Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 47 patients (46 children and 1 adult) with unilateral and bilateral retinoblastoma, the titer of the carcinoembryonic antigen (CEA) was determined. The CEA titer of children with active retinoblastomas was 1.44 +/- 0.26 ng/ml (x +/- SEM). Those patients whose retinoblastoma was inactivated by therapy did not show a significantly lower CEA titer. In the group of children with one eye removed because of a unilateral retinoblastoma, the CEA titer was significantly (P less than 0.1) lower. The globes of 25 children were examined histologically. In those cases with invasion of the optic nerve or choroid, the CEA titer was significantly higher (P less than 0.1) as compared with those where the tumor was limited to the retina alone.
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PMID:[Carcinoembryonic antigen in retinoblastomas (author's transl)]. 30 12

Tissue cultures were established from 6 retinoblastomas and the cultured cells examined by scanning electron microscopy. Cells from cultures of normal fetal retinal and glial tissue were also examined by SEM. Though a number of different cell types were found to coexist in the retinoblastoma cultures, most had the features of cells of either glial or neuronal origin. Evidence of further differentiation of cells in each series was seen. These findings indicate that the cell of origin in retinoblastoma is a multipotential stem cell which, though neoplastic, is still capable of differentiation into both glial and neuronal series.
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PMID:A scanning electron microscopic examination of retinoblastoma in tissue culture. 47 31

The levels of the glycolytic enzymes, phosphohexose isomerase, aldolase and LDH and its isozymes, were ascertained in the aqueous of human stillbirths and premature neonate dead (19-24 weeks gestation) and compared with those of older neonates (28-41 weeks) of low survival due mainly to respiratory failure. The fetal aqueous displayed a much greater LDH-P level (mean mU/ml +/- SEM: 45,600 +/- 2550; 72 eyes) in contrast to the near-term infant value (2420 +/- 615; 27 eyes) and 8-20 times higher aldolase and phosphohexose isomerase levels. LDH-P of the fetal vitreous was much lower (5820 +/- 860 mU/ml; 25 eyes) and for lens employed as a filtered homogenate in saline (1:20), amounted to 52.2 +/- 4.2 mU/mg lens (24 eyes). The distribution of LDH isozymes in the fetal vitreous and lens homogenate and the near-term neonate aqueous as determined by polyacrylamide disc electrophoresis, was similar to that of the fetal aqueous, LDH-1 and LDH-5 being least and LDH-3 and LDH-4, the highest. A few small but significant differences were apparent as compared to the fetal aqueous isozymes and included decrements in vitreous LDH-4, lens LDH-3 and neonatal aqueous LDH-3 and increases in vitreous LDH-2 and near-term aqueous LDH-4. The current findings may have application to retinoblastoma for which higher aqueous LDH levels have been reported and employed as a diagnostic adjunct. However, the fetal aqueous LDH values far exceed those encountered in this embryonal-type tumour.
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PMID:Glycolytic enzymes of human fetal and neonatal intraocular fluids. 404 Apr 54

Dysregulation of the cyclin D1-CDK4/CDK6 complex is frequently observed in almost all human cancer and contributes to aberrant cell proliferation and consequent tumorigenesis. Although many reports described the importance of CDK4/CDK6 in different set of human tumors, only few studies have been performed on leukemia. By gene expression analysis performed in a cohort of childhood patients affected by B-acute lymphoblastic leukemia (B-ALL) we found that both CDK4 and CDK6 are highly expressed. Moreover, reverse phase protein array (RPPA) analysis showed that cyclin D1 levels are higher in patients undergoing relapse. Starting from these considerations, we evaluated the effect of dual inhibition of CDK4/CDK6 in B-ALL and if this inhibition could enhance cytotoxic killing of leukemia cells after combination treatment with dexamethasone. We treated B-ALL cell lines with ribociclib, a highly specific CDK4/6 inhibitor. As expected, treatment with ribociclib induced growth inhibition of B-ALL cell lines, accompanied by strong cell cycle arrest in G1 phase, along with a dose-dependent decrease in phosphorylated retinoblastoma protein. Ribociclib exposure strongly synergizes with dexamethasone in SEM and RCH-ACV, two dexamethasone-resistant cell lines, along with a strong decrease in proliferation and a significant increase in apoptotic cell death. These results were also confirmed on primary cultures derived from bone marrow of pediatric patients affected by B-ALL. Immunoblot analysis showed a significant increase in glucocorticoid receptor (GR) along with some of its target genes, after combined treatment with ribociclib and dexamethasone. Altogether our findings support the concept that pharmacologic inhibition of CDK4/CDK6 may represent a useful therapeutic strategy to control cell proliferation in B-ALL and provide new insight in understanding potential mechanism of glucocorticoid resistance.
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PMID:Ribociclib, a Cdk4/Cdk6 kinase inhibitor, enhances glucocorticoid sensitivity in B-acute lymphoblastic leukemia (B-All). 2940 28