Relevant bibliographies by topics / BCR-ABL like

Contents

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

Academic literature on the topic 'BCR-ABL like'

Author: Grafiati
Published: 1 April 2023
Last updated: 31 July 2025

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 'BCR-ABL like.'

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 "BCR-ABL like"

1

Gross, Alec W., Xiaowu Zhang, and Ruibao Ren. "Bcr-Abl with an SH3 Deletion Retains the Ability To Induce a Myeloproliferative Disease in Mice, yet c-Abl Activated by an SH3 Deletion Induces Only Lymphoid Malignancy." Molecular and Cellular Biology 19, no. 10 (1999): 6918–28. http://dx.doi.org/10.1128/mcb.19.10.6918.

Full text
Abstract:
ABSTRACT The bcr-abl oncogene plays a critical role in the pathogenesis of chronic myelogenous leukemia (CML). The fusion of Bcr sequences to Abl constitutively activates the Abl protein tyrosine kinase. We have recently shown that expression of Bcr-Abl in bone marrow cells by retroviral transduction efficiently induces in mice a myeloproliferative disease resembling human CML and that Abl kinase activity is essential for Bcr-Abl to induce a CML-like myeloproliferative disease. However, it is not known if activation of the Abl kinase alone is sufficient to induce a myeloproliferative disease.
APA, Harvard, Vancouver, ISO, and other styles
2

He, Yiping, Jason A. Wertheim, Lanwei Xu, et al. "The coiled-coil domain and Tyr177 of bcr are required to induce a murine chronic myelogenous leukemia–like disease by bcr/abl." Blood 99, no. 8 (2002): 2957–68. http://dx.doi.org/10.1182/blood.v99.8.2957.

Full text
Abstract:
Abstract The bcr/abl fusion in chronic myelogenous leukemia (CML) creates a chimeric tyrosine kinase with dramatically different properties than intact c-abl. In P210 bcr/abl, the bcr portion includes a coiled-coil oligomerization domain (amino acids 1-63) and a grb2-binding site at tyrosine 177 (Tyr177) that are critical for fibroblast transformation, but give variable results in other cell lines. To investigate the role of the coiled-coil domain and Tyr177 in promoting CML, 4 P210 bcr/abl-derived mutants containing different bcr domains fused to abl were constructed. All 4 mutants, Δ(1-63) b
APA, Harvard, Vancouver, ISO, and other styles
3

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
4

Hao, Sheryl X., and Ruibao Ren. "Expression of Interferon Consensus Sequence Binding Protein (ICSBP) Is Downregulated in Bcr-Abl-Induced Murine Chronic Myelogenous Leukemia-Like Disease, and Forced Coexpression of ICSBP Inhibits Bcr-Abl-Induced Myeloproliferative Disorder." Molecular and Cellular Biology 20, no. 4 (2000): 1149–61. http://dx.doi.org/10.1128/mcb.20.4.1149-1161.2000.

Full text
Abstract:
ABSTRACT Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disorder resulting from the neoplastic transformation of a hematopoietic stem cell. The majority of cases of CML are associated with the (9;22) chromosome translocation that generates thebcr-abl chimeric gene. Alpha interferon (IFN-α) treatment induces hematological remission and prolongs life in 75% of CML patients in the chronic phase. It has been shown that mice deficient in interferon consensus sequence binding protein (ICSBP), a member of the interferon regulatory factor family, manifest a CML-like syndrome. We hav
APA, Harvard, Vancouver, ISO, and other styles
5

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
6

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.

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

Albers, Corinna, Anna L. Illert, Cornelius Miething, Christian Peschel, and Justus Duyster. "Grb10 Mediated Akt Activation Is Required for Induction of CML Like Myeloproliferative Disease in Mice by BCR-ABL." Blood 110, no. 11 (2007): 1012. http://dx.doi.org/10.1182/blood.v110.11.1012.1012.

Full text
Abstract:
Abstract Chronic myelogenous leukaemia (CML) results from the neoplastic transformation of hematopoietic stem cells (HSC) and is characterized by a chromosomal translocation t(9;22)(q34;q11). This aberration leads to the expression of the oncogenic tyrosine kinase BCR-ABL, which mediates signals for proliferation, transformation and anti-apoptosis via various signalling pathways. Grb10, a member of the growth factor bound proteins, is known to bind activated tyrosine kinases like BCR-ABL and might be involved in the activation of the Akt signalling pathway. Here we report the impact of Grb10 f
APA, Harvard, Vancouver, ISO, and other styles
8

Cross, Nick. "BCR-ABL Negative CML-Like Disorder." Clinical Lymphoma Myeloma and Leukemia 17 (September 2017): S107—S108. http://dx.doi.org/10.1016/j.clml.2017.08.052.

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

Mohi, M. Golam, Wayne W. Chan, Shaoguang Li, Benjamin Neel, and Richard A. Van Etten. "Distinct Gab2-Mediated Signaling Pathways Are Essential for Myeloid or Lymphoid Transformation and Leukemogenesis by BCR-ABL." Blood 112, no. 11 (2008): 570. http://dx.doi.org/10.1182/blood.v112.11.570.570.

Full text
Abstract:
Abstract The BCR-ABL oncogene encodes an activated fusion tyrosine kinase that causes chronic myelogenous leukemia (CML) and B-lymphoid acute lymphoblastic leukemia (B-ALL) in humans. An autophosphorylation site at Tyr 177 of BCR-ABL recruits Grb2 via its SH2 domain, and is required for efficient induction of CML-like myeloproliferative disease by BCR-ABL in a mouse BM retroviral transduction/transplantation model. We showed previously (Sattler et al., Cancer Cell2002;1:479) that the scaffolding/adapter protein Gab2 is recruited to Y177 of BCR-ABL via a Grb2/Gab2 complex, and in vitro transfor
APA, Harvard, Vancouver, ISO, and other styles
10

Albers, Corinna, Anna Lena Illert, Cornelius Miething, Christian Peschel, and Justus Duyster. "Raf1 Is Required for Induction of a Bcr-Abl Positive CML Like Myeloproliferative Disease in Mice." Blood 112, no. 11 (2008): 3207. http://dx.doi.org/10.1182/blood.v112.11.3207.3207.

Full text
Abstract:
Abstract Introduction: Chronic myelogenous leukemia (CML) results from neoplastic transformation of hematopoietic stem cells (HSC), characterized by a chromosomal translocation t(9;22)(q34;q11). This aberration leads to the expression of the oncogenic tyrosine kinase Bcr-Abl, which mediates signals for proliferation, transformation and anti-apoptosis via various different pathways including the Raf/MEK/ERK cascade. The cytoplasmic protein Raf1 is a key molecule within this cascade. Recent studies have revealed an additional function of the Raf-1 kinase that is independent of the activation of
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "BCR-ABL like"

1

MONTECCHINI, OKSANA. "TERAPIA DI PRECISIONE PER LA LEUCEMIA LINFOBLASTICA ACUTA PEDIATRICA BCR-ABL-LIKE: SVILUPPO DI UN SISTEMA IN VITRO PER LA DIAGNOSI E IL MONITORAGGIO CLINICO." Doctoral thesis, Università degli Studi di Trieste, 2021. http://hdl.handle.net/11368/2997554.

Full text
Abstract:
La leucemia linfoblastica acuta (LLA) pediatrica BCR-ABL like(BAL) è un nuovo sottotipo di leucemie identificato per similarità nell'espressione genica con la LLA positiva per BCR-ABL. Il BAL è associato all'attivazione delle pathways di ABL o JAK-STAT e ad un alto rischio di ricaduta, ma gli inibitori tirosin chinasici (TKI), potrebbero rappresentare una soluzione terapeutica. Qui riportiamo un saggio ELISA basato su un biosensore peptidico (PABL) in grado di valutare l’attività chinasica di ABL. La sequenza di PABL comprende un sito di fosforilazione della tirosina (Y) ABL e una sequenza di
APA, Harvard, Vancouver, ISO, and other styles
2

Drivet, Elsa. "Etude préclinique personnalisée d'une translocation rare T(1 ; 9)(Q24 ; Q34) "PH-LIKE" et perspectives d'optimisation des traitements contre les LAL-B de mauvais pronostic." Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0664.

Full text
Abstract:
La translocation t(1;9)(q24 ;q34), qui engendre la protéine de fusion RCSD1-ABL1, a été identifiés dans des cas de LAL de mauvais pronostic. Les propriétés oncogéniques du partenaire RCSD1, sa structure et son rôle dans l’activité et la signalisation de RCSD1-ABL1 restent inconnus. Nous avons récemment rapporté le cas d’une LAL-B t(1;9)(q24 ;q34) montrant une résistance à un grand nombre d’ITK, mais une sensibilité inattendue au ponatinib, en l’absence de mutation d’ABL1 susceptible d’expliquer ces réponses.Dans le but de caractériser la protéine RCSD1-ABL1, de comprendre ces profils de répons
APA, Harvard, Vancouver, ISO, and other styles
3

Okada, Masayuki. "A novel mechanism for imatinib mesylate-induced cell death of BCR-ABL positive human leukemic cells : caspase-independent, necrosis-like programmed cell death mediated by serine protease activity." Kyoto University, 2005. http://hdl.handle.net/2433/145297.

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

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
5

Nishihara, Toshio. "Effects of the Tyrosine Kinase Inhibitor, Imatinib Mesylate on a Bcr-Abl-Positive Cell Line : Suppression of Autonomous Cell Growth but No Effect on Decreased Adhesive Property and Morphological Changes." Kyoto University, 2004. http://hdl.handle.net/2433/147461.

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

Heurteau, Foulon Stéphanie. "Prévalence, qualité de vie et coût de la Leucémie Myéloïde Chronique en France Using healthcare claims data to analyze the prevalence of BCR-ABL-positive chronic myeloid leukemia in France: A nationwide population-based study Health state utility and quality of life measures in patients with chronic myeloid leukemia in France." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS574.

Full text
Abstract:
La leucémie myéloïde chronique (LMC) est une hémopathie maligne rare dont le pronostic a été transformé à partir des années 2000 par les inhibiteurs de tyrosine kinase (ITK). L’augmentation spectaculaire de l’espérance de vie des patients a conduit à une augmentation de la prévalence de la LMC. D’une maladie mortelle à moyen terme, la LMC est devenue une maladie chronique nécessitant la prise quotidienne d’ITK pendant plusieurs années. Les ITK sont des traitements onéreux qui, pris au long cours par un nombre croissant de patients, augmentent le fardeau économique de la maladie. Ces traitement
APA, Harvard, Vancouver, ISO, and other styles
7

山本, 起代子, and Kiyoko Yamamoto. "Functionally deregulated AML1/RUNX1 cooperates with BCR-ABL to induce a blastic phase-like phenotype of chronic myelogenous leukemia in mice." Thesis, 2013. http://hdl.handle.net/2237/19156.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Cheng, Hao-Yuan, and 鄭皓遠. "Combination of protein tyrosine kinase inhibitor AG1024 with paclitaxel enhances cell program death in BCR-ABL-mediated resistance of K562 cell line." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/30227831001776366712.

Full text
Abstract:
碩士<br>國立陽明大學<br>醫學生物技術研究所<br>93<br>Chronic myelogenous leukaemia (CML) is a clonal malignancy of the pluripotent haematopoietic stem cell, characterised by an uncontrolled proliferation and expansion of myeloid progenitors expressing a fusion oncogene, BCR-ABL, the molecular counterpart of the Ph1 chromosome. Many evidences showed that the tyrosine kinase activity of BCR-ABL is able to activate several major signalling pathways in malignant cells, including Ras, JAK/STAT and PI3K/Akt and also prevent cells apoptosis under some antineoplastic agents such as paclitaxel. Targeting these abnormali
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "BCR-ABL like"

1

Baccarani, Michele, Fausto Castagnetti, Gabriele Gugliotta, Francesca Palandri, Simona Soverini, and Gianantonio Rosti. "Prognostic factors of chronic myeloid leukaemia." In Oxford Specialist Handbook: Myeloproliferative Neoplasms. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0005.

Full text
Abstract:
Two decades following the successful introduction of the ABL tyrosine kinase inhibitors in clinics for the treatment of patients with chronic myeloid leukaemia (CML), the principal objective of treatment in chronic phase (CP) is survival, preferably without life-long therapy. In tandem, the methodology and tools for assessing the prognosis of the newly diagnosed patient with CML in CP has evolved substantially. Prior to the era of tyrosine kinase inhibitors (TKIs), risk assessment depended more on the response to treatment than on baseline characteristics. The Sokal score, introduced in 1984,
APA, Harvard, Vancouver, ISO, and other styles
2

Geyer, Holly L., Deepti Radia, Nicholas Sarlis, and Ruben A. Mesa. "Assessment of disease burden in patients with myeloproliferative neoplasms." In Oxford Specialist Handbook: Myeloproliferative Neoplasms. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198744214.003.0017.

Full text
Abstract:
The BCR-ABL-negative myeloproliferative neoplasms (MPN) collectively represent a diverse assortment of clonal myeloid malignancies with variability in both genotypic and phenotypic presentation. MPN subtypes including essential thrombocythaemia (ET), polycythaemia vera (PV), myelofibrosis (MF), systemic mast cell disorders have been best studied in terms of symptom profiles and heterogeneously incur disease burdens that impact treatment options, overall quality of life, and survival. Recent treatment strategies have aimed to incorporate disease burden assessment into the selection of therapeut
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "BCR-ABL like"

1

Tostes, Carine Pimenta Maurício Dantas, Kelly Costa De Almeida, Carolina V. A. Lutterbach De Carvalho, Gustavo Manso Fernandes, and Aislan Cristina R. F.Pascoal. "O EFEITO DA HIDROXIUREIA E MESILATO DE IMATINIBE NO TRATAMENTO DA LMC: RELATO DE CASO." In II Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/hematoclil/14.

Full text
Abstract:
INTRODUÇÃO: A leucemia mielóide crônica (LMC) é uma neoplasia mieloproliferativa relacionada à presença do gene de fusão BCR-ABL. É originada de uma célula-tronco hematopoiética anormal, que se caracteriza, como suas contrapartes normais. OBJETIVO: Avaliar o efeito do uso da hidroxiureia e mesilato de imatulibe nos parâmetros hematológicos em paciente diagnosticado com LMC. MATERIAL E MÉTODOS: Avaliação dos hemogramas realizados pelo paciente, após introdução das medicações. RESULTADOS: Paciente do sexo masculino, 57 anos, procurou auxílio médico após apresentar episódios recorrentes de cansaç
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

Silva, Danielle Cardoso da, Miguel A. Moreira, Raquel C. Maia, and Flavia C. Vasconcelos. "Abstract A58: Bcr-Abl independent activation of Erk1/2 in an imatinib resistant cell line." In Abstracts: AACR International Conference held in cooperation with the Latin American Cooperative Oncology Group (LACOG) on Translational Cancer Medicine; May 4-6, 2017; São Paulo, Brazil. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.tcm17-a58.

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

Bosso, Gabriela Jubilato, Letícia Cappellano, Luis Fernando Ventura Vilella, André Viu Matheus, and Ana Paula Pinto Batista. "LEUCEMIA MIELOIDE CRÔNICA EM ADOLESCENTE: RELATO DE CASO." In II Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/hematoclil/28.

Full text
Abstract:
Introdução: Rara em crianças e adolescentes, a leucemia mieloide crônica representa cerca de 2 a 3% dos casos de leucemia em menores de 15 anos. A doença mieloproliferativa é originada a partir da translocação dos cromossomos 9 e 22, dando origem ao cromossomo Philadelphia. O tratamento recomendado para crianças e adolescentes com LMC segue os protocolos de pacientes adultos pela falta de estudos na pediatria pela raridade da doença. O uso de inibidores de tirosina-quinase como o imatinibe tem mostrado bons resultados nos pacientes pediátricos. Objetivo: Relatar um caso de leucemia mieloide cr
APA, Harvard, Vancouver, ISO, and other styles
5

Lima, Luã De Morais De, and Cássia Bassetto Lorenzoni. "RECOMENDAÇÕES FARMACOLÓGICAS PARA TRATAMENTO DE LEUCEMIA MIELÓIDE CRÔNICA." In II Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/hematoclil/51.

Full text
Abstract:
Introdução: A Leucemia Mielóide Crônica (LMC) representa 14% das ocorrências de leucemia. Sua etiologia é relacionada a translocação 9:22 (cromossomo Filadélfia positivo). Assim, os tratamentos atuais para LMC vêm se mostrando promissores no incremento da sobrevida do paciente, a eles será dado foco neste resumo. Objetivos: Analisar as recomendações europeias para manejo da LMC e descrever os fármacos de primeira geração para tratamento da LMC. Material e métodos: O resumo sucedeu uma revisão da literatura mediante fontes qualitativas e ensaios clínicos. Nesse sentido, as bases de dados utiliz
APA, Harvard, Vancouver, ISO, and other styles
6

Vilella, Luis Fernando Ventura, Gabriela Jubilato Bosso, Leticia Cappellano, Natalia Marques Rodrigues, and André Viu Matheus. "LEUCEMIA MIELOIDE CRÔNICA (LMC) EM ADOLESCENTE DE 13 ANOS: RELATO DE CASO." In II Congresso Brasileiro de Hematologia Clínico-laboratorial On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/hematoclil/29.

Full text
Abstract:
Introdução:A Leucemia Mielóide Crônica (LMC) é uma patologia mieloproliferativa crônica e clonal; A doença é ocasionada pela translocação cromossomial, que ocorre entre os cromossomos 9 e 22 t(9;22) (q34;q11), originando uma nova configuração, denominada de Cromossomo Philadefia (Ph+), sendo este o desencadeante da inibição apoptótica, via Tirosino-Quinase. O protocolo de escolha para tratamento de LMC são justamente drogas que interferem no processo de proliferação celular das células hematopoiéticas, através da inibição da Tirosina-Quinase (iTK), e não drogas quimioterápicas que tem ação gen
APA, Harvard, Vancouver, ISO, and other styles
7

Soverini, Simona, Caterina De Benedittis, Alessandra Gnani, et al. "Abstract 1884: Resistance to second-line tyrosine kinase inhibitor treatment in imatinib-resistant Philadelphia-positive leukemia patients can be anticipated by ultra-deep sequencing of the BCR-ABL kinase domain using Roche 454 technology." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1884.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'BCR-ABL like' for particular source types:
Journal articles
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