Serum levels of glycosaminoglycans (GAGs) and insulin like growth factor-1 (IGF-1) as diagnostic markers for early hepatocellular carcinoma in cirrhotic patients with or without diabetes

Ibrahim, Suhaidah

doi:10.5897/jmld12.009

Cited by 6 publications

(3 citation statements)

References 57 publications

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“…Our results were in agreement with other reports demonstrating low IGF-1 levels in HCC patients (Ibrahim, Attia, Rabea, & El-Gayar, 2013). Reduced IGF-1 could be due to the increased oxidative damage in cirrhosis and HCC, leading to increased damage of parenchymal liver cell and decrease in IGF-1 synthesis (Ibrahim, Attia, Rabea, & El-Gayar, 2013). Another explanation was provided by Mazziotti et al (2002), who proposed that IGF-1 was low in HCC patients because of reduced ability of growth hormone to stimulate IGF-1 synthesis due to either a reduction of growth hormone receptors number in the diseased liver or a post receptor defect.…”

Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 93%

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Effect of Diet Intake Imbalance in Hepatocellular Carcinoma Progression

El-Bahrawy¹,

El-Ashmawy²,

Shamloula³

et al. 2014

IJB

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Incidence of hepatocellular carcinoma (HCC) has increased sharply in the last 10 years, with an especially high incidence in Egypt. This study was conducted to evaluate the impact of unbalanced diets on liver tumor through investigation of some biochemical mediators/pathways implicated in the pathogenesis of HCC. Male albino mice were divided into two major groups: Control group and Hepatocellular carcinoma (HCC) group; each group was further divided into four subgroups according to received diet: high fat (HF), low fat (LF), high carbohydrate (HC), and low carbohydrate (LC) groups. The results indicated that induction of HCC in mice showed marked body weight loss. Liver sections of HCC groups showed malignant giant cells and strong expression of p53. HCC mice groups kept on HF and LC diets showed the lowest survival rate, a significant increase in glucose-6-phosphate dehydrogenase (G6PDH), aldolase, and citrate synthase activities, a significant increase in serum E-cadherin as well as a significant decrease in insulin-like growth factor-1 (IGF-1) compared with LF diet. These results suggest that the molecular pathogenesis of HCC in mice correlates reduction of serum IGF-1 and elevated serum E-cadherin accompanied by reprogrammed metabolic profile shifted towards increased glycolysis and lipogenesis. These pathogenic changes were enhanced by over-consumption of carbohydrates, fats, and proteins, whereas dietary fat restriction could have a protective/ameliorative effect against the incidence of HCC.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 93%

Effect of Diet Intake Imbalance in Hepatocellular Carcinoma Progression

El-Bahrawy¹,

El-Ashmawy²,

Shamloula³

et al. 2014

IJB

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show abstract

“…In this context, applying a simple, noninvasive, low cost marker for liver reserve assessment will be helpful. [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Validation of an IGF-CTP scoring system for assessing hepatic reserve in egyptian patients with hepatocellular carcinoma

et al. 2015

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BackgroundThe Child-Turcotte-Pugh score (CTP) is the standard tool for hepatic reserve assessment in hepatocellular carcinoma (HCC). Recently, we reported that integrating plasma insulin-like growth factor-1 (IGF-1) level into the CTP score was associated with better patient risk stratification in two U.S. independent cohorts. Our current study aimed to validate the IGF-CTP score in patients who have different demographics and risk factors.Patients and MethodsWe prospectively recruited 100 Egyptian patients and calculated their IGF-CTP score compared to CTP score. C-index was used to compare the prognostic significance of the two scoring systems. Finally, we compared our results with our U.S. cohorts published data.ResultsIGF-CTP score showed significant better patient stratification compared to CTP score in the international validation cohort. Among CTP class A patients, who usually considered for active treatment and clinical trial enrollment, 32.5% were reclassified as IGF-CTP class B with significantly shorter OS than patients reclassified as class A with hazard ratio [HR] = 6.15, 95% confidence interval [CI] = 2.18-17.37.ConclusionIGF-CTP score showed significantly better patient stratification and survival prediction not only in the U.S. population but also in international validation population, who had different demographics and HCC risk factors.

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Biochemical/metabolic changes associated with hepatocellular carcinoma development in mice

et al. 2014

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Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related mortality after lung and stomach cancers. This work was undertaken to investigate some of the biochemical mediators/pathways associated with or implicated in the pathogenesis of HCC. Male albino mice were classified into two groups: normal control group and HCC group. Early stage HCC was induced by injection of diethylnitrosamine (DEN) i.p. 200 mg/kg as a single dose, and after 2 weeks, the mice were given i.p. injection of thioacetamide (TAA) 100 mg/kg twice per week for 4 weeks. Mice were left for further 2 weeks without any treatment, after which, mice were sacrificed; blood and liver samples were collected. Serum was used for determination of activities of glucose-6-phosphate dehydrogenase (G6PDH) and aldolase as well as levels of insulin-like growth factor-1 (IGF-1) and epithelial cadherin (E-cadherin). One portion of the liver was used for histopathological examination and immunohistochemical staining of the tumor suppressor p53 protein. Another portion of the liver was used for determination of citrate synthase activity. Induction of HCC in mice resulted in significant increase in G6PDH and aldolase activities, and E-cadherin level, but significant decrease in IGF-1. HCC mice group showed moderate expression of p53 protein. These results suggest that the molecular pathogenesis of HCC in mice involves reduction of serum level of IGF-1 and increased serum level of E-cadherin accompanied by dysregulation of p53 protein expression. HCC was also associated with reprogrammed metabolic profile shifted toward increased glycolysis and lipogenesis.

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Serum levels of glycosaminoglycans (GAGs) and insulin like growth factor-1 (IGF-1) as diagnostic markers for early hepatocellular carcinoma in cirrhotic patients with or without diabetes

Cited by 6 publications

References 57 publications

Effect of Diet Intake Imbalance in Hepatocellular Carcinoma Progression

Effect of Diet Intake Imbalance in Hepatocellular Carcinoma Progression

Validation of an IGF-CTP scoring system for assessing hepatic reserve in egyptian patients with hepatocellular carcinoma

Biochemical/metabolic changes associated with hepatocellular carcinoma development in mice

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