Relevant bibliographies by topics / Proteine bcr-abl

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Proteine bcr-abl'

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

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Proteine bcr-abl.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Proteine bcr-abl"

1

Tsukahara, Fujiko, and Yoshiro Maru. "Bag1 directly routes immature BCR-ABL for proteasomal degradation." Blood 116, no. 18 (2010): 3582–92. http://dx.doi.org/10.1182/blood-2009-10-249623.

Full text
Abstract:
Abstract Degradation of BCR-ABL oncoproteins by heat shock protein 90 (Hsp90) inhibitors in chronic myelogenous leukemia is expected to overcome resistance to ABL tyrosine kinase inhibitors. However, the precise mechanisms still remain to be uncovered. We found that while c-Cbl E3 ligase induced ubiquitin-dependent degradation of mature and phosphorylated BCR-ABL proteins, another E3 ligase CHIP (carboxyl terminus of the Hsc70-interacting protein) degraded immature BCR-ABL proteins and efficiently suppressed BCR-ABL–dependent leukemic growth. Interestingly, Bag1 (Bcl-2-associated athanogene-1)
APA, Harvard, Vancouver, ISO, and other styles
2

Gorre, Mercedes E., Katharine Ellwood-Yen, Gabriela Chiosis, Neal Rosen, and Charles L. Sawyers. "BCR-ABL point mutants isolated from patients with imatinib mesylate–resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90." Blood 100, no. 8 (2002): 3041–44. http://dx.doi.org/10.1182/blood-2002-05-1361.

Full text
Abstract:
Clinical resistance to imatinib mesylate is commonly observed in patients with advanced Philadelphia chromosome– positive (Ph+) leukemias. Acquired resistance is typically associated with reactivation of BCR-ABL due to kinase domain mutations or gene amplification, indicating that BCR-ABL remains a viable target for inhibition in these patients. Strategies for overcoming resistance can be envisioned through exploitation of other molecular features of the BCR-ABL protein, such as its dependence on the molecular chaperone heat shock protein 90 (Hsp90). To determine whether inhibition of Hsp90 co
APA, Harvard, Vancouver, ISO, and other styles
3

Chen, Ying, Nicole Froehlich, and Stefan K. Bohlander. "Towards the In Vivo Identificaton of Leukemogenic Fusion Proteins." Blood 104, no. 11 (2004): 2970. http://dx.doi.org/10.1182/blood.v104.11.2970.2970.

Full text
Abstract:
Abstract Currently there are no methods available to identifiy leukemogenic fusion proteins in vivo. All available methods, like Southern blotting, PCR, FISH or Western blotting, require the destruction of the cells that are assayed. A method for the in vivo detection of leukemogenic fusion proteins would be highly desirable because it would open up new approaches to study leukemia and might lead to novel treatment strategies. We have developed a strategy for the in vivo detection of the BCR/ABL fusion protein. BCR/ABL is found in virtually all cases chronic myeloid leukemia (CML) and a large
APA, Harvard, Vancouver, ISO, and other styles
4

Perazzona, Bastianella, Yan Wang, and Ralph B. Arlinghaus. "Role of BCR in Down-Modulation of BCR-ABL Oncogenicity in CML." Blood 112, no. 11 (2008): 3210. http://dx.doi.org/10.1182/blood.v112.11.3210.3210.

Full text
Abstract:
Abstract Bcr-Abl acquires its transforming ability through its up-regulated Abl tyrosine kinase activity. Bcr is a phosphoprotein with a novel serine/threonine kinase activity encoded by its first exon. Over-expression of BCR in K562 cells produces a phosphoserine form of Bcr and interferes with the oncogenic effects of BCR-ABL in mice (Lin et al., Oncogene 2001). We have recently shown the inhibitory effects of Bcr on Bcr-Abl, in a nude mouse solid tumor model. Expression of BCR/GFP in TonB210 cells used for injection delayed tumor formation and tumors were 50% smaller compared to the TonB210
APA, Harvard, Vancouver, ISO, and other styles
5

Zheng, Xiaomin, Saskia Güller, Gesine Bug, et al. "The Reciprocal t(9;22)-Translocation Products ABL/BCR Have Leukemogenic Potential Independently from BCR/ABL." Blood 104, no. 11 (2004): 214. http://dx.doi.org/10.1182/blood.v104.11.214.214.

Full text
Abstract:
Abstract In 95% of chronic myeloid leukemia (CML) and in 25% of acute lymphatic leukemia (ALL) the t(9;22) translocation fuses the bcr gene on chromosome 22 to the abl gene on chromosome 9 and vice versa. On 22+ the different breakpoints leads to the formation of two different major fusion genes: the major breakpoint (M-bcr) related to CML and the minor (m-bcr) related to ALL. The chimaeric fusion gene on 22+ (Philadelphia-chromosome) encodes for the BCR/ABL protein, the p210(BCR/ABL) in CML and the p185(BCR/ABL) in Ph+ALL. The fusion gene on 9+ encodes for the reciprocal ABL/BCR proteins, the
APA, Harvard, Vancouver, ISO, and other styles
6

Weerkamp, Floor, E. Dekking, Vincent H. J. Van der Velden, et al. "Flow Cytometric Detection of BCR-ABL Fusion Proteins in Leukemia Patients Via An Immunobead Assay." Blood 112, no. 11 (2008): 2533. http://dx.doi.org/10.1182/blood.v112.11.2533.2533.

Full text
Abstract:
Abstract The BCR-ABL fusion gene results from the translocation t(9;22). It is the hallmark of chronic myeloid leukemia (CML) and is present in a poor-risk subgroup of precursor B cell acute lymphoblastic leukemia (ALL), which represents 25–30% of adult ALL and 3–5% of childhood ALL. Consequently the detection of the BCR-ABL aberration is of utmost importance for diagnosis and classification of leukemia patients and can also be used as marker for monitoring of BCR-ABL+ leukemias to evaluate treatment effectiveness. So far, the BCR-ABL aberration has been detected by cytogenetics, FISH or PCR,
APA, Harvard, Vancouver, ISO, and other styles
7

Wohlbold, Lara, Heiko van der Kuip, Alexandra Moehring, et al. "Repeated Application of Sequence-Specific SiRNA Molecules Leads to an Effective Downmodulation of All Clinically Relevant bcr-abl Gene Variants." Blood 104, no. 11 (2004): 4319. http://dx.doi.org/10.1182/blood.v104.11.4319.4319.

Full text
Abstract:
Abstract Fusion transcripts such as bcr-abl encoding pathological oncogenic proteins represent ideal targets for a tumor-specific RNA interference (RNAi) approach. The aim of the present study was to optimize the efficacy of bcr-abl RNAi. We evaluated several synthetic siRNAs targeting the fusion sites of all common bcr-abl transcript variants (e14a2, e13a2, or e1a2). Significant knock-down of p210Bcr-abl and p190Bcr-abl fusion proteins was successfully achieved in bcr-abl expressing 32D cells and human leukemic K562 and MEG-01 cells. Repeated application of siRNA proved to be significantly mo
APA, Harvard, Vancouver, ISO, and other styles
8

Million, Ryan P., and Richard A. Van Etten. "The Grb2 binding site is required for the induction of chronic myeloid leukemia-like disease in mice by the Bcr/Abl tyrosine kinase." Blood 96, no. 2 (2000): 664–70. http://dx.doi.org/10.1182/blood.v96.2.664.014k52_664_670.

Full text
Abstract:
The BCR/ABL oncogene results from a balanced translocation between chromosomes 9 and 22 and is found in patients with chronic myeloid leukemia (CML) and in some patients with acute B-lymphoid leukemia. The Bcr/Abl fusion protein is a constitutively active tyrosine kinase that stimulates several intracellular signaling pathways, including activation of Ras through direct binding of the SH2-containing adapter protein Grb2 to Bcr tyrosine 177. A tyrosine-to-phenylalanine mutation (Y177F) at this site blocks the co-association of Bcr/Abl and Grb2 in vivo and impairs focus formation by Bcr/Abl in f
APA, Harvard, Vancouver, ISO, and other styles
9

Castro, Fabiola A., Gabriela Brumatti, and Gustavo P. Amarante-Mendes. "Expression of BCR-ABL Does Not Inhibit Apoptosis In Vitro, on a B Lymphoblastoid Cell Line." Blood 104, no. 11 (2004): 4242. http://dx.doi.org/10.1182/blood.v104.11.4242.4242.

Full text
Abstract:
Abstract The bcr-abl oncogene is generated by the Philadelphia chromosome (Ph) translocation, fusing the BCR gene to the ABL gene and occurs mainly in two different forms. In chronic myelogenous leukemia (CML) a 210kDa Bcr-Abl protein is associated with proliferation and accumulation of myeloid cells and their precursors, whereas a 185kDa form is responsible for the pathogenesis of acute lymphocytic leukemia (ALL). Bcr-Abl not only induces cellular transformation but also regulates cell proliferation and confers resistance to a variety of apoptosis-inducing agents. Much attention has been focu
APA, Harvard, Vancouver, ISO, and other styles
10

Wohlbold, Lara, Heiko van der Kuip, Cornelius Miething, et al. "Inhibition of bcr-abl gene expression by small interfering RNA sensitizes for imatinib mesylate (STI571)." Blood 102, no. 6 (2003): 2236–39. http://dx.doi.org/10.1182/blood-2002-12-3899.

Full text
Abstract:
Abstract Bcr-Abl proteins are effective inducers of the leukemic phenotype in chronic myeloid leukemia (CML) and distinct variants of acute lymphoblastic leukemia (ALL). Targeting bcr-abl by treatment with the selective tyrosine kinase inhibitor imatinib has proved to be highly efficient for controlling leukemic growth. However, it is unclear whether imatinib is sufficient to eradicate the disease because of primary or secondary resistance of leukemic cells. Therefore, targeting Bcr-Abl with an alternative approach is of great interest. We demonstrate that RNA interference (RNAi) with a breakp
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Proteine bcr-abl"

1

Cotteret, Sophie. "Induction de la résistance à l'apoptose par Bcr-Abl : amplification génique, inhibition des voies dépendante et -indépendante de l'activation des caspases." Bordeaux 2, 2000. http://www.theses.fr/2000BOR28733.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Hess, Patricia M. "Role of c-Jun NH-terminal Kinase in Bcr/Abl Induced Cell Transformation: a dissertation." eScholarship@UMMS, 2003. https://escholarship.umassmed.edu/gsbs_diss/88.

Full text
Abstract:
The c-Jun NH2-terminal kinase (JNK) group of kinases include ten members that are created by alternative splicing of transcripts derived from Jnk1, Jnk2 and Jnk3 genes. The JNK1 and JNK2 protein kinases are ubiquitously expressed while JNK3 is expressed in a limited number of tissues. The JNK signaling pathway is implicated in multiple physiological processes including cell transformation. There is growing evidence that JNK signaling is involved in oncogenesis. Nevertheless, the role that JNK plays in malignant transformation is still unclear. The aim of this thesis is to examine the role of J
APA, Harvard, Vancouver, ISO, and other styles
3

Silva, Ana Elisa Barreiros Bueno da. "Aspectos moleculares da transformação celular induzida por Bcr-Abl." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-03062008-153936/.

Full text
Abstract:
As leucemias cromossomo Ph-positivas estão intimamente associadas à expressão da tirosina-quinase Bcr-Abl. Esta oncoproteína promove independência de fatores de crescimento, alterações na adesão e inibição da apoptose por mecanismos ainda não totalmente elucidados. O objetivo desse estudo foi avaliar a contribuição da atividade quinase de Bcr-Abl para seu potencial anti-apoptótico e identificar alterações moleculares envolvidas na transformação celular induzida por essa proteína. Nossos resultados sugerem que a resistência à apoptose não depende da manutenção constante da atividade tirosina-qu
APA, Harvard, Vancouver, ISO, and other styles
4

Marusyk, Andriy. "Decreased cellular fitness as a tumor promoter /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.

Find full text
Abstract:
Thesis (Ph.D. in Molecular Biology) -- University of Colorado at Denver and Health Sciences Center, 2006.<br>Typescript. Includes bibliographical references (leaves 124-145). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;
APA, Harvard, Vancouver, ISO, and other styles
5

Petrola, Maria Juracy Solon. "Perfil do estresse oxidativo em pacientes portadores de Leucemia MielÃide CrÃnica." Universidade Federal do CearÃ, 2011. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=10856.

Full text
Abstract:
Chronic myeloid leukemia (CML) is characterized by clonal expansion of hematopoietic progenitor cells, result from the translocation (9:22). The oncogene BCR-ABL, in the Ph chromosome, is transcribed and translated into a fusion protein BCR / ABL. The ABL tyrosine kinase (TK) in the fusion protein is constitutively activated and is needed for the initial leukemogenic event of CML and its activity induces production of reactive oxygen species (ROS). Of particular relevance to CML is the fact that an increase of ROS can have consequences, facilitating genomic instability may contribute to diseas
APA, Harvard, Vancouver, ISO, and other styles
6

Gurjar, Purujit. "Design and Synthesis of Anti Cancer Agents that Inhibit Cysteine Proteases, Limit Oxidative Stress or Terminate Proliferation of BCR-ABL Expressing Cells." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1535635261401718.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Coppo, Paul. "Mise au point d'un modèle de cellules souches transformées par l'oncogène BCR-ABL : conséquences sur la différenciation et l''autorenouvellement." Paris 7, 2006. http://www.theses.fr/2006PA077224.

Full text
Abstract:
La leucémie myéloïde chronique (LMC) est une affection maligne clonale de la cellule souche hématopoïétique caractérisée par la présence du chromosome Philadelphie (ou Phi), issu de la translocation entre les chromosomes 9 et 22. Celui-ci génère l'oncoprotéine BCR-ABL ayant une activité tyrosine kinase constitutive. Actuellement, les mécanismes précis de l'expansion myéloïde, de l'autorenouvellement du clone leucémique, et du blocage de la différenciation lors de la crise blastique observés dans la LMC restent inconnus. Afin d'étudier les mécanismes par lesquels BCR-ABL pourrait orienter la de
APA, Harvard, Vancouver, ISO, and other styles
8

Eiring, Anna Marie. "Altered mRNA Metabolism in Chronic Myelogenous Leukemia: Loss of MicroRNA-328 Decoy Activity is Important for Blastic Transformation of Leukemic Progenitors." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1250701551.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
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 t
APA, Harvard, Vancouver, ISO, and other styles
10

Bewry, Nadine N. "STAT3 Contributes to Resistance Towards BCR-ABL Inhibitors in a Bone Marrow Microenvironment Model of Drug Resistance in Chronic Myeloid Leukemia Cells." [Tampa, Fla] : University of South Florida, 2009. http://purl.fcla.edu/usf/dc/et/SFE0002892.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Proteine bcr-abl"

1

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Proteine bcr-abl"

1

Bracco, Enrico, M. Shahzad Ali, Stefano Magnati, and Giuseppe Saglio. "The Paradigm of Targeting an Oncogenic Tyrosine Kinase: Lesson from BCR-ABL." In Advances in Precision Medicine Oncology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97528.

Full text
Abstract:
The aberrant tyrosine phosphorylation, either due to constitutive tyrosine kinases (TKs) or to inactivation of protein tyrosine phosphatases (PTPs), is a widespread feature of many cancerous cells. The BCR-ABL fusion protein, which arises from the Philadelphia chromosome, is a molecular distinct and peculiar trait of some kind of leukemia, namely Chronic Myeloid and Acute Lymphoblastic Leukemia, and displays constitutive tyrosine kinase activity. In the chapter, we will highlight the milestones that had led to the identification of the BCR-ABL fusion gene and its role as the only molecular pathogenic event sufficient to elicit and sustain chronic myeloid leukemia. We will also discuss the effort made to unveil the molecular mechanisms of action of the chimeric tyrosine kinase that eventually lead to aberrant cell proliferation and impaired cell-death. Furthermore, we will also review the lesson learned from the selective inhibition of BCR-ABL which currently represent a breakthrough in the treatment of several tumors characterized by defective tyrosine kinase activity.
APA, Harvard, Vancouver, ISO, and other styles
2

Egan, Daniel, and Jerald P. Radich. "Monitoring efforts in myeloproliferative neoplasms." In Oxford Specialist Handbook: Myeloproliferative Neoplasms. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0015.

Full text
Abstract:
Targeted therapy with tyrosine kinase inhibitors (TKI) has transformed the therapy of chronic myeloid leukaemia (CML), and is increasingly playing a role in the management of the myeloproliferative neoplasms (MPN), as a whole. In CML, the Philadelphia chromosome drives disease pathogenesis, and is the basis of both therapy (aimed at the BCR-ABL protein) and monitoring (the BCR-ABL chimeric mRNA). The efficacy of tyrosine kinase inhibitor therapy in CML is now accessed by reaching treatment milestones based on the BCR-ABL mRNA levels. In MPN, the landscape of genetic mutations associated with essential thrombocytosis (ET), polycythaemia vera (PV), and primary myelofibrosis (PMF) is ongoing. However, the recent discoveries of the JAK2 V617F and calreticulin mutations (for example) have a similar potential for disease targeting and monitoring as in CML.
APA, Harvard, Vancouver, ISO, and other styles
3

Cui, Qingbin, Pranav Gupta, Lei Zhang, and Zhe-Sheng Chen. "BCR-ABL Inhibitors as Sensitizing Agents for Cancer Chemotherapy." In Protein Kinase Inhibitors as Sensitizing Agents for Chemotherapy. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-816435-8.00002-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

"BCR/ABL protein domain function and signaling Ann Marie Pendergast." In Chronic Myeloid Leukemia. CRC Press, 2001. http://dx.doi.org/10.3109/9780203213018-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Kerr, David J., Daniel Haller, and Jaap Verweij. "Principles of chemotherapy." In Oxford Textbook of Cancer Biology, edited by Francesco Pezzella, Mahvash Tavassoli, and David J. Kerr. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0028.

Full text
Abstract:
Systemic cancer treatment stems initially from empirically discovered DNA synthesis inhibitors, which either deplete the cell of nucleotides, induce cross-link, or cause DNA single and double strand breaks or impair the cellular machinery of DNA repair, using mechanistically diverse drugs. A period of enlightenment followed, with anticancer drug development driven by an increased understanding of enzymes and pathways involved in cell signalling, control of angiogenesis, and epigenetics. This provided a parallel path towards precision cancer medicine where specific drugs can be targeted to patients with particular mutations. These include point mutations in RAS, which are used to exclude colorectal cancer patients from being treated with epidermal growth factor inhibitors; chromosomal translocations encoding fusion proteins which are cancer specific and serve as novel drug targets (e.g. BCR/ABL and imatinib, or EML4-ALK fusion oncogene and crizotinib). More recently, there has been a reanimation of immune approaches to cancer therapy with the clinical introduction of immune checkpoint inhibitors, designer T cells, and patient-specific antitumour vaccines. What next? It may be that next-generation sequencing provides an endless stream of so-called actionable mutations that permits tailored application of mutation-specific drugs, but so far there is little evidence of clinical benefit from such therapies.
APA, Harvard, Vancouver, ISO, and other styles
6

Gupta, Pranav, Yunali V. Ashar, Charles R. Ashby, Lusheng Lin, and Zhe-Sheng Chen. "The Oncogenic Protein, Breakpoint Cluster (BCR)-Abelson Kinase (ABL) and Chronic Myelocytic Leukemia (CML): Insight Into the Drug Resistance Mechanisms and Approaches for Targeting BCR-ABL in CML." In Reference Module in Biomedical Sciences. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-820472-6.00047-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Proteine bcr-abl"

1

Pereira, Washington A., Érica C. M. Nascimento, and João B. L. Martins. "Estudo QM/MM da proteína tirosina Bcr-Abl mutada T315I." In VIII Simpósio de Estrutura Eletrônica e Dinâmica Molecular. Universidade de Brasília, 2020. http://dx.doi.org/10.21826/viiiseedmol2020148.

Full text
Abstract:
Bcr-Abl tyrosine kinase protein activates the substrate starting kinase signaling cascade that results in cell division. When in excess this activation can lead to chronic myeloid leukemia. Currently, the treatment of this disease is achieved through drugs developed by rational drug design, e.g., imatinib. In this work we study descriptors of the following molecules: imatinib, nilotinib and ponatinib, together with a mutated protein. To characterize interactions between the residues of the active site against those inhibitors, a QM/MM study was carried out, using the hybrid method ONIOM, throu
APA, Harvard, Vancouver, ISO, and other styles
2

Jesus, Anderson Avelino de, Samuel Santana Moura, Rebeca Santos Da Silva, Raqueline Pastor De Santana E. Santana, and Irlandia Oliveira Almeida. "LEUCEMIA MIELÓIDE CRÔNICA: O CROMOSSOMO PHILADELPHIA E O GENE BCR-ABL." In I Congresso Nacional Multidisciplinar de Oncologia On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1529.

Full text
Abstract:
Introdução: A Leucemia Mieloide Crônica (LMC) foi a primeira neoplasia humana relacionada a uma alteração cromossômica. Primeiros casos foram descritos em 1845. Porém, somente em 1960 quando Peter C. Nowell, estudando células de medula óssea de pacientes com LMC observou a presença de um pequeno cromossomo denominado Philadelphia (Ph) nestas células, sendo considerado um marco para a citogenética. Objetivo: Levantar relações da Leucemia Mieloide Crônica com o gene BCR-ABL e o cromossomo Philadelphia. Material e métodos: Trata-se de um estudo bibliográfico com abordagem descritiva e qualitativa
APA, Harvard, Vancouver, ISO, and other styles
3

Rocha, Kelvyn M. L., Érica C. M. Nascimento, and João B. L. Martins. "Estudo de Docking da Bcr-Abl (PDB, 1OPJ) com Inibidores de Segunda Geração: Dasatinibe e Afatinibe." In VIII Simpósio de Estrutura Eletrônica e Dinâmica Molecular. Universidade de Brasília, 2020. http://dx.doi.org/10.21826/viiiseedmol2020151.

Full text
Abstract:
Chronic myeloid leukemia is a type of cancer which affects hematopoetic cells, causing excessive proliferation of white blood cells which eventually leads to loss of function and resistance to apoptosis (stage known as acute leukemia). Researchers have shown that many CML cases are associated with mutant transcripts of the Philadelphia chromosome (i.e. BCR-ABL), whose effects are pharmacologically treated. The first successful drug in that matter is imatinib, a competitive inhibitor which caused groundbreaking advances in the treatment of CML. However, many patients develop resistance to the t
APA, Harvard, Vancouver, ISO, and other styles
4

Pereira, Washington A., Érica C. M. Nascimento, and João B. L. Martins. "Estudo de estrutura eletrônica da interação de inibidores da proteína Tirosina Quinase Abl-Bcr na forma mutada frente a forma selvagem." In VII Simpósio de Estrutura Eletrônica e Dinâmica Molecular. Editora Letra1, 2018. http://dx.doi.org/10.21826/9788563800374084.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Bruno, Benjamin J., and Carol S. Lim. "Abstract 2641: Inhibition of Bcr-Abl in human leukemic cells with a coiled coil protein delivered by a leukemia-specific cell penetrating peptide." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2641.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Rosso, Valentina, Monica Pradotto, Sonia Carturan, et al. "Abstract 4771: The oncogenic kinase Bcr-Abl regulates splicing of Bcl-x trough a quaternary complex coordinated by Nck-beta and Sam68 adapter proteins." 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.am2011-4771.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Proteine bcr-abl' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography