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PubMed2005

Myeloid sarcoma involving the breast.

CONTEXT: Myeloid sarcoma is a neoplasm of myeloid cells that can arise before, concurrent with, or following acute myeloid leukemia. Rarely, it can also occur as an isolated mass. OBJECTIVE: To describe the clinicopathologic features of 6 patients with myeloid sarcoma involving the breast. DESIGN: Clinical information for all 6 patients was obtained from the medical record. Routine hematoxylin-eosin-stained slides; naphthol AS-D chloroacetate stain; and immunohistochemical stains for myeloid, B-cell, and T-cell antigens were prepared. RESULTS: There were 6 women with a median age of 52 years (range, 31-73 years). Two patients presented with isolated tumors of the breast, with no history or subsequent development of acute myeloid leukemia. In 3 patients, the breast tumors represented relapse of acute myeloid leukemia. One patient who presented initially with myeloid sarcoma involving the breast, skin, and spleen was lost to follow-up. Histologically, these tumors were classified as well differentiated (n = 3), poorly differentiated (n = 2), and blastic (n = 1). Naphthol AS-D chloroacetate esterase was positive in all 3 cases assessed. Immunohistochemistry showed that myeloperoxidase (n = 5) and CD43 (n = 3) were positive, and CD3 (n = 5) and CD20 (n = 5) were negative in all cases assessed. Lysozyme was positive in 4 (80%) of 5; CD117 was positive in 2 (67%) of 3; and single cases were positive for CD45 (1/3), TdT (1/2), CD79a, and the PAX5 gene product. CONCLUSIONS: Myeloid sarcoma involving the breast is uncommon. In the literature, as in this study, these tumors most often represent relapse or the initial presentation of acute myeloid leukemia. However, 2 of the cases we report presented with isolated masses, without a history or subsequent development of acute myeloid leukemia at last follow-up. Immunohistochemical studies are extremely helpful for recognizing isolated myeloid sarcoma.

Acute Disease↗
PubMed1992

NTP Toxicology and Carcinogenesis Studies of Monochloroacetic Acid (CAS No. 79-11-8) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

Monochloroacetic acid, a colorless crystalline material, is used as a postemergence contact herbicide and as an intermediate in the synthesis of other organic compounds. Toxicology and carcinogenicity studies were conducted by administering monochloroacetic acid (99% pure) in deionized water by gavage to groups of F344/N rats and B6C3F1 mice of each sex once daily, 5 days per week for 16 days, 13 weeks, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, mouse lymphoma L5178Y cells, Chinese hamster ovary cells, and Drosophila melanogaster. 16-Day Studies: Groups of five rats of each sex received 0, 7.5, 15, 30, 60, or 120 mg monochloroacetic acid/kg body weight. Doses administered to mice were 0, 15, 30, 60, 120, or 240 mg/kg to groups of five males and 0, 30, 60, 120, 240, or 480 mg/kg to groups of five females. One of five male rats given 120 mg/kg died during the studies. Clear nasal discharge, lacrimation, or both, were observed in all groups of male and female rats receiving monochloroacetic acid. No compound-related gross lesions were observed in rats. All male mice given 240 mg/kg and all females given 240 or 480 mg/kg died during the studies. Hypoactivity, piloerection, ataxia, and lacrimation were observed in mice given 240 or 480 mg/kg. No compound-related gross lesions were observed in mice at necropsy. 13-Week Studies: Groups of 20 rats of each sex received 0, 30, 60, 90, 120, or 150 mg/kg monochloroacetic acid, and groups of 20 mice of each sex received doses of 0, 25, 50, 100, 150, or 200 mg/kg. Three to five animals in each dose group were killed at weeks 4 and 8 for the evaluation of hematology parameters. Compound-related deaths occurred in rats in the three highest dose groups (all males given 120 or 150 mg/kg, 9/10 males given 90 mg/kg, and all females given 90 to 150 mg/kg) and in mice given 200 mg/kg (all males and 2/10 females). Final mean body weights of surviving rats and mice receiving monochloroacetic acid were similar to those of controls. In rats, dose-related increases in blood urea nitrogen, alanine aminotransferase, and aspartate aminotransferase levels were observed, and relative liver and kidney weights were elevated. There were no compound-related changes in the various hematologic or clinical pathology parameters in mice. A dose-related increase in the incidence and severity of cardiomyopathy was observed in male and female rats receiving monochloroacetic acid, and hepatocellular cytoplasmic vacuolization was observed in the high-dose mice that died during the studies. 2-Year Studies: Based on the mortality and compound-related histopathologic lesions observed in the 13-week studies, doses selected for the 2-year studies of monochloroacetic acid were 0, 15, or 30 mg/kg, administered to groups of 70 rats of each sex, and 0, 50, or 100 mg/kg, administered to groups of 60 mice of each sex. Interim evaluations were conducted on 10 rats per dose group after 6 months of treatment with monochloroacetic acid and on seven rats per dose group after 15 months of treatment. Body Weight and Survival in the 2-Year Studies: Mean body weights of low- and high-dose female and low-dose male rats receiving monochloroacetic acid were within 10% of those of controls throughout the studies; however, after week 30, the mean body weights of high-dose male rats were 4% to 8% less than those of controls. In mice, the mean body weights of dosed males were similar to controls, but those of low- and high-dose females were 6% to 10% less than control values after week 52. Survival of high-dose male and dosed female rats and high-dose male mice was significantly lower than that of controls (male rats: control, 27/53; low-dose, 21/53; high-dose, 16/53; female rats: 37/53; 19/53; 26/53; male mice: 46/60; 39/60; 21/60; female mice: 42/60; 40/60; 44/60). Neoplasms and Nonneoplastic Lesions in the 2-Year Studies: There was no compound-related increase in the incidence of neoplasms or nonneoplastic lesions in rats given monochloroacetic acid for 2 years. The incidence of uterine stromal polypss. The incidence of uterine stromal polyps in low- and high-dose female rats was slightly higher than that in controls (2/60; 7/57; 10/60). However, the incidence in the controls was unusually low, and those in the dosed groups were well within the range for NTP historical controls (mean: 21%, range: 10%-38%). Further, because the only malignant stromal neoplasm occurred in a control animal, the polyps were not considered to be related to the administration of monochloroacetic acid. Similarly, there was no monochloroacetic acid-related increase in the incidence of neoplasms in male or female mice, and malignant lymphoma occurred with a significant negative trend in dosed female mice. Increases in the incidence of inflammation of the mucosa of the nasal passages, respiratory epithelial metaplasia of the olfactory epithelium of the nose, and focal squamous cell hyperplasia of the forestomach occurred in dosed male and female mice. Genetic Toxicology: Monochloroacetic acid was not mutagenic in Salmonella typhimurium strains TA100, TA1535, TA1537, or TA98, with or without exogenous metabolic activation (S9). It induced trifluorothymidine resistance in L5178Y cells in the absence of S9 and induced sister chromatid exchanges without S9 in Chinese hamster ovary cells. Monochloroacetic acid did not induce a significant increase in chromosomal aberrations in Chinese hamster ovary cells, with or without S9. Monochloroacetic acid administered in feed was negative for the induction of sex-linked recessive lethal mutations in germ cells of male Drosophila melanogaster; however, when it was administered by injection, the results were equivocal. Conclusions: Under the conditions of these 2-year gavage studies, there was no evidence of carcinogenic activity for monochloroacetic acid in male or female F344/N rats given 15 or 30 mg/kg. There was no evidence of carcinogenic activity for monochloroacetic acid in male or female B6C3F1 mice given 50 or 100 mg/kg. Monochloroacetic acid administration was associated with inflammatory lesions of the nasal mucosa, metaplasia of the olfactory epithelium, and squamous cell hyperplasia of the forestomach in male and female mice. Synonyms: Chloroacetic acid, a-chloroacetic acid, chloroethanoic acid

Journal Article↗
PubMed1992

Morphologic and cytochemical characteristics of blood cells from the desert tortoise (Gopherus agassizii).

Morphologic and cytochemical staining characteristics of erythrocytes, leukocytes, and thrombocytes of the desert tortoise (Gopherus agassizii) were evaluated, using blood smears prepared from 23 healthy tortoises of Kern County, Calif. Special emphasis was placed on differentiating features of the various leukocytes and thrombocytes. A variety of cytochemical stains, including benzidine peroxidase, Sudan black B, chloroacetate esterase, alpha-naphthyl butyrate esterase, acid phosphatase, leukocyte alkaline phosphatase, periodic acid-Schiff, and toluidine blue were used. Heterophils had a characteristic, large, focal area of positive staining with chloroacetate esterase, alpha-naphthyl butyrate esterase, and acid phosphatase. Eosinophils stained diffusely positive with benzidine peroxidase, allowing differentiation of this leukocyte from heterophils. Thrombocytes stained focally positive with periodic acid-Schiff, allowing differentiation of these cells from lymphocytes, which stained uniformly negative. An intracytoplasmic body, commonly observed within erythrocytes, was considered ultrastructurally to represent a degenerate organelle.

Animals↗
PubMed1978

Cytochemical demonstration of esterases in peripheral blood leukocytes.

Cytochemical methods for alpha naphthyl acetate esterase and chloroacetate esterase have been used to identify human monocytes and granulocytes. In this study, a standard procedure for staining alpha naphthyl acetate and chloroacetate esterase activities was modified by extending the range of pH of the incubation mixture and the duration of staining and was applied to cat, dog, goat, guinea pig, hamster, human, pig, rabbit, rat, and sheep leukocytes. The results for both enzymes showed (1) incubation time and pH had discrete effects on staining and (2) species differences for in vitro conditions to demonstrate esterase activity were pronounced.

Acetates↗
PubMed1985

Formation of glutathione conjugates by reactive metabolites of vinylidene chloride in microsomes and isolated hepatocytes.

Oxidation of the vinyl halide carcinogen and hepatotoxin vinylidene chloride (VDC) by microsomal cytochrome P-450 yields 2,2-dichloroacetaldehyde, 2-chloroacetyl chloride, 2-chloroacetic acid, and 1,1-dichloroethylene oxide. The roles of these metabolites in covalent modification of proteins and reduced glutathione (GSH) were examined. 2-Chloroacetyl chloride reacted with model thiols at least 10(3)-fold faster than did 1,1-dichloroethylene oxide and at least 10(5)-fold faster than did 2,2-dichloroacetaldehyde or 2-chloroacetic acid. Microsomal covalent binding of [14C]VDC was inhibited by GSH but not by lysine, suggesting that protein thiols, rather than amino groups, are major targets. Liver microsomes catalyzed the formation of three GSH:VDC metabolite conjugates, identified as S-(2,2-dichloro-1-hydroxy)ethylglutathione, 2-(S-glutathionyl)acetate, and S-(2-glutathionyl)acetylglutathione, a novel conjugate containing both stable (thioether) and labile (thioester) linkages. The latter two conjugates also were formed in isolated rat hepatocytes and measurable amounts of 2-(S-glutathionyl)acetate were released into the incubation medium. Both 2-(S-glutathionyl)acetate and S-(2-glutathionyl)acetylglutathione were formed with [35S]GSH added to the hepatic medium, indicating that reactive VDC metabolites are capable of crossing the plasma membrane to react with extracellular targets. Unlabeled S-(2-glutathionyl)-acetylglutathione underwent carbonyl substitution with added [35S]GSH, suggesting that this conjugate may participate in modification of protein thiols. This conjugate also underwent hydrolysis with a half-life of approximately 3 hr. GSH:VDC metabolite conjugates may serve as accessible models for labile covalent adducts formed between VDC metabolites and protein thiols.

Animals↗
PubMed1976

Evidence for significant hematopoiesis in the human thymus.

Earlier studies on fetal thymus suggested that certain of the large pyroninophilic cells found there might have a hemopoietic role, and it was decided to determine the nature of these cells using histochemical and immunohistochemical methods. Thymic tissue from aborted fetuses, stillbirths, and neonatal deaths was examined histochemically using methods for the detection of chloroacetate esterase, peroxidase, and pseudoperoxidase, and by staining techniques for mast cells and eosinophils. Tissue was also examined using the indirect immunoperoxidase method for the presence of hemoglobin A (HbA) and F (HbF), for lysozyme (muramidase) and immunoglobins alpha, mu, gamma, kappa, lambda. Positive staining to some degree was seen in cells in the connective tissue stroma using all methods, and the cells stained corresponded to one or another of the types of pyroninophilic cells present. The finding of large cells with positive chloroacetate esterase and antilysozyme indicates the presence of granulopoiesis. Similarly, the presence of large nucleated cells with pseudoperoxidase and anti-hemoglobin (A and F) staining indicates the presence of erythropoiesis. Plasma cells were present in small numbers.

Antibody Specificity↗
PubMed1984

Phorbol ester-induced differentiation of a non-T/non-B human leukemic cell line (REH) to macrophage-like cells.

Treatment of non-T/non-B human leukemic cell line REH with 5 X 10(-9) M 12-O-tetradecanoylphorbol-13-acetate (TPA) at 37 degrees resulted in their adherence to culture flasks by 24 to 36 hr and, after 72 hr, the entire surface of the flask/coverslips became covered with macrophage-like cells containing pseudopodia. Wright-Giemsa-stained untreated cells had blast morphology, whereas TPA-treated cells (adherent or excess cells remaining in suspension) had characteristic morphology of macrophages and phagocytized large numbers of latex beads. Untreated REH cells were negative for nitroblue tetrazolium reduction, Sudan Black B, and peroxidase, and they were weakly positive for periodic acid-Schiff, acid phosphatase, chloroacetate esterase (pH 6.8), and nonspecific (naphthol AS-D acetate, pH 6.8) esterase, whereas TPA-treated cells (adherent or in suspension) gave strong reaction for these stains except for peroxidase and chloroacetate esterase which showed moderate reaction. Furthermore, the nonspecific esterase activity of TPA-treated cells and weak activity in 10% of untreated cells was strongly inhibited by NaF, a characteristic of monocytic series of cells. Lysozyme activity was not detected in culture supernatant from control or TPA-treated cells. No cytoplasmic immunoglobulin was detected in untreated or TPA-treated cells, and the monocyte/granulocyte antigen (detected by MCS-2 monoclonal antibody) which was absent from untreated REH cells was expressed in TPA-treated cells. TPA-treated cells lost common acute lymphoblastic leukemia antigen but showed significantly elevated expression of histocompatibility locus DR antigen. Terminal transferase estimated by immunofluorescence and biochemical assay was high in untreated REH cells, whereas TPA-treated cells were negative in terminal transferase immunofluorescence and had only negligible terminal transferase activity in biochemical assay. All these changes in REH cells observed on TPA treatment represent the differentiation of a human leukemic non-T/non-B-cell line to macrophage-like cells for the first time which indicates that some non-T/non-B acute lymphoblastic leukemia cells may have latent monocyte-like phenotype.

Cell Differentiation↗
PubMedDate not supplied

Identification of hematopoietic progenitor cells in human amniotic fluid before the 12th week of gestation.

Due to technical difficulties in performing amniocentesis before the 12th week of pregnancy, very little is known about the components of human amniotic fluid before that time. Amniocentesis was performed between the 7th-11th week of gestation in 25 informed and consenting patients, who had to undergo therapeutic interruption of pregnancy. The cells from the amniotic fluid were stained, counted on a hemocytometer, and checked for vitality. The origin of these cells was determined from cellular cultures the intracellular content of the hemoglobin and the chloroacetate esterase content of the hemoglobin and the chloroacetate esterase contents were also studied. Taking advantage of the "in vitro" adhesive properties of these cells to the bone marrow stromal feeder layer, we obtained clonal growth of an erythroid nature from 18 out of 33 samples. At the 17th week of gestation, an increased number of cells and a decrease in their vitality was found. Between the 7th and 12th week, the cellular composition of the fluid was totally different from that found later in the pregnancy. Small nucleated, round cells were identified as hematopoietic progenitor cells. At the beginning of the 11th week, a cellular population, typically used to perform prenatal diagnosis of chromosomal abnormalities from the 14th week of pregnancy appeared. Since hematopoietic progenitor cells were found in the amniotic fluid before the 12th week of gestation, these cells most probably come from the hematopoietic cells of the yolk sac through the thin membrane of the yolk sac at this time.

Amniotic Fluid↗
PubMed1997

Bone marrow mastocytosis associated with an undifferentiated extramedullary tumor of hemopoietic origin.

The case of a 62-year-old man who presented with acute abdominal pain and a widespread tumor involving the retroperitoneum is described. Three weeks after initial presentation, the patient died suddenly of acute cardiac failure with signs of arrhythmia. Autopsy revealed a disseminated tumor with infiltration of the retroperitoneal fat, as well as nodules in the left testis and the right atrium. The tumor cells were reactive for CD45, vimentin, and chloroacetate esterase, but were unreactive with a broad spectrum of antibodies against myelomonocytic and lymphocytic antigens and with antibodies against tryptase and c-kit (CD117), which are characteristic markers for mast cells. However, the bone marrow exhibited the typical picture of mastocytosis, with disseminated clusters of differentiated spindle-shaped cells that stained strongly for tryptase, c-kit, and chloroacetate esterase. No infiltrates of well-differentiated mastocytosis could be detected in any of the extramedullary tissues investigated. A diagnosis of bone marrow mastocytosis with an associated undifferentiated extramedullary tumor of hemopoietic origin was established. By definition, the extramedullary tumor could not be diagnosed as a granulocytic sarcoma or (differentiated) mastocytoma, but the possibility that a mast cell progenitor could be involved in the evolution of both tumors cannot be ruled out.

Bone Marrow Diseases↗
PubMed1997

Systemic mast cell disease (mastocytosis). General aspects and histopathological diagnosis.

Systemic mast cell disease/mastocytosis (SMCD) is best defined as a multitopic proliferation of cytologically and/or functionally abnormal tissue mast cells (TMC). SMCD preferentially involves the bone marrow, skin, spleen, liver, and lymph nodes. The histopathological diagnosis of SMCD may be very difficult to make, and the disease is often not considered in the differential diagnosis of lymphoreticular neoplasia. In suspected cases of SMCD, basic dyes such as Giemsa and toluidine blue are useful to demonstrate the specific metachromatic granules of TMC. The naphthol AS-D chloroacetate esterase reaction has also proved to be very reliable for enzyme-histochemical identification of TMC. Major diagnostic problems may arise in cases of malignant or "aggressive" SMCD exhibiting tissue infiltrates consisting predominantly of highly atypical, non-metachromatic TMC, which are usually also only weakly reactive for chloroacetate esterase. Immunostaining with antibodies against the mast cell-specific proteases tryptase and chymase has proved to be of great value of establishing the correct diagnosis in such cases. Anti-tryptase antibodies have major diagnostic significance due to their extremely high sensitivity and specificity. The classification of SMCD is controversial, but there is increasing support for the differentiation of at least two major subtypes that differ in prognosis: (i) a benign or "indolent" variant in which skin involvement (urticaria pigmentosa-like skin lesions) is usual, but associated malignant hematological disorders are rare; and (ii) a malignant or "aggressive" variant where skin involvement is usually absent but concomitant malignant hematological disorders (myelodysplastic and myeloproliferative syndromes and acute non-lymphocytic leukemias) are very common. Preliminary molecular biological studies of a few cases of malignant SMCD using the recently developed HUMARA assay have yielded evidence that the disease is monoclonal.

Animals↗
PubMed1997

Induction of differentiation of U-937 cells by 2-chloro-3-amino-1,4-naphthoquinone.

Naphthoquinone compounds have various pharmacological effects such as antiviral, antifungal and anticancer activities. We demonstrated the differentiation of the inducing effect of a naphthoquinone derivative, 2-chloro-3-amino-1,4-nahpthoquinone (NQCA) on the human leukemia cell line U-937. When U-937 cells were treated with NQCA for 4 days, phenotypes indicative of differentiation such as nitroblue tetrazolium (NBT)-reducing activity and phagocytosis were induced. To evaluate the route of differentiation of U-937 cells induced by NQCA, we determined naphthol AS-D chloroacetate esterase and alpha-naphthyl acetate esterase activities. Four days treatment of U-937 cells with NQCA increased alpha-naphthyl acetate esterase activity about 63.5% but naphthol AS-D chloroacetate esterase was not detected. These results indicate that NQCA caused differentiation of U-937 cells into macrophage-like cells. Since protein kinase C (PKC) and protein kinase A (PKA) have important roles in cell-differentiation and proliferation, we employed a PKC inhibitor NA-382 and a PKA inhibitor H-89 to examine the effects of each kinase on the differentiation of U-937 cells. The PKC inhibitor NA-382 decreased the effect of NQCA on U-937 cells, while the PKA inhibitor H-89 did not. Also glutathione (GSH) inhibited the effect of NQCA. It is concluded that the differentiation-inducing effect of NQCA on U-937 cells may be attributed to PKC activation followed by production of free radicals.

Alkaloids↗
PubMed1996

Central nervous system granulocytic sarcoma in a patient with essential thrombocythemia.

We report a rare case of central nervous system granulocytic sarcoma (GS) in a patient with essential thrombocythemia (ET). The diagnosis of GS was established by morphological and cytochemical findings (peroxidase and naphthol-AS-D-chloroacetate esterase positivity) of neoplastic cells. GS was detected as an intracranial frontal mass 7 months before the transformation of ET in acute myeloid leukemia and relapsed as two extradural spinal masses during the course of leukemic evolution.

Acute Disease↗
PubMed1998

Chloromethyl ketones are insulin-like stimulators of lipid synthesis in locust fat body.

N alpha-tosyl-L-lysine chloromethyl ketone (TLCK) stimulates lipid synthesis in locust fat body in vitro, and is able to reverse the inhibitory effects of AKH-I on lipid synthesis. Effective stimulatory concentrations of TLCK were in the range of 0.2-1.0 mM. Similar stimulatory effects were also achieved with phenylalanine chloromethyl ketone (PheCK) and leucine chloromethyl ketone (LeuCK), but not with tosyl-phenylalanine chloromethyl ketone (TPCK), dansyl-glu-gly-arg-CK, chloroacetone, chloroacetic acid, chloroacetamide, chloroacetaldehyde, chloroacetyl-L-leucine or acetylated or fluorescamine-labelled TLCK, PheCK, and LeuCK. The level of stimulation caused by TLCK was dependent on incubation time, so that after a 5-h preincubation of fat body tissue with TLCK the stimulated rate was severalfold higher than the control. TLCK also increased the rate of uptake of trehalose and uridine, but not glucose, deoxyglucose or glycine. Increasing concentrations of bovine serum albumin (BSA) in the incubation medium caused a reduction in the rate of TLCK-stimulated acetate uptake, such that levels of uptake were no higher with 1% BSA than in the controls. A range of more specific protease and kinase inhibitors was tested, but none caused stimulation; thus the mode of action of TLCK on the stimulation of acetate uptake has yet to be identified. Elucidation of the mode of action of TLCK may facilitate the development of novel compounds for insect pest control.

Adipose Tissue↗
PubMed1999

Synthesis and hypnotic activity of new 4-thiazolidinone and 2-thioxo-4,5-imidazolidinedione derivatives.

Conveniently accessible 4-[(2-(3,4-dimethoxyphenyl)ethyl]-3-thiosemicarbazide (2) was converted to new 1-substituted benzylidene/furfurylidene-4- [2-(3,4-dimethoxyphenyl)ethyl]-3-thiosemicarbazides (3) which furnished 2-(substituted benzylidene/furfurylidene) hydrazono-3-[2-(3,4-dimethoxyphenyl)ethyl]thiazolidin-4-ones (4) and 1-(substituted benzylidene/furfurylidene)-amino -3-[2-(3,4-dimethoxyphenyl)ethyl]-2-thioxo-4,5-imidazolidinedio nes (5) on reaction with chloroacetic acid and oxalyl chloride, respectively. The structure of 5 was confirmed by X-ray diffraction studies performed on 5a. 4 and 5 were evaluated for their potentiating effects on pentobarbital induced hypnosis. Most of the compounds caused remarkable increases in pentobarbital sleeping time.

Animals↗
PubMed1975

"Pure" monocytic or histiomonocytic leukemia: a revised concept.

In a series of 130 cases of acute leukemia studied by cytochemical staining techniques, 10 cases cytochemically diagnosed as "pure" monocytic leukemia were seen. Cytochemical staining of bone marrow aspirates from these patients revealed all leukemic cells to be Sudan black negative. No positive reactions were observed for peroxidase or naphthol AS-D chloroacetate esterase. All cases demonstrated strong alpha-naphthyl acetate esterase positivity; and fluoride-inhibited naphthol AS-D acetate esterase positivity was observed in 8 of 9 cases tested. The P.A.S. reaction showed diffuse fine to coarse granules. Oil red O stain was positive in 8 of 9 cases, and the beta-glucuronidase activity was strong in 5 of 9 cases. Light microscopy revealed cells with monocytic or histiocytic morphology. Electron microscopic studies in 2 cases demonstrated features consistent with leukemic monocytic or histiocytic morphology; none was suggestive of granulocytic or lymphocytic leukemia. Five of 6 patients treated with drug regimens including prednisone and vincristine entered a complete remission; the other obtained a partial remission. Two patients achieved complete remission after treatment with Adriamycin, 1 following a relapse. Three patients who received cytosine arabinoside as their only therapy died soon after treatment was commenced. It is suggested that the cytochemical similarity but morphological differences in those patients may be objectively used to group them as cases of histiomonocytic leukemia.

Adolescent↗
PubMed1978

Granulocytic sarcoma of the uterus.

The presenting features of vaginal bleeding and abnormal cytologic smears in a elderly patient with simultaneously occurring acute myelogenous leukemia (AML), were due to massive infiltration of the uterine cervix and endometrium by immature myeloid elements or granulocytic sarcoma. The abnormal cytologic smears and uterine mass were initially believed to represent a poorly differentiated lymphocytic lymphoma. The diagnosis of granulocytic sarcoma was confirmed with the naphthol AS-D chloroacetate stain that demonstrated activity in the cytoplasm of the neoplastic cells.

Diagnosis, Differential↗
PubMed1979

Granulocytic sarcoma preceding acute leukemia: a report of six cases.

An unusual case of granulocytic sarcoma presenting in a pericardial effusion following trauma and preceding acute myelogenous leukemia (AML) by 8 months is presented. Five additional cases of granulocytic sarcoma preceding leukemia collected by the author are also tabulated. Granulocytic sarcoma in a nonautopsy population of myelogenous leukemic patients was found to be 2.9%. When presenting in an extramedullary site, especially preceding peripheral blood and bone marrow manifestations of leukemia, a misdiagnosis of histiocytic lymphoma may result. In questionable cases, other techniques including the naphthol-ASD-chloroacetate stain, touch imprints, immunoperoxidase stain for lysozyme, and electron microscopy should be utilized. Although only a small series, the most recent cases have shown induction/remission and survival characteristics of AML patients without granulocytic sarcoma.

Adolescent↗
PubMed1979

Acute myeloblastic leukemia developing in patients with mediastinal lymphoblastic lymphoma.

Of three patients with mediastinal malignant lymphoma, lymphoblastic type, at the time of diagnosis one also had acute myeloblastic leukemia (AML), and the other two had blood and bone marrow findings indicative of acute lymphoblastic leukemia (ALL). The latter two patients developed the hematologic picture of AML less than eight months later. In all cases, AML was confirmed by cytochemical studies of peripheral blood and bone marrow cells. Autopsy of two of the patients revealed only AML. The myeloid nature of the proliferative cells was demonstrated with the naphthol-ASD-chloroacetate stain (NCA) on postmortem tissue sections. This study further supports the hypothesis of a common origin of neoplastic lymphoid and myeloid cells from pluripotent bone marrow stem cells.

Adult↗