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Journal articles on the topic 'BCR-ABL like'

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Published: 1 April 2023

Last updated: 31 July 2025

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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.

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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.

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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.

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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

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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.

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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

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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.

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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

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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.

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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

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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.

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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

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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.

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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

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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.

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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.

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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

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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.

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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

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11

Pelletier, Shawn D., Daniel S. Hong, Yiguo Hu, Yuhua Liu, and Shaoguang Li. "Lack of the adhesion molecules P-selectin and intercellular adhesion molecule-1 accelerate the development of BCR/ABL-induced chronic myeloid leukemia-like myeloproliferative disease in mice." Blood 104, no. 7 (2004): 2163–71. http://dx.doi.org/10.1182/blood-2003-09-3033.

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Abstract In vitro studies show that BCR/ABL-expressing hematopoietic cells exhibit altered adhesion properties. No in vivo studies show whether the altered adhesion properties affect BCR/ABL leukemo-genesis. Using mice with homozygous inactivation of genes encoding the 2 adhesion molecules P-selectin and intercellular adhesion molecule-1 (ICAM1), we show that the mutant mice develop BCR/ABL-induced chronic myeloid leukemia (CML)-like leukemia at a significantly faster rate than do wild-type (WT) mice. Lack of P-selectin and ICAM1 did not have a significant effect on the development of B-cell a

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12

Fredericks, Jessica, Chaitali Parikh, Ramesh Subrahmanyam, and Ruibao Ren. "The RALGEF Pathway Contributes to the Pathogenesis of Chronic Myelogenous Leukemia by BCR/ABL." Blood 112, no. 11 (2008): 3208. http://dx.doi.org/10.1182/blood.v112.11.3208.3208.

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Abstract Selected inhibitors of the BCR/ABL tyrosine kinase have shown a remarkable clinical activity in patients with chronic myelogenous leukemia (CML). However, these drugs do not completely eradicate leukemic cells and drug resistance emerges. Identification of additional contributors to the pathogenesis of CML remains to be important for developing strategies for overcoming resistance to BCR/ABL kinase inhibitors and for eradicating leukemic cells. We and others have previously shown that expression of BCR/ABL in mouse bone marrow cells by retroviral transduction and transplantation (BMT)

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13

Mian, Afsar, Isabella Haberbosch, Oliver G. Ottmann, and Martin Ruthardt. "Transphosphorylation of Endogenous BCR Mediates the Effect of T315I on the Transformation Potential of BCR/ABL." Blood 124, no. 21 (2014): 4523. http://dx.doi.org/10.1182/blood.v124.21.4523.4523.

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Abstract Targeting of BCR/ABL by ABL-kinase inhibitors (AKI) such as Imatinib, Nilotinib, or Dasatinib is a proven concept in Philadelphia chromosome positive (Ph+ ) leukemia. In the majority of cases the acquisition of resistance is related to point mutations in BCR/ABL, such as the E255K, Y253F/H (P-loop), H396R (activation loop) or the T315I (gatekeeper). Noteworthy, Ph+ leukemias, both CML and Ph+ ALL, never emerge at diagnosis with a BCR/ABL harboring a resistance mutation even if the clone with the mutation is already existing and detectable by very sensitive methods. This indicates that

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14

Million, Ryan P., Jon Aster, D. Gary Gilliland, and Richard A. Van Etten. "The Tel-Abl (ETV6-Abl) tyrosine kinase, product of complex (9;12) translocations in human leukemia, induces distinct myeloproliferative disease in mice." Blood 99, no. 12 (2002): 4568–77. http://dx.doi.org/10.1182/blood-2001-12-0244.

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Several patients with clinical features of chronic myeloid leukemia (CML) have fusion of the TEL (ETV6) gene on 12p13 with ABL on 9q34 and express a chimeric Tel-Abl protein that contains the same portion of the Abl tyrosine kinase fused to Tel, an Ets family transcription factor, rather than Bcr. In a murine retroviral bone marrow transduction-transplantation model, a Tel (exon 1-5)–Abl fusion protein induced 2 distinct illnesses: a CML-like myeloproliferative disease very similar to that induced by Bcr-Abl but with increased latency and a novel syndrome characterized by small-bowel myeloid c

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15

Minami, Yosuke, Scott Stuart, Tomokatsu Ikawa та ін. "Imatinib-Resistant Activation of β-Catenin by BCR-ABL in a Murine Model of Chronic Myelogenous Leukemia Stem Cells." Blood 108, № 11 (2006): 2126. http://dx.doi.org/10.1182/blood.v108.11.2126.2126.

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Abstract [INTRODUCTION] Chronic myelogenous leukemia (CML) is effectively treated with imatinib, a small molecule inhibitor of the BCR-ABL tyrosine kinase that is expressed in the hematopoietic compartment including stem and progenitor cells in CML patients. While imatinib induces disease remission, it does not eradicate BCR-ABL-positive stem cells. Recently, granulocyte-macrophage progenitors (GMP) with nuclear β-catenin and an aberrant potential for self-renewal were detected in CML blast crisis (Jamieson et al, NEJM, 2004). We have established a murine model that generates BCR-ABL-positive

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Zafar, Usva, Mohammed Yusuf, Rikhia Chakraborty, El-Nasir M. A. Lalani, and Afsar Ali Mian. "The ''Gatekeeper'' Mutation T315I in BCR/ABL Confers Additional Oncogenic Activities to Philadelphia Chromosome Positive Leukemia." Blood 134, Supplement_1 (2019): 5196. http://dx.doi.org/10.1182/blood-2019-131694.

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Chronic myeloid leukemia (CML) and 30% of adult acute lymphatic leukemia (ALL) are characterized by the Philadelphia chromosome (Ph+), having a (9;22) chromosomal translocation. The BCR/ABL fusion protein is the hallmark of Ph+ leukemia. BCR/ABL is characterized by deregulated and constitutively activated ABL tyrosine kinase activity that determines its transformation potential. Tyrosine kinase inhibitors (TKI) have greatly improved the overall prognosis of these diseases, particularly by altering the natural history of chronic phase (CP) CML and preventing the previously inexorable progressio

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17

Hantschel, Oliver D., Eva Eckelhart, Ines Kaupe, et al. "Bcr-Abl Directly Activates Stat5 Independent of Jak2." Blood 116, no. 21 (2010): 511. http://dx.doi.org/10.1182/blood.v116.21.511.511.

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Abstract Abstract 511 Persistent activation of the transcription factor Stat5 is a signaling hallmark of Chronic Myelogenous Leukemia (CML). In mouse models, Stat5 was required for initial myeloid and lymphoid transformation (by Bcr-Abl p210 or p185 and v-Abl). Most importantly, we and others recently showed that Stat5 was also required for maintenance of Bcr-Abl-dependent leukemia in vivo and for engraftment and reconstitution of Bcr-Abl p210-positive leukemia in secondary recipients. Therefore, Stat5 is of central functional importance in the Bcr-Abl signaling network and represents a possib

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18

Crawford, Lisa, Philip Windrum, Laura Magill, et al. "Bcr-Abl Positive Cells Display Increased Proteasome Activity and Greater Sensitivity to Proteasome Inhibition." Blood 112, no. 11 (2008): 3192. http://dx.doi.org/10.1182/blood.v112.11.3192.3192.

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Abstract Chronic myeloid leukemia (CML) is a malignant disorder of the hematopoietic stem cell, characterised by the constitutively active tyrosine kinase BCR-ABL. The current first-line therapy for CML is the tyrosine kinase inhibitor imatinib. Although imatinib induces durable responses, a number of patients develop resistance to this treatment, highlighting the need to identify new molecular targets in this disease. Proteasome inhibition has recently emerged as a novel anti-cancer therapy. There is evidence to suggest that the proteasome is a valid target in CML. We have previously reported

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Sha, Xiaojin, Dan Liebermann, and Barbara Hoffman. "Loss of Gadd45b Accelerates BCR-ABL-Driven CML." Blood 132, Supplement 1 (2018): 5138. http://dx.doi.org/10.1182/blood-2018-99-114890.

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Abstract Gadd45b is a member of Gadd45 stress sensor protein family that also includes Gadd45a & Gadd45g. To investigate the effect of Gadd45b in bcr-abl oncogene driven chronic myeloid leukemia (CML) development, syngeneic wild type lethally irradiated mice were reconstituted with either wild type or Gadd45b null myeloid progenitors transduced with a retroviral vector expressing BCR-ABL. Loss of Gadd45b was observed to accelerate BCR-ABL driven CML development with shortened median mouse survival time. BCR-ABL Gadd45b deficient CML progenitors exhibited increased proliferation and decreas

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20

Zhang, Bin, Yin Wei Ho, Sung-UK Lee, Takahiro Maeda, Claudia Huettner, and Ravi Bhatia. "Characterization of Leukemia-Initiating Cells in a Transgenic Model of Chronic Phase Chronic Myelogenous Leukemia (CML)." Blood 114, no. 22 (2009): 858. http://dx.doi.org/10.1182/blood.v114.22.858.858.

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Abstract Abstract 858 In normal hematopoiesis, only a small population of lin-Sca-1+c-kit+ (LSK) cells with Flt3-CD150+48− immunophenotype has long-term hematopoietic stem cell (LT-HSC) capacity, whereas Flt3-CD150+CD48+ and Flt3-CD150-CD48+ LSK cells represent more differentiated multipotent progenitors (MPP1 and MPP2) without long-term engrafting capacity. Despite extensive investigation into BCR-ABL induced leukemogenesis, the impact of BCR-ABL expression on LSK subpopulations and the specific subpopulation with leukemia-initiating capacity remain unknown. Targeted expression of the BCR-ABL

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Hantschel, Oliver D., Florian Grebien, Ines Kaupe, et al. "The Bcr-Abl SH2-Kinase Domain Interface Is Critical for Leukemogenesis and An Additional Therapeutic Target in CML." Blood 114, no. 22 (2009): 37. http://dx.doi.org/10.1182/blood.v114.22.37.37.

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Abstract Abstract 37 We previously showed that the Abl SH2 domain is an allosteric activator of c-Abl tyrosine kinase activity and substrate phosphorylation (Filippakopoulos et al. (2008) Cell 134(5), 793-803). This effect is exerted directly by docking of the SH2 domain onto the N-lobe of the kinase domain in the active conformation of c-Abl. We also showed that the same structural mechanism is a critical factor for full activation of the oncogenic fusion kinase Bcr-Abl. Disruption of binding of the SH2 domain to the kinase domain in Bcr-Abl by the Ile164Glu mutation in the SH2 domain, led to

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Kennedy, Vanessa E., Cheryl A. C. Peretz, Andrew Koh, et al. "Multiomic Single-Cell Sequencing May Distinguish BCR-ABL-Mutated Acute Myeloid Leukemia (AML) from Blast Crisis Chronic Myelogenous Leukemia (BC-CML)." Blood 142, Supplement 1 (2023): 4334. http://dx.doi.org/10.1182/blood-2023-182454.

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Introduction The existence of BCR-ABL+ AML as an entity distinct from BC-CML is controversial. The WHO recently recognized BCR-ABL+ AML, but with the caveat that it is poorly characterized (Khoury, 2022). Clinically, BCR-ABL+ AML is associated with high risk of relapse (Neuendorff, 2018). Further, acquired BCR-ABL mutations have been identified as a cause of relapse on FLT3 inhibitors (McMahon, 2019). We hypothesize that BCR-ABL+ AML can be distinguished as a distinct biologic entity from BC-CML by the observation of BCR-ABL as a sub-clonal rather than a founder mutation in leukemogenesis. Met

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Moore, James C., Chi Ly, Halbur Luke, and S. Tiong Ong. "Enhanced Killing of Chronic Myelogenous Leukemia Cells by Rapamycin and Imatinib Is Associated with Differential Inhibition of 4E-BP1 and eIF4E Phosphorylation and Decreased Protein Expression by Non-Overlapping Mechanisms." Blood 104, no. 11 (2004): 1993. http://dx.doi.org/10.1182/blood.v104.11.1993.1993.

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Abstract The Bcr-abl tyrosine kinase is known to promote transformation by dysregulating gene transcription, but its role in dysregulating translation is less well documented. Our recent work has implicated the mammalian target of rapamycin (mTOR) signaling as a downstream target of Bcr-Abl, since we find that the mTOR effectors, 4E-BP1 and S6, are phosphorylated in a Bcr-Abl kinase-dependent manner (Ly et al., Cancer Research, 2003). Because mTOR is a central regulator of eukaryotic translation, and inhibitors of mTOR act synergistically with imatinib mesylate (imatinib) to kill CML cells, th

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Burgess, Gem S., Elizabeth A. Williamson, Larry D. Cripe, et al. "Regulation of the c-jun Gene in p210 BCR-ABL Transformed Cells Corresponds With Activity of JNK, the c-jun N-Terminal Kinase." Blood 92, no. 7 (1998): 2450–60. http://dx.doi.org/10.1182/blood.v92.7.2450.

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Abstract Activity of the c-jun N-terminal kinase (JNK) has been shown in hematopoietic cells transformed by p210 BCR-ABL. However, analysis has not been reported for hematopoietic cells on the consequences of this activity for c-jun promoter regulation within its distinctive proximal 8-base consensus CRE-like element, an element linked to JNK-mediated increase in c-jun transcription. In the present study, regulation of the proximal c-jun promoter was studied in murine myeloid cells transformed by p210 BCR-ABL. Promoter regulation in p210 BCR-ABL transformed cells was compared with regulation o

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Burgess, Gem S., Elizabeth A. Williamson, Larry D. Cripe, et al. "Regulation of the c-jun Gene in p210 BCR-ABL Transformed Cells Corresponds With Activity of JNK, the c-jun N-Terminal Kinase." Blood 92, no. 7 (1998): 2450–60. http://dx.doi.org/10.1182/blood.v92.7.2450.2450_2450_2460.

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Activity of the c-jun N-terminal kinase (JNK) has been shown in hematopoietic cells transformed by p210 BCR-ABL. However, analysis has not been reported for hematopoietic cells on the consequences of this activity for c-jun promoter regulation within its distinctive proximal 8-base consensus CRE-like element, an element linked to JNK-mediated increase in c-jun transcription. In the present study, regulation of the proximal c-jun promoter was studied in murine myeloid cells transformed by p210 BCR-ABL. Promoter regulation in p210 BCR-ABL transformed cells was compared with regulation of the pro

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Pear, Warren S., Juli P. Miller, Lanwei Xu, et al. "Efficient and Rapid Induction of a Chronic Myelogenous Leukemia-Like Myeloproliferative Disease in Mice Receiving P210 bcr/abl-Transduced Bone Marrow." Blood 92, no. 10 (1998): 3780–92. http://dx.doi.org/10.1182/blood.v92.10.3780.

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Abstract Expression of the 210-kD bcr/abl fusion oncoprotein can cause a chronic myelogenous leukemia (CML)-like disease in mice receiving bone marrow cells transduced by bcr/abl-encoding retroviruses. However, previous methods failed to yield this disease at a frequency sufficient enough to allow for its use in the study of CML pathogenesis. To overcome this limitation, we have developed an efficient and reproducible method for inducing a CML-like disease in mice receiving P210 bcr/abl-transduced bone marrow cells. All mice receiving P210 bcr/abl-transduced bone marrow cells succumb to a myel

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Pear, Warren S., Juli P. Miller, Lanwei Xu, et al. "Efficient and Rapid Induction of a Chronic Myelogenous Leukemia-Like Myeloproliferative Disease in Mice Receiving P210 bcr/abl-Transduced Bone Marrow." Blood 92, no. 10 (1998): 3780–92. http://dx.doi.org/10.1182/blood.v92.10.3780.422k15_3780_3792.

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Expression of the 210-kD bcr/abl fusion oncoprotein can cause a chronic myelogenous leukemia (CML)-like disease in mice receiving bone marrow cells transduced by bcr/abl-encoding retroviruses. However, previous methods failed to yield this disease at a frequency sufficient enough to allow for its use in the study of CML pathogenesis. To overcome this limitation, we have developed an efficient and reproducible method for inducing a CML-like disease in mice receiving P210 bcr/abl-transduced bone marrow cells. All mice receiving P210 bcr/abl-transduced bone marrow cells succumb to a myeloprolifer

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Li, Shaoguang, Robert L. Ilaria, Ryan P. Million, George Q. Daley, and Richard A. Van Etten. "The P190, P210, and P230 Forms of the BCR/ABL Oncogene Induce a Similar Chronic Myeloid Leukemia–like Syndrome in Mice but Have Different Lymphoid Leukemogenic Activity." Journal of Experimental Medicine 189, no. 9 (1999): 1399–412. http://dx.doi.org/10.1084/jem.189.9.1399.

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The product of the Philadelphia chromosome (Ph) translocation, the BCR/ABL oncogene, exists in three principal forms (P190, P210, and P230 BCR/ABL) that are found in distinct forms of Ph-positive leukemia, suggesting the three proteins have different leukemogenic activity. We have directly compared the tyrosine kinase activity, in vitro transformation properties, and in vivo leukemogenic activity of the P190, P210, and P230 forms of BCR/ABL. P230 exhibited lower intrinsic tyrosine kinase activity than P210 and P190. Although all three oncogenes transformed both myeloid (32D cl3) and lymphoid (

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Illert, Anna Lena, Cornelius Miething, Rebekka Grundler, et al. "Interferon Regulatory Factor 4 Is Not Required for Induction of Chronic Myeloid Leukaemia-Like Myeloproliferative Disease by Bcr/Abl in Mice." Blood 106, no. 11 (2005): 2866. http://dx.doi.org/10.1182/blood.v106.11.2866.2866.

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Abstract Interferon regulatory factors (IRF) are activating and/or repressing transcription factors induced by treatment with type I and II Interferon (IFN), other cytokines, receptor cross-linking and viral infection. In contrast to IRF-1 and IRF-2, which are widely expressed, IRF-4 and IRF-8 are tissue-restricted factors. IRF-8 is expressed mainly in cells of haematopoietic origin and has recently been shown to inhibit mitogenic activity of p210 Bcr/Abl-transformed myeloid progenitor cells by activating several genes that interfere with the c-Myc pathway. IRF-4 is most homologous with IRF-8

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le Coutre, Philipp, Elena Tassi, Marileila Varella-Garcia, et al. "Induction of resistance to the Abelson inhibitor STI571 in human leukemic cells through gene amplification." Blood 95, no. 5 (2000): 1758–66. http://dx.doi.org/10.1182/blood.v95.5.1758.005a41_1758_1766.

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The 2-phenylaminopyrimidine derivative STI571 has been shown to selectively inhibit the tyrosine kinase domain of the oncogenicbcr/abl fusion protein. The activity of this inhibitor has been demonstrated so far both in vitro with bcr/abl expressing cells derived from leukemic patients, and in vivo on nude mice inoculated with bcr/abl positive cells. Yet, no information is available on whether leukemic cells can develop resistance to bcr/ablinhibition. The human bcr/abl expressing cell line LAMA84 was cultured with increasing concentrations of STI571. After approximately 6 months of culture, a

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Demirel, Özlem, Olivier Balló, Hubert Serve, and Christian H. Brandts. "The Role Of SOCS1 In BCR-ABL Mediated Transformation and Leukemogenesis." Blood 122, no. 21 (2013): 2507. http://dx.doi.org/10.1182/blood.v122.21.2507.2507.

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Abstract The BCR-ABL oncogene activates several signaling pathways, most notably by constitutive phosphorylation of the signal transducer and activator of transcription protein 5 (STAT5). After phosphorylation and nuclear translocation, STAT5 transcriptionally activates numerous genes responsible for proliferation, survival and differentiation of hematopoietic stem and progenitor cells. Among the STAT5 target genes are suppressor of cytokine signaling (SOCS) proteins. SOCS proteins inhibit JAK kinases by multiple mechanisms, thereby terminating cytokine signaling in a classical negative feedba

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Krause, Daniela S., Ulrich H. von Andrian, and Richard A. Van Etten. "Selectins and Their Ligands Are Required for Homing and Engraftment of BCR-ABL+ Leukemia-Initiating Cells." Blood 106, no. 11 (2005): 697. http://dx.doi.org/10.1182/blood.v106.11.697.697.

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Abstract Autologous hematopoietic stem cell (HSC) transplantation is a feasible form of treatment for many types of leukemias and lymphomas, including chronic myeloid leukemia (CML). Malignant cells contaminating the graft, however, can engraft and lead to relapse of the original disease. Previous studies have demonstrated that BCR-ABL+ leukemic progenitors have defects in the adhesive function of beta-1 integrins and in their response to the chemokine SDF-1alpha, pathways that are critical for homing and engraftment of normal HSC. We hypothesized that BCR-ABL-expressing leukemic stem cells di

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Zhao, Xingwang, Hengyi Xie, Meng Zhao, et al. "Fc receptor–like 1 intrinsically recruits c-Abl to enhance B cell activation and function." Science Advances 5, no. 7 (2019): eaaw0315. http://dx.doi.org/10.1126/sciadv.aaw0315.

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B cell activation is regulated by the stimulatory or inhibitory co-receptors of B cell receptors (BCRs). Here, we investigated the signaling mechanism of Fc receptor-like 1 (FcRL1), a newly identified BCR co-receptor. FcRL1 was passively recruited into B cell immunological synapses upon BCR engagement in the absence of FcRL1 cross-linking, suggesting that FcRL1 may intrinsically regulate B cell activation and function. BCR cross-linking alone led to the phosphorylation of the intracellular Y281ENV motif of FcRL1 to provide a docking site for c-Abl, an SH2 domain-containing kinase. The FcRL1 an

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Mian, Afsar, Anahita Rafiei, Claudia Oancea, Oliver G. Ottmann, and Martin Ruthardt. "The Functional Interplay Between the t(9;22)-Associated Fusion Proteins BCR/ABL and ABL/BCR in Philadelphia Chromosome Positive Acute Lymphatic Leukemia." Blood 124, no. 21 (2014): 2402. http://dx.doi.org/10.1182/blood.v124.21.2402.2402.

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Abstract The successful targeting of BCR/ABL by selective ABL-kinase inhibitors (AKI) such as Imatinib, Nilotinib, or Dasatinib alone is unable to eradicate the leukemic clone in Philadelphia chromosome positive (Ph+ ) leukemia. The t(9;22)(q34;q11) is a balanced translocation. Der22 involves the BCR (breakpoint cluster region) gene locus with two principal breaks: the M-bcr, encoding for the p210BCR/ABL and the m-bcr, encoding for the 185BCR/ABL fusion proteins, respectively. The constitutively activated BCR/ABL kinase is responsible for the leukemic transformation through an aberrant activat

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35

Sha, Xiaojin, Dan A. Liebermann, and Barbara Hoffman. "Loss of Growth Arrest DNA Damage 45a,b (GADD45a,b) Enhances Oncogenicity in BCR/ABL-Driven Chronic Myelogenous Leukemia." Blood 114, no. 22 (2009): 3264. http://dx.doi.org/10.1182/blood.v114.22.3264.3264.

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Abstract 3264 Poster Board III-1 The bcr/abl oncogene causes chronic myelogenous leukemia (CML) in human. BCR/ABL induces the transformation of myeloid lineage through MAPK, JNK/SAPK, PI3K signaling pathways. Growth arrest DNA damage 45A (GADD45A) and GADD45B are upregulated during myeloid lineage terminal differentiation. They are involved in G2/M cell cycle arrest and apoptosis in response to exogenous stress stimuli through MAPK and JNK/SAPK pathways. To investigate the effect of GADD45A and GADD45B in the development of CML, syngeneic wild type lethally irradiated mice were reconstituted w

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Eiring, Anna M., Paolo Neviani, Ramasamy Santhanam, et al. "Requirement of the E2F3 Transcription Factor for BCR/ABL Leukemogenesis." Blood 110, no. 11 (2007): 33. http://dx.doi.org/10.1182/blood.v110.11.33.33.

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Abstract Several RNA binding proteins (RBPs) have been implicated in the progression of chronic myelogenous leukemia (CML) from the indolent chronic phase to the aggressively fatal blast crisis. In the latter phase, expression and function of specific RBPs are altered at transcriptional or post-translational levels by the increased constitutive kinase activity of the BCR/ABL oncoprotein, resulting in enhanced resistance to apoptotic stimuli, growth advantage and differentiation arrest of CD34+ CML blast crisis (CML-BC) progenitors. In the current study, we identified by RIP (RNA immunoprecipit

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37

Slupianek, Artur, Stanislaw Jozwiakowski, Ewa Gurdek, Michal O. Nowicki, and Tomasz Skorski. "BCR/ABL Regulates the Expression and Interacts with Werner Syndrome Helicase/Exonuclease To Modulate Its Biochemical Properties." Blood 106, no. 11 (2005): 2873. http://dx.doi.org/10.1182/blood.v106.11.2873.2873.

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Abstract A genome-wide screen suggested that BCR/ABL kinase might stimulate WRN, a member of the RecQ-like DNA helicases family. The Werner syndrome protein (WRN) exerts DNA helicase and 3′-5′ exonuclease activities. Inactivating mutations in the WRN gene causes Werner syndrome, characterized by premature aging, genomic instability and cancer predisposition. The WRN helicase unwinds unusual DNA structures, which can occur physiologically, or can be accidentally generated during DNA repair (double-stranded DNA with mismatched tails, bimolecular G4 quartets and Holliday junctions). In addition,

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Yu, Chuanjiang, Sivahari Prasad Gorantla, Tony Mueller, et al. "Beclin-1 Phosphorylation By BCR-ABL Is Crucial for CML Leukemogenesis By Suppression of Autophagy." Blood 126, no. 23 (2015): 16. http://dx.doi.org/10.1182/blood.v126.23.16.16.

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Abstract The constitutively activated chimeric Tyrosine kinase BCR-ABL is critical for initiation, progression and maintenance of chronic myelogenous leukemia (CML). Imatinib and second generation BCR-ABL tyrosine kinase inhibitors (TKIs) serve now as standard therapies for Ph+-patients. However, disease persistence occurs frequently and insensitivity of CML stem cells to TKI treatment is discussed as one major reason for this. Recent evidence accumulates, that autophagy, a genetically-regulated process of adaptation to metabolic stress, is involved in TKI-induced cell death. It is hypothesize

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Cuiffo, Benjamin, and Ruibao Ren. "Dominant Negative Effect of Palmitoylation-Deficient NRAS In Suppression of BCR/ABL Leukemogenesis." Blood 116, no. 21 (2010): 3157. http://dx.doi.org/10.1182/blood.v116.21.3157.3157.

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Abstract Abstract 3157 RAS mutations are found in ∼30% of all human cancers, with NRAS being the RAS isoform found most frequently mutated in hematological malignancies including acute myelogenous leukemia (AML) and chronic myelomonocytic leukemia (CMML). We have previously shown that expression of oncogenic NRAS efficiently induces a CMML- or AML-like disease in mice. Like all RAS proteins, NRAS must undergo a series of post-translational modifications for differential targeting to distinct cellular membrane microdomains. We have previously found that palmitoylation, in addition to prenylatio

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Krause, Daniela S., Katherine Lazarides, Ulrich H. von Andrian, and Richard A. Van Etten. "CD44 Is Selectively Required for the Homing and Engraftment of BCR-ABL-Expressing Leukemic Stem Cells." Blood 108, no. 11 (2006): 743. http://dx.doi.org/10.1182/blood.v108.11.743.743.

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Abstract In chronic myeloid leukemia (CML) patients treated by autologous hematopoietic stem cell (HSC) transplantation, malignant progenitors in the graft can contribute to relapse of leukemia (Deisseroth et al., Blood1994; 83:3068), but the mechanisms of homing and engraftment of leukemic CML stem cells are unknown. Although the frequency of autografting in CML has decreased following the introduction of imatinib, most imatinib-responsive patients harbor residual BCR-ABL-expressing stem cells (Graham et al., Blood2002; 99:319) and some will develop progressive leukemia. Autografting with cel

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Hsieh, Mo-Ying, та Richard A. Van Etten. "Distinct Roles for the NF-κB Pathway In Myeloid and Lymphoid Transformation and Leukemogenesis by BCR-ABL." Blood 116, № 21 (2010): 1225. http://dx.doi.org/10.1182/blood.v116.21.1225.1225.

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Abstract Abstract 1225 The BCR-ABL tyrosine kinase, product of the t(9;22) Ph chromosome, activates multiple signaling pathways in leukemic cells from patients with chronic myeloid leukemia (CML) and Ph+ B-cell acute lymphoblastic leukemia (B-ALL). Previous studies have shown that NF-κB is activated in BCR-ABL-expressing cell lines and contributes to transformation of primary B-lymphoid cells by BCR-ABL (Reuther et al., Genes Dev. 1998;12:968), but the mechanism of activation has not been defined (Kirchner et al., Exp. Hematol. 2003;31:504), and importance of NF-kB to myeloid and lymphoid leuk

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Sanchez-Aguilera, Abel, Ami tava Sengupta, Joseph P. Mastin, Kyung H. Chang, David A. Williams, and Jose A. Cancelas. "Rac2 GTPase Activation Is Necessary for Development of p190-BCR-ABL-Induced B-Cell Acute Lymphoblastic Leukemia." Blood 112, no. 11 (2008): 3790. http://dx.doi.org/10.1182/blood.v112.11.3790.3790.

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Abstract The fusion gene BCR-ABL, resulting from t(9;22) reciprocal chromosomal translocations, encodes a constitutively active tyrosine kinase. Two different isoforms of BCR-ABL, p190 and p210, are associated to two completely different diseases. In the tyrosine kinase inhibitor (TKI) era, while p210-BCR-ABL-induced CML is highly responsive to TKI, p190-BCR-ABL still induces a poor prognosis B-cell acute lymphoblastic leukemia (B-ALL). The only difference between these two forms of BCR-ABL is the existence of a DH/Cdc24/PH domain in p210-BCR-ABL, which acts as a guanine nucleotide exchange fa

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43

Nardi, Valentina, Olaia Naveiras, Mohammad Azam, and George Q. Daley. "A Critical Role for CCL Chemokines in the Immuno-Protection Induced by Type I Interferons and IRF8/ICSBP Against Bcr/Abl-Induced Leukemia." Blood 110, no. 11 (2007): 1001. http://dx.doi.org/10.1182/blood.v110.11.1001.1001.

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Abstract Until recently, the mainstay of Chronic Myelogenous Leukemia (CML) therapy was Interferon (IFN) alpha, which in a minority of patients induces long lasting cytogenetic remission. While the exact mechanism of action of IFN alpha in CML is still obscure, it is clear that the clinical response to IFN alpha correlates with immune system reactivity against leukemic clones. As minimal molecular disease often persists despite the use of imatinib and new Bcr-Abl inhibitors, immunotherapy remains an appealing adjunct to molecularly targeted inhibitors in CML therapy. We have shown that IRF8/IC

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Yamamoto, Kiyoko, Shinobu Tsuzuki, Tomoki Naoe, and Masao Seto. "Deregulated Activity of AML1/RUNX1 Cooperates with BCR-ABL to Immortalize Hematopoietic Progenitor Cells and Induces Blast Crisis-Like Disease of Chronic Myelogenous Leukemia in Mice,." Blood 118, no. 21 (2011): 3749. http://dx.doi.org/10.1182/blood.v118.21.3749.3749.

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Abstract Abstract 3749 Since the introduction of imatinib treatment for chronic myeloid leukemia (CML), most patients in the chronic phase (CP) achieve long-lasting hematologic remission. However, some patients acquire resistance or intolerance to imatinib, which results in disease progression to blast crisis (BC). Although it is known that BCR-ABL induces genomic instability, which results in leukemia cells creating multiple gene defects, genes inducing the progression to BC in CML are largely unknown. Moreover, mutations in the AML1/RUNX1 gene and overrepresentation of AML1/RUNX1 in BC compa

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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.

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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

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Uchida, Naoya, Hideki Hanawa, Koiti Inokuchi, Kazuo Dan, and Takashi Shimada. "Leukemogenesis of the b2a2 Type p210 BCR/ABL in a Bone Marrow Transplantation Mouse Model Using a Lentivirus Vector." Blood 106, no. 11 (2005): 2875. http://dx.doi.org/10.1182/blood.v106.11.2875.2875.

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Abstract [INTRODUCTION] BCR/ABL induces the chronic phase of chronic myeloid leukemia (CML). The three main principal forms (p190, p210 and p230 BCR/ABL) of the BCR/ABL gene are found in distinct forms of leukemia and have shown to be different leukemogenic activities in mice. The BCR breakpoint locations of p210 BCR/ABL falls either between the exons b2 and b3 (b2a2) or between the exons b3 and b4 (b3a2). Though the leukemogenic activity of the b3a2 type gene had been shown in mice, the leukemogenesis of the b2a2 type has not been tested yet. [PURPOSE] The purpose of this study is to evaluate

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Peng, Cong, Julia Brain, Yiguo Hu, et al. "IPI-504, a Novel, Orally Active HSP90 Inhibitor, Prolongs Survival of Mice with BCR-ABL T315I CML and B-ALL." Blood 108, no. 11 (2006): 2183. http://dx.doi.org/10.1182/blood.v108.11.2183.2183.

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Abstract Development of mutations within the kinase domain is a major drug-resistance mechanism for tyrosine kinase inhibitors (TKIs) in cancer therapy. In CML (chronic myeloid leukemia), a disease driven by the constitutively active BCR-ABL oncoprotein, no available TKIs have been effective in treating patients with the BCR-ABL T315I mutation. Heat shock protein 90 (Hsp90) is a highly conserved, constitutively expressed molecular chaperone that facilitates folding of client proteins like BCR-ABL, and affects the stability of these proteins. Several labs have shown that Hsp90 inhibition in vit

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Gleixner, Karoline V., Harald Herrmann, Barbara Peter, et al. "The Multi-Kinase/ABL Inhibitor R763/AS703569 Induces DNA Endoreduplication and Apoptosis In Imatinib-Resistant CML Cells and Synergizes with Nilotinib, Dasatinib, and the Plk-1 Inhibitor BI 2536, In Producing Growth Inhibition." Blood 116, no. 21 (2010): 3394. http://dx.doi.org/10.1182/blood.v116.21.3394.3394.

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Abstract Abstract 3394 Resistance to imatinib is a major clinical problem and challenge in advanced chronic myeloid leukemia (CML). In most patients, drug-resistant mutants of BCR/ABL are detectable. Although most of these mutants still are responsive to second generation BCR/ABL kinase inhibitors (KI) such as nilotinib or dasatinib, drug responses are often short-lived. The BCR/ABL mutant T315I confers resistance against all available BCR/ABL KI, including nilotinib and dasatinib. More recent data suggest that several Aurora kinase (AuK) inhibitors block the kinase activity of BCR/ABL T315I.

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Gabert, Jean A., Christophe Picard, Sandrine Hayette, et al. "Prospective Multicentric Molecular Study for Poor Prognosis Fusion Transcripts at Diagnosis in Adult ALL Patients - The LALA94 Experience." Blood 106, no. 11 (2005): 4476. http://dx.doi.org/10.1182/blood.v106.11.4476.4476.

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Abstract From 1994 to 2000, 984 adults aged from 15 to 55 years with newly diagnosed Acute Lymphoblastic Leukemia (ALL) were eligible for randomization in the multicentric LALA-94 clinical protocol. The t(9;22), t(1;19) and t(4;11) translocations corresponding to BCR-ABL, E2A-PBX1 and MLL-AF4 fusion gene transcripts respectively, were considered as independent poor prognostic factors. Standardized RT-PCR analysis of these fusion gene transcripts were performed by 17 laboratories in order to provide data before the second randomization (J35) on 787 patients. In this multicentric study, validate

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Singh, Aditya, and Prateek Bhatia. "Effective Downregulation of BCR-ABL Tumorigenicity by RNA Targeted CRISPR-Cas13a." Current Gene Therapy 21, no. 3 (2021): 270–77. http://dx.doi.org/10.2174/1566523221666210217155233.

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Aim: To induce BCR-ABL gene silencing using CRISPR Cas13a. Background: CML is a clonal myeloproliferative disorder of pluripotent stem cells driven by a reciprocal translocation between chromosomes 9 and 22 forming a BCR-ABL fusion gene. Tyrosine- kinase inhibitor drugs like imatinib are the mainstay of treatment and cases resistant to these drugs have a poor prognosis in the absence of a compatible stem-cell donor. However with rapid advancements in gene-editing technologies most studies are now focusing on developing a translational model targeting single-gene disorders with a prospective pe

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