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

Children with cancer represent a high-risk group for protein-energy malnutrition due to side effects associated with treatment. Assessment of nutritional status at the time of diagnosis and during treatment is, therefore, essential for planning nutritional intervention. We studied the nutritional status of 25 children with leukemia [9 newly diagnosed/relapsed (D/R) leukemic patients and 16 children with leukemia in remission (REM)]. Plasma proteins (prealbumin, PA; albumin, Alb; transferrin, Tr; retinol-binding protein, RBP) and acute phase-reactant proteins (alpha 1-acid glycoprotein, AGP; C-reactive protein, CRP; ceruloplasmin, CER) were measured by radial immunodiffusion. Results show that there were no significant deficits in anthropometric measurements among leukemic children. In contrast, the mean levels of all plasma proteins, especially PA (P < 0.005), were significantly lower in the D/R group than in the REM group. All D/R children, compared to 59% of those in remission, had PA levels < 20 mg/dl. Only the D/R group had abnormal levels of RBP, Tr, and Alb. Children who were treated with prednisone had significantly higher mean levels of PA, RBP, and AGP than those who were not receiving prednisone. The mean levels of acute phase-reactant proteins in these leukemic children were comparable to those of healthy children. We conclude that mild/moderate malnutrition is common in leukemic patients at D/R and that PA seems to be the most sensitive indicator of visceral protein status.
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PMID:Nutritional status of children with leukemia. 907 29

Induction of apoptosis by chemotherapeutic drugs involves the sphingomyelin-ceramide (SM-CER) pathway. This signaling is critically dependent on reactive oxygen species (ROS) generation and p53/p56 Lyn activation. In this study, we have investigated the influence of protein kinase C (PKC) zeta overexpression on the SM-CER pathway in U937 human leukemia cell line. We show that PKCzeta overexpression resulted in delayed apoptosis and significant resistance to both 1-beta-D-arabinofuranosylcytosine (ara-C) and daunorubicin (DNR), but there was no significant protection against cell-permeant C(6)-CER. Moreover, PKCzeta overexpression abrogated drug-induced neutral sphingomyelinase stimulation and CER generation by inhibiting ROS production. We further investigated p53/p56 Lyn activation in PKCzeta-overexpressing U937 cells treated with ara-C or DNR. We demonstrate that PKCzeta inhibited p53/p56 Lyn phosphorylation and stimulation in drug- or H(2)O(2)-treated cells, suggesting that p53/p56 Lyn redox regulation is altered in PKCzeta-overexpressing cells. Finally, we show that PKCzeta-overexpressing U937 cells displayed accelerated H(2)O(2) detoxification. Altogether, our study provides evidence for the role of PKCzeta in the negative regulation of drug-induced SM-CER pathway.
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PMID:Overexpression of protein kinase Czeta confers protection against antileukemic drugs by inhibiting the redox-dependent sphingomyelinase activation. 1243 13