Neutral glycolipids in leukemic and nonleukemic leukocytes by J. HILDEBRAND, P. STRYCKMANS, P. STOFFYN

“…Group I consisted of leukocytes from nonleukemic patients; group II, from patients with chronic myelogenous leukemia; group III, from patients with chronic lymphocytic leukemia; and group IV, from patients with acute leukemia.Two neutral glycolipids were found in nonleukemic mixed leukocyte populations. …”
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Single-Cell Transcriptomics Reveals the Expression of Aging- and Senescence-Associated Genes in Distinct Cancer Cell Populations by Dominik Saul, Robyn Laura Kosinsky

“…In this study, we aimed to analyze aging-associated transcriptional patterns in publicly available bulk mRNA-seq and single-cell RNA-seq (scRNA-seq) datasets for chronic myelogenous leukemia (CML), colorectal cancer (CRC), hepatocellular carcinoma (HCC), lung cancer (LC), and pancreatic ductal adenocarcinoma (PDAC). …”
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Nonreceptor Tyrosine Kinases in Prostate by Cancer Yu-Ming Chang, Hsing-Jien Kung, Christopher P. Evans

“…Underscoring NRTK's and, specifically, Src's importance in cancer is the recent approval by the US Food and Drug Administration of dasatinib, the first commercial Src inhibitor for clinical use in chronic myelogenous leukemia (CML). In this review we will focus on NRTKs and their roles in the biology of CaP. …”
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Spred2 modulates the erythroid differentiation induced by imatinib in chronic myeloid leukemia cells. by Yuefeng Yang, Xiaoyun Liu, Fengjun Xiao, Shuya Xue, Qinqin Xu, Yue Yin, Huiyan Sun, Jie Xu, Hengxiang Wang, Qunwei Zhang, Hua Wang, Lisheng Wang

“…Differentiation induction is currently considered as an alternative strategy for treating chronic myelogenous leukemia (CML). Our previous work has demonstrated that Sprouty-related EVH1 domainprotein2 (Spred2) was involved in imatinib mediated cytotoxicity in CML cells. …”
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A multiple reaction monitoring (MRM) method to detect Bcr-Abl kinase activity in CML using a peptide biosensor. by Tzu-Yi Yang, Christie L Eissler, Mark C Hall, Laurie L Parker

“…The protein kinase Bcr-Abl plays a major role in the pathogenesis of chronic myelogenous leukemia (CML), and is the target of the breakthrough drug imatinib (Gleevec™). …”
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Knocking down low molecular weight protein tyrosine phosphatase (LMW-PTP) reverts chemoresistance through inactivation of Src and Bcr-Abl proteins. by Paula A Ferreira, Roberta R Ruela-de-Sousa, Karla C S Queiroz, Ana Carolina S Souza, Renato Milani, Ronaldo Aloise Pilli, Maikel P Peppelenbosch, Jeroen den Hertog, Carmen V Ferreira

“…The development of multidrug resistance (MDR) limits the efficacy of continuous chemotherapeutic treatment in chronic myelogenous leukemia (CML). Low molecular weight protein tyrosine phosphatase (LMW-PTP) is up-regulated in several cancers and has been associated to poor prognosis. …”
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Early Growth Response Factor 1 in Aging Hematopoietic Stem Cells and Leukemia by Rohan Kulkarni

“…However, dysregulation of Egr1 is associated with hematological malignancies such as acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), and chronic myelogenous leukemia (CML). Here, we summarize the current understanding of the role of EGR1 in the regulation of HSC functionality and the manifestation of leukemia. …”
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Lactic Acid Bacteria from Kefir Increase Cytotoxicity of Natural Killer Cells to Tumor Cells by Takuya Yamane, Tatsuji Sakamoto, Takenori Nakagaki, Yoshihisa Nakano

“…In this study, we found that a mixture of the six lactic acid bacteria from kefir increased the cytotoxicity of human natural killer KHYG-1 cells to human chronic myelogenous leukemia K562 cells and colorectal tumor HCT116 cells. …”
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Early recognition of intraventricular hemorrhage in the setting of thrombocytosis in the emergency department by Charles M, Fontoura R, Sugalski G

“…Studies have shown that when hemorrhage is present in patients with thrombocytosis, it is most often seen in the setting of chronic myelogenous leukemia and essential thrombocythemia. In essential thrombocythemia, the overall risk of bleeding and thrombosis is 0.33% per patient-year and 6.6% per patient-year, respectively. …”
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Induction of Neuronal Morphology in the 661W Cone Photoreceptor Cell Line with Staurosporine. by Alex F Thompson, Megan E Crowe, Christopher J Lieven, Leonard A Levin

“…METHODS:661W and RGC-5 cells, non-neuronal retinal astrocytes, retinal endothelial cells, retinal pericytes, M21 melanoma cells, K562 chronic myelogenous leukemia cells, and Daudi Burkitt lymphoma cells, were differentiated with staurosporine. …”
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Changing the subcellular location of the oncoprotein Bcr-Abl using rationally designed capture motifs. by Dixon, A, Constance, J, Tanaka, T, Rabbitts, T, Lim, C

“… PURPOSE: Bcr-Abl, the causative agent of chronic myelogenous leukemia (CML), localizes in the cytoplasm where its oncogenic signaling leads to proliferation of cells. …”

Relationship of cytokines and cytokine signaling to immunodeficiency disorders in the mouse by Morawetz R.A., Giese N.A., Gabriele L., Rothman P., Horak I., Ozato K., Morse III H.C.

“…Unexpectedly, however, the ICSBP-/- mice also develop a syndrome with many similarities to chronic myelogenous leukemia in humans. The chronic phase of this disease is followed by a fatal blast crisis characterized by clonal expansions of undifferentiated cells. …”
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Emodin reverses leukemia multidrug resistance by competitive inhibition and downregulation of P-glycoprotein. by Hongping Min, Miaomiao Niu, Weilin Zhang, Jia Yan, Jiachang Li, Xiying Tan, Bo Li, Mengxiang Su, Bin Di, Fang Yan

“…Development of multidrug resistance (MDR) is a continuous clinical challenge partially due to the overexpression of P-glycoprotein (P-gp) for chronic myelogenous leukemia (CML) patients. Herein, we evaluated the inhibitory potency of emodin, a natural anthraquinone derivative isolated from Rheum palmatum L, on P-gp in P-gp positive K562/ADM cells. …”
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Identification of small molecules that disrupt signaling between ABL and its positive regulator RIN1. by Pamela Y Ting, Robert Damoiseaux, Björn Titz, Kenneth A Bradley, Thomas G Graeber, Virneliz Fernández-Vega, Thomas D Bannister, Peter Chase, Reji Nair, Louis Scampavia, Peter Hodder, Timothy P Spicer, John Colicelli

“…Constitutively active BCR-ABL kinase fusions are causative mutations in the pathogenesis of hematopoietic neoplasias including chronic myelogenous leukemia (CML). Although these fusions have been successfully targeted with kinase inhibitors, drug-resistance and relapse continue to limit long-term survival, highlighting the need for continued innovative drug discovery. …”
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Tuberculous and Non-Tuberculous Granulomatous Lymphadenitis in Patients Receiving ImatinibMesylate (Glivec) for Metastatic Gastrointestinal Stromal Tumor by Abbas Agaimy, Valeska Brueckl, Daniela Schmidt, Stephanie Krieg, Evelyn Ullrich, Norbert Meidenbauer

“…Background: Imatinib mesylate (IM) is the standard treatment for BCR-ABL-positive chronic myelogenous leukemia (CML) and is the first-line adjuvant and palliative treatment for metastatic and inoperable gastrointestinal stromal tumor (GIST). …”
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The teratogenic effects of imatinib mesylate on rat fetuses by M.M. El Gendy, A.M. Kandil, M.A. Helal, F.M. Zahou

“…Imatinib mesylate, a selective tyrosine kinase inhibitor, is the first line treatment against chronic myelogenous leukemia and gastrointestinal stromal tumors. …”
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Genetic mechanism of human neutrophil antigen 2 deficiency and expression variations. by Yunfang Li, David C Mair, Randy M Schuller, Ling Li, Jianming Wu

“…In addition, the percentages of HNA-2 positive neutrophils vary significantly among individuals and HNA-2 expression variations play a role in human diseases such as myelodysplastic syndrome, chronic myelogenous leukemia, and gastric cancer. The underlying genetic mechanism of HNA-2 deficiency and expression variations has remained a mystery. …”
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Past, present, and future of Bcr-Abl inhibitors: from chemical development to clinical efficacy by Federico Rossari, Filippo Minutolo, Enrico Orciuolo

“…Although the specific targeting of that oncoprotein, several Bcr-Abl-dependent and Bcr-Abl-independent mechanisms of resistance to imatinib arose after becoming first-line therapy in chronic myelogenous leukemia (CML) treatment. Consequently, new specific drugs, namely dasatinib, nilotinib, bosutinib, and ponatinib, were rationally designed and approved for clinic to override resistances. …”
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Signaling Pathways in Cancer: Therapeutic Targets, Combinatorial Treatments, and New Developments by Hon Yan Kelvin Yip, Antonella Papa

“…Small molecule inhibitors and monoclonal antibodies directed at relevant cancer-related proteins have been instrumental in delivering successful treatments of some blood malignancies (e.g., imatinib with chronic myelogenous leukemia (CML)) and solid tumors (e.g., tamoxifen with ER positive breast cancer and trastuzumab for HER2-positive breast cancer). …”
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Quantitative structure–activity relationship modeling for predication of inhibition potencies of imatinib derivatives using SMILES attributes by Hamideh Hamzehali, Shahram Lotfi, Shahin Ahmadi, Parvin Kumar

“…Abstract Chronic myelogenous leukemia (CML) which is resulted from the BCR-ABL tyrosine kinase (TK) chimeric oncoprotein, is a malignant clonal disorder of hematopoietic stem cells. …”
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