Oncogene addiction.
By Andrew K. Joe, I. Weinstein. Cancer Research, 2008
690 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/14a96bc3d27ea7c06b2917c775447684e67227b5
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- Arkaitz Carracedo
- Dean W. Felsher
- P. Pandolfi
- G. J. Yoshida
- Yulin Li
- Aik Choon Tan
- Karen A. Ryall
- Meital Gabay
In Oncology
Citations in the corpus
- Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, neutral): “The heightened state of dependency of cancer cells on oncogenes and the loss of tumor suppressors led to the terms “oncogene addiction” (OA) and “tumor suppressor gene hypersensitivity” (Weinstein, 2002; Weinstein and Joe, 2008).”
- MYC activation is a hallmark of cancer initiation and maintenance. (2014, background): “Given that many experimental models demonstrated a dependency on continuous MYC expression for tumor progression, the key challenge to understanding MYC oncogene addiction is the delineation of the mechanisms underlying this dependency (Weinstein 2002; Sharma and Settleman 2007; Felsher 2008; Weinst”
- Metabolic reprogramming: the emerging concept and associated therapeutic strategies (2015, background): “This is a typical example of metabolic reprogramming in cancer cells with oncogene-addiction [62, 63], suggesting a potential “Achilles’ heel” of tumor cells that are addicted to glutamine metabolism in manner that is mediated by c-Myc.”
- Systems biology approaches for advancing the discovery of effective drug combinations (2015, background): “Combinations of drugs could potentially overcome these resistance strategies by limiting the potential of escape mutations and pathways [14].”
- The MAPK pathway across different malignancies: A new perspective (2014, background): “Differentiation of targetable driver mutations from genetic and genomic noise and passenger mutations is 1 of the most important goals of genome and epigenome analysis.(2,3) Driver mutations lead to dysregulation of signaling pathways, increasing malignant behavior.”
- The PTEN–PI3K pathway: of feedbacks and cross-talks (2008, background): “These data have been rationalized putting forward the hypothesis that tumor cells are addicted to oncogenic events (Weinstein and Joe, 2008).”