene expression or DNA methylation may play an important role. Hence, the aim of this thesis was to use novel methods to investigate genome-wide gene expression and DNA methylation patterns in a large collection of primary ALL cells from pediatric patients. With these studies

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17

Rehe, Klaus. "Diversity of cancer stem cells in acute lymphoblastic leukaemia." Thesis, University of Newcastle Upon Tyne, 2012. http://hdl.handle.net/10443/1777.

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For many cancers research led to controversial results regarding frequency and identity of cancer stem cells, cells that self-renew and are able to reconstitute the full phenotype of the original malignancy. In some malignancies such as acute myeloid leukaemia the hierarchical stem cell model that suggests that only rare and immunophenotypically immature blasts exhibit stem cell characteristics, resembling the normal physiological haematopoietic hierarchy, has been well established. In contrast to that, the stochastic model states that all or at least a substantial proportion of malignant cell

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18

Aldhafiri, Fahad Khalid. "Weight status during and after childhood acute lymphoblastic leukaemia." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4500/.

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Background: This thesis sits within the arena of weight status during and after childhood acute lymphoblastic leukaemia (ALL), with a particular focus on the prevalence of unhealthy weight status amongst (ALL), Saudi and UK populations. Each chapter in the thesis explores different aspects of unhealthy weight status in ALL which had been highlighted as gaps in the literature at a conference in Puebla, Mexico, at the end of 2006. A summary of each study is given below. Study 1: Background: This study estimated prevalence of unhealthy weight status and metabolic syndrome (MS) amongst Saudi survi

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19

卓大治 and Tai-chi Cheuk. "Childhood acute lymphoblastic leukaemia with TEL-AML1 gene fusion." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31969690.

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20

Sulong, Sarina. "Determination of allelic imbalance in childhood acute lymphoblastic leukaemia." Thesis, University of Newcastle Upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.445581.

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21

Sundaresh, A. "Aberrant transcriptional pathways in t(12;21) Acute Lymphoblastic Leukaemia." Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1522624/.

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The single most frequent chromosomal translocation associated with childhood Acute Lymphoblastic Leukaemia is the t(12;21) rearrangement, that creates a fusion gene between TEL (ETV6) and AML1 (RUNX1). Although TELAML1+ patients have a very good prognosis, relapses occur in up to 20% of cases and many patients face long-term side effects of chemotherapy. Our laboratory has previously shown that TEL-AML1 regulates Signal Transducer and Activator of Transcription 3 (STAT3) activation, which is critical for survival of the leukaemic cells. In this study, inhibition of STAT3 in TEL-AML1+ cells res

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22

Ede, Benjamin Christopher. "Improving therapies for childhood T cell acute lymphoblastic leukaemia." Thesis, University of Bristol, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.752757.

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23

Robinson, Hazel M. "Acquired abnormalities of chromosome 21 in acute lymphoblastic leukaemia." Thesis, University of Southampton, 2008. https://eprints.soton.ac.uk/161483/.

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The intrachromosomal amplification of chromosome 21 (iAMP21) was identified as a novel and prognositically important acquired chromosomal abnormality in childhood acute lymphoblastic leukaemia (ALL). It is defined by multiple copies of the RUNX1 gene, as seen by fluorescence in situ hybridisation (FISH), localised to a single abnormal duplicated chromosome 21 [dup(21)]. The morphological form of this chromosome is highly variable between patients and currently the only reliable method of detection is FISH with probes to RUNX1. Studies of 48 iAMP21 patients using detailed FISH techniques and ar

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24

Thörn, Ingrid. "Minimal Residual Disease Assessment in Childhood Acute Lymphoblastic Leukemia." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-101028.

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25

Cheuk, Tai-chi. "Childhood acute lymphoblastic leukaemia with TEL-AML1 gene fusion." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22264619.

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26

Basnett, Jordan. "Characterisation of Resistance to Everolimus in Acute Lymphoblastic Leukemia." Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/16332.

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Acute Lymphoblastic Leukemia (ALL) is the most common childhood cancer. Disease relapse following treatment still occurs in a significant minority of children and the majority of adult patients. The inability to further intensify current treatments due to dose limiting toxicities of chemotherapeutic agents demands the development of new agents. One exciting new treatment, is the mTOR inhibitor everolimus. Preclinical studies using everolimus, while promising, revealed that resistance can emerge following prolonged treatment in vivo. This study uses ALL xenografts that have developed resistance

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27

LIPKIN, VASQUEZ MARINA. "Unveiling the heterogeneity within chilhood Ph+ acute lymphoblastic leukemia." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2011. http://hdl.handle.net/10281/20633.

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In the past two decades, childhood acute lymphoblastic leukemia (ALL) cure rate has reached over 80% due to treatment advances, but some resistant ALL subtypes, such as those that carry the Philadelphia (Ph+) chromosome, still don’t respond to therapy. The presence of BCR-ABL in ALL children is correlated to a very poor prognosis, nevertheless, several long-scale studies have shown that Ph+ ALL is heterogeneous in terms of clinical parameters and patients respond differently to the therapy, what suggests the presence of additional mechanisms of leukemogenesis. A set of international studies wi

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28

Wright, Adrienne M. P. "A role for nucleoside transport processes in the cytotoxicity of 2-chlorodeoxyadenosine in leukemic lymphoblasts from children with acute lymphoblastic leukemia." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23091.pdf.

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29

Heidari, Mansour. "Investigation of the molecular function of the nuclear oncoprotein HOX11 in human t-cell leukaemia." Thesis, Heidari, Mansour (2003) Investigation of the molecular function of the nuclear oncoprotein HOX11 in human t-cell leukaemia. PhD thesis, Murdoch University, 2003. https://researchrepository.murdoch.edu.au/id/eprint/71/.

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HOXll, the prototypical member of the HOXll family (HOX11, HOXllLl and HOXllL2) was originally discovered as a transcriptional regulator aberrantly expressed in tumours with an immature T-cell phenotype (T-ALL) as a result of specific chromosomal translocations involving T-cell receptor loci. Subsequently, it was revealed that HOXll is required for normal spleen development since newborn Hoxll-/- mice exhibit asplenia. In both its normal and abnormal roles, HOXll has been postulated to function by binding regulatory elements within specific target genes to control gene transcription. However,

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30

Heidari, Mansour. "Investigation of the molecular function of the nuclear oncoprotein HOX11 in human t-cell leukaemia." Murdoch University, 2003. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20060815.123509.

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HOXll, the prototypical member of the HOXll family (HOX11, HOXllLl and HOXllL2) was originally discovered as a transcriptional regulator aberrantly expressed in tumours with an immature T-cell phenotype (T-ALL) as a result of specific chromosomal translocations involving T-cell receptor loci. Subsequently, it was revealed that HOXll is required for normal spleen development since newborn Hoxll-/- mice exhibit asplenia. In both its normal and abnormal roles, HOXll has been postulated to function by binding regulatory elements within specific target genes to control gene transcription. However,

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31

Lee, Andrew John. "Augmentation of the immunogenicity of acute lymphoblastic leukaemia in vitro." Thesis, University of Leicester, 2000. http://hdl.handle.net/2381/29362.

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Acute lymphoblastic leukaemia (ALL) is a heterogeneous disease of different immuno-phenotypically defined subtypes. Although successful conventional therapies are available, for a proportion of patients (approximately 30%) these are ultimately unsuccessful. ALL relapse is a result of the failure of the immune system to recognise these malignant cells and down regulation of crucial molecules required for cognate CD4+ T-cell recognition has been postulated as a means of immune escape. This study has concentrated on the augmentation of the immunogenicity of B-cell ALL to facilitate the generation

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32

Liaw, Tracy Yun En Children's Cancer Institute Australia for Medical Research Faculty of Medicine UNSW. "Characterisation of novel anticancer agents in childhood acute lymphoblastic leukaemia." Publisher:University of New South Wales. Children's Cancer Institute Australia for Medical Research, 2009. http://handle.unsw.edu.au/1959.4/43558.

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Tubulin-binding agents (TBAs) are employed widely in cancer treatment, including childhood acute lymphoblastic leukaemia (ALL). Despite their success, resistance to TBAs can be a major clinical problem. Mechanisms mediating resistance to TBAs that target the colchicine-binding site on β-tubulin, along with novel therapeutic strategies were investigated. 2-Methoxyestradiol (2ME2) is a multi-targeted TBA active in various cancer types, yet its efficacy and mechanisms(s) of action in haematological malignancies are not well evaluated. To improve understanding of mechanisms(s) of action and drug r

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33

Gottardo, Nicholas G. "Oncogenes and prognosis in childhood T-cell acute lymphoblastic leukaemia." University of Western Australia. School of Paediatrics and Child Health, 2008. http://theses.library.uwa.edu.au/adt-WU2009.0039.

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[Truncated abstract] The treatment of childhood acute lymphoblastic leukaemia (ALL) is one of the great success stories of paediatric oncology, transforming a universally fatal disease into one where 75 to 90% of children are now cured. Although in the past survival for children with T-cell ALL (T-ALL) lagged behind that of children with pre-B ALL, the use of contemporary intensified treatment strategies has significantly diminished this difference, with many investigators reporting similar cure rates for both groups of patients. Despite these marked improvements, numerous challenges still fac

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34

Larery, Angela R. D. McGill Jerry C. "Hierarchical neuropsychological functioning among pediatric survivors of acute lymphoblastic leukemia." [Denton, Tex.] : University of North Texas, 2007. http://digital.library.unt.edu/permalink/meta-dc-3949.

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35

Van, Vlierberghe Pieter. "Moleciular-genetic insights in pediatric T-cell acute lymphoblastic leukemia." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/12225.

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36

Chou, J.-L. "In vitro induction of differentiation of human lymphoblastic leukaemic cells." Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377217.

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37

Breen, Marie Elizabeth. "The erythropoietin receptor in TEL-AML1 positive acute lymphoblastic leukaemia." Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.579773.

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The TEL-AMLl fusion is the result of t(12;21) (p13;q22), the most frequent chromosomal translocation in childhood B-cell ALL. Recent studies have found a positive correlation with TEL-AMLl and EpoR expression. Three possible mechanisms of up-regulation were investigated in this study: Gene expression analysis, DNA methylation and microRNAs. Microarray analysis compared TEL-AMLl positive and negative gene expression profiles to identify differentially expressed genes. Genes with well known roles in haematopoiesis were also examined. GATA-2 showed a similar expression profile to EpoR, with a hig

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38

Thornton, Nadia. "L-alanosine : selective treatment in relapsed childhood acute lymphoblastic leukaemia." Thesis, University of Newcastle Upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440588.

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39

Inman, Louise. "The c-Kit signalling pathway and acute non-lymphoblastic leukaemogenesis." Thesis, University of the West of England, Bristol, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365066.

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40

Reid, George. "Mammalian asparaginases of possible therapeutic significance in acute lymphoblastic leukaemia." Thesis, University of Strathclyde, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303368.

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41

Steele, Jeremey Peter Charles. "The severe combined immune deficient model of acute lymphoblastic leukaemia." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298191.

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42

Srisukkham, Worawut. "An intelligent decision support system for acute lymphoblastic leukaemia detection." Thesis, Northumbria University, 2017. http://nrl.northumbria.ac.uk/36140/.

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The morphological analysis of blood smear slides by haematologists or haematopathologists is one of the diagnostic procedures available to evaluate the presence of acute leukaemia. This operation is a complex and costly process, and often lacks standardized accuracy owing to a variety of factors, including insufficient expertise and operator fatigue. This research proposes an intelligent decision support system for automatic detection of acute lymphoblastic leukaemia (ALL) using microscopic blood smear images to overcome the above barrier. The work has four main key stages. (1) Firstly, a modi

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43

Lindqvist, Carl Mårten. "Genomic characterization of pediatric acute lymphoblastic leukemia by deep sequencing." Doctoral thesis, Uppsala universitet, Molekylär medicin, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-269760.

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Acute Lymphoblastic Leukemia (ALL) is the most common cancer in children, with close to 200 cases per year in the Nordic countries. Despite recent advances in modern chemotherapies, 20% of the ALL patients experience a relapse. ALL has traditionally been stratified into subtypes with different risk classification and therapy using large genomic aberrations such as translocations and aneuploidies. In recent years technological advances have enabled the detection of smaller genetic variants, such as point mutations and small insertions/deletions. This thesis focuses on the detection of these sma

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44

Borssén, Magnus. "DNA methylation as a prognostic marker i acute lymphoblastic leukemia." Doctoral thesis, Umeå universitet, Patologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-127225.

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Acute lymphoblastic leukemia (ALL) is the most common childhood malignancy. Most ALL cases originate from immature B-cells (BCP-ALL) and are characterized by reoccurring structural genetic aberrations. These aberrations hold information of the pathogenesis of ALL and are used for risk stratification in treatment. Despite increased knowledge of genetic aberrations in pediatric T-cell ALL (T-ALL), no reliable molecular genetic markers exist for identifying patients with higher risk of relapse. The lack of molecular prognostic markers is also evident in patients with relapsed ALL. During the last

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Dormon, Katherine Louise. "Investigating the evolution of dexamethasone resistance in acute lymphoblastic leukaemia." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3737.

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The evolution of ALL from presentation to relapse is often accompanied by the emergence of resistance to commonly used chemotherapeutics, including dexamethasone (Dex), a synthetic glucocorticoid that has been the backbone of ALL treatment since the 1950s. In order to investigate the evolution of drug resistance we focused on the L707 cells, a matched Dex-sensitive presentation and Dex-resistant relapse pair from a patient with t(17;19) B ALL. A major genetic difference between presentation and relapse is a 5q deletion spanning 6 genes, including NR3C1, the glucocorticoid receptor and the site

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46

Rocchetti, Francesca. "Study of calcineurin pro-oncogenic role in acute lymphoblastic leukemia." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC166.

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Malgré les avancés thérapeutiques, le pronostic des leucémies aiguës lymphoblastiques (LAL) reste mauvais. Notre laboratoire a montré que la calcineurine (Cn) est requise pour le maintien à long terme des LAL-T. Sa délétion est associée à la dérégulation de l'expression de plusieurs gènes, dont TRNP1 et NFIB, qui sont nouveaux dans le contexte des LAL-T. Nous avons montré que la suppression de leur expression a un effet délétère sur les cellules leucémiques de LAL-T in vitro et in vivo. Cn est aussi activée dans les LAL-B BCR-ABL+. Des travaux publiés ont proposé que son inhibition par la cycl

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47

Larery, Angela R. D. "Hierarchical neuropsychological functioning in pediatric survivors of acute lymphoblastic leukemia." Thesis, University of North Texas, 2007. https://digital.library.unt.edu/ark:/67531/metadc3949/.

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Acute lymphocytic leukemia (ALL) is one of the most common types of pediatric cancers. Improvements in treatment within the last 20 years have resulted in reduced mortality and a greater focus upon quality of life. Several researchers have documented neuropsychological impairments in children following treatment for ALL; however, there have not been any comparative studies documenting differences in neuropsychological functioning based upon treatment modality despite the documented effects of radiation therapy and combined radiation/chemotherapy upon the developing brain. In addition, past stu

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48

Berks, Richard. "In vitro models of TEL/AML1-positive acute lymphoblastic leukaemia." Thesis, University of York, 2012. http://etheses.whiterose.ac.uk/3160/.

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Acute lymphoblastic leukaemia (ALL) is the most common cancer in children, and is characterised by the proliferation of immature lymphoid cells in the bone marrow. The fusion gene TEL/AML1, generated by the chromosome translocation t(12;21), is the most common single genetic aberration in B-lineage ALL, and is formed from the transcription factors TEL and AML1 (coded for by the genes ETV6 and RUNX1, respectively). However, it is still not clear how the presence of TEL/AML1 causes the development of leukaemia. In addition, the importance of a common secondary mutation in TEL/AML1+ leukaemia, th

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49

Lund, Bendik. "Host Genome Variation and Toxicity in Childhood Acute Lymphoblastic Leukaemia." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for laboratoriemedisin, barne- og kvinnesykdommer, 2014. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-24171.

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Kreft er den vanligste medisinske dødsårsaken hos barn mellom 1 og 15 år. Akutt lymfatisk leukemi (ALL) er den vanligste kreftformen hos barn og i Norge får ca. 30-40 barn ALL hvert år. Behandlingen strekker seg over 2,5 år og består av 6-12 ulike cellegifter i forskjellige kombinasjoner i tillegg til støttebehandling og overvåkning. Behandlingen medfører mange bivirkninger, bl.a. nedsatt immunforsvar som gir økt risiko for infeksjoner. Den totale overlevelsen for barn med ALL er i dag på ca. 80-85%. Av de som dør etter å ha fått diagnosen skyldes dette for ca. 75% kreftsykdommen i seg selv hv

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Withycombe, Janice Squires. "Early Weight Gain and Obesity in Childhood Acute Lymphoblastic Leukemia." Diss., The University of Arizona, 2012. http://hdl.handle.net/10150/223340.

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Abstract:

Obesity is a recognized problem for children treated for acute lymphoblastic leukemia (ALL) and is present in roughly one fourth of children by the end of therapy. Obesity may lead to immediate health threats, such as an increased risk for cancer relapse, or may cause future heath issues such as diabetes, metabolic syndrome, hypertension, additional cancers, depression or cardiovascular disease. The purpose of this study was to determine if weight gain during two individual cycles of therapy (Induction or Delayed Intensification Cycle 1) were predictive of obesity (defined as body mass index ≥

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