RAS oncogenes: weaving a tumorigenic web

By Y. Pylayeva-Gupta, Elda Grabocka, D. Bar-Sagi. Nature Reviews. Cancer, 2011

1,751 citations recorded by the source corpus.

RAS proteins are essential components of signalling pathways that emanate from cell surface receptors. Oncogenic activation of these proteins owing to missense mutations is frequently detected in several types of cancer. A wealth of biochemical and genetic studies indicates that RAS proteins control a complex molecular circuitry that consists of a wide array of interconnecting pathways. In this Review, we describe how RAS oncogenes exploit their extensive signalling reach to affect multiple cellular processes that drive tumorigenesis.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/e4602484112b56a500797ace51579560f5594001

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

1. Jie Zheng
2. William C. Hahn
3. T. Jacks
4. K. Yu
5. T. Roberts

In Oncology

1. D. Bar-Sagi
2. Y. Pylayeva-Gupta
3. Jie Zheng
4. William C. Hahn
5. Kyoung Eun Lee
6. G. Miller
7. T. Jacks
8. C. Hajdu

Citations in the corpus

• Risk Factors and Preventions of Breast Cancer (2017, background): “The proteins encoded by these genes are extremely homologous, and they belong to the small guanosine triphosphate (GTP)-binding protein (G protein) superfamily [46].”
• Targeting KRAS Mutant Cancers with a Covalent G12C-Specific Inhibitor. (2018, background): “…at codon 12 aberrantly activates the protein into a hyperexcitable state by attenuating its GTPase activity resulting in accretion of GTPbound activated KRAS (Lito et al., 2016; Patricelli et al., 2016; Pylayeva-Gupta et al., 2011) and activation of downstream signaling pathways (Downward, 2003).”
• Oncogenic Kras-induced GM-CSF production promotes the development of pancreatic neoplasia (2012, background): “…June 12, 2012 ª2012 Elsevier Inc. contributes to the genesis and progression of PDA have not been fully elucidated, the proliferative and survival advantages conferred on epithelial cells by the expression of endogenous oncogenic Kras have been clearly implicated (Pylayeva-Gupta et al., 2011).”
• KRAS and YAP1 converge to regulate EMT and tumor survival (2014, background): “…KRAS activates pleiotropic signaling pathways that contribute to tumor initiation and maintenance including the Mitogen-Activated Protein Kinase (MAPK), Phosphatidylinositol 3-Kinase (PI3K), and Ral Guanine nucleotide Exchange Factor (RalGEF) signaling pathways (Pylayeva-Gupta et al., 2011).”
• Revisiting the hallmarks of cancer. (2017, neutral): “[29] Pylayeva-Gupta Y, Grabocka E and Bar-Sagi D.”
• Energy metabolism of cancer: Glycolysis versus oxidative phosphorylation (Review). (2012, background): “Many intermediates from glycolysis, truncated TCA and glutaminolysis are used in cell biosynthesis during the cancer cell metabolic switch to glycolysis by Ras and Myc (40,57).”
• KRAS: feeding pancreatic cancer proliferation (2014, neutral): “Constitutive activation of Ras results in the persistent stimulation of its multitude of downstream signaling partners, which results in many of the phenotypic hallmarks of cancer including increased proliferation, the suppression of apoptosis, altered metabolism, alteration of the tumor microenviro”
• Fundamental Limits to Cellular Sensing (2015, background): “And many cellular signaling pathways, including two-component systems in bacteria [74], GTP-ase cycles as in the Ras system [63], phosphorylation cycles as in MAPK cascades [19], are driven out of thermal equilibrium via the turnover of fuel.”