Modelling the molecular circuitry of cancer
By William C. Hahn, R. Weinberg. Nature Reviews. Cancer, 2002
1,006 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/338fbe4af9c90d960173d36c294db8b8cef61658
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
- Brent R. Stockwell
- René Bernards
- R. Weinberg
- T. Brummelkamp
- Bharat B. Aggarwal
- S. Shukla
- Sanjay Gupta
- Reuven Agami
In Oncology
- Brent R. Stockwell
- R. Weinberg
- Annapoorni Rangarajan
- Sanjay Gupta
- S. Shukla
- Sue-Jean Hong
- A. Gifford
- William C. Hahn
Citations in the corpus
- Apigenin: A Promising Molecule for Cancer Prevention (2010, positive): “myricetin in (1) inhibiting chymotrypsin-like activity of purified 20S proteasome and of 26S proteasome, (2) accumulating putative ubiquitinated forms of two proteasome target proteins, Bax and IκBα, and (3) inducing activation of caspase-3 and cleavage of poly (ADP-ribose) polymerase in Jurkat T ce”
- Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, neutral): “Many of these phenotypic traits can be brought about by genetic alterations that involve the gain-of-function mutation, amplification, and/or overexpression of key oncogenes together with the loss-of-function mutation, deletion, and/ or epigenetic silencing of key tumor suppressors (Hahn and Weinber”
- ATM and related protein kinases: safeguarding genome integrity (2003, background): “Phosphorylation of serines 635 and 645 of human Rad17 is cell cycle regulated and is required for G(1)/S checkpoint activation in response to DNA damage.”
- Chronic lymphocytic leukemia requires BCL2 to sequester prodeath BIM, explaining sensitivity to BCL2 antagonist ABT-737. (2007, background): “Discussion It has been hypothesized that cancer cells, due to their numerous physiologic aberrancies, require a block in the normal apoptotic pathways in order to survive (30, 31).”
- Identification of genotype-selective antitumor agents using synthetic lethal chemical screening in engineered human tumor cells. (2003, background): “…in BJ-TERT/LT/ST/RASV12 cells were as well as others that disrupt of the function of p53, RB, and subsequently tested in a 2-fold dilution series in BJ and BJPP2A (Hahn et al., 1999, 2002; Hahn and Weinberg, 2002; Less- TERT/LT/ST/RASV12 cells to identify compounds that display nick et al., 2002).”
- Targeting the mitogen-activated protein kinase cascade to treat cancer (2004, background): “Anchorage-independent cell-cycle progression is one hallmark of the neoplastic phenotyp”
- Cancer is a Preventable Disease that Requires Major Lifestyle Changes (2008, background): “Although all cancers are a result of multiple mutations (9, 10), these mutations are due to interaction with the environment (11, 12).”
- Endocrine-disrupting chemicals: an Endocrine Society scientific statement. (2009, background): “A majority of researchers support the idea that cancer is due to the accumulation of mutations in a cell [the somatic mutation theory (121)].”
- Stable suppression of tumorigenicity by virus-mediated RNA interference. (2002, background): “There-continued activity of certain oncogenes is required for tumor growth (Hahn and Weinberg, 2002).”
- Species- and cell type-specific requirements for cellular transformation. (2004, background): “Introduction human cell types to undergo transformation to a tumorigenic state (Hahn et al., 1999; Hahn and Weinberg, 2002b).”