Two genetic hits (more or less) to cancer
By A. Knudson. Nature Reviews. Cancer, 2001
1,208 citations recorded by the source corpus.
Subfields: Cancer Research, Oncology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/6df24c6a7bb82c6f2ea3162d63140961ba4c8252
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- P. Pandolfi
- Matthew Meyerson
- Gad Getz
- M. Lawrence
- A. Gimenez-Roqueplo
- W. Marston Linehan
- D. Hoon
- Christopher Sander
In Oncology
- Padmanee Sharma
- Arkaitz Carracedo
- James P. Allison
- John N. Weinstein
- Christopher Sander
- A. Richmond
- Nikolaus Schultz
- Peter W. Laird
In Pathology and Forensic Medicine
- John N. Weinstein
- James P. Allison
- Padmanee Sharma
- Peter W. Laird
- Peter A. Jones
- R. Jirtle
- S. Baylin
- Michael K. Skinner
Citations in the corpus
- Subtle variations in Pten dose determine cancer susceptibility (2010, background): “Three decades ago, Alfred Knudson, a pioneer of cancer genetics, proposed a groundbreaking model for tumorigenesis, suggesting that cancer growth is initiated as a result of two genetic alterations of a single TS”
- Pathogenic germline variants in 10,389 adult cancers (2018, background): “For example, allele fraction derived from sequencing analysis of matched tumor and normal samples can validate whether variants of tumor suppressors are undergoing positive selection in the context of the classic two-hit model (Knudson, 1971; Knudson, 2001; Lu et al., 2015), and mRNA analysis can va”
- Epigenetic Determinants of Cancer. (2016, background): “The idea that both copies of a TSG have to be incapacitated in a malignant cell line was proposed by Knudson (2001) in his “two- or multiple-hit” hypothesis and has found wide acceptance.”
- Immune Checkpoint Targeting in Cancer Therapy: Towards Combination Strategies with Curative Potential (2015, background): “…mutations that result in activation of genes that are normally involved in regulation of cell division and programmed cell death, as well as inactivation of genes involved in protection against DNA damage or driving apoptosis (Bishop, 1991; Solomon et al., 1991; Weinberg, 1991; Knudson, 2001).”
- Role of chemokines in tumor growth. (2007, background): “Tumor cells with “gain of function” mutations [15], equipped with constitutive activation of anti-apoptotic and proliferative pathways, begin to evolve and modify their microenvironment.”
- Environmental epigenomics and disease susceptibility (2007, background): “Consequently, the silenced allele of an imprinted gene has been equated to the 'first hit', as proposed by Knudso”