Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 30-year-old man was referred because of slight leukocytosis. The hematological findings, including those of the bone marrow, showed no evidence of leukemia. The level of neutrophil alkaline phosphatase (NAP) in the peripheral blood was normal, as were the chromosomes from bone marrow cells. Fifteen months later, the disease was diagnosed as M2 (according to the French-American-British classification) showing a t(8;21)(q22;q22) and a low NAP level as two markers of M2 cells. This is probably the first case of acute leukemia in which the cytogenetic analysis was performed before and after the appearance of a specific chromosome abnormality.
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PMID:Appearance time of leukemic cells with t(8;21) in bone marrow. 225 82

Stromal cell numbers from subjects with no haematological disease and those with acute myeloid leukaemia (AML), chronic granulocytic leukaemia (CGL), acute lymphatic leukaemia (ALL) and non-Hodgkin's lymphoma (NHL) were compared to determine their role in malignancy. Frozen sections of trephine biopsy specimens from iliac crests were stained for endogenous alkaline phosphatase activity, endogenous acid phosphatase activity, and, using immunocytochemical methods, for endothelial cells (anti-factor-VIII related antigen) and macrophages and related cells (EBM/11). In granulocytic malignancies, whether acute or chronic, alkaline phosphatase positive reticulum cells (AL-RC) and vascular endothelial cells were generally increased. In lymphoid malignancies, the numbers of AL-RC were generally reduced. Numbers of vascular endothelial cells seemed to be normal in ALL but reduced in foci of NHL. Macrophages are numerous in normal marrow, and their numbers seemed to be normal in granulocytic lesions but were more variable and sometimes reduced in ALL and NHL. Lymphoid malignancies, therefore, have a destructive effect on some stromal elements; granulocytic malignancies are associated with normal or increased numbers of stromal cells. A possible consequence of depleted stromal cells might be slower reconstitution of normal haemopoiesis after treatment. The large numbers in granulocytic malignancies raises the possibility of synergistic stimulation between stromal and neoplastic cells.
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PMID:Bone marrow stromal cell changes in haematological malignancies. 226 66

This study examines the effect of cytosine arabinoside (Ara-C) on CFU-GM progenitor cells grown in methylcellulose culture from normal and myelodysplastic subjects and patients with acute non-lymphoblastic leukaemia. Light density marrow cells were incubated during culture with Ara-C concentrations ranging from 10(-4) M to 10(-12) M. After counting, colonies were cytospun and cells within the colonies examined for alkaline phosphatase positivity and expression of HLA-DR antigen, as indices of differentiation. Monocytes/macrophages were also enumerated in colonies using the monoclonal antibody CD14. In all subjects, 10(-4) M to 10(-6) M Ara-C caused significant reduction in CFU-GM colony formation compared with control (no Ara-C). In no instance did colony numbers increase. Ara-C across the dose curve had no effect on myeloid differentiation markers in any of the groups studied. Similarly, percentages of CD14 positive cells in colonies were not altered by exposure to Ara-C. Using this clonogenic model, these data suggest that Ara-C does not induce differentiation of CFU-GM stem cells in normal subjects or patients with myelodysplasia/acute non lymphoblastic leukemia.
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PMID:Cytosine arabinoside does not cause differentiation in vitro of CFU-GM in marrow from normal, myelodysplastic or ANLL subjects. 231 14

9-[5'-(2-Oxo-1,3,2-oxazaphosphorinan-2-yl)-beta-D-arabinosyl]adeni ne (1c) and 9-[5'-(2-oxo-1,3,2-dioxaphosphorinan-2-yl)-beta-D-arabinosyl]adeni ne (1d) were synthesized by reaction of 9-[beta-D-arabinofuranosyl]adenine with phosphoryl chloride with 1-amino-3-propanol and 1,3-propanediol, respectively. 1c consisted of a mixture of diastereomers, while 1d was enantiomerically homogeneous. The structures of these compounds were established by spectral (1H NMR, MS, UV) and elemental analyses. Both 1c and 1d were resistant to degradation by 5'-nucleotidase, alkaline phosphatase, venom phosphodiesterase, crude snake venom, adenosine deaminase, and adenylate deaminase. Neither compound was significantly biotransformed by mouse hepatic microsomal preparations in the presence of an NADPH-generating system. Compound 1c was marginally effective at prolonging the life span of mice bearing P-388 leukemia; compound 1d, however, was inactive.
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PMID:Synthesis and biological evaluation of 9-[5'-(2-oxo-1,3,2-oxazaphosphorinan-2-yl)-beta-D-arabinosyl]ade nine and 9-[5'-(2-oxo-1,3,2-dioxaphosphorinan-2-yl)-beta-D-arabinosyl]ade nine: potential neutral precursors of 9-[beta-D-arabinofuranosyl]adenine 5'-monophosphate. 241 27

The hematopoietic cells in blood and/or bone marrow from 20 leukemic dogs and 22 control dogs were characterized using a battery of cytochemical stains. The results of cytochemical staining led to modification of the diagnoses based on clinical, hematologic and histologic findings in seven (35%) of the leukemias. Sudan black B and chloroacetate esterase served as granulocytic markers in both the control and leukemic groups. Peroxidase activity was present in the granulocytes and monocytes of control animals but not the blasts of leukemic dogs. Alkaline phosphatase-positive staining of granulocytic precursors was a consistent finding in granulocytic and myelomonocytic leukemia, and alkaline phosphatase-positive lymphoblasts were seen in 38% of lymphocytic leukemias. Diffuse alpha naphthyl butyrate esterase-positive staining marked monocytes in both control and leukemic dogs. Cytochemical staining was found to be a valuable diagnostic aid in the classification of leukemias in the dog.
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PMID:Cytochemical characterization of leukemic cells from 20 dogs. 241 32

The present study describes 11 cases (10 carcinomas, one rhabdomyosarcoma) in which immuno-alkaline phosphatase labelling with monoclonal antibodies was used to demonstrate metastatic cells in routine smears of aspirated bone marrow. Carcinoma cells were detected using antibodies against epithelial cytokeratins, milk fat globule membrane antigen and carcinoembryonic antigen, and rhabdomyosarcoma cells with monoclonal anti-desmin. In four of the carcinoma cases it had not been possible to identify malignant cells in routinely stained marrow smears, whilst the case of disseminated rhabdomyosarcoma had initially been diagnosed (and treated) as a case of acute lymphoblastic leukaemia. The anti-cytokeratin antibody was found to be the most valuable of the anti-epithelial reagents used, since it labelled malignant cells in all of the 10 cases of carcinoma and gave the strongest reactions. These results suggest that immunocytochemical labelling should be used in cases of suspected carcinoma whenever conventional examination of marrow smears yields negative results, and furthermore (as illustrated by the case of rhabdomyosarcoma) that the technique is of value for identifying the true nature of poorly differentiated neoplasms in bone marrow.
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PMID:Detection of metastatic tumour cells in routine bone marrow smears by immuno-alkaline phosphatase labelling with monoclonal antibodies. 241 78

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hematopoietic stem cell disorder in which the blood cells demonstrate aberrant interactions with serum complement. In part, this is due to the absence of the complement regulatory protein, decay accelerating factor (DAF). A small number of patients with PNH have gone on to develop acute nonlymphocytic leukemia, which is thought to arise from the injured marrow as a second hematopoietic disorder. We have studied a patient with PNH who developed acute myeloblastic leukemia (AML); the blasts from this patient were found to lack DAF as measured by polyclonal antibody binding and fluorescence flow cytometry as well as by immunoblotting. The blasts from 11 other patients with AML bound anti-DAF antibody in amounts similar to normal mononuclear cells from healthy donors. Cells of the human leukemia cell lines HL-60, K562, U937, and HEL also bound anti-DAF antibody. In addition to DAF deficiency, blasts from the PNH patient had undetectable alkaline phosphatase activity, in contrast to human leukemia cell lines. These data suggest that the leukemic cells of the PNH patient arose out of the PNH clone and that AML in the setting of PNH is not a separate disorder.
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PMID:Acute myeloblastic leukemia in paroxysmal nocturnal hemoglobinuria. Evidence of evolution from the abnormal paroxysmal nocturnal hemoglobinuria clone. 243 90

Recent studies have demonstrated by Northern blot analysis that both the c-fms proto-oncogene and the CSF-1 gene are expressed during human monocytic differentiation. In order to examine c-fms and CSF-1 expression at the cellular level, we have applied alkaline phosphatase detection of biotinylated v-fms and CSF-1 cDNA probes in situ. Using this approach, we demonstrate that c-fms and CSF-1 transcripts are detectable in HL 60 cells induced along the monocytic lineage but not in uninduced cells. The specific detection of these transcripts is further supported by the absence of histochemical staining in RNase-treated cells and when using pBR322 plasmid without insert as the biotinylated probe. Finally, the results indicate that most of the induced HL-60 cells have detectable levels of both c-fms and CSF-1 RNA. This approach should be useful for studying expression of these genes in populations of leukemic blasts and normal hematopoietic cells.
Leukemia 1987 Jun
PMID:Detection of c-fms and CSF-1 RNA by in situ hybridization. 244 33

The concomitant presence of B antigens and of the antigen recognized by the monoclonal antibody Leu-M5 (CD11c) on neoplastic lymphoid cells has been reported to be largely restricted to hairy cell leukemia (HCL). The authors studied Leu-M5 reactivity of neoplastic cells from 59 patients whose specimens were referred with a stated diagnosis of HCL by using the alkaline phosphatase anti-alkaline phosphatase technique on peripheral blood (PB) and bone marrow (BM) specimens. Tartrate-resistant acid phosphatase (AcP-T) activity was also studied. In 49 patients, HCL had been confirmed previously by BM biopsy, and specimens were evaluated for disease status during or after therapy with interferon (IFN) or 2'-deoxycoformycin. The remaining ten patients were newly referred for confirmation of the diagnosis of HCL before therapy. In all 55 patients in whom the BM biopsy demonstrated HCL, virtually every leukemic cell was Leu-M5 reactive, and the reaction proved, in some cases, to be helpful in the detection of small numbers of hairy cells in PB or BM preparations. AcP-T reactivity was demonstrated in the neoplastic cells of 52 of these 55 patients, including all but 3 of those receiving IFN, and was helpful in confirming persistent leukemia when interpretation of BM biopsy sections was difficult because the numbers of hairy cells were small. However, in four of the ten newly referred patients, BM biopsy showed features of splenic lymphoma with villous lymphocytes, rather than HCL. The neoplastic cells of these four patients were of B-cell origin and in three were Leu-M5 reactive. The authors' study indicates that Leu-M5 is present in nearly all hairy cells, but its presence in conjunction with other B-cell markers is not specific for HCL.
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PMID:Evaluation of Leu-M5 (CD11c) in hairy cell leukemia by the alkaline phosphatase anti-alkaline phosphatase technique. 245 31

The mouse lymphocyte surface alloantigen, Ly-31, defined by monoclonal antibody N1.10 (IgG2b,k) and controlled by a gene locus closely linked to the Akp-2 locus on chromosome 4, was biochemically investigated. By employing a quantitative immunoassay system, it was found that the Ly-31.1-specific antibody detected an allotypic determinant of mouse alkaline phosphatase. Ly-31.1, i.e., mouse alkaline phosphatase, was expressed predominantly in kidney and bone and was also detected in placenta, lung, and testis. Concerning tumor cell lines, they varied in the amount of antigen present, with both T and B lymphoid lineages selectively possessing the antigen. In normal lymphoid tissues, lesser amounts of antigen were detected. The binding of mouse alkaline phosphatase to Ly-31.1-specific monoclonal antibodies was specific in nature. The Ly-31.1 antigen was immunoprecipitated from the lysates of surface-radiolabeled YAC-1 moloney leukemia cells, and appeared as a single band of about 78,000 under both reduced and nonreduced conditions on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Furthermore, treatment of tumor cell lines with phosphatidylinositol-specific-phospholipase C resulted in the removal of Ly-31 antigen from the cell surface. These results suggest that a gene cluster containing the Ly-31 and Akp-2 loci which control the alkaline phosphatase is formed on mouse chromosome 4. The Ly-31 antigen is the first enzyme demonstrated to be a lymphocyte surface alloantigen.
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PMID:Mouse Ly-31.1 is an alloantigenic determinant of alkaline phosphatase predominantly expressed in the kidney and bone. 246 81


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