Up-Regulation of the Vitamin D Pathway in Acute Myeloid Leukemia

A Novel Cause of Hypercalcemia

Joshua M. L. Casan, S. Ghoth, A. H. Wei, S. B. Ting, S. Morgan

Research output: Contribution to journalArticleOtherpeer-review

Abstract

We report the first documented occurrence of hypercalcemia due to excessive production of calcitriol in acute myeloid leukemia (AML). The patient presented with severe hypercalcemia and renal failure accompanying a new diagnosis of AML. This extremely rare AML complication proved refractory to conventional hypercalcemia treatments but responded promptly to chemotherapy. Subsequent PCR studies performed on the leukemia blasts for vitamin D-related genes revealed dramatic up-regulation compared to healthy CD34+ cells and other primary AML cells. Recent data highlight a role for vitamin D in hematopoietic cell proliferation. Accordingly, this case may highlight another aspect of molecular heterogeneity in AML.
Original languageEnglish
Article number1141
JournalAnnals of Hematology and Oncology
Volume4
Issue number3
Publication statusPublished - 2017

Cite this

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title = "Up-Regulation of the Vitamin D Pathway in Acute Myeloid Leukemia: A Novel Cause of Hypercalcemia",
abstract = "We report the first documented occurrence of hypercalcemia due to excessive production of calcitriol in acute myeloid leukemia (AML). The patient presented with severe hypercalcemia and renal failure accompanying a new diagnosis of AML. This extremely rare AML complication proved refractory to conventional hypercalcemia treatments but responded promptly to chemotherapy. Subsequent PCR studies performed on the leukemia blasts for vitamin D-related genes revealed dramatic up-regulation compared to healthy CD34+ cells and other primary AML cells. Recent data highlight a role for vitamin D in hematopoietic cell proliferation. Accordingly, this case may highlight another aspect of molecular heterogeneity in AML.",
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journal = "Annals of Hematology and Oncology",
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Up-Regulation of the Vitamin D Pathway in Acute Myeloid Leukemia : A Novel Cause of Hypercalcemia. / Casan, Joshua M. L.; Ghoth, S.; Wei, A. H.; Ting, S. B.; Morgan, S.

In: Annals of Hematology and Oncology, Vol. 4, No. 3, 1141, 2017.

Research output: Contribution to journalArticleOtherpeer-review

TY - JOUR

T1 - Up-Regulation of the Vitamin D Pathway in Acute Myeloid Leukemia

T2 - A Novel Cause of Hypercalcemia

AU - Casan, Joshua M. L.

AU - Ghoth, S.

AU - Wei, A. H.

AU - Ting, S. B.

AU - Morgan, S.

PY - 2017

Y1 - 2017

N2 - We report the first documented occurrence of hypercalcemia due to excessive production of calcitriol in acute myeloid leukemia (AML). The patient presented with severe hypercalcemia and renal failure accompanying a new diagnosis of AML. This extremely rare AML complication proved refractory to conventional hypercalcemia treatments but responded promptly to chemotherapy. Subsequent PCR studies performed on the leukemia blasts for vitamin D-related genes revealed dramatic up-regulation compared to healthy CD34+ cells and other primary AML cells. Recent data highlight a role for vitamin D in hematopoietic cell proliferation. Accordingly, this case may highlight another aspect of molecular heterogeneity in AML.

AB - We report the first documented occurrence of hypercalcemia due to excessive production of calcitriol in acute myeloid leukemia (AML). The patient presented with severe hypercalcemia and renal failure accompanying a new diagnosis of AML. This extremely rare AML complication proved refractory to conventional hypercalcemia treatments but responded promptly to chemotherapy. Subsequent PCR studies performed on the leukemia blasts for vitamin D-related genes revealed dramatic up-regulation compared to healthy CD34+ cells and other primary AML cells. Recent data highlight a role for vitamin D in hematopoietic cell proliferation. Accordingly, this case may highlight another aspect of molecular heterogeneity in AML.

M3 - Article

VL - 4

JO - Annals of Hematology and Oncology

JF - Annals of Hematology and Oncology

SN - 2375-7965

IS - 3

M1 - 1141

ER -