Insulin and insulin-like growth factor signalling in neoplasia

By Michael Pollak. Nature Reviews. Cancer, 2008

2,106 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/aa290ad31c77c81edbdd5dc3b89dfde592d556e8

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrinology, Diabetes and Metabolism

1. Prashanth Rawla
2. R. Huang
3. M. Nieto
4. J. P. Thiery
5. H. Acloque
6. R. Shaw
7. D. Shackelford
8. R. Bergenstal

In Molecular Biology

1. J. P. Thiery
2. M. Nieto
3. R. Huang
4. R. Shaw
5. H. Acloque
6. B. Spiegelman
7. Prashanth Rawla
8. D. Shackelford

Citations in the corpus

• Palmitic Acid: Physiological Role, Metabolism and Nutritional Implications (2017, background): “Changes in the correct balance of fuels and/or signal transduction pathways that concern nutrient utilization may trigger the cancer predisposition related to metabolic diseases such as diabetes and obesity (Calle andKaaks, 2004; Pollak, 2008).”
• A chromatin-mediated reversible drug tolerant state in cancer cell subpopulations (2010, background): “Notably, IGF-1R activation has been linked to drug resistance and poor prognosis in several cancer settings (reviewed in Casa et al., 2008; Pollak, 2008).”
• Glycemic index, glycemic load and glycemic response: An International Scientific Consensus Summit from the International Carbohydrate Quality Consortium (ICQC). (2015, positive): “If real, such associations would be explained by the higher impact of high GI/GL foods on glycemia, insuline-mia and insulin-like growth factors which may promote tumor growth [98].”
• The LKB1-AMPK pathway: metabolism and growth control in tumor suppression (2009, background): “Importantly, compounds that activate AMPK will not only affect tumour incidence through cell-autonomous effects on cell growth downstream of AMPK, but perhaps also through non-cell autonomous effects of lowering plasma insulin levels, which itself contributes to cancer risk and incidenc”
• Causes, consequences, and reversal of immune system aging. (2013, neutral): “A concern with the use of some agents is that neoplastic cells might also express receptors resulting in tumor growth (115).”
• The tumor microenvironment underlies acquired resistance to CSF1R inhibition in gliomas (2016, background): “S8B) (35–37), it is a known mediator of tissue repair and neuroprotection (38–41), and one of its canonical downstream signaling pathways is PI3K/Akt (42).”
• Epithelial-mesenchymal transitions in development and disease. (2009, methodology): “the IGF/IGFR pathway were recently reviewed, including the use of receptor-specific antibodies, kinase inhibitors, or activators of the AMP-activated protein kinase such as metformin (Pollak, 2008).”
• Diabetes and Cancer (2010, positive): “IGF-I has more potent mitogenic and anti-apoptotic activities than insulin (58) and could act as a growth stimulus in preneoplastic and neoplastic cells that express insulin, IGF-I, and hybrid receptors (49).”
• Epidemiology of Prostate Cancer (2019, background): “The IGF family is composed of two receptors (insulin receptor (INSR), IGF-1 receptor (IGF-1R) and mannose 6-phosphate receptor (M6P/ IGF-2R)), three ligands (insulin, IGF-1 and IGF-2) and six known types of circulating IGF-binding proteins (IGFBP1-6) that modulate the bioavailability and bioactivity”
• Molecular mechanisms of cancer development in obesity (2011, background): “IGF1 and IGF2 are hormones that are primarily produced in the liver and they share sequence homology with insuli”