Timothy P. Hughes

ORCID: 0000-0002-0910-3730
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About
Contact & Profiles
Research Areas
  • Chronic Myeloid Leukemia Treatments
  • Chronic Lymphocytic Leukemia Research
  • Eosinophilic Disorders and Syndromes
  • Acute Lymphoblastic Leukemia research
  • Acute Myeloid Leukemia Research
  • Lymphoma Diagnosis and Treatment
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Click Chemistry and Applications
  • HER2/EGFR in Cancer Research
  • Lung Cancer Treatments and Mutations
  • Hematopoietic Stem Cell Transplantation
  • Fungal Plant Pathogen Control
  • Immune Cell Function and Interaction
  • Quinazolinone synthesis and applications
  • Mast cells and histamine
  • Gastrointestinal Tumor Research and Treatment
  • CAR-T cell therapy research
  • Monoclonal and Polyclonal Antibodies Research
  • T-cell and B-cell Immunology
  • HIV/AIDS drug development and treatment
  • Bone health and treatments
  • Protein Tyrosine Phosphatases
  • PI3K/AKT/mTOR signaling in cancer
  • RNA Research and Splicing
  • Immune cells in cancer

South Australian Health and Medical Research Institute
2016-2025

South Australia Pathology
2015-2024

The University of Adelaide
2015-2024

Royal Adelaide Hospital
2015-2024

Charité - Universitätsmedizin Berlin
2006-2024

Institute of Hematology & Blood Diseases Hospital
2024

Cancer Research Institute
2024

Chinese Academy of Medical Sciences & Peking Union Medical College
2024

Jena University Hospital
2011-2024

Australasian Leukaemia and Lymphoma Group
2014-2024

Imatinib, a selective inhibitor of the BCR-ABL tyrosine kinase, produces high response rates in patients with chronic-phase chronic myeloid leukemia (CML) who have had no to interferon alfa. We compared efficacy imatinib that alfa combined low-dose cytarabine newly diagnosed CML.

10.1056/nejmoa022457 article EN New England Journal of Medicine 2003-03-13

The cause of chronic myeloid leukemia (CML) is a constitutively active BCR-ABL tyrosine kinase. Imatinib inhibits this kinase, and in short-term study was superior to interferon alfa plus cytarabine for newly diagnosed CML the phase. For 5 years, we followed patients with who received imatinib as initial therapy.We randomly assigned 553 receive then evaluated them overall event-free survival; progression accelerated-phase or blast crisis; hematologic, cytogenetic, molecular responses;...

10.1056/nejmoa062867 article EN New England Journal of Medicine 2006-12-06

Nilotinib has been shown to be a more potent inhibitor of BCR-ABL than imatinib. We evaluated the efficacy and safety nilotinib, as compared with imatinib, in patients newly diagnosed Philadelphia chromosome-positive chronic myeloid leukemia (CML) phase.In this phase 3, randomized, open-label, multicenter study, we assigned 846 chronic-phase CML 1:1:1 ratio receive nilotinib (at dose either 300 mg or 400 twice daily) imatinib once daily). The primary end point was rate major molecular...

10.1056/nejmoa0912614 article EN New England Journal of Medicine 2010-06-06

Philadelphia chromosome–like acute lymphoblastic leukemia (Ph-like ALL) is characterized by a gene-expression profile similar to that of BCR–ABL1–positive ALL, alterations lymphoid transcription factor genes, and poor outcome. The frequency spectrum genetic in Ph-like ALL its responsiveness tyrosine kinase inhibition are undefined, especially adolescents adults.

10.1056/nejmoa1403088 article EN New England Journal of Medicine 2014-09-11

In a randomized trial, 1106 patients with chronic myeloid leukemia (CML) in phase were assigned to imatinib or interferon alfa plus cytarabine as initial therapy. We measured levels of BCR-ABL transcripts the blood all this trial who had complete cytogenetic remission.Levels by quantitative real-time polymerase-chain-reaction assay. Results expressed relative median level 30 untreated CML phase.In remission, after 12 months treatment fallen at least 3 log 57 percent those group and 24 given...

10.1056/nejmoa030513 article EN New England Journal of Medicine 2003-10-08

Imatinib, a selective BCR-ABL1 kinase inhibitor, improved the prognosis for patients with chronic myeloid leukemia (CML). We conducted efficacy and safety analyses on basis of more than 10 years follow-up in CML who were treated imatinib as initial therapy.In this open-label, multicenter trial crossover design, we randomly assigned newly diagnosed phase to receive either or interferon alfa plus cytarabine. Long-term included overall survival, response treatment, serious adverse events.The...

10.1056/nejmoa1609324 article EN New England Journal of Medicine 2017-03-08

Ponatinib is a potent oral tyrosine kinase inhibitor of unmutated and mutated BCR-ABL, including BCR-ABL with the inhibitor–refractory threonine-to-isoleucine mutation at position 315 (T315I). We conducted phase 2 trial ponatinib in patients chronic myeloid leukemia (CML) or Philadelphia chromosome–positive acute lymphoblastic (Ph-positive ALL).

10.1056/nejmoa1306494 article EN New England Journal of Medicine 2013-11-01

In the phase 3 Evaluating Nilotinib Efficacy and Safety in Clinical Trials-Newly Diagnosed Patients (ENESTnd) study, nilotinib resulted earlier higher response rates a lower risk of progression to accelerated phase/blast crisis (AP/BC) than imatinib patients with newly diagnosed chronic myeloid leukemia (CML-CP). Here, patients' long-term outcomes ENESTnd are evaluated after minimum follow-up 5 years. By years, more half all each arm (300 mg twice daily, 54%; 400 52%) achieved molecular 4.5...

10.1038/leu.2016.5 article EN cc-by-nc-nd Leukemia 2016-02-03

Dasatinib is a BCR-ABL inhibitor, 325-fold more potent than imatinib against unmutated in vitro. Phase II studies have demonstrated efficacy and safety with dasatinib 70 mg twice daily chronic-phase (CP) chronic myelogenous leukemia (CML) after treatment failure. In phase I, responses occurred once-daily administration despite only intermittent inhibition. Once-daily resulted less toxicity, suggesting that toxicity results from continuous inhibition of unintended targets. Here, dose-...

10.1200/jco.2007.14.9260 article EN Journal of Clinical Oncology 2008-06-10
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