Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0023418 (
leukemia
)
93,477
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Rats bearing Reuber H-35 or Novikoff hepatomas and mice bearing L1210 or L5178Y murine leukemias exhibited elevated serum levels of fetuin : N-acetylneuraminic acid transferase (EC 2.4.99.1) activity. The serum transferase activity could be correlated with the growth rate of the tumor; in animals bearing the more rapidly growing Novikoff hepatoma, activity was higher than in animals bearing the Reuber H-35 hepatoma. Higher transferase levels were also found in L1210 leukemic mice than in mice with the slightly slower growing L5178Y
leukemia
. Serum from rats bearing Reuber H-35 hepatoma and mice bearing L1210 murine
leukemia
had elevated levels of alpha- and
beta-glucosidase
(EC 3.2.1.20 and
EC 3.2.1.21
), alpha- and beta-galactosidase (EC 3.2.1.22 and (3.2.1.23), beta mannosidase (EC 3.2.1.25), alpha- and beta-fucosidase (EC 3.2.1.- and EC 3.2.1.38), beta-N-acetylglucosaminidase (EC 3.2.1.30) and acid phosphatase (EC 3.1.3.2); alpha-mannosidase (EC 3.2.1.24), beta-N-acetylgalactosaminidase (EC 3.2.2.-) and beta-xylosidase (EC 3.2.1.37) were not elevated. In animals bearing Reuber H-35 hepatoma, host liver levels of glycosidases, beta-glucuronidase (EC 3.2.1.31) and acid phosphatase were elevated over both the control and the hepatoma values. The data are interpreted to mean that the tumors or various host tissues release large quantities of enzymes into the serum and that enzyme levels in host organs may also be affected by the tumor.
...
PMID:Serum and host liver activities of glycosidases and sialyltransferases in animals bearing transplantable tumors. 17 98
Amygdalin MF was evaluated alone and in combination with an activating agent,
beta-glucosidase
, against three transplantable rodent tumors; Ridgway osteogenic sarcoma, Lewis lung carcinoma, and P388
leukemia
. In dose-response studies up to the LD20 in normal mice, amygdalin MF alone did not demonstrate significant antitumor activity against any of these three tumor systems. Similarly, at doses not exceeding the LD10 in normal mice, amygdalin MF plus
beta-glucosidase
did not demonstrate antitumour activity against any of these three tumor systems. Potentiation of the lethal toxicity of amygdalin MF by
beta-glucosidase
was observed in all studies where the two agents were given in simultaneous combination.
...
PMID:Experimental studies of the antitumor activity of amygdalin MF (NSC-15780) alone and in combination with beta-glucosidase (NSC-128056). 106 May 11
The ultrastructural localization of four acid hydrolases (acid phosphatase, beta-glucuronidase, beta-glucosaminidase and alpha-naphthylacetate esterase) has been studied in lymphocytes from 16 patients with three types of chronic T-cell
leukaemia
, namely, T-prolymphocytic
leukaemia
(T-PLL), T-chronic lymphocytic leukaemia (T-CLL) and adult T-cell lymphoma
leukaemia
(ATLL). Different patterns of enzyme distribution were observed in the leukaemic T-cells from these disorders. In T-PLL, reactivity for the four acid hydrolases was confined to single or a few large granules. Gall bodies were reactive for beta-glucuronidase, b-glucosaminidase and alpha-naphthylacetate esterase but apparently unreactive for acid phosphatase. In T-CLL, scattered small- to medium-size cytoplasmic granules and many parallel tubular arrays were strongly reactive for acid phosphatase, beta-glucuronidase and
beta-glucosidase
but showed no reactivity for alpha-naphthylacetate esterase. Intermediate features were observed in ATLL. The observed differences in enzyme reactivity reflect a different content of lysosomal granules in the various types of leukaemic T-cells. They also suggest that similar differences may be found in normal T-lymphocyte subsets.
...
PMID:Ultrastructural cytochemistry of chronic T-cell leukaemias. A study with four acid hydrolases. 660 30
The effect of amygdalin on human acute myelogenous leukemia cells and normal bone marrow granulocyte-monocyte precursors was studied in vitro using soft-gel culture. A pharmaceutical and a clinical source of amygdalin were tested and
beta-glucosidase
was added to selected cultures to promote the hydrolysis of amygdalin. Acute myelogenous leukemia cells were obtained from two human cell lines designated KG-1 and HL-60. A 50% inhibition of colony formation by both normal and leukemic cells was observed at an amygdalin concentration of 3.5 mg/ml using both drug sources. We found the colony-forming cells from the leukemic cell lines and normal marrow to be relatively resistant to amygdalin and its metabolites in vitro, and there was no selective kill of clonogenic cells from the human
leukemia
cell lines as compared to normal bone marrow.
...
PMID:Amygdalin (Laetrile): effect on clonogenic cells from human myeloid leukemia cell lines and normal human marrow. 692 26
A patient with coexistent Gaucher disease and Philadelphia positive chronic granulocytic leukemia (CGL), who subsequently developed myeloblastic
leukemia
, is described. The diagnosis of CGL was established according to standard clinical, morphological, biochemical, and cytogenetic data, while the diagnosis of true Gaucher disease was based on biochemical data and the presence of Gaucher cells with typical ultrastructural features in the bone marrow and spleen. Enzyme studies showed low activity of ceramide-
beta-glucosidase
in the patient's peripheral blood leukocytes, skin fibroblasts, and splenic tissue and the presence of increased amounts of ceramide-beta-glucoside in the spleen. This case is reported in order to draw attention to the possible coexistence of these two diseases in the same patient, as opposed to the well-recognized finding of "Gaucher-like" cells in the bone marrow of patients with CGL. Enzyme studies enable distinction between these two situations.
...
PMID:Coexistence of Gaucher Disease and Philadelphia positive chronic granulocytic leukemia. 695 8