Sonya I. Haslam

University of Aberdeen

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Stuart H. Ralston

MRC Institute of Genetics and Molecular Medicine

Wim Van Hul

University of Antwerp

Neva E. Haites

University of Aberdeen

Kiyoshi Nakatsuka

Osaka City University

J. L. San-Millan

Instituto Cajal

Paul Chrisp

Optum (United States)

P J Willems

Erasmus University Rotterdam

Wendy Balemans

Janssen (Belgium)

Antonio Morales‐Piga

Instituto de Salud Carlos III

Cooperative Institutions

University of Antwerp

Antwerp University Hospital

Leiden University Medical Center

Academic Center for Dentistry Amsterdam

National Medical Research Center of Dentistry and Maxillofacial Surgery

Instituto Cajal

Aalborg University

Charité - Universitätsmedizin Berlin

University Hospital Ulm

Universität Ulm

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The genetics of Pagetʼs disease of bone

Current Opinion in Orthopedics (1998)

Sonya I. Haslam Stuart H. Ralston

Log in or Register Get new issue alertsGet alerts Enter your Email address: Wolters Kluwer Health may email you for journal alerts and information, but is committed to maintaining your privacy and will not share your personal information without your express consent. For more information, please refer to our Privacy Policy. Subscribe to eTOC Secondary Logo Journal Logo All Articles Images Videos Podcasts Blogs Advanced Search Toggle navigation Register Login HomeCurrent IssuePrevious Issues Current Orthopaedic PracticeCurrent Opinion in Orthopaedics (1999-2007)Clinical Orthopaedics and Related Research (1976-2007) Published Ahead-of-PrintCOP eNewsMy CollectionsJournal Info About the JournalEditorial BoardInformation for AuthorsAdvertisingOpen AccessSubscription ServicesReprintsRights and Permissions All Articles Images Videos Podcasts Blogs Advanced Search

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10.1097/00001433-199810000-00004

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Citations (3)

Dasatinib: the emerging evidence of its potential in the treatment of chronic myeloid leukemia

Core evidence (2005)

Sonya I. Haslam

Dasatinib: the emerging evidence of its potential in the treatment of chronic myeloid leukemia Sonya HaslamCore Medical Publishing, Mere House, Brook Street, Knutsford, Cheshire WA16 8GP, UKIntroduction: Current therapy options for chronic myeloid leukemia (CML) include conventional chemotherapy, allogeneic stem cell transplant, interferon-alfa, and imatinib mesylate, which has recently achieved gold standard status. Although the majority of patients initially respond well to treatment with imatinib, wider clinical experience with this drug has resulted in the development of imatinib resistance being increasingly documented. There is therefore an unmet medical need for novel therapies to override imatinib resistance in CML.Aims: This review summarizes the emerging evidence for the potential use of dasatinib in the treatment of imatinib-resistant CML. Disease and treatment: Dasatinib is a novel small molecule that has shown potent antileukemic activity in imatinib-resistant cell lines, malignant marrow cells isolated from patients with imatinib-resistant CML, and in mouse xenograft models of imatinib-resistant CML. Preliminary data from an initial phase I dose escalation trial have been encouraging, indicating that dasatinib is generally well tolerated and produces hematologic and cytogenetic responses in patients with imatinib-resistant CML in all phases of the disease. The maximum tolerated dose (MTD) has not yet been reached, and dose escalation continues to determine the dose range that yields optimal results.Profile: Although dasatinib is still in the early stages of development, the potential impact of this molecule on the treatment of CML could be revolutionary, not only providing a much needed treatment option for patients with imatinib-resistant CML, but also, combined with imatinib, could possibly prove useful in delaying the onset of resistance to treatment. Furthermore, combined with other agents active in CML, dasatinib could have potential utility in purging residual leukemic cells in patients whose disease is controlled by imatinib.Key words: dasatinib, BMS-354825, BCR-ABL, SRC-ABL kinase inhibitor, chronic myeloid leukemia (CML), imatinib resistance, treatment,evidence, outcomes

Imatinib Mesylate

Chronic myelogenous leukemia

10.2147/ce.s6402

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Bevacizumab: the evidence for its clinical potential in the treatment of nonsmall cell lung cancer

Core evidence (2007)

Sonya I. Haslam Paul Chrisp

Lung cancer is the leading cause of cancer-related mortality. Platinum-based chemotherapy is the usual first-line treatment for advanced nonsmall cell lung cancer (NSCLC), although an efficacy plateau has been reached with this approach. Bevacizumab is a recombinant, humanized, monoclonal antibody to vascular endothelial growth factor, which inhibits tumor angiogenesis and is being evaluated as a different mechanism to improve outcomes in patients with stage IIIB/stage IV (metastatic) NSCLC.

Carboplatin

10.2147/ce.s7418

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Paget's Disease of Bone: Evidence for a Susceptibility Locus on Chromosome 18q and for Genetic Heterogeneity

Journal of Bone and Mineral Research (1998)

Sonya I. Haslam Wim Van Hul Antonio Morales‐Piga Wendy Balemans J. L. San-Millan

Abstract Paget's disease of bone is a common condition characterized by bone pain, deformity, pathological fracture, and an increased incidence of osteosarcoma. Genetic factors play a role in the pathogenesis of Paget's disease but the molecular basis of the disease remains unclear. Previous genetic linkage studies have mapped the rare Paget's disease-like bone dysplasia familial expansile osteolysis (FEO) to chromosome 18q21–22, and recent work has shown evidence of linkage between this locus and Paget's disease in one family. Here we studied the relationship between the 18q21–22 locus and Paget's disease in eight large multiplex families from diverse ethnic backgrounds with inherited Paget's disease. Paget's disease was inherited as an autosomal dominant trait in all families, with high penetrance by the sixth decade. Analysis of seven highly polymorphic markers from chromosome 18q21–22 showed positive summated two-point log10 odds ratio (lodscores) of +2.97 with the marker D18S42 at a recombination fraction (θ) = 0.05, and of +2.95 with the marker D18S60 at θ = 0.00, values which are close to the cut-off of +3.0, which is generally accepted as evidence of linkage. Segregation analysis of the haplotypes and formal statistical analysis using the HOMOG program provided evidence for genetic heterogeneity, however, with evidence for linkage in five families and against linkage in the remaining three families (chi square 8.82; df = 2; p < 0.025). Multipoint linkage analysis in the five linked families showed lodscores of above +3.5 across the whole susceptibility region and a maximum summated lodscore of 3.89 at the marker D18S465. In the three nonlinked families, negative multipoint results were obtained for the whole region, with lodscores below –2.0 in one family, excluding this as a candidate locus for the disease. Our studies demonstrate the importance of hereditary factors in the pathogenesis of Paget's disease and confirm evidence of linkage between Paget's disease and chromosome 18q21–22 in some families. This raises the possibility that Paget's disease and FEO may share a common molecular basis, perhaps due to different mutations in the same gene or family of genes. Data from three families did not support evidence of linkage to 18q21–22 however, indicating that Paget's disease is genetically heterogeneous and suggests the presence of at least one additional locus which remains to be discovered.

10.1359/jbmr.1998.13.6.911

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Citations (141)