Pulmonary embolus in acute myelocytic leukemia

Wiernik, Peter H.; Serpick, Arthur A.

doi:10.1002/1097-0142(196909)24:3<581::aid-cncr2820240324>3.0.co;2-9

Cited by 18 publications

(5 citation statements)

References 14 publications

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“…Malignant diseases, especially carcinoma, predispose to thrombosis (Lieberman et al, 1961;Miller et al, 1967;Wiernik and Serpick, 1969). In some types of carcinoma, especially carcinoma of the pancreas, the incidence is very high.…”

Section: Discussionmentioning

confidence: 99%

Thromboembolic Complications in Myelomatosis

Catovsky¹,

Ikoku²,

Pitney³

et al. 1970

BMJ

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Section: Discussionmentioning

confidence: 99%

Thromboembolic Complications in Myelomatosis

Catovsky¹,

Ikoku²,

Pitney³

et al. 1970

BMJ

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“…23 Throm bocytopenia in patients with AL does not prevent the development of thrombotic complications, and emboli in the pulmonary artery were reported in subjects with a very low platelet count. 24 Femoral thrombophlebi tis is often observed in patients despite a low platelet count and a low prothrombin level. However, there is a lack of studies elucidating the possible link between the thrombotic tendency and the DIC occurrence in a larger group of patients with AL.…”

Section: Aplmentioning

confidence: 99%

Disseminated Intravascular Coagulation in Acute Leukemia

Lisiewicz¹

1988

Semin Thromb Hemost

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The mechanisms of hemorrhage in acute leukemias (AL) are related to the direct effect of leukemic cells infiltrating the vascular walls and affecting the blood coagulation, causing damage to the megakaryo cyte system, changes in liver function, and subsequent decrease in the synthesis of some blood coagulation factors, increase in blood fibrinolytic activity, and the disseminated intravascular coagulation 1-4 (DIC). The effects of antileukemic agents on the blood coagula tion system in patients with leukemia represent sepa rate problems. Hemorrhagic diathesis is one of the most severe complications of AL and is often the direct cause of death. The basic difference between the particular forms lies in the cytologic type of leu kocytes undergoing the leukemic proliferation. There are, moreover, some differences in the clinical evolu tion and the response to therapy between AL of the myeloblastic and the lymphoblastic types. The mor phologic classification of AL is still a subject of dis cussion and in that regard the French-AmericanBritish (FAB) and World Health Organization (WHO) classifications should be mentioned. The FAB classi fication divides AL into six types of acute nonlymphocytic leukemias, that is, acute myeloblastic leukemias (AML), designed as M 1 to M 6 , and three types of acute lymphoblastic leukemia (ALL) corresponding to L 1 to L 3 . 5 However, currently several other AL classifications have been proposed and difficulties of reproducing the morphologic classification at dif ferent centers and the uncertainty about the impor tance of such classifications for prognosis is still un resolved. 6

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“…Adriamycin and daunorubicin are anthracycline antibiotics that have been unusually effective in the treatment of malignancy (1)(2)(3)(4). Biochemical studies indicate that the drugs inhibit both DNA-directed DNA synthesis (5) and DNA-directed RNA synthesis (6), presumably by their ability to interact with the DNA template primer (7,8).…”

mentioning

confidence: 99%

“…Biochemical studies indicate that the drugs inhibit both DNA-directed DNA synthesis (5) and DNA-directed RNA synthesis (6), presumably by their ability to interact with the DNA template primer (7,8). Although the drugs are structurally similar, they differ in their pharmacodynamics (9), therapeutic effectiveness (10), and clinical usefulness (1)(2)(3)(4). Some of these differences might be explained in terms of cellular drug uptake (9) and drug metabolism (11,12).…”

mentioning

confidence: 99%

Adriamycin and Daunorubicin Inhibition of Mutant T4 DNA Polymerases

Goodman

Bessman

Bachur

1974

Proc. Natl. Acad. Sci. U.S.A.

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The anticancer drugs, adriamycin and daunorubicin, as well as two other DNA reagents, ethidium bromide and 9-aminoacridine, all exert a differential inhibitory effect on nucleotide incorporation for purified DNA polymerases induced by mutant and wild-type bacteriophage T4. When compared with DNA polymerase of wild-type phage, antimutator enzymes are inhibited to a far greater extent and mutator enzymes to a lesser extent. In contrast, the polymerase-associated 3'-exonuclease activities of wild type and mutants are also inhibited by the compounds but nondifferentially.Adriamycin and daunorubicin are anthracycline antibiotics that have been unusually effective in the treatment of malignancy (1-4). Biochemical studies indicate that the drugs inhibit both DNA-directed DNA synthesis (5) and DNA-directed RNA synthesis (6), presumably by their ability to interact with the DNA template primer (7,8). Although the drugs are structurally similar, they differ in their pharmacodynamics (9), therapeutic effectiveness (10), and clinical usefulness (1-4). Some of these differences might be explained in terms of cellular drug uptake (9) and drug metabolism (11,12). However, no direct comparison of the effect of the two agents on purified enzymes has been reported.The DNA polymerase (EC 2.7.7.7; deoxynucleoside triphosphate-DNA deoxynucleotidyltransferase) induced by T4 bacteriophage catalyzes both addition of deoxynucleoside triphosphates to the 3'-hydroxyl end of the primer, directed by DNA template, as well as the removal of nucleotides from this end. An interesting feature of the mutant DNA polymerases studied by us (13) is that, by comparison with the wild-type enzyme, nuclease-to-polymerase ratios are higher for those from mutants carrying antimutator genes and lower for those from mutants carrying mutator genes. In this report we show another difference among these enzymes; that is, their differential reponse to the antitumor drugs, adriamycin and daunorubicin, and to two other intercalating agents, ethidium bromide and 9-aminoacridine. The results are of interest in terms of the recent report by Springgate and Loeb (14), who show that the DNA polymerase of leukemic cells has mutator characteristics. MATERIALS AND METHODSNucleotides and Test Compounds. All nonradioactive nucleotides were purchased from P-L Biochemicals, and radioactive nucleotides form Schwarz-Mann. Adriamycin-HCl was obtained from the Farmitalia Co., Milan, Italy, and daunorubicin-HCl was provided by Drug Research and Development Branch, DCT, NCI, NIH. The concentrations of the antibiotics in aqueous solutions were determined spectrally from their absorbance at 485 nm (9). They were stored at -20°as 3.4 mM aqueous solutions. Ethidium bromide was purchased from Sigma Chemical Co., and 9-aminoacridine was purchased from Aldrich Chemical Co.Nucleic Acids. Microorganisms. We are indebted to Dr. John W. Drake for all of the temperature-sensitive mutants in gene 43 used in these studies. They are described in refs. 17 and 18. Phage T4D were those used ...

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Pulmonary embolus in acute myelocytic leukemia

Cited by 18 publications

References 14 publications

Thromboembolic Complications in Myelomatosis

Thromboembolic Complications in Myelomatosis

Disseminated Intravascular Coagulation in Acute Leukemia

Adriamycin and Daunorubicin Inhibition of Mutant T4 DNA Polymerases

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