A Fibrosarcoma With Hypoglycæmia and a High Serum-Insulin Level

Oleesky, S.; Samols, Ellis; Bailey, Ian A.; Bilkus, David

doi:10.1016/s0140-6736(62)90231-3

Cited by 74 publications

(12 citation statements)

References 20 publications

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“…For while fasting plasma insulins are generally normal in other varieties of organic hypoglycaemia (Berson and YalQw,196 1; unpublished observations) exceptions have been observed in retroperitoneal fibrosarcomata and idiopathic hypoglycaemia (Whitney and Heller, 1961 ;Oleesky et al, 1962;Berson and Yalow, 1961). A normal plasma insulin does not exclude the diagnosis of an insulinoma.…”

Section: Discussionmentioning

confidence: 99%

Insulin Assay in Insulinomas

Samols¹,

Marks²

1963

BMJ

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Section: Discussionmentioning

confidence: 99%

Insulin Assay in Insulinomas

Samols¹,

Marks²

1963

BMJ

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“…Efforts to demonstrate activity in the plasma of these patients have been even less rewarding. In only one case (Whitney and Massey, 1961) has increased activity been demonstrated by bio-assay, and in two cases by immuno-assay (Oleesky et al, 1962;Samaan et al, 1965). Failure may be attributable, at least in part, to unsatisfactory extraction procedures.…”

Section: Hypoglycaemiamentioning

confidence: 99%

“…Samaan, Lal, Fraser, and Welbourn (1965) suggest that the tumours produce hypoglycaemia by stimulating the secretion of pancreatic insulin, and Stern (1960) has suggested that release of leucine from the tumour into the blood of a leucine-sensitive person is the mechanism by which this response is mediated. However, Miller et al (1959) cite a case in which pancreatectomy failed to maintain normoglycaemia, and Oleesky, Bailey, Samols, and Bilkus (1962) report leucine sensitivity in their patient with reversion to normality following radiotherapy to the tumour. Also leucine sensitivity is not invariably found in these patients (Butterfield et al, 1960).…”

Section: Hypoglycaemiamentioning

confidence: 99%

Review of endocrine syndromes associated with tumours of non-endocrine origin

Hobbs

Miller

1966

Journal of Clinical Pathology

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“…The insulin receptor (INSR) and the IGF-1R are both tyrosine kinase receptors and are structurally similar and activate almost identical intracellular signaling events. Insulin and IGFs receptors have been reported in various cancers including breast [1-9], lung [10], colon [11], melanoma [12], cervix [12], renal cell carcinoma [13], fibrosarcoma [14], Hodgkin’s lymphoma [15], insulinoma [16], as well as in one hematologic malignancy, lymphoblastic leukemia [14]. INSR and IGFRs have likewise been well characterized on the cell membranes of these cancers [11,17-19].…”

Section: Introductionmentioning

confidence: 99%

Modulation of insulin/IGFs pathways by sirtuin-7 inhibition in drug-induced chemoreistance

2014

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BackgroundInsulin and insulin-like growth factors (IGFs) are key regulators of metabolism and growth. Recent evidences suggest a key role of these pathways in non-classical tissues and the metabolic pathways by which these hormones exert their effects in neoplasia is unclear.AimsTo study insulin/IGFs pathways in drug sensitive and resistant cancer cells representing breast cancer (MCF-7), osteosarcoma (SaOS-2), and ovarian cancer (A2780) and to examine the effect of Sirtuin-7 (Sirt7) inhibition on insulin/IGFs pathways in MCF-7 cell line.MethodsDrug resistant cells were generated by continuous incubation of parental cell lines with stepwise increases in Doxorubicin or Cisplatin over a period of 3 to 6 months. MCF-7 cells were transfected with cloned hairpin siRNA template for Sirt7 using the Amaxa GmbH transfection system. mRNA expression of Sirt7, INSR, IRS-1, IRS-2, IRS-4, IGF-1, IGF-2, MDR-1, MRP-1, BCRP was measured by qPCR and Sirt7 by standard Western blotting. FITC-insulin uptake was imaged with Leica Confocal Microscope.ResultsInsulin receptor (INSR), insulin receptor substrate-1 (IRS-1) were inhibited in drug-induced resistance, whereas IRS-2 was significantly induced in all the chemoresistant cells tested when compared to their parental counterparts. IGF-1 and IGF-2 were also upregulated in all the drug resistant cells tested. Sirt7 was significantly reduced in all chemoresistant cells tested. Knockdown of Sirt7 expression in human breast MCF-7 cell line by siRNA induced premature senescence-like phenotype and multi-drug resistance, suggesting that this gene may play an active role in regulating cancer cell response to stress. Suppression of Sirt7 selectively inhibited INSR and IRS-1, whereas it had minimal effect on that of IRS-2. Sirt7 suppression in MCF-7 also inhibited insulin uptake. Additionally, Sirt7 inhibition upregulated IGF-1, IGF-2 and IGFR expression.ConclusionOur data demonstrate that stress-induced Sirt7 inhibition significantly increases stress resistance and modulates insulin/IGF-1 signaling pathways. More importantly, this study links Sir2 family proteins to insulin/IGF signaling in drug-induced stress resistance in neoplasia.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1135426681234493

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A Fibrosarcoma With Hypoglycæmia and a High Serum-Insulin Level

Cited by 74 publications

References 20 publications

Insulin Assay in Insulinomas

Insulin Assay in Insulinomas

Review of endocrine syndromes associated with tumours of non-endocrine origin

Modulation of insulin/IGFs pathways by sirtuin-7 inhibition in drug-induced chemoreistance

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