Results 51 to 60 of about 9,645 (157)

Peptides spanning the junctional region of both the abl/bcr and the bcr/abl fusion proteins bind common HLA class I molecules [PDF]

Leukemia, 2000
The Philadelphia (Ph) chromosome, resulting from the t(9;22) translocation, is characteristic of chronic myeloid leukemia (CML). As a result of this translocation, two novel chimeric genes are generated and the bcr/abl and abl/bcr fusion proteins expressed.
Berke, Z., Andersen, M.H., Pedersen, M., Fugger, L., Zeuthen, J.and, Haurum, J.S.   +5 more
openaire   +4 more sources

Targeting the oligomerization of BCR/ABL by membrane permeable competitive peptides inhibits the proliferation of Philadelphia Chromosome positive leukemic cells [PDF]

, 2013
The BCR/ABL fusion protein is the hallmark of Philadelphia Chromosome positive (Ph+) leukemia. The constitutive activation of the ABL-kinase in BCR/ABL cells induces the leukemic phenotype.
Beißert, Tim, Goldblum, Amiram, Mahajna, Jamal, Mian, Afsar Ali, Najajreh, Yousef, Oancea, Claudia, Ottmann, Oliver Gerhard, Ruthardt, Martin, Schüll, Marion   +8 more
core  

Targeting self-renewal pathways in myeloid malignancies [PDF]

, 2013
A fundamental property of hematopoietic stem cells (HSCs) is the ability to self-renew. This is a complex process involving multiple signal transduction cascades which control the fine balance between self-renewal and differentiation through ...
Copland, M., Sands, W.A., Wheadon, H.
core   +2 more sources

Insights into the clinical, platelet and genetic landscape of inherited thrombocytopenia with malignancy risk

British Journal of Haematology, EarlyView.
Inherited thrombocytopenia (IT) caused by germline variants in RUNX1, ETV6 or ANKRD26 carries a high risk of developing haematological malignancy. This study examined the clinical, platelet and molecular characteristics of 66 patients with these conditions, who carried 24 distinct genetic variants in the corresponding genes.
Ana Marín‐Quílez, Ana Sánchez‐Fuentes, Ana Zamora‐Cánovas, Pedro Luis Gómez‐González, Lorena Diaz‐Ajenjo, Rocío Benito, Agustín Rodríguez‐Alén, Teresa Sevivas, Thais Murciano, Laura Murillo, Nora V. Butta, Nuria Revilla, Rosa Campos, Paola Escribano, Jordi Esteve, Nuria Fernández‐Mosteirin, Francisca Ferrer‐Marín, Laura Hernández, Jorge Huerta‐Aragonés, Antonio León, Mónica López‐Duarte, Eugenia López, Mónica Martín‐Salces, Meritxell Nomdedeu, Raquel Oña, Irene Peláez‐Pleguezuelos, Fernando Ramos, Elena Sebastián, Claudia Serrano, Cristina Sierra‐Aisa, Rosa Vidal‐Laso, José Ramón González‐Porras, María Luisa Lozano, José María Bastida, José Rivera   +34 more
wiley   +1 more source

The COOH terminus of the c-Abl tyrosine kinase contains distinct F- and G-actin binding domains with bundling activity [PDF]

, 1994
The myristoylated form of c-Abl protein, as well as the P210bcr/abl protein, have been shown by indirect immunofluorescence to associate with F-actin stress fibers in fibroblasts. Analysis of deletion mutants of c-Abl stably expressed in fibroblasts maps
Baltimore, David, Jackson, Peter K., Janmey, Paul A., Matsudaira, Paul T., Sanders, Mitchell C., Van Etten, Richard A.   +5 more
core   +4 more sources

Deletions of the derivative chromosome 9 occur at the time of the Philadelphia translocation and provide a powerful and independent prognostic indicator in chronic myeloid leukemia [PDF]

, 2001
Chronic myeloid leukemia (CML) is characterized by formation of the BCR-ABL fusion gene, usually as a consequence of the Philadelphia (Ph) translocation between chromosomes 9 and 22.
Bench, AJ, Campbell, LJ, Grace, C, Green, AR, Huntly, BJP, Nacheva, EP, Prince, HM, Reid, AG, Shepherd, P, Szer, J, Telford, N, Turner, P   +11 more
core   +1 more source

Apoptosis resistance in chronic myelogenous leukemia [PDF]

Einstein (São Paulo), 2005
The chronic myeloid leukemia (CML) is the three-phasemyeloproliferative disorder, dependent on the expression of theoncoprotein Bcr-Abl, which is the product of the reciprocaltranslocation between chromosomes 9 and 22, resulting in thePhiladelphia ...
Fabíola Attié de Castro, Jacqueline de Fátima Jacysyn, Ana Elisa Bueno-da-Silva, Nelson Hamerschlak, Gustavo Pessini Amarante-Mendes   +4 more
doaj  

TP‐0903 Suppresses Aurora A–PLK1 Signaling to Inhibit Proliferation of a Myelodysplastic Syndrome‐Derived Cell Line

Cancer Science, EarlyView.
TP‐0903 exerts the antitumor effects through diverse cell‐specific mechanisms, including apoptosis, ferroptosis, and cell cycle disruption. These insights underline the potential of TP‐0903 as a therapeutic agent for hematological malignancies and emphasize the need for further research to fully elucidate the molecular targets of TP‐0903 and optimize ...
Tomoko Kimura‐Hyoda, Mikuri Ryu, Ryosuke Yuta, Saori Fukumoto, Kentaro Hosokawa, Hisayuki Yao, Yoko Yasuda, Koichi Miura, Kaoru Tohyama, Fumio Arai, Takeshi Uchiumi   +10 more
wiley   +1 more source

The role of miRNA in haematological malignancy [PDF]

, 2013
Currently, there are over 1,800 annotated human miRNAs, many of which have tissue-specific expression. Numerous studies have highlighted their role in haematopoietic differentiation and proliferation, acting as master regulators of haematopoietic stem ...
Chevassut, Timothy, Gounaris-Shannon, Stephanie   +1 more
core   +2 more sources

Characterization of three new imatinib-responsive fusion genes in chronic myeloproliferative disorders generated by disruption of the platelet-derived growth factor receptor β gene

Haematologica, 2007
Background and Objectives We sought to identify new fusion genes with involvement of the platelet-derived growth factor receptor β gene (PDGFRB) in three patients presenting with various subtypes of chronic myeloproliferative disorders associated with ...
Christoph Walz, Georgia Metzgeroth, Claudia Haferlach, Annette Schmitt-Graeff, Alice Fabarius, Volker Hagen, Otto Prümmer, Stefan Rauh, Rüdiger Hehlmann, Andreas Hochhaus, Nicholas C.P. Cross, Andreas Reiter   +11 more
doaj   +1 more source