Epigenetic inactivation of RASSF1A in lung and breast cancers and malignant phenotype suppression.
By D. Burbee, É. Forgács, S. Zöchbauer-Müller, L. Shivakumar, K. Fong, B. Gao, Dwight Randle, M. Kondo, A. Virmani, S. Bader and 9 more. Journal of the National Cancer Institute, 2001
822 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/4e223560b305b92f93a8b77282ba625b629e1386
How researchers see this paper
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In Molecular Biology
- S. Baylin
- Peter A. Jones
- A. Maitra
- Adi F. Gazdar
- Dan E. Arking
- Manel Esteller
- Peter W. Laird
- A. Bird
In Oncology
Citations in the corpus
- Epigenetic Determinants of Cancer. (2016, background): “Examples include RasFF1a and FHIT, located on chromosome arm 3p, frequently deleted in lung and other types of tumors (Dammann et al. 2000; Burbee et al. 2001).”
- Genomic alterations in cultured human embryonic stem cells (2005, background): “Epigenetic silencing of RASSF1 gene by promoter methylation is a feature of many human cancers, whereas most non-neoplastic cell types are characterized by unmethylated promoter”
- RAS oncogenes: weaving a tumorigenic web (2011, background): “There is an indication that such a pro-apoptotic function of RAS might be selected against in cancer, as the expression of either RASSF1 or RASSF5 in tumours is frequently suppressed either owing to promoter hypermethylation or — in the case of RASSF1 — owing to the deletion of the chromosomal”