Cancer and hepatic steatosis

Paternostro, Rafael; Trauner, Michael; Pinter, Matthias

doi:10.1016/j.esmoop.2021.100185

Cited by 13 publications

(12 citation statements)

References 100 publications

(189 reference statements)

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“…Similar conclusions have been reported; for example, a major morbidity rate of 40% was observed after liver resection in obese or overweight patients[ 31 , 32 ]. There is evidence to explain this phenomenon, namely, hepatic steatosis associated with obesity may adversely affect the regeneration of liver remnants and thus influence morbidity[ 33 ]. During the perioperative period, obese patients should be instructed by dieticians to adjust their dietary habits and properly match their nutritional structure.…”

Section: Discussionmentioning

confidence: 99%

Postoperative morbidity adversely impacts oncological prognosis after curative resection for hilar cholangiocarcinoma

Liu¹,

Chen²,

Zhang³

et al. 2022

WJG

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BACKGROUND Postoperative morbidity after curative resection for hilar cholangiocarcinoma (HCCA) is common; however, whether it has an impact on oncological prognosis is unknown. AIM To evaluate the influence of postoperative morbidity on tumor recurrence and mortality after curative resection for HCCA. METHODS Patients with recently diagnosed HCCA who had undergone curative resection between January 2010 and December 2017 at The First Affiliated Hospital of Army Medical University in China were enrolled. The independent risk factors for morbidity in the 30 d after surgery were investigated, and links between postoperative morbidity and patient characteristics and outcomes were assessed. Postoperative morbidities were divided into five grades based on the Clavien-Dindo classification, and major morbidities were defined as Clavien-Dindo ≥ 3. Univariate and multivariate Cox regression analyses were used to evaluate the risk factors for recurrence-free survival (RFS) and overall survival (OS). RESULTS Postoperative morbidity occurred in 146 out of 239 patients (61.1%). Multivariate logistic regression revealed that cirrhosis, intraoperative blood loss > 500 mL, diabetes mellitus, and obesity were independent risk factors. Postoperative morbidity was associated with decreased OS and RFS (OS: 18.0 mo vs 31.0 mo, respectively, P = 0.003; RFS: 16.0 mo vs 26.0 mo, respectively, P = 0.002). Multivariate Cox regression analysis indicated that postoperative morbidity was independently associated with decreased OS [hazard ratios (HR): 1.557, 95% confidence interval (CI): 1.119-2.167, P = 0.009] and RFS (HR: 1.535, 95%CI: 1.117-2.108, P = 0.008). Moreover, major morbidity was independently associated with decreased OS (HR: 2.175; 95%CI: 1.470-3.216, P < 0.001) and RFS (HR: 2.054; 95%CI: 1.400-3.014, P < 0.001) after curative resection for HCCA. CONCLUSION Postoperative morbidity (especially major morbidity) may be an independent risk factor for unfavorable prognosis in HCCA patients following curative resection.

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Section: Discussionmentioning

confidence: 99%

Postoperative morbidity adversely impacts oncological prognosis after curative resection for hilar cholangiocarcinoma

Liu¹,

Chen²,

Zhang³

et al. 2022

WJG

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“…Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) develop in patients with metabolic syndromes including obesity, IR and diabetes ( 9 , 10 ) whereas alcoholic liver disease (ALD) and ASH (alcoholic steatohepatitis) are caused by excessive alcohol drinking which also contributes to lipid metabolic dysfunction ( 11 , 12 ). While simple fatty liver is reversible by lifestyle changes, ASH and NASH can progress to more morbid forms of liver pathologies including fibrosis/cirrhosis and is highly associated with liver cancer ( 13 ).…”

Section: Contribution Of Steatosis To Liver Cancermentioning

confidence: 99%

Hepatic macrophage mediated immune response in liver steatosis driven carcinogenesis

Alba

Datta

et al. 2022

Front. Oncol.

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Obesity confers an independent risk for carcinogenesis. Classically viewed as a genetic disease, owing to the discovery of tumor suppressors and oncogenes, genetic events alone are not sufficient to explain the progression and development of cancers. Tumor development is often associated with metabolic and immunological changes. In particular, obesity is found to significantly increase the mortality rate of liver cancer. As its role is not defined, a fundamental question is whether and how metabolic changes drive the development of cancer. In this review, we will dissect the current literature demonstrating that liver lipid dysfunction is a critical component driving the progression of cancer. We will discuss the involvement of inflammation in lipid dysfunction driven liver cancer development with a focus on the involvement of liver macrophages. We will first discuss the association of steatosis with liver cancer. This will be followed with a literature summary demonstrating the importance of inflammation and particularly macrophages in the progression of liver steatosis and highlighting the evidence that macrophages and macrophage produced inflammatory mediators are critical for liver cancer development. We will then discuss the specific inflammatory mediators and their roles in steatosis driven liver cancer development. Finally, we will summarize the molecular pattern (PAMP and DAMP) as well as lipid particle signals that are involved in the activation, infiltration and reprogramming of liver macrophages. We will also discuss some of the therapies that may interfere with lipid metabolism and also affect liver cancer development.

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“…Ведущую роль в фиброгенезе играют провоспалительные цитокины [33], а также возникновение локальной иммуносупрессии -промоутера гепатокарциногенеза [34].…”

Section: в печень как онкогенный матриксunclassified

Hepatocellular cancer. Current aspects of carcinogenesis

Шапошников¹,

Nepomnyashchaya²,

Yurieva³

2022

Clin. Exp. Morphology

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The modern concept of general carcinogenesis is built on the basic knowledge of exogenous and endogenous factors. They change the body–organ–cell homeostatic and tissue basis and lead to genetic and molecular alterations followed by uncontrolled abnormal cell growth. We studied hepatocellular carcinoma (HCC) as an example of malignant neoplasm carcinogenesis. The article presents some major molecular and genetic alterations resulting in HCC as well as their association with immune microenvironment that mostly determines the onset and further tumor development. These are morphological, molecular, and genetic factors on which the HCC classification we propose is based. It involves 2 tumor classes (proliferating and nonproliferating) and will enable for determining the upcoming prospects for diagnosis of and treatment for this condition. Keywords: exogenous and endogenous risk factors, molecular and genetic and structural liver alterations, classification of hepatocellular carcinoma

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Cancer and hepatic steatosis

Cited by 13 publications

References 100 publications

Postoperative morbidity adversely impacts oncological prognosis after curative resection for hilar cholangiocarcinoma

Postoperative morbidity adversely impacts oncological prognosis after curative resection for hilar cholangiocarcinoma

Hepatic macrophage mediated immune response in liver steatosis driven carcinogenesis

Hepatocellular cancer. Current aspects of carcinogenesis

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