Non-Hodgkin’s Lymphoma Terminating in Acute Myelogenous Leukemia

Cavalli, F.; Sonntag, R; Zimmermann, Andreas; Deubelbeiss, Kurt; Ryssel, Hans-Jörg

doi:10.1159/000207721

Cited by 10 publications

(4 citation statements)

References 10 publications

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“…25) In addition, other less frequent toxic effects, such as hepatotoxicity, ototoxicity and neuropathy, can occur and adversely affect patients given high doses of cisplatin. 26) Cisplatin induces mitochondrial dysfunctions, particularly inhibition of the electron transfer system, resulting in the enhanced production of superoxide anions, hydrogen peroxide and hydroxyl radicals. 27) There are evidences suggesting that cisplatin-induced renal and liver damage is closely associated with the increase in lipid peroxidation and GSH depletion by these reactive oxygen species 2194 Vol.…”

Section: Discussionmentioning

confidence: 99%

Effects of the Licorice Extract against Tumor Growth and Cisplatin-Induced Toxicity in a Mouse Xenograft Model of Colon Cancer

Lee

Park

Lim

et al. 2007

Biological & Pharmaceutical Bulletin

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Cisplatin (cis-diamminedichloroplatinum II) is a platinum coordinated complex that is widely used as an antineoplastic agent for the treatment of many solid tumors, including cancers of the ovary, testis, lung, bladder, head and neck, cervix and endometrium.1) Despite its excellent anticancer activity, the clinical use of cisplatin is often limited by its undesirable side effects, such as severe nephrotoxicity and hepatotoxicity. 2,3) Although the precise mechanism for this cisplatin-induced toxicity is not well understood, cisplatin is taken up preferentially and accumulates in the human liver and kidney cells, 4) resulting in the enhanced production of reactive oxygen species (ROS) and the decrease in the antioxidant enzymes.5,6) Therefore, antioxidants have been administered before a cisplatin treatment to protect against nephrotoxicity. 7)Licorice is an esteemed crude drug in both the Orient and Occident that is originated from the dried roots of several Glycyrrhiza species, including Glycyrrhiza uralensis FISCHER, G. glabra LINNE and G. inflata BATALIN. 8,9) In Chinese traditional medicine, licorice remains one of the most commonly prescribed herbs and has been used in the treatment of various ailments ranging from tuberculosis to peptic ulcers.10) Licorice has also been employed as a flavoring and sweetening agent, as well as a demulcent and expectorant in Western countries.11) The chemical constituents of licorice include glycyrrhizin and its aglycone, glycyrrhetinic acid, which are originally isolated from aqueous extracts and are used in the treatment of hyperlipemia, atherosclerosis, viral diseases, allergic inflammation and hepatotoxicity.12,13) The acetone or ethanol extract of licorice has species-specific flavonoids, such as liquiritin, isoliquiritin and their corresponding aglycones, glabridin, glabrol, glabrene, hispaglabridin A and hispaglabridin B.14,15) These flavonoids exhibit antioxidative, 16) superoxide scavenging 16) and anticarcinogenic activities.17) However, in vivo antitumor activity of a licorice extract and its protective activity on cisplatin-induced toxicity have not yet been studied.In the present study to assess the antitumor activity of a licorice extract and whether it has the potential to serve as a beneficial supplement during cisplatin chemotherapy, we examined the inhibitory effect of the licorice extract alone and in combination with cisplatin on the tumor growth, and its protective effect against cisplatin-induced nephrotoxicity and hepatotoxicity in mice xenografted with mouse colon carcinoma cells. MATERIALS AND METHODSChemical Cisplatin, phenylmethylsulfonyl fluoride (PMSF), sodium nitrite, 1,1,3,3-tetramethoxypropane, reduced glutathione (GSH), 5,5Ј-dithiobis(2-nitrobenzoic acid) (DTNB), glutathione reductase, reduced nicotinamide adenine dinucleotide phosphate (NADPH), superoxide dismutase (SOD), xanthine oxidase, a-naphthylamine, sulfanilic acid, xanthine, catalase and 4-amino-3-hydrazino-5-mercapto-1,2,4-triazole (purpald ® ) were purchased from SigmaAldrich Chem...

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Section: Discussionmentioning

confidence: 99%

Effects of the Licorice Extract against Tumor Growth and Cisplatin-Induced Toxicity in a Mouse Xenograft Model of Colon Cancer

Lee

Park

Lim

et al. 2007

Biological & Pharmaceutical Bulletin

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“…In spite of its significant anticancer activity, the clinical use of cisplatin is often limited by its undesirable side effects such as nephrotoxicity (Madias and Harrington, 1978). Hepatotoxicity can also occur when cisplatin is administered at high doses (Cavalli et al, 1978;Cersosimo, 1993;Pollera et al, 1987). Oxidative stress appears to play an important role in cisplatininduced hepatotoxicity.…”

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confidence: 99%

Cisplatin-Induced Hepatotoxicity Is Enhanced by Elevated Expression of Cytochrome P450 2E1

Cederbaum

2005

Toxicological Sciences

176

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In this study, the possible potentiation of cisplatin-induced hepatotoxicity by cytochrome P450 2E1 (CYP2E1) was examined both in vitro and in vivo. Transfected HepG2 cells expressing CYP2E1 (E47 cells) and not expressing CYP2E1 (C34 cells) were used as an in vitro model, and mice drinking 2% acetone for 7 days to induce CYP2E1 were used as an in vivo model. Exposure of E47 cells to cisplatin caused a much greater loss of cell viability, more striking depletion of reduced glutathione (GSH), and higher reactive oxygen species (ROS) production as compared with C34 cells. The prooxidant L-buthionine-[R,S]-sulfoximine (BSO), which depletes GSH, enhanced cisplatin-induced loss of cell viability, whereas the antioxidant glutathione ethyl ester, or the iron chelator deferoxamine mesylate (DFO) protected against the cisplatin-induced loss of E47 cell viability. Diallyl sulfide (DAS), an inhibitor of CYP2E1, also protected against the cisplatin toxicity in the E47 cells. After being injected with cisplatin (ip, 45 mg/kg), mice drinking 2% acetone with increased CYP2E1 levels exhibited elevated levels of serum ALT and AST, liver caspase-3 activity and positive staining of TUNEL increased, and histopathology indicated the presence of necrotic foci in livers of acetone plus cisplatin-treated mice. Lipid peroxidation and protein oxidation as indicated by carbonyl formation, staining of 3-nitrotyrosine (3-NT) and iron were higher in the cisplatin plus acetone group, compared with cisplatin alone group. Both in vitro and in vivo results indicate that elevated CYP2E1 enhances cisplatin-induced hepatotoxicity, and the mechanism may involve increased production of ROS and oxidative stress.

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“…A thorough review of the literature [3,4,[12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] through 1979 uncovered a total of 58 documented cases, of which only four (7%) occurred in patients 20 years of age or younger.…”

Section: Discussionmentioning

confidence: 99%

Acute myeloblastic leukemia following non‐hodgkin lymphoma in an adolescent. A report of a case with preleukemic syndrome, and review of the literature

Kaur

Miller

Andreeff

et al. 1981

Med. Pediatr. Oncol.

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Reports of acute nonlymphoblastic leukemia occurring after successful treatment of Hodgkin and non-Hodgkin lymphoma (NHL) are appearing with increasing frequency. Two years after completion of LSA2-L2 therapy for stage III, poorly differentiated lymphocytic lymphoma, a 16-year-old boy developed a preleukemic state characterized by a refractory macrocytic anemia with excess blasts, dyshematopoiesis, abnormal cluster:colony ratio on in vitro bone marrow culture, and acquired deficiencies of erythrocyte pyruvate kinase, triose phosphate isomerase, and adenylate kinase. Four months later acute myeloblastic leukemia was evident. The RNA index determined by flow cytofluorometry was increased. Four marker chromosomes were found and involved complex translocation of chromosomes 11 and 17 (t11;l17) in 100% of the cells, and chromosomes 4 (t4q;4) in 10% of the cells. A thorough literature search uncovered four other reports of acute nonlymphoblastic leukemia occurring in children treated for NHL and a total of 58 cases in the adult and pediatric age groups. Over 50% of the patients had AML, were mean over 50 years of age, and were treated with radiotherapy and chemotherapy. It is anticipated that additional cases of second malignancies will be reported in this population of patients whose outlook for the curability of the primary malignancy is 75%.

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Non-Hodgkin’s Lymphoma Terminating in Acute Myelogenous Leukemia

Cited by 10 publications

References 10 publications

Effects of the Licorice Extract against Tumor Growth and Cisplatin-Induced Toxicity in a Mouse Xenograft Model of Colon Cancer

Effects of the Licorice Extract against Tumor Growth and Cisplatin-Induced Toxicity in a Mouse Xenograft Model of Colon Cancer

Cisplatin-Induced Hepatotoxicity Is Enhanced by Elevated Expression of Cytochrome P450 2E1

Acute myeloblastic leukemia following non‐hodgkin lymphoma in an adolescent. A report of a case with preleukemic syndrome, and review of the literature

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