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PubMed1998

Reaction mechanism of fluoroacetate dehalogenase from Moraxella sp. B.

Fluoroacetate dehalogenase (EC 3.8.1.3) catalyzes the dehalogenation of fluoroacetate and other haloacetates. The amino acid sequence of fluoroacetate dehalogenase from Moraxella sp. B is similar to that of haloalkane dehalogenase (EC 3.8.1.5) from Xanthobacter autotrophicus GJ10 in the regions around Asp-105 and His-272, which correspond to the active site nucleophile Asp-124 and the base catalyst His-289 of the haloalkane dehalogenase, respectively (Krooshof, G. H., Kwant, E. M., Damborský, J., Koca, J., and Janssen, D. B. (1997) Biochemistry 36, 9571-9580). After multiple turnovers of the fluoroacetate dehalogenase reaction in H218O, the enzyme was digested with trypsin, and the molecular masses of the peptide fragments formed were measured by ion-spray mass spectrometry. Two 18O atoms were shown to be incorporated into the octapeptide, Phe-99-Arg-106. Tandem mass spectrometric analysis of this peptide revealed that Asp-105 was labeled with two 18O atoms. These results indicate that Asp-105 acts as a nucleophile to attack the alpha-carbon of the substrate, leading to the formation of an ester intermediate, which is subsequently hydrolyzed by the nucleophilic attack of a water molecule on the carbonyl carbon atom. A His-272 --> Asn mutant (H272N) showed no activity with either fluoroacetate or chloroacetate. However, ion-spray mass spectrometry revealed that the H272N mutant enzyme was covalently alkylated with the substrate. The reaction of the H272N mutant enzyme with [14C]chloroacetate also showed the incorporation of radioactivity into the enzyme. These results suggest that His-272 probably acts as a base catalyst for the hydrolysis of the covalent ester intermediate.

Acetates↗

PubMedDate not supplied

Measurement of haloacetic acids and their decomposition in wine by capillary gas chromatography.

A method has been developed for the analysis of haloacetic acids in wine involving solid-phase extraction followed by methylation and quantification by capillary gas chromatography with electron capture detection. Recoveries from spiked samples were greater than 85% for each of the acids and the limits of detection of the method were 100, 10 and 5 micrograms/litre for the chloroacetic, bromoacetic and iodoacetic acids, respectively. The haloacetic acids were not detected in a survey of over 30 retail samples. Separate stability studies showed that the concentration of chloroacetic acid added to wine was essentially unaffected by up to 90 days storage at 30 degrees C. Under the same conditions, however, less than 20% of bromoacetic acid and iodoacetic acid remained.

Acetates↗

PubMed1991

Validated methods for degrading hazardous chemicals: some halogenated compounds.

Two techniques were investigated for degrading a number of halogenated compounds of commercial and research importance. Reductive dehalogenation with nickel-aluminum alloy in potassium hydroxide solution was used to degrade iodomethane, chloroacetic acid, trichloroacetic acid, 2-chloroethanol, 2-bromoethanol, 2-chloroethylamine, 2-bromoethylamine, 1-bromobutane, 1-iodobutane, 2-bromobutane, 2-iodobutane, 2-bromo-2-methylpropane, 2-iodo-2-methylpropane, 3-chloropyridine, fluorobenzene, chlorobenzene, bromobenzene, iodobenzene, 4-fluoroaniline, 2-chloroaniline, 3-chloroaniline, 4-chloroaniline, 4-fluoronitrobenzene, 2-chloronitrobenzene, 3-chloronitrobenzene, 4-chloronitrobenzene, benzyl chloride, benzyl bromide, alpha,alpha-dichlorotoluene, and 3-aminobenzotrifluoride. The products were generally those obtained by replacing the halogen with hydrogen although concomitant reduction of the other groups was also observed. Bibenzyl was produced during the reduction of benzyl chloride, benzyl bromide, and alpha,alpha-dichlorotoluene. Refluxing with ethanolic potassium hydroxide was used to degrade iodomethane, chloroacetic acid, 2-fluoroethanol, 2-chloroethanol, 2-bromoethanol, 1-chlorobutane, 1-bromobutane, 1-iodobutane, 2-bromobutane, 2-iodobutane, 2-bromo-2-methylpropane, 2-iodo-2-methylpropane, benzyl chloride, benzyl bromide, 1-bromononane, 1-chlorodecane, and 1-bromodecane. The products were the corresponding ethyl ethers. 2-Methylaziridine was cleaved with nickel-aluminum alloy in potassium hydroxide solution to a mixture of isopropylamine and n-propylamine. In all cases, the compounds were completely degraded and only nonmutagenic reaction mixtures were produced.

Hazardous Substances↗

PubMed1984

A morphologic and cytochemical study of acute myelomonocytic leukemia with abnormal marrow eosinophils associated with inv(16)(p13q22).

Nineteen patients with acute nonlymphocytic leukemia were found to have a pericentric inversion of chromosome 16. All were classified as having acute myelomonocytic leukemia (M4) according to French-American-British Cooperative Group (FAB) criteria. Consistent abnormalities of marrow eosinophils were present. In 15 of the 19 patients, the number of eosinophils was increased. Morphologic abnormalities of eosinophils were present in all patients, the most striking being the presence of large basophilic staining granules in 18 of the 19 patients. In most cases we also found a population of cells with morphologic features of both eosinophils and monocytes. Eosinophils showed atypical cytochemical reactions with PAS in ten of ten cases studied, with naphthol ASD Chloroacetate in ten of ten cases, and with combined naphthol ASD Chloroacetate esterase- chlorazol fast pink in seven of nine cases tested. The presence of inv(16) defines a distinct subset of ANLL with consistent morphologic and cytochemical features.

Adolescent↗

PubMed2000

Identification and kinetics of leukocytes after severe ischaemia/reperfusion renal injury.

BACKGROUND: Leukocyte adhesion/infiltration in response to renal ischaemia/reperfusion (I/R) injury is a well-known but poorly understood phenomenon. The identification, kinetics, and exact role of these inflammatory cells in I/R injury and regeneration are still matters of debate. METHODS: Uninephrectomized rats were submitted to 60 min renal ischaemia by clamping of renal vessels. RESULTS: Severe acute renal failure was observed, with maximum functional impairment on day 2. By 12 h after the ischaemic event, up to 80% of proximal tubular cells in the outer stripe of outer medulla (OSOM) were already severely damaged. Proliferation (proliferating cell nuclear antigen (PCNA) staining) started after 24 h, reaching maximum activity on day 3. Regeneration of tubular morphology started on the 3rd day, and after 10 days 50% of tubules had regenerated completely. Interstitial leukocytes (OX-1 immunohistochemical staining) were already prominent at day 1, thereafter gradually increasing with time. The so-called neutrophil-specific identification methods (myeloperoxidase (MPO), chloroacetate esterase, mAb HIS-48) proved to be non-specific, since they also stained for macrophages, as demonstrated by flow cytometry and the combination of these stainings with the macrophage-specific ED-1 staining. MPO activity was already significantly increased at 1 h post-I/R (439+/-34%, P<0.005), reaching its maximum activity after 12 h of I/R (1159+/-138%, P<0.0005), declining thereafter. On the other hand, neutrophil presence investigated by H&E staining revealed only a few neutrophils in glomeruli, medullary rays, and OSOM at 24 h after the ischaemic event (4.7+/-4.2 cells/mm(2) vs controls=2.3+/-2.0 cells/mm(2) (n.s.)), and remained unchanged over the next 10 days. In contrast, significant monocyte/macrophage adhesion/infiltration (ED-1 staining) occurred at the OSOM at 24 h post-ischaemia (at 24 h, 120+/-46 cells/mm(2) vs. sham=18+/-4 cells/mm(2) (P<0.05)), became prominent at day 5 (1034+/-161 cells/mm(2) vs sham=18+/-18 cells/mm(2) (P<0.05)), and almost disappeared after 10 days. CD4(+) cells (W3/25) gradually increased from day 5, reaching a maximum at day 10. A few CD8(+) cells (OX-8) were apparent from days 3 until 10, but no B-cells (OX-33) were observed. CONCLUSIONS: After severe warm I/R renal injury, a pronounced acute tubular necrosis occurs during the first 12-24 h in the absence of a marked cellular infiltrate, but with an important renal MPO activity, reflecting the activation of the adhering inflammatory cells (polymorphonuclear cells (PMNs) and mainly monocytes/macrophages). Only later at the time and site (OSOM) of regeneration a sequential accumulation of monocytes/macrophages and T cells becomes prominent, in contrast with the low number of neutrophils found in the kidney during the 10-day post-ischaemic period. The non-specificity of the so-called neutrophil-specific identification methods (MPO activity, naphthol AS-D chloroacetate esterase, or mAb HIS-48 staining), cross-reacting with monocytes/macrophages, explains the controversy in literature concerning the number of PMNs in post-ischaemic injury.

Animals↗

PubMed1983

Quantitative cytochemistry of blood neutrophils in acute myeloid leukaemia.

Blood neutrophils were studied by quantitative cytochemistry in patients with acute myeloid leukemia at diagnosis (17 patients), during remission (17 patients) and in relapse (seven patients). Scanning and integrating microdensitometry was used to quantify components of azurophilic granules (myeloperoxidase, chloroacetate esterase, beta-glucuronidase, acid phosphatase, acid mucosubstance) and also specific granules (lactoferrin). At diagnosis, neutrophil myeloperoxidase, chloroacetate esterase, and lactoferrin were significantly decreased, compared with normal neutrophils from 25 controls, with 13 of the 17 patients showing a partial or complete deficiency of at least one granule constituent. Five of seven patients, followed serially from remission into relapse, showed a fall in activity of azurophilic or specific granule components before overt blast cell infiltration of the marrow had occurred and this may predict relapse.

Acid Phosphatase↗

PubMed1983

Esterase cytochemistry in primary myelodysplastic syndromes and megaloblastic anaemias: demonstration of abnormal staining patterns associated with dysmyelopoiesis.

Acid alpha naphthyl acetate esterase (ANAE) and combined ANAE-chloroacetate esterase cytochemistry was performed on 121 bone marrow aspirates from primary myelodysplastic syndromes (MDS) and a secondary dysplasia-megaloblastic anaemia (MA). The investigation demonstrated the presence of abnormal ANAE positive granulocyte populations in a significant proportion of cases. These cells, in which the staining patterns were characterized by atypical granular ANAE positivity and double ANAE-chloroacetate reactions, were shown immunologically to lack the receptor and antigenic characteristics of monocytes and morphologically to be granulocytes. Isoelectric focusing, however, indicated that the atypical esterase cytochemistry of these granulocytes was due to the presence of markedly increased concentrations of ANAE isoenzymes usually found in monocytes. Atypical ANAE-staining granulocytes were particularly evident in MDS marrows showing sideroblastic erythroid changes, whilst in MA they were mainly seen in cases of intermediate severity. It is suggested that these cells are associated with dysmyelopoietic changes in both malignant and non-malignant conditions.

Anemia↗

PubMed1989

Diagnosis of acute myeloid leukaemia with the use of monoclonal anti-neutrophil elastase (NP57) reactive with routinely processed biopsy samples.

The reactivity of a monoclonal anti-neutrophil elastase antibody (NP57) with routinely processed biopsy samples from various acute leukaemias has been examined and compared with that of chloroacetate esterase and CD15 (hapten X), two other myeloid cell-associated markers detectable in paraffin sections. No staining was seen with these markers in 14 cases of acute lymphoblastic leukaemia. In contrast the neoplastic cells in 27 of 37 acute myeloid leukaemias were NP57 positive. Twenty of these were also positive for chloroacetate esterase, whereas CD15 was expressed in only six cases. These results indicate that detection of elastase with monoclonal NP57 forms a useful supplement to traditional methods for the histopathological diagnosis of acute myeloid leukaemias.

Antibodies, Monoclonal↗

PubMed1978

Evidence for multiple reactive forms of papain.

The pH-dependence of the second-order rate constants of acylation and alkylation reactions of the -SH group of papain were determined by using neutral and charged reactants under identical conditions. From these pH rate profiles, in contrast to previous claims, different pKa values were obtained with different groups of reactants. In the case of charged reactants, like chloroacetate (pKa = 3.6) and arginine derivatives (pKa = 4.3), the pKa differences can be attributed to electrostatic effects. However, the fact that a pKa of 3.25 was found with methyl and ethyl bromoacetate, and a pKa of 4.0 was obtained with bromoacetamide and a number of neutral substrates, is inconsistent with the theories put forth hitherto for the meaning of such pKa values, because they all consider only one reactive enzyme form. The different pKa values obtained here with neutral reactants are explained in terms of various reactive papain forms. The perturbation of pKa by electrostatic effects was examined by reacting simple thiol compounds containing different charges, like 2-mercaptoacetate, 2-mercaptoethylamine, 2-mercaptoethanol and glutathione, with the neutral chloroacetamide and with the negatively charged chloroacetate. Differences in pKa can be interpreted in terms of intramolecular and intermolecular electrostatic interactions.

Acylation↗

PubMed2002

Cytoprotective properties of novel nonpeptide calpain inhibitors in renal cells.

Calpains are cytosolic, Ca(2+)-activated, neutral cysteine proteases. Rabbit renal proximal tubule (RPT) cells express both mu- and m-calpain. Although multiple calpain inhibitors protect against RPT cell death, most calpain inhibitors lack specificity, membrane permeability, and/or potency. A group of novel catalytic site-directed calpain inhibitors, including chloroacetic acid N'-[6,7-dichloro-4-(4-methoxy-phenyl)-3-oxo-3,4-dihydroquinoxalin-2-yl]hydrazide (SJA7019) and chloroacetic acid N'-(6,7-dichloro-4-phenyl-3-oxo-3,4-dihydroquinoxalin-2-yl) hydrazide (SJA7029), were identified to be potent calpain inhibitors in vitro. The goals of this study were to determine the action of these two compounds on 1) RPT calpain activity using fluorescein isothiocyanate-casein zymography, 2) antimycin A-induced RPT extracellular (45)Ca(2+) influx and cell death, and 3) hypoxia/reoxygenation-induced RPT cellular dysfunction and death. The results showed that the SJA compounds inhibited RPT mu- and m-calpain with equal potency (approximate IC(50), 30 microM) and efficacy, and blocked antimycin A-induced extracellular Ca(2+) influx and cell death. In addition, SJA7029 blocked cell death and allowed the recovery of mitochondrial function and active Na(+) transport in RPTs subjected to hypoxia/reoxygenation. In summary, the SJA compounds 1) were more potent inhibitors of calpains than catalytic site-directed peptide inhibitors in this model, 2) prevented extracellular Ca(2+) influx during the late phase of cell death, and 3) are true cytoprotectants and allow recovery of RPT cellular functions after injury.

Animals↗

PubMed1995

A meta cleavage pathway for 4-chlorobenzoate, an intermediate in the metabolism of 4-chlorobiphenyl by Pseudomonas cepacia P166.

Bacterial degradation of biphenyl and polychlorinated biphenyls proceeds by a well-studied pathway which produces benzoate and 2-hydroxypent-2,4-dienoate (or, in the case of polychlorinated biphenyls, the chlorinated derivatives of these compounds). Pseudomonas cepacia P166 utilizes 4-chlorobiphenyl for growth and produces 4-chlorobenzoate as a central intermediate. In this study we found that strain P166 further transforms 4-chlorobenzoate to 4-chlorocatechol, which is mineralized by a meta cleavage pathway. Key metabolites which we identified include the meta cleavage product (5-chloro-2-hydroxymuconic semialdehyde), 5-chloro-2-hydroxymuconate, 5-chloro-2-oxopent-4-enoate, 5-chloro-4-hydroxy-2-oxopentanoate, and chloroacetate. Chloroacetate accumulated transiently, and slow but stoichiometric dehalogenation was observed.

Biodegradation, Environmental↗

PubMed1983

In vitro generation of mast cell-like cells from human peripheral mononuclear phagocytes.

An in vitro culture method, previously shown to induce the transformation of rat macrophages to mast cells, has been adapted to humans. Adherent peripheral human blood mononuclear cells were cultured in a medium supplemented with 30% L-cell supernatant and 30% horse serum. During the first week of culture, the cells were phagocytic (80%), lacked histamine, were not metachromatic and stained faintly for naphthol-AS-D-chloroacetate esterase, primarily in a paranuclear location. During the first 2 weeks of culture, the cells grew in size, synthesized DNA, became nonadherent and developed cytoplasmic chloroacetate esterase staining which was strongly positive in 50-60% of the cells during the third week. Intracellular histamine levels increased steadily during culture, and electron-dense metachromatic cytoplasmic granules were present during the third week. Human peripheral blood mononuclear cells contain therefore a subpopulation of cells that can differentiate into mast cells-like cells under specific in vitro culture conditions.

Cell Differentiation↗

PubMed1990

Sequential appearance of basophils and mast cells from human bone marrow in long-term suspension culture.

Human bone marrow cells grown in liquid culture in the presence of conditioned medium from concanavalin A stimulated peripheral blood mononuclear cells, from mixed lymphocyte reactions, or from an osteogenic sarcoma tumor line gave rise to basophils which were maximal in number at 1-3 weeks. Basophils had a multilobed nucleus, contained large cytoplasmic granules of variable size which stained metachromatically with acid, but not neutral toluidine blue, were negative for chloroacetate esterase, and did not contain human mast cell tryptase. In long-term cultures, mast cells were detected after 5-6 weeks. Mast cells had cytoplasmic granules that stained with acid and neutral toluidine blue, were positive for chloroacetate esterase, and contained human mast cell tryptase. It, therefore, appears that in liquid cultures even in the absence of feeder layers, human bone marrow cell cultures can give rise initially to basophils, and then to mast cells.

Animals↗

PubMedDate not supplied

Dissimilar characteristics of N-methyl-N-nitrosourea-initiated foci and tumors promoted by dichloroacetic acid or trichloroacetic acid in the liver of female B6C3F1 mice.

Dichloroacetic acid (DCA) and trichloroacetic acid (TCA) are metabolites of the industrial solvent and environmental contaminant trichloroethylene (TCE), as well as contaminants of chlorinated drinking water. Human exposure to these chemicals is of concern as all three have been shown to increase liver tumor incidence in mice. Differences in dose-response curves, progression to cancer, and postexposure regression of lesions suggest that TCA and DCA work through different mechanisms. The purpose of this study was to further characterize the proliferative hepatocellular lesions promoted by TCA and DCA using biomarkers of cell growth, differentiation, and metabolism in liver sections to better delineate the distinctions in the mechanism of the two chloroacetates. Fifteen-day-old female mice were initiated with 25 mg/kg N-methyl-N-nitrosourea. The initiated mice were administered DCA or TCA (20.0 mmol/L) in drinking water from age 49 days until euthanasia at age 413 days. The pathologic assessment showed that the foci of altered hepatocytes and tumors occurring in the animals promoted with DCA were eosinophilic and positive immunohistochemically for TGF-alpha, c-jun, c-myc, CYP 2E1, CYP 4A1, and glutathione S-transferase-pi (GST-pi). The DCA lesions also were essentially negative for c-fos and TGF-beta, but nontumor hepatocytes were consistently TGF-beta-positive. In contrast, tumors promoted by TCA were predominantly basophilic, lacked GST-pi, and stained variably; usually, more than 50% of the tumor hepatocytes were essentially negative for the other biomarkers. This study demonstrates some striking differences in certain molecular biomarkers of cell growth, differentiation, and metabolism between DCA and TCA. The results also suggest some potential growth signal transduction pathways that may contribute to the DCA promotion of tumors, further support the premise that these two chloroacetates promote hepatocarcinogenesis in different ways, and provide a rational basis for a similar comparison with TCE. Such a comparison should give some insight as to whether DCA, TCA, or both are playing a significant role in the murine liver carcinogenesis of the parent compound, TCE.

Animals↗

PubMed1996

Differentiation inducing effects of 2-chloro-3-amino-1,4-naphthoquinone on human leukemia HL-60.

There are some highly cytotoxic anticancer compounds inducing differentiation of cancer cells to normal cells at below highly cytotoxic concentration. Naphthoquinone derivatives having cytotoxic effects on cancer cell were tested to learn whether they have differentiation inducing activity in human leukemia HL-60 cells or not. When HL-60 cells were treated with 2-chloro-3-amino-1,4-naphthoquinone (CANQ) for four days, differentiation-related phenotypes such as nitrobluetetrazolium (NBT)-reducing ability and phagocytosis were induced. These differentiation markers were increased by cotreatment with 1,25-dihydroxyvitamin D3 which is a well-known inducer of differentiation in HL-60 cells. To evaluate the route of differentiation induced by CANQ, we examined naphthol AS-D chloroacetate esterase and alpha-naphthylacetate esterase activities and changes in cellular size and granulation. Treatment of HL-60 cells with CANQ for four days resulted in an 82.4% increase in alpha-naphthylacetate esterase activity in spite of a 0.2% increase in naphthol AS-D chloroacetate esterase activity. The size of cells in cell mass was larger and granulation was more decreased than untreated cells. These results indicate that HL-60 cells were induced to differentiate into macrophage-like cells.

Calcitriol↗

PubMed1983

2-Haloacid dehalogenase from a 4-chlorobenzoate-degrading Pseudomonas spec. CBS 3.

Pseudomonas spec. CBS 3 contains a 2-haloacid dehalogenase induced by chloroacetate. The enzyme was purified about 25-fold to electrophoretic homogeneity by ammonium sulfate fractionation, hydroxyapatite, DEAE-cellulose and gel filtration. The relative molecular masses, as determined by Sephadex G-75 gel filtration and dodecyl sulfate polyacrylamide gel electrophoresis, were 41 000 and 28 000, respectively. The enzyme dehalogenated all monohaloacetates except fluoroacetate. Low activities were found against dichloroacetate and 2,2-dichloropropionate. The enzyme was inactive against trichloroacetate and 3-chloropropionate, it catalysed the stereospecific dehalogenation of L-2-chloropropionate to D-lactate, the rate of dehalogenation being about 20% of the rate of chloroacetate dechlorination. The enzyme activity was not affected by chelating agents and thiol reagents.

Acetates↗

PubMed1996

Unsuspected gastric granulocytic sarcoma in a patient with myelodysplastic syndrome.

Granulocytic sarcoma (GS) is an uncommon and localized extramedullary tumor composed of immature granulocytic cells. Most GS reported in large series were not associated with overt acute myelogenous leukemia. Gastric perforation occurred during prednisolone therapy in a 72-year-old Japanese male with a four-month history of a myelofibrosis-like state. Subtotal gastrectomy was performed for a suspected gastric ulcer perforation. Gastric histologic, immunohistochemical and cytochemical examination revealed diffuse infiltration by sheets of myeloblasts and promyelocytes with scant or moderately abundant cytoplasm including a few eosinophilic myelocytes. Bone marrow study done in one month after the operation disclosed refractory anemia with excess of blasts (RAEB). Leukemic transformation occurred two months later, and a subcutaneous tumor appeared on the forehead. The forehead tumor predominantly consisted of myeloblasts without evidence of maturation. Both the stomach and forehead tumors were examined immunohistochemically with a panel of monoclonal antibodies (LCA, L26, MT1, UCHL1, OPD4, LN-1, LN-2, LN-3, MB1, Leu-M1, PM) and polyclonal antibodies (lysozyme, alpha 1-antitrypsin, alpha 1-antichymotrypsin, S-100 protein, lactoferrin), as well as naphthol-ASD-chloroacetate esterase staining to investigate and characterize the reliable marks for GS, and the patient was diagnosed as GS. We found that gastric GS may occur in a myelofibrosis-like state followed by RAEB of myelodysplastic syndrome and that naphthol-ASD-chloroacetate esterase staining and immunohistochemical detection of MT1, lysozyme, and alpha 1-antitrypsin were the most reliable markers for confirming the diagnosis of GS.

Aged↗

PubMed2005

Myeloid sarcoma of appendix mimicking acute appendicitis.

CONTEXT: Myeloid sarcoma is a neoplasm of immature myeloid cells involving an extramedullary anatomic site that is usually, although not always, associated with acute myeloid leukemia. Any extramedullary site can be involved by myeloid sarcoma, but involvement of the cecal appendix is uncommon, and symptoms mimicking acute appendicitis as a result of appendiceal involvement are rare. OBJECTIVE: To describe the clinicopathologic features of 2 patients with myeloid sarcoma involving the appendix who presented with right lower quadrant pain suggestive of acute appendicitis and prompting appendectomy. DESIGN: Clinical information for both patients was obtained from the medical record. Routine hematoxylin-eosin-stained slides, naphthol-ASD-chloroacetate stain, and immunohistochemical stains for myeloid, B-cell, and T-cell antigens were prepared. RESULTS: Peripheral blood and bone marrow were infiltrated by coexistent acute myeloid leukemia in case 1 but were negative for leukemia in case 2. In case 2, the patient had a history of acute myeloid leukemia that had been treated by an allogenic bone marrow transplant 7 months earlier. Histologic examination of the appendix revealed poorly differentiated myeloid sarcoma in both cases. Each neoplasm was positive for chloroacetate esterase, myeloperoxidase, lysozyme, and CD43 and was negative for CD3 and CD20. CONCLUSIONS: Myeloid sarcoma involving the appendix can rarely cause pain or other symptoms mimicking acute appendicitis. A high index of suspicion combined with the use of cytochemical and immunohistochemical studies are helpful in establishing the diagnosis.

Abdomen↗