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Tytuł:
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Low-dose deoxycoformycin in lymphoid malignancy.
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Autorzy:
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Grever MR
Leiby JM
Kraut EH
Wilson HE
Neidhart JA
Wall RL
Balcerzak SP
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Źródło:
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Journal of clinical oncology : official journal of the American Society of Clinical Oncology [J Clin Oncol] 1985 Sep; Vol. 3 (9), pp. 1196-201.
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Typ publikacji:
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Journal Article; Research Support, U.S. Gov't, P.H.S.
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Język:
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English
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Imprint Name(s):
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Publication: 2003- : Alexandria, VA : American Society of Clinical Oncology
Original Publication: New York, N.Y. : Grune & Stratton, c1983-
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MeSH Terms:
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Adenosine Deaminase Inhibitors*
Coformycin/*administration & dosage
Leukemia, Lymphoid/*drug therapy
Lymphoma, Non-Hodgkin/*drug therapy
Nucleoside Deaminases/*antagonists & inhibitors
Ribonucleosides/*administration & dosage
B-Lymphocytes/enzymology ; Candidiasis/chemically induced ; Coformycin/adverse effects ; Coformycin/analogs & derivatives ; Coformycin/therapeutic use ; Conjunctivitis/chemically induced ; Drug Administration Schedule ; Gastrointestinal Diseases/chemically induced ; Herpesviridae Infections/chemically induced ; Humans ; Leukemia, Lymphoid/enzymology ; Liver Function Tests ; Lymphoma, Non-Hodgkin/enzymology ; Middle Aged ; Pentostatin ; Respiratory Tract Infections
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Grant Information:
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P30 CA 16058-10 United States CA NCI NIH HHS; R01 36331-01 United States PHS HHS
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Substance Nomenclature:
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0 (Adenosine Deaminase Inhibitors)
0 (Ribonucleosides)
11033-22-0 (Coformycin)
395575MZO7 (Pentostatin)
EC 3.5.4.- (Nucleoside Deaminases)
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Entry Date(s):
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Date Created: 19850901 Date Completed: 19851011 Latest Revision: 20170210
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Update Code:
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20240104
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DOI:
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10.1200/JCO.1985.3.9.1196
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PMID:
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2993534
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Deoxycoformycin (dCF), a potent inhibitor of adenosine deaminase (ADA), was explored for its antineoplastic potential in 28 patients with advanced lymphoid malignancy. Both normal and malignant B lymphocytes have low levels of ADA activity, and low doses of dCF profoundly inhibit this enzyme in the peripheral blood of patients with chronic lymphocytic leukemia (CLL). The low doses of dCF administered in this trial (4 mg/m2) were not associated with prohibitive toxicity. Five of 28 patients had an objective response. Four additional patients had clinical improvement. No significant difference in the pretreatment ADA activity existed between responding patients and treatment failures. The demonstration of responses to dCF following failure on standard alkylating agents suggests that dCF may not be cross-resistant with current agents used to treat CLL. Additional studies should be pursued using low-dose dCF in patients with advanced malignancy.