Capecitabine in advanced hepatocellular carcinoma: A multicenter experience

Pelizzaro, Filippo; Sammarco, Alessandro; Dadduzio, Vincenzo; Pastorelli, Davide; Giovanis, Petros; Soldà, Caterina; Rizzato, Mario Domenico; Lombardi, Giuseppe; Peserico, Giulia; Imondi, A.; Sartori, Anna; Maddalo, G.; Farinati, Fabio

doi:10.1016/j.dld.2019.06.015

Cited by 20 publications

(12 citation statements)

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“…In this case, we expect that the same applies to the levels of NF-YAs, which correlate to the TP53 status. Due to the overall modest efficacy of these drugs in the long term management of patients, other drugs have been tested [65,66]. Thus, a possible outcome of our analysis is the evaluation of efficacies of established and novel drugs based on modifications of NF-YA levels, even tested in vitro, as well the development of anti-NF-Y compounds, as we have recently started to do, based on in silico screenings and in vitro testing [67].…”

Section: Discussionmentioning

confidence: 99%

NF-Y Overexpression in Liver Hepatocellular Carcinoma (HCC)

Bezzecchi

Ronzio

Mantovani

et al. 2020

IJMS

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NF-Y is a pioneer trimeric transcription factor formed by the Histone Fold Domain (HFD) NF-YB/NF-YC subunits and NF-YA. Three subunits are required for DNA binding. CCAAT-specificity resides in NF-YA and transactivation resides in Q-rich domains of NF-YA and NF-YC. They are involved in alternative splicing (AS). We recently showed that NF-YA is overexpressed in breast and lung carcinomas. We report here on the overexpression of all subunits in the liver hepatocellular carcinoma (HCC) TCGA database, specifically the short NF-YAs and NF-YC2 (37 kDa) isoforms. This is observed at all tumor stages, in viral-infected samples and independently from the inflammatory status. Up-regulation of NF-YAs and NF-YC, but not NF-YB, is associated to tumors with mutant p53. We used a deep-learning-based method (DeepCC) to extend the partitioning of the three molecular clusters to all HCC TCGA tumors. In iCluster3, CCAAT is a primary matrix found in promoters of up-regulated genes, and cell-cycle pathways are enriched. Finally, clinical data indicate that, globally, only NF-YAs, but not HFD subunits, correlate with the worst prognosis; in iCluster1 patients, however, all subunits correlate. The data show a difference with other epithelial cancers, in that global overexpression of the three subunits is reported and clinically relevant in a subset of patients; yet, they further reinstate the regulatory role of the sequence-specific subunit.

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Section: Discussionmentioning

confidence: 99%

NF-Y Overexpression in Liver Hepatocellular Carcinoma (HCC)

Bezzecchi

Ronzio

Mantovani

et al. 2020

IJMS

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“…[20][21][22][23][24][25] When patients underwent multiple treatments, they were classified according to the most effective one using the following hierarchy: LT, liver resection (LR), percutaneous ablation (ABL), transarterial chemoembolisation/embolisation or radioembolisation (IAT, intra-arterial therapies), sorafenib (SOR) and other therapies or best supportive care (OTHER/BSC). [25][26][27]…”

Section: Staging and Treatment Of Hccmentioning

confidence: 99%

Epidemiological trends and trajectories of MAFLD-associated hepatocellular carcinoma 2002–2033: the ITA.LI.CA database

Vitale

Svegliati‐Baroni

Ortolani

et al. 2021

Gut

Self Cite

107

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BackgroundMetabolic dysfunction-associated fatty liver disease (MAFLD) represents a new inclusive definition of the whole spectrum of liver diseases associated to metabolic disorders. The main objective of this study was to compare patients with MAFLD and non-MAFLD with hepatocellular carcinoma (HCC) included in a nationally representative cohort.MethodsWe analysed 6882 consecutive patients with HCC enrolled from 2002 to 2019 by 23 Italian Liver Cancer centres to compare epidemiological and future trends in three subgroups: pure, single aetiology MAFLD (S-MAFLD); mixed aetiology MAFLD (metabolic and others, M-MAFLD); and non-MAFLD HCC.ResultsMAFLD was diagnosed in the majority of patients with HCC (68.4%). The proportion of both total MAFLD and S-MAFLD HCC significantly increased over time (from 50.4% and 3.6% in 2002–2003, to 77.3% and 28.9% in 2018–2019, respectively, p<0.001). In Italy S-MAFLD HCC is expected to overcome M-MAFLD HCC in about 6 years. Patients with S-MAFLD HCC were older, more frequently men and less frequently cirrhotic with clinically relevant portal hypertension and a surveillance-related diagnosis. They had more frequently large tumours and extrahepatic metastases. After weighting, and compared with patients with non-MAFLD, S-MAFLD and M-MAFLD HCC showed a significantly lower overall (p=0.026, p=0.004) and HCC-related (p<0.001, for both) risk of death. Patients with S-MAFLD HCC showed a significantly higher risk of non-HCC-related death (p=0.006).ConclusionsThe prevalence of MAFLD HCC in Italy is rapidly increasing to cover the majority of patients with HCC. Despite a less favourable cancer stage at diagnosis, patients with MAFLD HCC have a lower risk of HCC-related death, suggesting reduced cancer aggressiveness.

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“…Capecitabine is an orally administered 5-FU prodrug that is absorbed in an intact form via the gastrointestinal tract. Capecitabine has been investigated in the treatment of advanced HCC using either convention [ 79 ].…”

Section: Genes Associated With Capecitabine/5-fu Resistancementioning

confidence: 99%

Evaluation and Application of Drug Resistance by Biomarkers in the Clinical Treatment of Liver Cancer

Huang

Wang

et al. 2023

Cells

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Liver cancer is one of the most lethal cancers in the world, mainly owing to the lack of effective means for early monitoring and treatment. Accordingly, there is considerable research interest in various clinically applicable methods for addressing these unmet needs. At present, the most commonly used biomarker for the early diagnosis of liver cancer is alpha-fetoprotein (AFP), but AFP is sensitive to interference from other factors and cannot really be used as the basis for determining liver cancer. Treatment options in addition to liver surgery (resection, transplantation) include radiation therapy, chemotherapy, and targeted therapy. However, even more expensive targeted drug therapies have a limited impact on the clinical outcome of liver cancer. One of the big reasons is the rapid emergence of drug resistance. Therefore, in addition to finding effective biomarkers for early diagnosis, an important focus of current discussions is on how to effectively adjust and select drug strategies and guidelines for the treatment of liver cancer patients. In this review, we bring this thought process to the drug resistance problem faced by different treatment strategies, approaching it from the perspective of gene expression and molecular biology and the possibility of finding effective solutions.

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Capecitabine in advanced hepatocellular carcinoma: A multicenter experience

Cited by 20 publications

References 50 publications

NF-Y Overexpression in Liver Hepatocellular Carcinoma (HCC)

NF-Y Overexpression in Liver Hepatocellular Carcinoma (HCC)

Epidemiological trends and trajectories of MAFLD-associated hepatocellular carcinoma 2002–2033: the ITA.LI.CA database

Evaluation and Application of Drug Resistance by Biomarkers in the Clinical Treatment of Liver Cancer

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