7 results match your criteria: "The University of Michigan Hospital and Health Systems[Affiliation]"
Clin Biochem
January 2018
Dept. of Pathology & Lab. Medicine, Division of Biochemistry, University of Ottawa, Canada.
Clin Biochem
January 2018
Department of Hematology, Odense University Hospital, Odense, Denmark.
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.
View Article and Find Full Text PDFJ Transl Med
September 2015
Department of Pathology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA, 02115, USA.
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.
Blood Cancer J
August 2015
Division of Hematology-Oncology, Department of Internal Medicine, Comprehensive Cancer Center, The University of Michigan Hospital and Health Systems, Ann Arbor, MI, USA.
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.
View Article and Find Full Text PDFJAMA Pediatr
May 2015
Department of Anesthesiology, The University of Michigan Hospital and Health Systems, C. S. Mott Children's Hospital, Ann Arbor.
Obstet Gynecol
April 2014
Dr. Pearlman is from the Department of Obstetrics and Gynecology at the University of Michigan Hospital and Health Systems, Ann Arbor, Michigan; e-mail:
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.