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Tessa L. Holyoake
University of Glasgow
292Publications
52H-index
15.4kCitations
Publications 292
Newest
#1Pablo Baquero (Glas.: University of Glasgow)H-Index: 5
#2Amy Dawson (Glas.: University of Glasgow)H-Index: 1
Last.Michael C. Nicastri (UPenn: University of Pennsylvania)H-Index: 3
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In chronic myeloid leukemia (CML), tyrosine kinase inhibitor (TKI) treatment induces autophagy that promotes survival and TKI-resistance in leukemic stem cells (LSCs). In clinical studies hydroxychloroquine (HCQ), the only clinically approved autophagy inhibitor, does not consistently inhibit autophagy in cancer patients, so more potent autophagy inhibitors are needed. We generated a murine model of CML in which autophagic flux can be measured in bone marrow-located LSCs. In parallel, we use cel...
#1Francesca Pellicano (Glas.: University of Glasgow)H-Index: 15
#2Laura Park (Glas.: University of Glasgow)H-Index: 3
Last.Alan Hair (Glas.: University of Glasgow)H-Index: 5
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Chronic myeloid leukemia (CML) stem/progenitor cells (SPCs) express a transcriptional program characteristic of proliferation, yet can achieve and maintain quiescence. Understanding the mechanisms by which leukemic SPCs maintain quiescence will help to clarify how they persist during long-term targeted treatment. We have identified a novel BCR-ABL1 protein kinase–dependent pathway mediated by the upregulation of hsa-mir183 , the downregulation of its direct target early growth response 1 (EGR1),...
#1Bin Zhang (City of Hope National Medical Center)H-Index: 15
#2Le Xuan Truong Nguyen (City of Hope National Medical Center)H-Index: 2
Last.Yu Lin Su (City of Hope National Medical Center)H-Index: 1
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In chronic myelogenous leukemia, leukemia stem cell function requires a microRNA that is provided by bone marrow endothelial cells.
#1Hein Than (UofU: University of Utah)
#2Anthony D. Pomicter (UofU: University of Utah)H-Index: 8
Last.Thomas O'Hare (UofU: University of Utah)H-Index: 34
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Chronic myeloid leukemia (CML) is a hematopoietic stem cell malignancy driven by BCR-ABL1 tyrosine kinase and effectively managed with tyrosine kinase inhibitors (TKIs) such as imatinib. Reactivation of BCR-ABL1 through mutations in the kinase is a common mechanism of resistance, but fails to explain clinical resistance in a significant proportion of cases, a situation referred to as BCR-ABL1-independent resistance. Additionally, most patients require continuous TKI therapy to avoid recurrence o...
#1Marzia Vezzalini (University of Verona)H-Index: 10
#2Andrea Mafficini (University of Verona)H-Index: 19
Last.Cristina Tecchio (University of Verona)H-Index: 21
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Background Protein tyrosine phosphatase receptor gamma (PTPRG) is a ubiquitously expressed member of the protein tyrosine phosphatase family known to act as a tumor suppressor gene in many different neoplasms with mechanisms of inactivation including mutations and methylation of CpG islands in the promoter region. Although a critical role in human hematopoiesis and an oncosuppressor role in chronic myeloid leukemia (CML) have been reported, only one polyclonal antibody (named chPTPRG) has been d...
#1Lorna JacksonH-Index: 1
Last.Xu HuangH-Index: 35
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Oncogene addiction is the dependence seen in some types of cancer cells on the presence or activity of an oncogene. Chronic myeloid leukaemia (CML) is driven by the BCR-ABL1 oncogene. CML has become a paradigm for targeted therapies, as the disease is effectively managed in most patients by BCR-ABL1 inhibitors. Although the symptom-causing leukaemic progenitor cells depend on the kinase activity of BCR-ABL1 for survival, the more primitive leukaemia stem cells (LSCs) responsible for disease main...
#1Elodie M. KuntzH-Index: 3
#2Pablo BaqueroH-Index: 5
Last.Eyal GottliebH-Index: 54
view all 8 authors...
Treatment with tyrosine kinase inhibitors results in a survival benefit in patients with chronic myeloid leukemia (CML). However, relapse due to persistent leukemic stem cells (LSCs) requires additional selective targets for efficient eradication of the disease. Metabolomic analyses on patient-derived CML LSCs reveal that these have an increased dependency on oxidative metabolism that renders them sensitive to treatment with tigecycline, an FDA-approved inhibitor of mitochondrial translation. Th...
#1Isabel Ben Batalla (UHH: University of Hamburg)H-Index: 3
#2Robert ErdmannH-Index: 3
Last.Richard E. Clark (RLUH: Royal Liverpool University Hospital)H-Index: 49
view all 22 authors...
Purpose:BCR-ABL kinase inhibitors are employed successfully for chronic myeloid leukemia (CML) treatment. However, resistant disease and persistence of BCR-ABL1-independent leukemia stem and progenitor cells (LSPC) remain clinical challenges. The receptor tyrosine kinase Axl can mediate survival and therapy resistance of different cancer cells. We investigated the therapeutic potential of Axl inhibition in CML. Experimental Design:We used primary cells from CML patients and TKI-sensitive and -re...
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