A genetic explanation of Slaughter's concept of field cancerization: evidence and clinical implications.
By B. Braakhuis, M. Tabor, J. Kummer, C. R. Leemans, Ruud H. Brakenhoff. Cancer Research, 2003
1,268 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/25b9fcdd52110b417175f36a4a3bb88600e14b80
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- P. Bossi
- S. Sell
- L. Licitra
- F. Perrone
- L. Mariani
- Konrad Basler
- P. Olmi
- E. Moreno
Citations in the corpus
- dMyc transforms cells into super-competitors. (2004, background): “…give rise to various subclones that eventually evolve phological alterations and can rescue lethal dmyc alleles. into primary and “second field tumors” that share a Adult 4xdmyc/2xdmyc Clones Larvae of the genotype y w Dp(1;1)Co hsp70-GFP hsp70-flpcommon clonal origin (Braakhuis et al., 2003).”
- Stem cell origin of cancer and differentiation therapy. (2004, background): “When such a situation is recognized clinically, it is advisable not only to remove any obvious tumors, but also to remove the surrounding “cancerized” field, if possible [130].”
- High-risk human papillomavirus affects prognosis in patients with surgically treated oropharyngeal squamous cell carcinoma. (2006, background): “One may speculate about the reasons involved in the uneventful behavior of HPV-related cancers within the framework of the head and neck cancer genetic progression model(46,47) and the most recent proposed interpretations of the genetic mechanisms at the basis of the Slaughter’s cancerization concep”