Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with chronic myeloid leukaemia developed bone marrow granulomas during treatment with interferon alpha-2b. Some granulomas had necrotic centres and giant cells and there was marked eosinophilia surrounding them. The granulomas disappeared when the interferon treatment was discontinued. Mycobacteriosis was ruled out. The most likely explanation for the granuloma formation was drug hypersensitivity.
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PMID:Granulomatous bone marrow inflammation during treatment of chronic myeloid leukaemia with interferon alpha-2b. 749 Mar 29

Leukemia is the most common childhood cancer. Trisenox, the active ingredient of which is trivalent arsenic, is the first line of treatment for acute promyelocytic leukemia. Since drug action usually requires uptake of the drug, it is of importance to determine the transport system responsible for Trisenox uptake. Recently, human aquaglyceroporin 9 (AQP9) has been shown to transport As(III) in Xenopus oocytes. In this study we report to show that AQP9 expression modulates the drug sensitivity of leukemic cells. AQP9 was transfected into the chronic myelogenous leukemia cell line K562. The transfectants became hypersensitive to Trisenox and Sb(III). The promyelocytic leukemia cell line HL60 treated with vitamin D showed higher expression of AQP9 and hypersensitivity to Trisenox and Sb(III). This sensitivity was due to higher rates of uptake of the trivalent metalloids by the cell lines overexpressing AQP9. Trisenox hypersensitivity results from increased expression of AQP9 drug uptake system. The possibility of using pharmacological agents to increase expression of AQP9 gene delivers the promise of new therapies for the treatment of leukemia. Thus, drug hypersensitivity can be correlated with increased expression of the drug uptake system. This is the first demonstration that AQP9 can modulate drug sensitivity in cancer.
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PMID:Drug uptake and pharmacological modulation of drug sensitivity in leukemia by AQP9. 1533 39

Imatinib mesylate (IM) is used in the targeted therapy of chronic myelogenous leukemia and gastrointestinal stromal tumors. It is well tolerated and leads to no higher incidence of hemorrhagic events than other therapies. Of 87 patients we treated with IM for a minimum of 3 months, 10 patients (11%) developed unilateral or bilateral conjunctival hemorrhage (CH). No other hemorrhagic events were observed during follow-up, except for CH recurrence in 6 cases (7%). Because there was no other obvious reason for such a high incidence of CH, we hypothesize drug hypersensitivity or ocular irritation induced by IM treatment.
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PMID:Conjunctival hemorrhagic events associated with imatinib mesylate. 1819 4

Keratosis pilaris (KP) is a disorder of follicular keratinization that is characterized by keratin plugs in the hair follicles with surrounding erythema. A 46-year-old man with chronic myelogenous leukemia (CML) was started on nilotinib, a second generation tyrosine kinase inhibitor (TKI). Two months later the patient noticed red bumps on the skin and patchy hair loss on the arms, chest, shoulders, back, and legs. Cutaneous reactions to nilotinib are the most frequent non-hematologic adverse effects reported. However, it is important to distinguish KP-like eruptions from more severe drug hypersensitivity eruptions, which can necessitate discontinuing the medication. Also, it is important to classify the cutaneous eruptions in patients on TKI according to the morphology instead of labeling them all as "chemotherapy eruption" to be able to better manage these adverse effects.
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PMID:Nilontinib induced keratosis pilaris atrophicans. 2761 40