Is hepatocellular carcinoma the same disease in children and adults? Comparison of histology, molecular background, and treatment in pediatric and adult patients

Weeda, Víola B.; Aronson, Daniël C.; Verheij, Joanne; Lamers, Wouter H.

doi:10.1002/pbc.27475

Cited by 22 publications

(21 citation statements)

References 48 publications

(153 reference statements)

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“…44 Moreover, not only are risk factors for childhood HCC 4 very different to HB, 9,12 but also differ from adult population. 4,16 In addition, as Nonetheless, several studies suggested that the temporal increase in incidence of the embryonal tumour HB may be attributable to population-level secular trends in pregnancy characteristics especially low birthweight, 30,36,37,39,40,42 which has been consistently associated with childhood HB. 12,15 Improved survival of preterm infants, who may be more susceptible to HB, 14 was another commonly proposed driver of observed trends.…”

Section: Discussionmentioning

confidence: 99%

“…It can develop either in the context of the underlying liver disease or as "de novo HCC" without pre-existing liver disease. 4,16 A key risk factor for HCC is hepatitis B virus (HBV) infection with a higher incidence of childhood HCC in regions with endemic HBV. 4 Monitoring of temporal changes in cancer incidence has an established role in epidemiological research to help identify high-risk populations, develop hypotheses regarding plausible explanatory factors, and motivate aetiological research, especially when there is evidence of rapidly rising incidence.…”

Section: Introductionmentioning

confidence: 99%

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Global trends in incidence rates of childhood liver cancers: A systematic review and meta‐analysis

Dasgupta

Henshaw

Youlden

et al. 2020

Paediatric Perinatal Epid

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Background Childhood liver cancers are relatively rare, hence inferences on incidence trends over time are limited by lack of precision in most studies. Objective To conduct a systematic review and meta‐analysis of published contemporary trends on childhood liver cancer incidence rates worldwide. Data sources PubMed, EMBASE, CINAHL, Web of Science. Study selection and data extraction English‐language peer‐reviewed articles published from 1 January 2008 to 1 December 2019 that presented quantitative estimates of incidence trends for childhood liver cancer and diagnostic subgroups. Review was conducted per PRISMA guidelines. Two authors independently extracted data and critically assessed studies. Synthesis Random effects meta‐analysis models were used to estimate pooled incidence trends by diagnostic subgroups. Heterogeneity was measured using the Q and I2 statistics and publication bias evaluated using Egger’s test. Results Eighteen studies were included, all based on population‐based cancer registries. Trends were reported on average for 18 years. Overall pooled estimates of the annual percentage change (APC) were 1.4 (95% confidence interval [CI] 0.5, 2.3) for childhood liver cancers, 2.8 (95% CI 1.8, 3.8) for hepatoblastoma and −3.0 (95% CI −11.0, 4.9) for hepatocellular carcinoma. Sub‐group analysis by region indicated increasing trends for childhood liver cancers in North America/Europe/Australia (APC 1.7, 95% CI 0.7, 2.8) whereas corresponding trends were stable in Asia (APC 1.4, 95%CI −0.3, 2.7). Publication bias was not detected for any of these analyses. The I2 statistic indicated that the heterogeneity among included studies was low for combined liver cancers, moderate for hepatoblastoma and high for hepatocellular carcinoma. Conclusions Incidence is increasing for childhood liver cancers and the most commonly diagnosed subgroup hepatoblastoma. Lack of knowledge of the etiology of childhood liver cancers limited the ability to understand the reasons for observed incidence trends. This review highlighted the need for ongoing monitoring of incidence trends and etiological studies.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Global trends in incidence rates of childhood liver cancers: A systematic review and meta‐analysis

Dasgupta

Henshaw

Youlden

et al. 2020

Paediatric Perinatal Epid

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“…84 As is seen in hepatocellular carcinoma, hemorrhage, necrosis, and bile staining may be prominent. 85 Hepatoblastoma can be variable in size, and it often presents at a late stage, and with nonspecific symptoms. Multinodular tumors may contain different histologic components and should be adequately sampled.…”

Section: Manifestations Of the Hepatobiliary System Hepatoblastomamentioning

confidence: 99%

Familial Adenomatous Polyposis Syndrome: An Update and Review of Extraintestinal Manifestations

Dinarvand

Davaro

Doan³

et al. 2019

Archives of Pathology &Amp; Laboratory Medicine

105

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Context.— Familial adenomatous polyposis (FAP) is a rare genetic disorder with autosomal dominant inheritance, defined by numerous adenomatous polyps, which inevitably progress to colorectal carcinoma unless detected and managed early. Greater than 70% of patients with this syndrome also develop extraintestinal manifestations, such as multiple osteomas, dental abnormalities, and a variety of other lesions located throughout the body. These manifestations have historically been subcategorized as Gardner syndrome, Turcot syndrome, or gastric adenocarcinoma and proximal polyposis of the stomach. Recent studies, however, correlate the severity of gastrointestinal disease and the prominence of extraintestinal findings to specific mutations within the adenomatous polyposis coli gene ( APC), supporting a spectrum of disease as opposed to subcategorization. Advances in immunohistochemical and molecular techniques shed new light on the origin, classification, and progression risk of different entities associated with FAP. Objective.— To provide a comprehensive clinicopathologic review of neoplastic and nonneoplastic entities associated with FAP syndrome, with emphasis on recent developments in immunohistochemical and molecular profiles of extraintestinal manifestations in the thyroid, skin, soft tissue, bone, central nervous system, liver, and pancreas, and the subsequent changes in classification schemes and risk stratification. Data Sources.— This review will be based on peer-reviewed literature and the authors' experiences. Conclusions.— In this review we will provide an update on the clinicopathologic manifestations, immunohistochemical profiles, molecular features, and prognosis of entities seen in FAP, with a focus on routine recognition and appropriate workup of extraintestinal manifestations.

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“…Hepatocellular carcinoma (HCC) is the second most common primary liver malignancy of childhood (27%) [ 1 ]. Pediatric HCC may arise in the context of cirrhosis related to underlying metabolic or genetic diseases or in livers without chronic disease (CLD) [ 2 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

Focal Adhesion Kinase (FAK) Over-Expression and Prognostic Implication in Pediatric Hepatocellular Carcinoma

Francalanci

Giovannoni

Stefanis

et al. 2020

IJMS

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Focal adhesion kinase (FAK) is over-expressed and is correlated with aggressiveness in adult hepatocellular carcinoma (HCC). Inhibition of FAK decreases HCC invasiveness by down-regulating Enhancer of Zeste homolog 2 (EZH2), an epigenetic controller, that acts in transcriptional repression of a large number of genes via histone 3 methylation of lysine 27 (H3K27me3). Here, we investigated the hepatic expression of total FAK, EZH2, H3K27me3, and proliferating cell nuclear antigen (PCNA) in 17 pediatric HCCs and 8 healthy livers (CTRL). Quantitative imaging analysis showed that FAK gene/protein expression is up-regulated in HCCs compared to CTRL and, among tumor samples the levels of this gene/protein are significantly higher in cirrhotic HCCs than in a healthy milieu. Accordingly, the protein levels of EZH2 were also significantly increased in HCCs from a cirrhotic background. Intriguingly, the protein expression of FAK, EZH2, and PCNA significantly inversely correlated with tumor size. Finally, in HCC samples, mainly in cirrhotic background, the up-regulation of FAK gene positively correlated with that observed in β-Catenin gene. Conclusion: FAK gene/protein is over-expressed in pediatric HCCs concomitantly to EZH2 protein and β-Catenin gene, with a more significant up-regulation in a cirrhotic background. This triad of interactors deserves further investigations for translational application.

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Is hepatocellular carcinoma the same disease in children and adults? Comparison of histology, molecular background, and treatment in pediatric and adult patients

Cited by 22 publications

References 48 publications

Global trends in incidence rates of childhood liver cancers: A systematic review and meta‐analysis

Global trends in incidence rates of childhood liver cancers: A systematic review and meta‐analysis

Familial Adenomatous Polyposis Syndrome: An Update and Review of Extraintestinal Manifestations

Focal Adhesion Kinase (FAK) Over-Expression and Prognostic Implication in Pediatric Hepatocellular Carcinoma

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