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: EC:3.5.1.1 (
asparaginase
)
2,695
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Nutrients as therapy for patients with cancer are important as adjunctive therapy, i.e., adequate nutrition may be important for the success of whatever form of therapy is administered. Diets deficient in certain amino acids have some selectivity when tested against experimental tumors propagated in vivo. Such diets have had limited clinical trial and have been characterized by poor patient acceptance. Enzymes that produce deficiencies of certain amino acids, e.g.,
asparaginase
, glutaminase, methioninase appear to offer a more reasonable approach to development of selective amino acid deficiencies in man. Trace metals in excessive amounts may be toxic or carcinogenic to the host. Two heavy metal salts, Cis-diamine dichloroplatinum and gallium nitrate, have recently been shown to have anti-neoplastic effects in man. There is no conclusive evidence that vitamins, administered in large doses, have significant antineoplastic effects although large doses of vitamin A, vitamin C, and vitamin B12 have been used for this purpose. In contrast, certain vitamin analogs such as folate antimetabolites can cause tumor regression and are useful clinical treatment. An enzyme, carboxypeptidase G1, by splitting naturally occurring folates, may also have promise as a method of producing enzymic
folate deficiency
.
...
PMID:Nutrients, vitamins and minerals as therapy. 37 10
Plasma homocysteine was determined in 12 children with acute lymphoblastic leukemia. The patients were investigated prior to chemotherapy (stage I), during seven weeks of induction chemotherapy (stage II), and thereafter during intermittent high-dose methotrexate (HD-MTX) therapy (stage III). The patients were followed for a period of three to 15 months, and the study included a total of 80 HD-MTX courses. Before start of chemotherapy (stage I), the average plasma homocysteine level in the children with leukemia was 13.18 +/- 6.23 (SD) mumol/liter, which is significantly (P less than 0.001) higher than the level in control children (6.52 +/- 1.21 mumol/liter). The plasma homocysteine level in the patients was positively correlated with the peripheral white blood cell count (P less than 0.01) and negatively correlated with serum folate (P less than 0.02). The serum folate was normal or subnormal in these patients. During induction therapy with cytotoxic drugs such as vincristine,
asparaginase
, and intrathecal MTX (stage II), there was a drastic change in plasma homocysteine as a function of time. A reciprocal alteration in serum folate was observed, suggesting fluctuating intracellular folate status at this stage of therapy. At the end of stage II (about seven weeks), there was a significant (P less than 0.01) reduction in total homocysteine (to 7.08 +/- 3.84 mumol/liter). HD-MTX (8 g/m2) therapy with 5-formyltetrahydrofolate "rescue" (stage III) was usually begun about seven weeks after start of chemotherapy, and the patients were followed for two to eight courses separated by three to eight weeks. Plasma homocysteine showed a transient increase (26-64%) following each MTX infusion. After three MTX infusions, basal total plasma homocysteine was reduced to 5.56 +/- 1.12 mumol/liter. During most MTX infusions, there was a variable reduction (17-56%) in plasma methionine followed by a rebound increase. It is concluded that plasma homocysteine in children with acute lymphoblastic leukemia is elevated prior to therapy, probably because of occasional
folate deficiency
and increased burden of proliferating cells. During induction therapy, monitoring plasma homocysteine and serum folate both suggest a labile folate homeostasis, usually a deficiency state. HD-MTX induced a temporary intracellular folate depletion before 5-formyl-tetrahydrofolate was administered, as judged by a transient homocysteinemia. The methionine depletion may interfere with the antileukemic effect of MTX.
...
PMID:Plasma homocysteine in children with acute lymphoblastic leukemia: changes during a chemotherapeutic regimen including methotrexate. 198 22