Cyclin D dysregulation: an early and unifying pathogenic event in multiple myeloma.
By P. Bergsagel, W. Kuehl, F. Zhan, J. Sawyer, B. Barlogie, J. Shaughnessy. Blood, 2005
705 citations recorded by the source corpus.
Subfields: Genetics, Hematology
View Paper: https://www.semanticscholar.org/paper/14408da1d565c0be5634f56acb52bf1fd1af3567
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Citations in the corpus
- DEPTOR is an mTOR Inhibitor Whose Frequent Overexpression in Multiple Myeloma Cells Promotes their Survival (2009, background): “It is curious that DEPTOR is overexpressed mostly in MMs characterized bychromosomal translocations instead of those that are hyperdiploid because of aneuploidy (Figure 6B) (Bergsagel et al., 2005).”
- Cyclin-dependent kinase pathways as targets for cancer treatment. (2006, background): “Similar translocations targeting D cyclins have been described in multiple myeloma.(42,43) Gene amplification is another common mechanism leading to aberrant overexpression of cyclin D1, although overexpression occurs commonly in the absence of amplification as well.”
- Selective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers (2013, background): “Cyclin D2 (CCND2) is deregulated in many human cancers, including MM (Bergsagel et al., 2005; Musgrove et al., 2011).”
- Promiscuous mutations activate the noncanonical NF-kappaB pathway in multiple myeloma. (2007, background): “However, both groups are characterized by dysregulation of a cyclin D gene, which appears to be an early and unifying event in MM pathogenesis (Bergsagel et al., 2005).”
- Clonal competition with alternating dominance in multiple myeloma. (2012, background): “Notably, the presence of cytogenetic marks commonly associated with high-risk disease18 [t(4;14), t(14;16), t(14;20), del(17p13)] was significantly associated (P .”