Dissertations / Theses on the topic 'Lymphoblastic'
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Paganin, Maddalena. ""High Risk" Acute Lymphoblastic Leukemia." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3427207.
Full textLa leucemia linfoblastica acuta (LLA) è una neoplasia caratterizzata da una proliferazione abnorme, clonale ed auto-mantenuta di cellule linfoidi. In questi tre anni di dottorato ho cercato di aggiungere qualche nozione per la comprensione dei complessi meccanismi molecolari che sottendono a questa malattia. L'attività di ricerca si è svolta presso il Laboratorio di Oncoematologia Pediatrica, Dipartimento di Pediatria dell'Università degli Studi di Padova e per tre mesi presso il Laboratorio del Prof. A. A. Ferrando, Columbia University Irving Cancer Research Center, New York. Ogni linfocita è contraddistinto a livello dei siti di ricombinazione, inserzione e delezione dei segmenti genici delle regioni variabili delle immunoglobuline (Ig) e del recettore delle cellule T (TCR), da una regione giunzionale detta N-region. Le regioni giunzionali possono essere considerate un fingerprint-marker specifico di ogni linfocita e di ogni neoplasia linfoide ed essere utilizzate per studiare le caratteristiche biologiche della leucemia o per l'analisi della malattia residua minima (MRD). I primi mesi di dottorato sono stati dedicati allo studio della LLA positiva per t(4;11) in 32 pazienti pediatrici di età superiore a 1 anno attraverso l'analisi dell'immunofenotipo, riarrangiamenti Ig/TCR e prognosi. Dall'analisi è stato identificato un pattern di riarrangiamenti diverso tra i pazienti pediatrici e gli infant dovuto alla diversa maturità della cellula nelle due classi di pazienti come se la maggiore età dei pazienti andasse a pari passo con lo stadio maturativo del blasto leucemico (Capitolo 1.1). Fondamentale per l'analisi dei riarrangiamenti Ig/TCR è la disponibilità di materiale per l'estrazione del DNA e l'esecuzione del pannello di PCR di screening. Se si ha una quantità limitata di DNA non è quindi sempre possibile ricavare il pattern di clonalità . Abbiamo eseguito uno studio per valutare la possibilità di eseguire le PCR di screening della regione Ig/TCR su DNA amplificato con una tecnica di "whole genome amplification" basata sull'utilizzo della DNA polimerasi ?29 e di random primer. Il DNA utilizzato era estratto da cellule in sospensione di asiprato midollare, anche in quantità limitata, o da cellule su vetrino non colorato. Abbiamo eseguito 476 PCR prima e dopo "whole genome amplification". Il confronto dei risultati, dopo sequenziamento dei prodotti di PCR, ha mostrato una concordanza dei risultati del 98%. L'amplificazione dell'intero genoma non ha inficiato i risultati di PCR nella regione Ig/TCR (Capitolo 1.2). Il principale campo di interesse in questi anni di dottorato è stata lo studio del valore prognostico della MRM nei pazienti pediatrici LLA ricaduti. La quasi totalità dei pazienti pediatrici con leucemia linfoblastica acuta raggiunge la remissione completa continua ma esiste ancora un 20% di questi che va incontro ad una recidiva di malattia. Il protocollo AIEOP LAL REC 2003 stratifica i pazienti ricaduti in classi di rischio: basso-medio (S1-S2) e alto (S3-S4) a seconda dell'immunofenotipo, del tempo e della sede di ricaduta. Abbiamo valutato il valore prognostico della malattia residua minima durante la terapia nella classe di pazienti ad alto rischio. Sono stati studiati 60 pazienti ricaduti classificati come S3-S4, arruolati nel protocollo AIEOP LAL REC 2003. Per ogni paziente E' stato analizzato il profilo di clonalità con PCR di screening e l'analisi heteroduplex dei riarrangiamenti Ig/TCR; è stata analizzata la malattia residua minima (MRM) attraverso RQ-PCR in diverse fasi della terapia: dopo l'induzione (TP1), dopo la re-induzione (TP2) e dopo il consolidamento (TP3) post-ricaduta. L'EFS a tre anni è del 73, 45 e 19% rispettivamente per i pazienti con MRD al TP1 negativa, positiva non quantificabile (MRD < 10-4) o positivo (MRD ? 10-4), (P < 0.05). Il valore prognostico predittivo statisticamente significativo dell'MRD è stato confermato dall'analisi multivariata. Abbiamo dimostrato che la quantificazione delle malattia residua minima permette di differenziare i pazienti precocemente e in modo efficace comprendendo quali pazienti rispondono alla terapia convenzionale e possano ricevere il trapianto di cellule staminali allogeniche e quali invece necessitino di terapie innovative (Capitolo 2.1). La ricaduta midollare è attualmente definita secondo criteri morfologici quando la conta dei blasti è ?25% dopo che il paziente ha raggiunto la remissione completa. Abbiamo valutato il potere della presenza di MRM come indicatore di successiva ricorrenza ematologica di ALL determinando se vi siano livelli critici di MRM predittivi di ricaduta. Abbiamo trovato che rilevare un prelievo positivo quantificabile durante il follow-up del paziente è associato a una cumulative relapse incidence dell'85.7%. Questo dato ha valore statisticamente significativo se confrontato con il valore predittivo di un prelievo negativo o positivo non quantificabile per MRM. Identificare anticipatamente la ricaduta potrebbe aiutare nel progettare un trattamento terapeutico preventivo di ricaduta morfologica (Capitolo 2.1). Nella prospettiva di comprendere su quali vie si potrebbero spostare le future strategie terapeutiche per pazienti che presentino caratteristiche di alto rischio, abbiamo abbracciato l'ipotesi attuale che l'origine di molte neoplasie maligne risieda in una ristretta popolazione di cellule staminali tumorali responsabile della crescita, diffusione tumorale e resistenza alla terapia. Nella LLA questa popolazione non è stata ancora chiaramente identificata e caratterizzata anche se studi recenti spingono l'attenzione sulle subpopolazioni caratterizzate dagli antigeni di superficie CD34/CD38/CD19. Abbiamo analizzato in 10 pazienti il profilo di clonalità Ig/TCR delle popolazioni CD34+CD38-CD19+ e CD34+CD38-CD19- dopo sorting, confrontandolo con quello identificato nella popolazione totale dei blasti leucemici del paziente. In 9/10 pazienti le subpopolazioni di progenitori, isolate e analizzate, condividevano almeno un riarrangiamento genico clonale (fingerprint- marker) con i blasti leucemici. Questa è una dimostrazione diretta, attraverso un marcatore genetico, e non funzionale, dell'origine del blasti leucemici dalla popolazione CD34+CD38-, nel 90% dei casi nella sottopolazione CD34+CD38-CD19- (Capitolo 3.1). Abbiamo inoltre studiato se la frequenza del compartimento CD34+CD38- all'esordio LLA correlasse con il livello di MRM dopo chemioterapia. Abbiamo analizzato 133 pazienti LLA rilevando che una percentuale <1% di CD34+CD38- correla in modo statisticamente significativo con un basso livello di MRM rilevato dopo 33 giorni di terapia (Capitolo 3.1). Durante gli ultimi mesi di dottorato mi sono avvicinata allo studio di WT1, un fattore di regolazione dello sviluppo. I meccanismi molecolari implicati nello sviluppo e nella ricaduta della LLA ad immunofenotipo T sono scarsamente compresi. Partendo dall'osservazione che nel 10% dei pazienti con LLA-T il gene WT1 è mutato, abbiamo approcciato lo studio di questo fattore dal punto di vista genico e proteico, per comprendere il suo coinvolgimento nello sviluppo della leucemia. La parte del lavoro a cui ho contribuito ha riguardato l'analisi dello stato di metilazione del promotore del gene WT1 (Capitolo 4.1).
Kuchinskaya, Ekaterina. "Genetic studies of acute lymphoblastic leukemia /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-337-5/.
Full textCartwright, 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.
Full textLo, 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.
Full textTitle from first page of PDF file (viewed July 22, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 63-69).
Elmantaser, Musab Elmabrouk M. "Bone health in children with acute lymphoblastic leukaemia." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4447/.
Full textWilson, 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.
Full textBomken, Simon Nicholas. "Investigating leukaemic propagation in childhood acute lymphoblastic leukaemia." Thesis, University of Newcastle Upon Tyne, 2013. http://hdl.handle.net/10443/1865.
Full textSorour, 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.
Full textMangolini, M. "Oncogenic signalling in t(12;21) Acute Lymphoblastic Leukaemia." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1415780/.
Full textJackson, Rosanna Katherine. "Personalisation of dexamethasone in childhood acute lymphoblastic leukaemia." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3940.
Full textKanerva, Jukka. "Prognostic factors in childhood acute lymphoblastic leukemia (ALL)." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/kanerva/.
Full textOliveira, Tiago M. "The importance of glycosylation in Acute Lymphoblastic Leukemia." Thesis, Griffith University, 2021. http://hdl.handle.net/10072/410463.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Institute for Glycomics
Griffith Health
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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.
Full textAkers, 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.
Full textTitle from document title page. Document formatted into pages; contains x, 102 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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.
Full textNordlund, 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.
Full textRehe, Klaus. "Diversity of cancer stem cells in acute lymphoblastic leukaemia." Thesis, University of Newcastle Upon Tyne, 2012. http://hdl.handle.net/10443/1777.
Full textAldhafiri, Fahad Khalid. "Weight status during and after childhood acute lymphoblastic leukaemia." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4500/.
Full text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.
Full textSulong, 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.
Full textSundaresh, 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/.
Full textEde, 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.
Full textRobinson, Hazel M. "Acquired abnormalities of chromosome 21 in acute lymphoblastic leukaemia." Thesis, University of Southampton, 2008. https://eprints.soton.ac.uk/161483/.
Full textThörn, 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.
Full textCheuk, 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.
Full textBasnett, Jordan. "Characterisation of Resistance to Everolimus in Acute Lymphoblastic Leukemia." Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/16332.
Full textLIPKIN, 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.
Full textWright, 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.
Full textHeidari, 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/.
Full textHeidari, 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.
Full textLee, Andrew John. "Augmentation of the immunogenicity of acute lymphoblastic leukaemia in vitro." Thesis, University of Leicester, 2000. http://hdl.handle.net/2381/29362.
Full textLiaw, 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.
Full textGottardo, 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.
Full textLarery, 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.
Full textVan, 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.
Full textChou, 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.
Full textBreen, 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.
Full textThornton, 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.
Full textInman, 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.
Full textReid, 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.
Full textSteele, 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.
Full textSrisukkham, Worawut. "An intelligent decision support system for acute lymphoblastic leukaemia detection." Thesis, Northumbria University, 2017. http://nrl.northumbria.ac.uk/36140/.
Full textLindqvist, 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.
Full textBorssén, 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.
Full textDormon, 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.
Full textRocchetti, Francesca. "Study of calcineurin pro-oncogenic role in acute lymphoblastic leukemia." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC166.
Full textAlthough acute Iymphoblastic leukemia (ALL) cure rates improved in the last decades, outcome for primary resistant and relapsed patients remains poor. Our laboratory showed that calcineurin (Cn) is essential to T-ALL Leukemia Initiating Cells activity. Its deletion is associated with strong anti-leukemic effects and to the deregulation of several genes, including TRNP1 and NFIB, which have never been reported in T-ALL. Here, we demonstrate that silencing of these genes is deleterious to T-ALL cells both in vitro and in vivo, unravelling new actors involved in leukemogenesis. Cn is activated in BCR-ABL+ B-ALL (Ph+ B-ALL) as well and its inhibition by cyclosporin A (CsA) was reported to sensitize leukemic cells to BCR-ABL inhibitors in a mouse model of the disease. We demonstrate here that this sensitization is due to off-target effects of CsA, since Cn genetic deletion did not affect BCR-ABL-induced B-ALL maintenance and propagation in two mouse models of the disease. Moreover, CsA similarly sensitized Cn+ and Cn- leukemic cells to BCR-ABL inhibitors in vitro. The outcome of B-ALL is particularly poor when patients present deletions of IKZF1, the gene encoding the transcription factor Ikaros, which are observed in >800/0 of Ph+ B-ALL cases. Using a mouse model of BCR-ABL-induced B-ALL in which one copy of Ikaros can be specifically deleted in pro-B cells, we observed acceleration of leukemia onset and a stem-cell/early progenitor-like transcriptomic signature. Thus, the loss of one copy of Ikaros allows the reprogramming of the pro/pre-B cell of origin towards a more primitive, undifferentiated state, likely explaining the increased aggressiveness of the disease
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/.
Full textBerks, Richard. "In vitro models of TEL/AML1-positive acute lymphoblastic leukaemia." Thesis, University of York, 2012. http://etheses.whiterose.ac.uk/3160/.
Full textLund, 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.
Full textCancer remains the leading cause of disease-related mortality among children aged 1-14 years in developed countries. Acute lymphoblastic leukaemia (ALL) is the most common malignancy in childhood and accounts for about 25% of all childhood cancers. In Norway about 30-40 children are diagnosed with ALL each year. Treatment comprises of a combination of 6-12 different chemotherapy drugs administered over a period of 2.5 years with additional supportive care. Side effects remain a great challenge for both patients and physicians. One of the most common side effects is immunosuppression which increases the risk of infection. Today, the overall survival rate in childhood ALL is 80-85%. About 75% of deaths related to ALL are caused by the disease itself, most after relapse, but about 25% of deaths are caused by treatment and are classified as treatment-related deaths (TRDs). In this study, the incidence, risk factors and causes of death were investigated for 88 TRDs among 2,700 patients in the Nordic countries Sweden, Denmark, Finland, Iceland and Norway. The incidence of TRD was 3.2%, which was stable in the two protocols, the Nordic Society of Paediatric Haematology and Oncology (NOPHO) ALL 1992 and ALL 2000 protocols. The risk factors identified were female gender, treatment risk-group, T-cell disease, Down syndrome and stem cell transplantation. Seventy-five percent of the deaths were related to infection, 10% to bleeding or thrombosis, 10% to organ failure and 5% to the tumour burden. We have no good explanation as to why some patients experience more severe infections than others, even when receiving the same drugs, drug dosage and supportive care. It is reasonable to believe that genetic factors play a role. In accordance with the increasing understanding of host genetic variation the past 10 years, we investigated 34,000 single nucleotide polymorphisms (SNPs) relevant in childhood ALL in a Danish ALL cohort including 69 children and detected 24 SNPs which associated with infections during induction treatment. Through CART-analysis (classification and regression tree) a four-SNP risk profile were identified as highly predictive of risk of infections during the 50 days induction treatment. The four SNPs belong to the genes R51F1, CBR1, POLDIP3 and CCL11 which regulate drug metabolism, cell-growth and inflammation. If these findings are replicated in larger studies, such knowledge may be useful for developing personalized medicine with more tailored therapy and supportive care, which will hopefully reduce the severity of side effects and increase overall survival. Studies involving multiple biological markers, such as SNPs and short tandem repeats (STRs), often use high-quality DNA extracted from blood samples. However, blood samples are not always easy to obtain from study participants, especially if the patient has died. Archival bone marrow samples from patients with leukaemia are available and represent a potential DNA source. We were interested in exploring whether such archival material is usable for the analysis and identification of multiple markers. DNA from 21 bone marrow smears and 13 bone marrow biopsies were extracted and quantified. Because of small amounts of DNA from each sample whole genome amplification (WGA) was applied. Ten different STR-markers and 34,000 SNPs were analysed and compared with corresponding blood samples. For the STR markers 90% detection rates were obtained. Shorter markers (107bp-242bp) from samples stored 0-3 years gave better results compared with longer markers (219bp-317bp) stored 4-10 years. Multiple SNP analysis was more complicated and only seven of 34 archival samples gave acceptable results (SNP call-rates above 50%). However, in two samples, nearly 100% of SNP-markers were detected. Although increasing the total amount of DNA, WGA reduced the analysis quality. In conclusion, DNA from archival bone-marrow samples might be used in multiple marker analysis, but adjustments of the laboratory set-up are essential to optimize this method.
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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