Abstract
The most frequent liver tumor in children is hepatoblastoma (HB), which derives from embryonic parenchymal liver cells or hepatoblasts. Hepatocellular carcinoma (HCC), which rarely affects young people, causes one fourth of deaths due to cancer in adults. In contrast, HB usually has better prognosis, but this is still poor in 20% of cases. Although more responsive to chemotherapy than HCC, the failure of pharmacological treatment used before and/or after surgical resection is an important limitation in the management of patients with HB. To advance in the implementation of personalized medicine it is important to select the best combination among available anti-HB drugs, such as platinum derivatives, anthracyclines, etoposide, tyrosine-kinase inhibitors, Vinca alkaloids, 5-fluorouracil, monoclonal antibodies, irinotecan and nitrogen mustards. This requires predicting the sensitivity to these drugs of each tumor at each time because, it should be kept in mind, that cancer chemoresistance is a dynamic process of Darwinian nature. For this goal it is necessary to improve our understanding of the mechanisms of chemoresistance involved in the refractoriness of HB against the pharmacological challenge and how they evolve during treatment. In this review we have summarized the current knowledge on the multifactorial and complex factors responsible for the lack of response of HB to chemotherapy.
Highlights
Hepatoblastoma (HB) is a rare tumor affecting less than 2 children per million, this is the most common pediatric liver cancer [1]
In the present review we have revised the available information regarding the role of these mechanisms of chemoresistance (MOCs) in the lack of response to drugs commonly used in first- and second-line regimens of HB treatment, i.e., platinum derivatives, anthracyclines, etoposide, tyrosine-kinase inhibitors (TKIs), Vinca alkaloids, 5-fluorouracil
Minor changes in the expression of genes included in MOC-4 were found in HB biopsies [29], but the same study demonstrated that the exposure of HepG2 cells to cisplatin upregulated excision repair cross-complementing 1 protein (ERCC1) and the product of Xeroderma pigmentosum group A (XPA) genes, suggesting that DNA repair mechanisms are induced by this pharmacological treatment
Summary
Hepatoblastoma (HB) is a rare tumor affecting less than 2 children per million (mainly under 3 years of age), this is the most common pediatric liver cancer [1]. Along with advances in surgical techniques, chemotherapy has contributed to achieve survival rates of up to 70–80% in contrast to the 20% obtained when patients were treated only with surgery [3]. Cancers 2019, 11, 407 followed by chemotherapy was allowed only if the tumor met strict resection criteria. The outcome after both therapeutic approaches seems to be similar. HB is poorer than that of patients with well differentiated HB, especially in the case of small cell undifferentiated HB, an uncommon subgroup associated with an adverse outcome [6]. In the present review we have revised the available information regarding the role of these MOCs in the lack of response to drugs commonly used in first- and second-line regimens of HB treatment, i.e., platinum derivatives, anthracyclines, etoposide, tyrosine-kinase inhibitors (TKIs), Vinca alkaloids, 5-fluorouracil (5-FU), irinotecan, bevacizumab and nitrogen mustards
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