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Hyperphosphatemia during spontaneous tumor lysis syndrome culminate in severe hyphosphatemia at the time of blast crisis of Ph<sup>neg</sup> CML to acute myelomoncytic leukemia

By Salomon Ophira, Holtzman Eli J, Beckerman Pazit, Avivi Camila, Trakhtenbrot Luba, Kneller Abraham, Tohami Tali, Kleinbaum Yeroham, Apter Sara, Amariglio Ninette, Grossman Ehud and Schiby Ginette

Abstract

<p>Abstract</p> <p>Extreme swing of phosphor from severe hyperphosphatemia to severe hypophosphatemia in a patient with blast crisis of myeloid origin was the result of imbalance between massive apoptosis of leukemic cells in the context of spontaneous tumor lysis syndrome and massive production of leukemic cells with only 1% of blast in peripheral blood. The mutated p53 protein suggested acting as oncogene in the presented case and possibly affecting phosphor status.</p

Topics: Acute leukemia, Tumor lysis syndrome, Apoptosis, Hypophosphatemia, Hyperphosphatemia, Diseases of the blood and blood-forming organs, RC633-647.5, Specialties of internal medicine, RC581-951, Internal medicine, RC31-1245, Medicine, R, DOAJ:Internal medicine, DOAJ:Medicine (General), DOAJ:Health Sciences, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, DOAJ:Oncology
Publisher: BioMed Central
Year: 2012
DOI identifier: 10.1186/2162-3619-1-24
OAI identifier: oai:doaj.org/article:37e10596fc7d4a498ae0b04ff7ab1b64
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