7 results match your criteria: "The University of Michigan Hospital and Health Systems[Affiliation]"

Protein electrophoresis and immunofixation are subject to a variety of analytical interferences that may affect monoclonal protein diagnostics performed in the context of monoclonal gammopathies. Interferences include endogenous substances, such as hemoglobin and fibrinogen, and exogenous compounds, such as radiocontrast dyes, antibiotics, and monoclonal antibody therapies. General approaches to managing interferences begin with recognition of the problem.

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Background: Progressive bone marrow fibrosis (BMF) is a cardinal feature of many myeloproliferative neoplasms (MPNs) and there is a documented association between the severity of BMF and overall prognosis. We conducted an exploratory analysis of sequential BMF data from two phase I studies of long-term treatment with the Janus kinase 2 (JAK2) inhibitor fedratinib in patients with myelofibrosis.

Methods: Bone marrow samples were obtained at baseline and after every six cycles (24 weeks) of daily fedratinib treatment.

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In this phase 2 open-label randomized study, 31 patients with intermediate-2 or high-risk myelofibrosis received fedratinib 300, 400 or 500 mg once daily in consecutive 4-week cycles. Mean spleen volume reductions at 12 weeks (primary end point) were 30.3% (300 mg), 33.

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The clinical phenotype of SDHC-associated hereditary paraganglioma syndrome (PGL3).

J Clin Endocrinol Metab

August 2014

Department of Internal Medicine, Divisions of Metabolism Endocrinology and Diabetes (T.E., R.J.A.), Molecular Medicine and Genetics (J.N.E., V.M.R.), and Gastroenterology (E.M.S.), Department of Human Genetics (M.L.M.), and Department of Otolaryngology-Head and Neck Surgery (H.A.A.) at the University of Michigan Hospital and Health Systems, Ann Arbor, Michigan 48109; and Norris Cancer Center (S.B.G.), University of Southern California, Los Angeles, California 90033.

Context: Mutations in the genes encoding subunits of the succinate dehydrogenase complex cause hereditary paraganglioma syndromes. Although the phenotypes associated with the more commonly mutated genes, SDHB and SDHD, are well described, less is known about SDHC-associated paragangliomas.

Objective: To describe functionality, penetrance, number of primary tumors, biological behavior, and location of paragangliomas associated with SDHC mutations.

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