Caspase 8 is deleted or silenced preferentially in childhood neuroblastomas with amplification of MYCN
By T. Teitz, T. Wei, Marcus B. Valentine, E. F. Vanin, J. Grenet, Virginia Valentine, F. Behm, A. Look, J. Lahti, Vincent J. Kidd. Nature Medicine, 2000
820 citations recorded by the source corpus.
Subfields: Molecular Biology, Neurology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/4ea8f5601688f1c491ed911be07bd21bc704ef02
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In Molecular Biology
Citations in the corpus
- Genomic targets of the human c-Myc protein. (2003, background): “An interesting example is CASP8, whose silencing in human childhood neuroblastomas correlated with N-Myc overexpression (Teitz et al. 2000).”
- Apoptosis A Link between Cancer Genetics and Chemotherapy (2002, background): “Silencing of INK4a/ARF, caspase-8, and Apaf-1 by DNA methylation has been linked to drug resistance Rather than attempting to reactivate the intrinsic apoptotic pathway, an alternative approach would be to(Robertson and Jones, 1998; Soengas et al., 2001; Teitz et al., 2000).”
- Caspase functions in cell death and disease. (2013, background): “2000), thus mutations leading to loss of caspase-8 function render neuroblastoma cell lines resistant to DRinduced apoptosis (Hopkins-Donaldson et al. 2000; Teitz et al. 2000; Eggert et al. 2001; Yang et al. 2003).”
- Tumor resistance to apoptosis (2009, background): “Further, homo- or heterozygous genomic deletions were found in some neuroblastoma.(42) In addition, caspase-8 expression can be transcriptionally regulated by splicing, for example in leukemia and neuroblastoma.”
- Causal relationship between the loss of RUNX3 expression and gastric cancer. (2002, neutral): “von Hippel-Lindau gene, CDKN2A (p16), CDKN2B (p15), E cadherin (E-cad), hMLH1, APC (reviewed by RUNX3 was found to be silenced frequently in gastric cancer by hypermethylation of CpG islands in the exon Jones and Laird, 1999), and the caspase 8 gene (Teitz et al., 2000).”