We are analyzing https://link.springer.com/article/10.1007/s40264-016-0485-y.

Title:
Hyperglycaemia Induced by Novel Anticancer Agents: An Undesirable Complication or a Potential Therapeutic Opportunity? | Drug Safety
Description:
Signalling pathways involving protein kinase, insulin-like growth factor 1, insulin receptors and the phosphoinositide 3 kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) system are critical in promoting oncogenesis. The use of anticancer agents that inhibit these pathways frequently results in hyperglycaemia, an on-target effect of these drugs. Hyperglycaemia induced by these agents denotes optimal inhibition of the desired pharmacological target. As hyperglycaemia can be treated successfully and effectively with metformin, managing this complication by reducing the dose of or discontinuing the anticancer drug may be counterproductive, especially if it is otherwise effective and clinically tolerated. The use of metformin to treat hyperglycaemia induced by anticancer drugs provides a valuable therapeutic opportunity of potentiating their clinical anticancer effects. Although evidence from randomised controlled trials is awaited, extensive preclinical evidence and clinical observational studies suggest that metformin has anticancer properties that improve overall survival in patients with diabetes and a variety of cancers. Metformin has also been reported to reverse resistance to epidermal growth factor receptor (EGFR)-inhibiting tyrosine kinase inhibitors. This review summarises briefly the role of the above signalling pathways in oncogenesis, the causal association between inhibition of these pathways and hyperglycaemia, and the effect of metformin on clinical outcomes resulting from its anticancer properties. The evidence reviewed herein, albeit almost exclusively from observational studies, provides support for a greater use of metformin not only in patients with cancer and diabetes or drug-induced hyperglycaemia but also potentially as an anticancer drug. However, prospective randomised controlled studies are needed in all these settings to better assess the effect on clinical outcomes of adding metformin to ongoing anticancer therapy.
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Keywords {🔍}

pubmed, cancer, article, google, scholar, cas, metformin, patients, central, diabetes, clin, oncol, lung, growth, study, inhibitors, review, kinase, receptor, phase, survival, advanced, treatment, factor, res, drug, type, metaanalysis, risk, inhibitor, insulin, tyrosine, cell, accessed, june, anticancer, therapy, pancreatic, carcinoma, inhibition, clinical, med, tumors, solid, information, target, drugs, outcomes, breast, pharmacol,

Topics {✒️}

eu/docs/en_gb/document_library/epar_-_product_information/human/000704/wc500032225 gov/downloads/advisorycommittees/committeesmeetingmaterials/drugs/oncologicdrugsadvisorycommittee/ucm494785 gov/downloads/advisorycommittees/committeesmeetingmaterials/drugs/oncologicdrugsadvisorycommittee/ucm496630 anti-igf-1r monoclonal antibodies anti-igf-1r monoclonal antibody dual igf-1r/insulin receptor month download article/chapter anti-igf-1r antibody cixutumumab small-molecule kinase inhibitors gov/ftp1/ctcae/ctcae_4 phosphatidylinositol 3-kinase/protein kinase extracellular signal-regulated kinase life-threatening hypoglycemia induced gov/drugsatfda_docs/label/2015/208434s000lbl gov/drugsatfda_docs/label/2014/202324s002lbl gov/drugsatfda_docs/label/2015/205755s003s004lbl gov/drugsatfda_docs/label/2015/202806s004lbl gov/drugsatfda_docs/label/2015/204114s004lbl gov/drugsatfda_docs/label/2015/206947s000lbl gov/drugsatfda_docs/label/2015/021938s028s029lbl gov/drugsatfda_docs/label/2014/022405s007lbl small-cell lung cancer metastatic soft-tissue sarcoma er-positive breast carcinoma targeting t790m-mediated resistance growth factor-1 receptor gov/drugsatfda_docs/nda/2015/208434orig1s000pharmr gov/drugsatfda_docs/nda/2014/205755orig1s000pharmr sunitinib-induced severe hypoglycemia akt inhibitor-induced hyperglycemia population-based cohort study pi3k/akt/mtor pathway pi3k/akt/mtor inhibitors igf-ir targeted therapy tgf-β signaling pathway surface-expressed insulin receptors severe resistant hypoglycemia pi3k-mtor pathway inhibition tyrosine kinase inhibitor develop everolimus-related hyperglycemia dual phosphatidylinositol-3-kinase tyrosine kinase inhibitors hepatocellular carcinoma—systematic review comprehensive pharmacokinetic/pharmacodynamics analysis insulin receptor inhibitors igf-1r/cd221 renal cell carcinoma review article published european economic area igf-1r inhibition

Questions {❓}

Can metformin change the prognosis of pancreatic cancer?
Can we unlock the potential of IGF-1R inhibition in cancer therapy?
Chronic inhibition of mammalian target of rapamycin signaling downregulates insulin receptor substrates 1 and 2 and AKT activation: a crossroad between cancer and diabetes?
Does metformin reduce cancer risks?
Hyperglycaemia Induced by Novel Anticancer Agents: An Undesirable Complication or a Potential Therapeutic Opportunity?
Hyperglycaemia Induced by Novel Anticancer Agents: An Undesirable Complication or a Potential Therapeutic Opportunity?
Insulin-like growth factor receptor inhibitors: baby or the bathwater?
Is there a survival benefit of first-line epidermal growth factor receptor tyrosine kinase inhibitor monotherapy versus chemotherapy in patients with advanced non-small-cell lung cancer?
Is there evidence for different effects among EGFR-TKIs?
Metformin: taking away the candy for cancer?
Tyrosine kinase inhibitors and diabetes: a novel treatment paradigm?
Were the IGF signaling inhibitors all bad?

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         description:Signalling pathways involving protein kinase, insulin-like growth factor 1, insulin receptors and the phosphoinositide 3 kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) system are critical in promoting oncogenesis. The use of anticancer agents that inhibit these pathways frequently results in hyperglycaemia, an on-target effect of these drugs. Hyperglycaemia induced by these agents denotes optimal inhibition of the desired pharmacological target. As hyperglycaemia can be treated successfully and effectively with metformin, managing this complication by reducing the dose of or discontinuing the anticancer drug may be counterproductive, especially if it is otherwise effective and clinically tolerated. The use of metformin to treat hyperglycaemia induced by anticancer drugs provides a valuable therapeutic opportunity of potentiating their clinical anticancer effects. Although evidence from randomised controlled trials is awaited, extensive preclinical evidence and clinical observational studies suggest that metformin has anticancer properties that improve overall survival in patients with diabetes and a variety of cancers. Metformin has also been reported to reverse resistance to epidermal growth factor receptor (EGFR)-inhibiting tyrosine kinase inhibitors. This review summarises briefly the role of the above signalling pathways in oncogenesis, the causal association between inhibition of these pathways and hyperglycaemia, and the effect of metformin on clinical outcomes resulting from its anticancer properties. The evidence reviewed herein, albeit almost exclusively from observational studies, provides support for a greater use of metformin not only in patients with cancer and diabetes or drug-induced hyperglycaemia but also potentially as an anticancer drug. However, prospective randomised controlled studies are needed in all these settings to better assess the effect on clinical outcomes of adding metformin to ongoing anticancer therapy.
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      description:Signalling pathways involving protein kinase, insulin-like growth factor 1, insulin receptors and the phosphoinositide 3 kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) system are critical in promoting oncogenesis. The use of anticancer agents that inhibit these pathways frequently results in hyperglycaemia, an on-target effect of these drugs. Hyperglycaemia induced by these agents denotes optimal inhibition of the desired pharmacological target. As hyperglycaemia can be treated successfully and effectively with metformin, managing this complication by reducing the dose of or discontinuing the anticancer drug may be counterproductive, especially if it is otherwise effective and clinically tolerated. The use of metformin to treat hyperglycaemia induced by anticancer drugs provides a valuable therapeutic opportunity of potentiating their clinical anticancer effects. Although evidence from randomised controlled trials is awaited, extensive preclinical evidence and clinical observational studies suggest that metformin has anticancer properties that improve overall survival in patients with diabetes and a variety of cancers. Metformin has also been reported to reverse resistance to epidermal growth factor receptor (EGFR)-inhibiting tyrosine kinase inhibitors. This review summarises briefly the role of the above signalling pathways in oncogenesis, the causal association between inhibition of these pathways and hyperglycaemia, and the effect of metformin on clinical outcomes resulting from its anticancer properties. The evidence reviewed herein, albeit almost exclusively from observational studies, provides support for a greater use of metformin not only in patients with cancer and diabetes or drug-induced hyperglycaemia but also potentially as an anticancer drug. However, prospective randomised controlled studies are needed in all these settings to better assess the effect on clinical outcomes of adding metformin to ongoing anticancer therapy.
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