Candace J. Poole

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Overexpression of MYC is a hallmark of many human cancers. The MYC oncogene has long been thought to execute its neoplastic functions by acting as a classic transcription factor, deregulating the expression of a large number of specific target genes. However, MYC's influence on many of these target genes is rather modest and there is little overlap between(More)
Rous sarcoma virus, an oncogenic avian retrovirus, readily causes morphological transformation of chick cells, but in infected rat cells transformation is rare because proviral transcription is inefficient. This constraint is not due to a lack of positive transcriptional factors, or an excess of negative ones, but reflects the site of proviral integration(More)
The fusion of a Rous sarcoma virus (RSV)-transformed rat fibroblast clone to at least 2 different human cell types reproducibly produces phenotypically normal hybrids. Analysis of such hybrids reveals that proviral silence is the result of transcriptional down-regulation, presumably by a trans-acting human molecule. Furthermore, this phenomenon seems to be(More)
Aberrant DNA methylation is a hallmark of cancer. However, our understanding of how tumor cell-specific DNA methylation patterns are established and maintained is limited. Here, we report that in T-cell acute lymphoblastic leukemia (T-ALL) and Burkitt's lymphoma the MYC oncogene causes overexpression of DNA methyltransferase (DNMT) 1 and 3B, which(More)
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