Relevant bibliographies by topics / Chronic myeloid leukemia gene therapy

Academic literature on the topic 'Chronic myeloid leukemia gene therapy'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Chronic myeloid leukemia gene therapy"

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Ghosn, Youssef, Mohammed Hussein Kamareddine, Antonios Tawk, Carlos Elia, Ahmad El Mahmoud, Khodor Terro, Nadia El Harake, Bachar El-Baba, Joseph Makdessi, and Said Farhat. "Inorganic Nanoparticles as Drug Delivery Systems and Their Potential Role in the Treatment of Chronic Myelogenous Leukaemia." Technology in Cancer Research & Treatment 18 (January 1, 2019): 153303381985324. http://dx.doi.org/10.1177/1533033819853241.

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Chronic myeloid leukemia is a myeloproliferative disease where cells of myeloid linage display a t(9;22) chromosomal translocation leading to the formation of the BCR/ABL fusion gene and the continuous activation of tyrosine kinases. This malignancy has a peak incidence at 45 to 85 years, accounting for 15% of all leukemias in adults. Controlling the activity of tyrosine kinase became the main strategy in chronic myeloid leukemia treatment, with imatinib being placed at the forefront of current treatment protocols. New approaches in future anticancer therapy are emerging with nanomedicine being gradually implemented. Setting through a thorough survey of published literature, this review discusses the use of inorganic nanoparticles in chronic myeloid leukemia therapy. After an introduction on the basics of chronic myeloid leukemia, a description of the current treatment modalities of chronic myeloid leukemia and drug-resistance mechanisms is presented. This is followed by a general view on the applications of nanostrategies in medicine and then a detailed breakdown of inorganic nanocarriers and their uses in chronic myeloid leukemia treatment.
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Jamieson, Catriona H. "Chronic Myeloid Leukemia Stem Cells." Hematology 2008, no. 1 (January 1, 2008): 436–42. http://dx.doi.org/10.1182/asheducation-2008.1.436.

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Abstract Chronic myeloid leukemia (CML) is typified by robust marrow and extramedullary myeloid cell production. In the absence of therapy or sometimes despite it, CML has a propensity to progress from a relatively well tolerated chronic phase to an almost uniformly fatal blast crisis phase. The discovery of the Philadelphia chromosome followed by identification of its BCR-ABL fusion gene product and the resultant constitutively active P210 BCR-ABL tyrosine kinase, prompted the unraveling of the molecular pathogenesis of CML. Ground-breaking research demonstrating that BCR-ABL was necessary and sufficient to initiate chronic phase CML provided the rationale for targeted therapy. However, regardless of greatly reduced mortality rates with BCR-ABL targeted therapy, most patients harbor quiescent CML stem cells that may be a reservoir for disease progression to blast crisis. While the hematopoietic stem cell (HSC) origin of CML was first suggested over 30 years ago, only recently have the HSC and progenitor cell–specific effects of the molecular mutations that drive CML been investigated. This has provided the impetus for investigating the genetic and epigenetic events governing HSC and progenitor cell resistance to therapy and their role in disease progression. Accumulating evidence suggests that the acquired BCR-ABL mutation initiates chronic phase CML and results in aberrant stem cell differentiation and survival. This eventually leads to the production of an expanded progenitor population that aberrantly acquires self-renewal capacity resulting in leukemia stem cell (LSC) generation and blast crisis transformation. Therapeutic recalcitrance of blast crisis CML provides the rationale for targeting the molecular pathways that drive aberrant progenitor differentiation, survival and self-renewal earlier in disease before LSC predominate.
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Deininger, Michael W. "Diagnosing and Managing Advanced Chronic Myeloid Leukemia." American Society of Clinical Oncology Educational Book, no. 35 (May 2015): e381-e388. http://dx.doi.org/10.14694/edbook_am.2015.35.e381.

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Clinical staging of chronic myeloid leukemia (CML) distinguishes between chronic phase (CP-CML), accelerated phase (AP-CML), and blastic phase (BP-CML), reflecting its natural history in the absence of effective therapy. Morphologically, transformation from CP-CML to AP/BP-CML is characterized by a progressive or sudden loss of differentiation. Multiple different somatic mutations have been implicated in transformation from CP-CML to AP/BC-CML, but no characteristic mutation or combination of mutations have emerged. Gene expression profiles of AP-CML and BP-CML are similar, consistent with biphasic evolution at the molecular level. Gene expression of tyrosine kinase inhibitor (TKI)–resistant CP-CML and second CP-CML resemble AP/BP-CML, suggesting that morphology alone is a poor predictor of biologic behavior. At the clinical level, progression to AP/BP-CML or resistance to first-line TKI therapy distinguishes a good risk condition with survival close to the general population from a disease likely to reduce survival. Progression while receiving TKI therapy is frequently caused by mutations in the target kinase BCR-ABL1, but progression may occur in the absence of explanatory BCR-ABL1 mutations, suggesting involvement of alternative pathways. Identifying patients in whom milestones of TKI response fail to occur or whose disease progress while receiving therapy requires appropriate molecular monitoring. Selection of salvage TKI depends on prior TKI history, comorbidities, and BCR-ABL1 mutation status. Despite the introduction of novel TKIs, therapy of AP/BP-CML remains challenging and requires accepting modalities with substantial toxicity, such as hematopoietic stem cell transplantation (HSCT).
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Trela, Ewelina, Sylwester Glowacki, and Janusz Błasiak. "Therapy of Chronic Myeloid Leukemia: Twilight of the Imatinib Era?" ISRN Oncology 2014 (January 30, 2014): 1–9. http://dx.doi.org/10.1155/2014/596483.

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Chronic myeloid leukemia (CML) results from the clonal expansion of pluripotent hematopoietic stem cells containing the active BCR/ABL fusion gene produced by a reciprocal translocation of the ABL1 gene to the BCR gene. The BCR/ABL protein displays a constitutive tyrosine kinase activity and confers on leukemic cells growth and proliferation advantage and resistance to apoptosis. Introduction of imatinib (IM) and other tyrosine kinase inhibitors (TKIs) has radically improved the outcome of patients with CML and some other diseases with BCR/ABL expression. However, a fraction of CML patients presents with resistance to this drug. Regardless of clinical profits of IM, there are several drawbacks associated with its use, including lack of eradication of the malignant clone and increasing relapse rate resulting from long-term therapy, resistance, and intolerance. Second and third generations of TKIs have been developed to break IM resistance. Clinical studies revealed that the introduction of second-generation TKIs has improved the overall survival of CML patients; however, some with specific mutations such as T315I remain resistant. Second-generation TKIs may completely replace imatinib in perspective CML therapy, and addition of third-generation inhibitors may overcome resistance induced by every form of point mutations.
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Warfvinge, Rebecca, Mikael Sommarin, Parashar Dhapola, Ulrich Pfisterer, Linda Geironson Ulfsson, Fatemeh Safi, Ram Krishna Thakur, Johan Richter, and Göran Karlsson. "Characterization of Leukemic Stem Cells Heterogeneity in Chronic Myeloid Leukemia." Blood 134, Supplement_1 (November 13, 2019): 4140. http://dx.doi.org/10.1182/blood-2019-130956.

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In chronic myeloid leukemia (CML), a rare subset of leukemic stem cells (LSC) persists in patients responding to conventional tyrosine kinase inhibitor (TKI) therapy. The failure to eradicate these LSCs results in indefinite therapy dependence and a risk of leukemic relapse. However, the conventional LSC compartment (Lin-CD34+CD38-) is highly heterogeneous where only a subpopulation is believed to be functional, TKI-insensitive LSCs. Previously, using single-cell gene expression analysis we characterized the heterogeneity within the LSC population (Lin-CD34+CD38-) in CML patients using a selected panel of 96 primers. Interestingly, by comparing LSC heterogeneity at diagnosis with the heterogeneity following 3 months of TKI therapy we uncovered a therapy-insensitive, quiescent subpopulation, which could be isolated at high-purity using a combination of the surface markers: Lin-CD34+CD38-CD45RA-cKIT-CD26+ (Warfvinge, Geironson, Sommarin et al., 2017). Here, we expand the single-cell analysis of CML LSC populations to include combined immunophenotype-/RNA sequencing analysis (CITE-seq). CITE-seq allows for unbiased, further in-depth transcriptome analysis as wells as immunophenotypic characterization by pre-staining cells with a panel of DNA-barcoded antibodies prior to sequencing. DNA-barcoded antibodies convert the protein expression into readable sequences through unique oligo-conjugates as identifiers. Using CITE-seq with a panel of 44 distinct surface markers designed to immunophenotypically differentiate between stem/progenitors cells and leukemic clones we simultaneously characterize the molecular and immunophenotypic heterogeneity within Lin-CD34+/Lin-CD34+CD38- CML stem/progenitor compartment at diagnosis. Additionally by comparing the LSCs transcriptome from patients with different therapeutic outcome after 12 months of therapy we describe how differences in heterogeneity and the presence of immunophenotypic therapy-insensitive LSCs at diagnosis (Lin-CD34+CD38-CD45RA-cKIT-CD26+) contribute to therapy response. Disclosures Richter: Novartis: Consultancy; Pfizer: Consultancy, Research Funding.
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Husnain, Muhammad, Trent Wang, Maikel Valdes, James Hoffman, and Lazaros Lekakis. "Multiple Myeloma in a Patient with ANKRD26-Related Thrombocytopenia Successfully Treated with Combination Therapy and Autologous Stem Cell Transplant." Case Reports in Hematology 2019 (June 2, 2019): 1–3. http://dx.doi.org/10.1155/2019/9357572.

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Ankyrin repeat domain-containing protein 26- (ANKRD26-) related thrombocytopenia is a rare, autosomal dominant condition caused by ANKRD26 gene mutation. ANKRD26-related thrombocytopenia is characterized by moderate thrombocytopenia with minimal bleeding, normal platelet size, and dysmegakaryopoiesis on bone marrow evaluation. ANKRD26 mutation has been previously associated with myeloid malignancies, including acute myeloid leukemia, myelodysplastic syndrome, and chronic myeloid leukemia. We report the first case of multiple myeloma in a patient with ANKRD26 related thrombocytopenia. The patient was successfully treated with contemporary combination therapy followed by melphalan-conditioned autologous stem cell transplant for his multiple myeloma despite preexisting thrombocytopenia.
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Gao, Liquan, Ilaria Bellantuono, Annika Elsässer, Stephen B. Marley, Myrtle Y. Gordon, John M. Goldman, and Hans J. Stauss. "Selective elimination of leukemic CD34+ progenitor cells by cytotoxic T lymphocytes specific for WT1." Blood 95, no. 7 (April 1, 2000): 2198–203. http://dx.doi.org/10.1182/blood.v95.7.2198.

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Abstract Hematologic malignancies such as acute and chronic myeloid leukemia are characterized by the malignant transformation of immature CD34+ progenitor cells. Transformation is associated with elevated expression of the Wilm's tumor gene encoded transcription factor (WT1). Here we demonstrate that WT1 can serve as a target for cytotoxic T lymphocytes (CTL) with exquisite specificity for leukemic progenitor cells. HLA-A0201– restricted CTL specific for WT1 kill leukemia cell lines and inhibit colony formation by transformed CD34+ progenitor cells isolated from patients with chronic myeloid leukemia (CML), whereas colony formation by normal CD34+ progenitor cells is unaffected. Thus, the tissue-specific transcription factor WT1 is an ideal target for CTL-mediated purging of leukemic progenitor cells in vitro and for antigen-specific therapy of leukemia and other WT1-expressing malignancies in vivo.
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Gao, Liquan, Ilaria Bellantuono, Annika Elsässer, Stephen B. Marley, Myrtle Y. Gordon, John M. Goldman, and Hans J. Stauss. "Selective elimination of leukemic CD34+ progenitor cells by cytotoxic T lymphocytes specific for WT1." Blood 95, no. 7 (April 1, 2000): 2198–203. http://dx.doi.org/10.1182/blood.v95.7.2198.007k38_2198_2203.

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Hematologic malignancies such as acute and chronic myeloid leukemia are characterized by the malignant transformation of immature CD34+ progenitor cells. Transformation is associated with elevated expression of the Wilm's tumor gene encoded transcription factor (WT1). Here we demonstrate that WT1 can serve as a target for cytotoxic T lymphocytes (CTL) with exquisite specificity for leukemic progenitor cells. HLA-A0201– restricted CTL specific for WT1 kill leukemia cell lines and inhibit colony formation by transformed CD34+ progenitor cells isolated from patients with chronic myeloid leukemia (CML), whereas colony formation by normal CD34+ progenitor cells is unaffected. Thus, the tissue-specific transcription factor WT1 is an ideal target for CTL-mediated purging of leukemic progenitor cells in vitro and for antigen-specific therapy of leukemia and other WT1-expressing malignancies in vivo.
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Xin, Jiajia, Dandan Yin, Wei Fu, Hui-Jie Zhang, Yaozhen Chen, Yazhou Wang, Mingkai Li, and Xingbin Hu. "A Novel Compound Inhibits Chronic Myeloid Leukemia Via Upregulating Apoptosis." Blood 126, no. 23 (December 3, 2015): 5559. http://dx.doi.org/10.1182/blood.v126.23.5559.5559.

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Abstract Chronic myeloid leukemia (CML) is a myeloid proliferative disorder mainly result from chimeric protein BCR-ABL1 encoded by a fusion gene at the t(9;22) (q34;q11) chromosomal translocation. Intrinsically, this recombined protein results in an increased tyrosine kinase (TK) activity that directly related to hematopoietic stem cell malignant proliferation. Consequently, the drugs derived from tyrosine kinase inhibitors (TKI) have been developed as an infective therapy, and greatly improved patients survival in clinic. Unfortunately, single TKI administration led to toxicities or tolerance in long-term treated CML patients. Even worse is, about 5% CML patients were not caused by bcr-abl gene mutation. Thus better medicines are badly needed to compensate CML therapy. Herein, we investigated the undefined function of a biscoumarins. The new synthesized compound exhibited a null toxicity on HUVECs but intensive toxicity on K562 leukemic cells. Subsequent results demonstrated that it efficiently inhibited the expansion of human CML cell line and bone marrow cells of SCL-tTA-BCL/ABL transgenic model mice via increased apoptosis. Critically, we also showed that CD34+ bone marrow leukemic cells collected from patients underwent more apoptosis after treated by the biscoumarins derivate. To extend these results into vivo, we observed a prolonged survival of bcr-abl transgenic mice treated by derivate mono-therapy or combination with imatinib compared to those of untreated or imatinib-treated CML mice. All together, these results indicated that this biscoumarins derivate may have novel potential as a therapeutic agent against CML. Disclosures No relevant conflicts of interest to declare.
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Deshmukh, Komal Galani, and Katalin Kelemen. "Lessons Learned from Donor Cell-Derived Myeloid Neoplasms: Report of Three Cases and Review of the Literature." Life 12, no. 4 (April 8, 2022): 559. http://dx.doi.org/10.3390/life12040559.

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Donor-cell derived myeloid neoplasm (DDMN), a rare complication after allogeneic hematopoietic cell transplantation (HCT), is of interest for its potential to reveal donor-derived and host-derived factors that contribute to the pathogenesis of leukemia. The accurate diagnosis of donor-derived leukemias has been facilitated by the more frequent use of molecular techniques. In this study, we describe three additional cases of DDMN; the first reported case of donor-derived chronic myelomonocytic leukemia (CMML), one acute myeloid leukemia (AML) with t(8;21)(q22;22); RUNX1-RUNX1T1 and one donor-derived MDS with deletion 5q. A review of the cytogenetic profiles of previously reported DDMN indicates a significant contribution of therapy-related myeloid neoplasms. Cases with direct evidence of donor- or recipient-dependent factors are rare; a role of direct transfer of leukemic cells, genomic instability of the donor, abnormal gene methylation in donor cells, proleukemic potential of abnormal stromal niche, and the role of immunological surveillance after transplantation has been observed. The role of additional potential pathogenetic factors that are without clinically observed evidence are also reviewed.
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Dissertations / Theses on the topic "Chronic myeloid leukemia gene therapy"

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Miller-Reynolds, Angela Rose-Marie. "Suicide gene therapy in murine models of chronic myeloid leukaemia." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412871.

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Yazdanparast, Haniyeh [Verfasser], and Viktor [Akademischer Betreuer] Umansky. "Myeloid cells and therapy resistance in Chronic Lymphocytic Leukemia / Haniyeh Yazdanparast ; Betreuer: Viktor Umansky." Heidelberg : Universitätsbibliothek Heidelberg, 2018. http://d-nb.info/1177385988/34.

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Roos, Cecilia. "Studies of leukotriene C4 synthase expression and regulation in chronic myeloid leukaemia /." Karlstad : Faculty of Technology and Science, Biomedical Science, Karlstads universitet, 2008. http://www.diva-portal.org/kau/abstract.xsql?dbid=1598.

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Olsson-Strömberg, Ulla. "Clinical and experimental studies in chronic myeloid leukemia : studies of treatment outcome, in vitro cellular drug resistance and gene expression /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7841.

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Mascarenhas, Cintia do Couto 1982. "Avaliação de mutações pontuais no gene ABL por metodo de cromatografia liquida desnaturante de alta performance (D-HPLC) em pacientes com leucemia mieloide cronica tratados com inibidores de tirosina quinase." [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308623.

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Orientadores: Carmino Antonio de Souza, Katia Borgia Barbosa Pagnano
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: O desenvolvimento da Leucemia Mielóide Crônica (LMC) tem como característica a formação do cromossomo Philadelphia que envolve a quebra do gene BCR gerando um rearranjo molecular denominado BCR-ABL, cujo produto final é uma proteína de fusão citoplasmática que determina a patogenia da doença. Esta proteína é uma tirosina quinase (TK) que possui capacidade de auto-ativação e para a inativação desta proteína, foram desenvolvidos os inibidores da tirosina quinase (ITK), que tem a capacidade de se ligar no mesmo sítio de ligação da molécula de ATP. Esta ligação impede a transferência dos grupos fosfatos aos substratos subseqüentes, bloqueando a cascata de transdução de sinais e prevenindo a ativação das vias mitogênica dependente da quinase Bcr-Abl e anti-apoptóticas levando à morte do fenótipo BCR-ABL.Um dos principais mecanismos de resistência ao tratamento com ITK são as mutações pontuais, sendo a T315I foco de estudos mais detalhados por tornar a proteína mutante altamente insensível a todas as drogas inibidoras da proteína TK disponíveis atualmente Foi utilizado neste trabalho a técnica de D-HPLC para fazer screening de mutações nos pacientes com LMC com resposta sub ótima ou falha de tratamento de acordo com os critérios da Leukemia Net. Para o screening do éxon 6 foram selecionados 93 pacientes com LMC: 5 eram intolerantes, 67 resistentes e 21 com resposta subótima. Como controle negativo foi usado o sangue periférico doadores de sangue do Hemocentro da UNICAMP. Para o screening de mutações de todo o gene BCR-ABL foram estudados 37 pacientes com LMC e como controle negativo, usamos a linhagem celular HL60 que não possui a translocação BCR-ABL. No screening do éxon 6, 23 amostras (25%) mostraram um perfil de eluição no D-HPLC anormal em relação ao controle, o que sugeriu a presença de mutação. A sobrevida global (OS) para todo grupo foi de 80% em uma mediana de tempo de observação de 30 meses. OS para pacientes sem mutações foi de 87% e para os pacientes com mutações foi de 56% em uma mediana de tempo de observação 37 e 10 meses, respectivamente (p <0,0001, RR = 68). No screening de todo o gene BCR-ABL 17 (46%) tiveram perfil cromatográfico diferente do controle Como estávamos estabelecendo a padronização do método, procedemos com o seqüenciamento de todas as amostras e os resultados obtidos foram comparados com a seqüência depositada no banco de dados GenBank (U07563). Das 17 amostras com alteração do perfil cromatográfico, observamos a presença de mutação em 13 amostras. Acreditamos que isso se deva a sensibilidade do método de D-HPLC que é capaz de identificar tanto polimorfismos quanto mutações com maior eficiência que o seqüenciamento. Em resumo, o D-HPLC demonstrou ser um método sensível e prático para o acompanhamento do aparecimento de mutações no domínio da quinase na rotina clínica. Mutações nessa região estudada são clinicamente relevantes e podem conferir um pior prognóstico. A detecção precoce pode ser uma ferramenta importante para otimizar a terapêutica na LMC.
Abstract: The development of chronic myeloid leukemia (CML) is the formation of the characteristic Philadelphia chromosome involving breach of the BCR gene generating a molecular rearrangement called BCR-ABL, whose final product is a cytoplasmic fusion protein that determines the pathogenesis of the disease. This is a protein tyrosine kinase (TK) that has self-ativaçãoe to inactivate this protein have developed the inhibitors of tyrosine kinase (ITK), which has ability to connect on the same site of binding of molecule of ATP. This connection prevents the transfer of phosphate groups to substrates subsequent, blocking the cascade of signal transduction and preventing the activation of mitogenic pathways dependent kinase BCR-ABL and anti leading to apoptotic death phenotype of BCR-ABL.One major mechanisms of resistance to treatment with ITK are mutations off, and the T315I focus of more detailed studies by making mutant protein highly insensitive to all drugs Inhibit TK protein currently available was used in this work to D-HPLC technique to screening for mutations in patients with CML with sub-optimal response or failure of treatment according to the criteria Leukemia Net For the screening of exon 6 were selected 93 CML patients: 5 were intolerant, 67 resistant and 21 with answer sub-optimal. The negative control we used the peripheral blood donors Blood from the blood of UNICAMP. For the screening of mutations throughout the BCR-ABL gene were studied 37 patients with CML and control negative, we used the HL60 cell line that does not have the translocation BCR-ABL. In the screening of exon 6, 23 samples (25%) showed a profile of the D-HPLC elution abnormal in the control, which suggested the presence of mutation. The overall survival (OS) for whole group was 80% in a median time of observation of 30 months. OS for patients with mutations was 87% and for patients with mutations was 56% in the median observation time of 37 and 10 months respectively (p <0.0001, RR = 68). In screening the entire gene BCR-ABL 17 (46%) had chromatographic profile different from the control we were setting the standardization of methods, procedures with the sequencing of all samples and the results were compared with the sequence deposited in the GenBank database (U07563). Of the 17 samples with change the chromatographic profile, we observed the presence of mutation in 13 samples. We believe that this is due to sensitivity of the method of D-HPLC is able to identify the mutations both polymorphisms with greater efficiency to the sequencing. In summary, the D-HPLC has proved a sensitive and practical method for monitoring the appearance of mutations in the kinase domain in the clinical routine. Mutations studied in this region are clinically relevant and may confer worse prognosis. Early detection can be a tool important to optimize therapy in CML.
Mestrado
Ciencias Basicas
Mestre em Clinica Medica
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Istook, Diana Lee. "Differential gene expression between patients with acute lymphocytic leukemia and patients with acute myeloid leukemia : the use of analysis of variance models in microarray data analysis /." Oklahoma City : [s.n.], 2004.

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Olsson-Strömberg, Ulla. "Clinical and Experimental Studies in Chronic Myeloid Leukemia : Studies of Treatment Outcome, In Vitro Cellular Drug Resistance and Gene Expression." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7841.

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The aims of the studies described in the thesis were to investigate different treatment strategies in chronic myeloid leukemia (CML) patients. Furthermore, activity of imatinib was investigated by in vitro cytotoxicity assay, and the gene expression pattern in interferon treated patients.

In a randomized prospective national study, we examined the influence of busulphan (n=89) versus hydroxyurea (n=90) treatment on time to blast crisis, and survival. There was no significant difference in survival between hydroxyurea and busulphan treated patients; median survival was 3.5 and 3.2 years, respectively. The 26 patients who underwent allogeneic stem cell transplantation had a significantly longer median survival (4.7 years) than those who were not transplanted.

We investigated the feasibility of mobilizing Philadelphia chromosome negative blood stem cells with intensive chemotherapy and lenograstim in CML patients. Twenty-three patients (62%) were successfully mobilized. Twenty-one of these patients underwent autologous stem cell transplantation later on, with a 5-year overall survival at 68%.

Fluorometric Microculture Cytotoxicity Assay was used to analyze 32 tumor cell samples from CML patients, (26 chronic phase and 6 blast crisis). Imatinib showed a higher in vitro activity and more positive drug interactions in cells from blast crisis than from chronic phase. Interferon, daunorubicin and arsenic trioxide had the greatest benefit from a combination with imatinib.

Microarray-based gene expression analyses were performed on diagnostic CML samples prior to interferon treatment. We identified six genes that were differentially expressed in responders and non-responders to interferon. It might prove possible to use gene expression analysis to predict future response to interferon.

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Mascarenhas, Cintia do Couto 1982. "Identificação e investigação de genes diferencialmente expressos entre pacientes com leucemia mielóide crônica e indivíduos controle." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308645.

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Orientadores: Carmino Antonio de Souza, Fernando Ferreira Costa
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A elucidação dos mecanismos moleculares envolvidos na fisiopatologia e tratamento das doenças hematológicas, bem como no entendimento do perfil de expressão gênica das linhagens celulares leucêmicas, tem sido objeto de numerosas investigações. Com o uso da técnica SSH (Subtractive Supression Hybridization ou Biblioteca Subtrativa Supressiva) foi possível identificar importantes genes que se encontram diferencialmente expressos em granulócitos de pacientes com Leucemia Mielóide Crônica e indivíduos controle. Foram encontrados 39 genes superexpressos e 173 com expressão diminuída em células de LMC. Ao relacionar esses genes com vias metabólicas que estão reguladas positiva (expressão aumentada) ou negativamente (expressão diminuída) nessa doença, verificou-se que a maioria dos genes estavam relacionados com a regulação de NF-kB, AKT, o Interferon e a IL-4 em células de controle. Entre os genes superexpressos encontrados na LMC, foi observado o SEPT5, RUNX1, MIER1, KPNA6 e FLT3, enquanto PAN3, TOB1 e ITCH estavam com expressão diminuída nessa doença em comparação com indivíduos controle. O TOB1 se mostrou promissor, uma vez que é um gene supressor tumoral, pode estar envolvido na proliferação de células leucêmicas e interage com vários outros genes encontrados neste estudo. Assim, devido à grande heterogeneidade de funções relacionadas com a expressão desse gene, foi investigada a relação entre a expressão de mRNA e as respostas aos ITK's na LMC. A avaliação foi realizada por PCR em tempo real em doentes com CCgR, PCgR, MINCgR e NOCgR após tratamento com TKI's e os resultados foram comparados com a expressão em granulócitos de indivíduos controle, observando que os pacientes NOCgR têm uma expressão de TOB1 significativamente inferior em comparação com doadores saudáveis e pacientes que alcançaram RCgC. Ao comparar pacientes não resistentes e resistentes a diferença foi significativa. Esses resultados sugerem que a expressão diminuída de TOB1 em pacientes NOCgR pode ser indicativo de desregulação da apoptose e de vias de sinalização importantes nessa doença incluindo a via da AKT, conduzindo assim a resistência a ITK's nesses pacientes. Outro objetivo deste trabalho foi caracterizar a função dos genes TOB1 e SEPT5 nos processos celulares e vias de sinalização de apoptose, proliferação, migração e ciclo celular em linhagens celulares leucêmicas. Ao realizar o silenciamento desses genes (utilizando partículas lentivirais) notou-se que o silenciamento de TOB1, como já descrito na literatura em outras doenças, interfere na proliferação celular, clonogenicidade, apoptose, ciclo celular e expressão de proteínas importantes da cascata de sinalização, o que salienta sua importância em células BCR-ABL positivas. Já o gene SEPT5 ao ser silenciado leva a algumas alterações como a apoptose e ciclo celular. Nesse contexto, o silenciamento destes genes chama atenção para as possibilidades de controle da proliferação celular, apoptose, ciclo celular e clonogenicidade em células BCR-ABL positivas. Foi realizada a avaliação da expressão desses genes em células de sangue periférico e medula óssea de pacientes com LMC e indivíduos controles, linhagens celulares de câncer humano e linhagens de murino. Os resultados mostraram um aumento significativo na expressão do gene SEPT5 em todos os tipos celulares analisados em pacientes com LMC. O mesmo padrão foi observado em células de murino que possuem a mutação T315I e em células humanas que possuem a translocação t(9;22) e estão relacionadas com a fase blástica da doença [K562, KU812, NALM]. Quando avaliada a expressão do gene TOB1 nota-se diminuição em todos os tipos celulares analisados em pacientes com LMC e em células BaF3T315I. Também foi observada uma baixa expressão em células com a t(9;22) e estão relacionadas com a fase blástica da doença[K562, KU812, NALM] quando comparadas a expressão em medula óssea controle. Outro resultado interessante foi obtido a partir da análise de adesão celular em granulócitos de pacientes com LMC e controles, evidenciando a diminuição da adesão em granulócitos de pacientes com LMC em relação aos de controles, levando a hipótese de que essa alteração nas propriedades adesivas dos granulócitos em pacientes com LMC pode estar diretamente ligada à liberação de células jovens pela matriz da medula óssea. A criação de estratégias que levam ao melhor entendimento da fisiopatologia da doença e avanço no tratamento da LMC deve ser focada em vários genes alvos e não apenas no BCR-ABL, pois no desenvolvimento da LMC há a ativação e desativação de várias vias de sinalização celular. Os resultados deste estudo podem ajudar na melhor compreensão dessas vias e também para identificar outros genes e vias úteis para a melhora no manejo terapêutico e criação de novas drogas para o tratamento dessa doença
Abstract: The elucidation of the molecular mechanisms involved in the pathophysiology and treatment of blood disorders, as well as the understanding of genes expression profiling of leukemia cell lines has been the focus of numerous investigations. The use of the SSH (Suppression Subtractive Hybridization Library or Suppression Subtractive) technique made available the identification of important genes which are differentially expressed in granulocytes from patients with chronic myeloid leukemia (CML) and healthy controls. 39 genes overexpressed were found, and 173 with decreased expression in CML cells. When correlating these genes with metabolic pathways that are regulated positively (increased expression) or negatively (decreased expression) in this disease, it was found that most of the genes were related to the regulation of NF-kB, AKT, Interferon and IL-4 in control cells. The following genes were found overexpressed in CML: SEPT5, RUNX1, MIER1, KPNA6 and FLT3, while PAN3, TOB1 and ITCH were found with decreased expression in this disease compared with controls. The TOB1 gene showed promising since it is a tumor suppressor, may be involved in the proliferation of leukaemic cells and interacts with several others genes found in this study. Thus, due to the great heterogeneity of functions related to this gene, was investigated the relationship between mRNA expression and TKI's responses. The evaluation was performed by real time PCR in patients with CCgR, PCgR, MINCgR and NOCgR after treatment with TKI and healthy controls. Was observed that patients that have NOCgR, the TOB1 expression is significantly lower compared with healthy donors and patients who achieved CCgR. When comparing non-resistant and resistant patients the difference also was significant. These results suggest that reduced expression of TOB1 in NOCgR patients may indicate apoptosis deregulation and changes in important signaling pathways of CML including the Akt pathway, thereby leading to TKI's resistance of these patients. Another aim of this work was to characterize the function of TOB1 and SEPT5 in cellular processes and signaling pathways of apoptosis, proliferation, migration and cell cycle in leukemic cell lines. After the silencing of these genes (using lentiviral particles), was noted that the silencing TOB1 - as described in the literature for other diseases - interferes in cell proliferation, clonogenicity, apoptosis, cell cycle and in expression of important proteins at signaling cascade, which emphasizes its importance in BCR-ABL positive cells. The SEPT5 silencing leads to some changes such as apoptosis and cell cycle. In this context, the silencing of these genes leads to attention of possibilities of control of cell proliferation, apoptosis, cell cycle and cell clonogenicity in BCR-ABL positive cells. Was assessed the expression of these genes in cells from peripheral blood and bone marrow of CML patients and controls, as well in human and murine cell lines. Results showed a significant increase in SEPT5 gene expression in patients with CML in all cell types evaluated. The same profile was observed in murine cells BAF3T315I and in human cells having the translocation t (9; 22) been related to blast crisis [K562, KU812, NALM]. When measuring expression of TOB1, was noted decrease in all cell types studied in CML patients and cells BaF3T315I. Another interesting result was obtained from the analysis of cell adhesion at granulocytes in CML patients and controls which showed decreased adhesion of granulocytes in CML patients compared to controls, leading to the hypothesis that the change in adhesive properties at CML can be directly linked to the release of young cells by bone marrow. The creation of strategies that lead to better understanding of the pathophysiology of the disease and advance in the treatment of CML should be focused on several target genes and not only in BCR-ABL, since in the development of CML there is an activation and deactivation of multiple signaling pathways . The results of this study may help to better understand these pathways and also to identify other genes and pathways useful for improving the management and development of new therapeutic drugs to treat this disease
Doutorado
Clinica Medica
Doutora em Clínica Médica
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Küpper, Maja Kim [Verfasser], Wolfgang [Akademischer Betreuer] Wagner, and Gerhard [Akademischer Betreuer] Müller-Newen. "STAT3-mediated therapy resistance of malignant stem cells in chronic myeloid leukemia (CML) / Maja Kim Küpper ; Wolfgang Wagner, Gerhard Müller-Newen." Aachen : Universitätsbibliothek der RWTH Aachen, 2019. http://d-nb.info/1194067107/34.

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Katsoulas, Athanasia. "Design and mechanism of action of novel agents termed "combi-molecules" engineered for tandem targeting for Bcr-abl expressing leukemia cells." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111884.

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Abstract:
Bcr-abl expression being associated with anti-apoptotic signaling and expression of DNA repair enzymes, we surmised that single molecules capable of blocking abl tyrosine kinase (TK) function and damaging DNA should lead to compounds with potency superior to that of GleevecRTM. To this end, we designed novel agents termed "combi-molecules" programmed to not only behave as bcr-abl inhibitors on their own, but also to further degrade to another inhibitor and a DNA damaging species. The released inhibitor was designed to sustain bcr-abl inhibition following degradation of the combi-molecule and the DNA damaging species to activate pathways leading to apoptosis. To model this strategy termed "combi-targeting", we synthesized ZRCM5 (a monoalkyltriazene) that showed antiproliferative activity superior to that of the classical DNA damaging agent TemodalRTM, but not to that of Gleevec RTM. This result was imputed to the rather weak bcr-abl inhibitory activity of ZRCM5 and its strong DNA damaging property. Another prototype designed to contain an aniline mustard moiety (AK04) was a strong bcr-abl inhibitor but a poor DNA alkylating agent. Its cytotoxic activity was again stronger than that of the clinical alkylating agent chlorambucil but inferior to that of GleevecRTM. Further chemical studies directed at structural modification of the benzamide moiety led to the synthesis of ZRF1 with strong potency against bcr-abl TK and strong DNA damaging property. This novel optimized combi-molecule showed a 1.6-3-fold greater potency than GleevecRTM against bcr-abl expressing cells. Further investigation with ZRF1, showed that its cytotoxic potency was dependent on the p53 wild-type status of the cells. In cells expressing wild-type p53, p21 transactivation was associated with cell cycle arrest and that of Bax with apoptosis. In addition to, the pro-apoptotic effect of bcr-abl inhibition, these multiple mechanisms of action may synergistically enhance the cytotoxic potency of ZRF1 in p53 wild-type cells. The study conclusively demonstrated that p53 is a major determinant for the cytotoxic advantage of the novel combi-molecular approach in chronic myelogenous leukemia (CML), a disease in which 70-85% of all cases express wild-type p53.
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Books on the topic "Chronic myeloid leukemia gene therapy"

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Weinberg, Robert A. (Robert Allan), 1942-, ed. The Philadelphia chromosome: A mutant gene and the quest to cure cancer at the genetic level. New York: The Experiment, LLC, 2013.

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1947-, Talpaz Moshe, and Kantarjian Hagop 1952-, eds. Medical management of chronic myelogenous leukemia. New York: Dekker, 1998.

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Wapner, Jessica. The Philadelphia Chromosome: A Mutant Gene and the Quest to Cure Cancer at the Genetic Level. Highbridge Audio and Blackstone Publishing, 2021.

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Weinberg, Robert A., and Jessica Wapner. Philadelphia Chromosome: A Genetic Mystery, a Lethal Cancer, and the Improbable Invention of a Lifesaving Treatment. Experiment LLC, The, 2014.

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(Editor), Jorge Cortes, and Michael Deininger (Editor), eds. Chronic Myeloid Leukemia. Informa Healthcare, 2006.

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Cortes, Jorge, and Michael Deininger. Chronic Myeloid Leukemia. Taylor & Francis Group, 2006.

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Cortes, Jorge, and Michael Deininger. Chronic Myeloid Leukemia. Taylor & Francis Group, 2006.

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Cortes, Jorge, and Michael Deininger. Chronic Myeloid Leukemia. Taylor & Francis Group, 2019.

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E, Cortés F. Jorge, and Deininger Michael, eds. Chronic myeloid leukemia. New York: Informa Healthcare, 2007.

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Cortes, Jorge, and Michael Deininger. Chronic Myeloid Leukemia. Taylor & Francis Group, 2006.

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Book chapters on the topic "Chronic myeloid leukemia gene therapy"

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Yong, Agnes S. M., and Junia V. Melo. "Pathophysiology of Chronic Myeloid Leukemia." In Leukemias: Principles and Practice of Therapy, 259–70. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444327359.ch21.

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Castro, Januario E., and Thomas J. Kipps. "Gene Therapy of Chronic Lymphocytic Leukemia." In Chronic Lymphocytic Leukemia, 329–40. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-412-2_18.

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Jabbour, Elias, and Jorge Cortes. "Targeted Therapies in Chronic Myeloid Leukemia." In Targeted Therapy in Translational Cancer Research, 111–20. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118468678.ch11.

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Corey, Seth J., and Jorge Cortes. "Chronic Myeloid Leukemia: Pathophysiology and Therapeutics." In Molecularly Targeted Therapy for Childhood Cancer, 139–53. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-0-387-69062-9_8.

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Hochhaus, Andreas. "Therapy of Newly Diagnosed and Chronic-Phase Chronic Myeloid Leukemia." In Leukemias: Principles and Practice of Therapy, 271–80. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444327359.ch22.

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Valencia-Serna, Juliana, Breanne Landry, Xiaoyan Jiang, and Hasan Uludag. "Potential of siRNA Therapy in Chronic Myeloid Leukemia." In Intracellular Delivery II, 435–73. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-8896-0_21.

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Pawelski, S., L. Konopka, K. Szczepanik, and H. Zdziechowska. "Therapy of Blastic Transformation of Chronic Myeloid Leukemia." In Leukemias, 249–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77083-8_45.

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Hiwase, Devendra K., and Timothy P. Hughes. "Therapy of Advanced-Stage and Resistant Chronic Myeloid Leukemia." In Leukemias: Principles and Practice of Therapy, 281–95. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444327359.ch23.

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Radich, Jerald. "The Detection and Quantification of bcr-abl in Chronic Myeloid Leukemia Following Marrow Transplantation." In Gene Quantification, 277–93. Boston, MA: Birkhäuser Boston, 1998. http://dx.doi.org/10.1007/978-1-4612-4164-5_16.

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Lussana, Federico, Tamara Intermesoli, Paola Stefanoni, and Alessandro Rambaldi. "Mechanisms of Resistance to Targeted Therapies in Chronic Myeloid Leukemia." In Mechanisms of Drug Resistance in Cancer Therapy, 231–50. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/164_2017_81.

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Conference papers on the topic "Chronic myeloid leukemia gene therapy"

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Bajpai, Prachi, A. Tripathi, and Deepa Agrawal. "Abstract B42: Polymorphism of CYP3A5 gene in Indian chronic myeloid leukemia patients." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-b42.

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Yi, Bin, Xiaobo Li, Wenjun Du, Gary A. Piazza, and Yaguang Xi. "Abstract 1848: Let-7 brings new insights into chronic myeloid leukemia therapy." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1848.

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Laurino, Marco, Maurizio Stano, Monica Betta, Gabriele Pannocchia, and Alberto Landi. "Combining pharmacological therapy and vaccination in Chronic Myeloid Leukemia via model predictive control." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6610403.

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Basak, Jayasri, Soma Mukhopadhyay, Sukanta Konar, and Ashis Mukhopadhyay. "Abstract A68: Molecular response of pediatric chronic myeloid leukemia (CML) with imatinib mesylate therapy." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-a68.

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Pemmaraju, Naveen, Hagop Kantarjian, Susan O'Brien, Raja Luthra, Elias Jabbour, Aflonso Quintas-Cardama, Gautam Borthakur, et al. "Abstract 4715: Dasatinib as initial therapy for patients with chronic myeloid leukemia (CML) in early chronic phase (CP)." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4715.

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Hostetler, Bryan, Olga Uchakina, and Robert McKallip. "Abstract 3848: Targeting hyaluronidase reduces stromal cell protection of chronic myeloid leukemia to imatinib therapy." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3848.

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Volz, C., A. Gottschalk, M. Krumbholz, C. Albert, S. Semper, M. Suttorp, I. Glauche, and M. Metzler. "Therapy assessment of pediatric chronic myeloid leukemia (CML) using combined analyses of RNA/DNA response dynamics." In 33. Jahrestagung der Kind-Philipp-Stiftung für pädiatr. onkolog. Forschung. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1709801.

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Dufva, Olli, Tiina Kasanen, Mohamed El Missiry, Judith Klievink, Hanna Lähteenmäki, and Satu Mustjoki. "Abstract A115: Tyrosine kinase inhibitor therapy modulates immune checkpoints and TCR repertoire diversity in chronic myeloid leukemia." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a115.

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Kaehler, Meike, Inga Nagel, Henrike Bruckmueller, Ruwen Boehm, Ole Ammerpohl, and Ingolf Cascorbi. "Abstract 5846: Drug resistance in chronic myeloid leukemia: Impact of methylation on gene expression in imatinib and nilotinib resistance." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5846.

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Oliveira, Ligia P., Rafael G. Ferro, and Ana CSS Galvão. "Abstract 1846: Gene expression analysis of P-glycoprotein and LMWPTP in chronic myeloid leukemia cells treated with metformin and imatinib mesylate." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1846.

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