Submit to Cancers Review for Cancers Propose a Special Issue

Journal Browser

► Journal Browser

Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers

Print Special Issue Flyer
Special Issue Editors
Special Issue Information
Keywords
Published Papers

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (10 December 2022) | Viewed by 31351

Share This Special Issue

Special Issue Editor

Dr. Cédric Coulouarn

E-Mail Website
Guest Editor

Inserm, Univ Rennes 1, OSS (Oncogenesis, Stress, Signaling) Laboratory, UMR_S 1242, Centre de Lutte contre le Cancer Eugène Marquis, F-35042 Rennes, France
Interests: hepatocellular carcinoma; cholangiocarcinoma; cell plasticity; TGFβ signaling; circular RNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Liver cancers, including hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), are deadly cancers associated with increased incidence worldwide and limited curative therapeutic options. Liver carcinogenesis is a long and multistep process associated with the accumulation of multiple molecular abnormalities, including DNA mutations, gain/loss of heterozygosity, and/or epigenetic alterations. These abnormalities contribute to modulating the activity of specific signaling pathways involved in tumor onset and progression. A better understanding of these molecular mechanisms underlying liver carcinogenesis should help in designing innovative therapeutic strategies and identifying innovative biomarkers for the management of patients’ liver cancer.

This Special Issue specifically aims at providing a review of the literature as well as emerging experimental evidence of the molecular mechanisms underlying tumor onset and progression in HCC and CCA. The description of multifaceted regulation of gene expression in liver cancers, notably at genetic, epigenetic, transcriptional, and post-transcriptional levels, will be taken into consideration. The specific topic of this Special Issue includes the regulation of signaling pathways involved in liver carcinogenesis.

This Special Issue should serve as a forum for molecular and cellular biologists to share their experimental data and theories that can help better understand the molecular mechanisms contributing to liver tumor onset and progression and open new opportunities for innovative therapeutics.

I am looking forward to your contributions to this Special Issue.

Prof. Cédric Coulouarn
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

hepatocellular carcinoma
cholangiocarcinoma
signaling pathways
mutations
gene expression
molecular signatures
liver cancer

Published Papers (12 papers)

Download All Papers

Editorial

Jump to: Research, Review, Other

3 pages, 204 KiB

Open AccessEditorial

The Molecular Mechanisms Underlying Onset and Progression of Liver Cancers

by Clara Le Breton and Cédric Coulouarn

Cancers 2023, 15(17), 4383; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers15174383 - 01 Sep 2023

Viewed by 805

Abstract

Liver cancers, including hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), are deadly cancers that have risen in frequency globally and have limited curative therapeutic options [...] Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers)

Research

Jump to: Editorial, Review, Other

16 pages, 3116 KiB

Open AccessArticle

Phosphorylation-Mediated Activation of β-Catenin-TCF4-CEGRs/ALCDs Pathway Is an Essential Event in Development of Aggressive Hepatoblastoma

by Ruhi Gulati, Margaret A. Hanlon, Maggie Lutz, Tyler Quitmeyer, James Geller, Gregory Tiao, Lubov Timchenko and Nikolai Timchenko

Cancers 2022, 14(24), 6062; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14246062 - 09 Dec 2022

Cited by 2 | Viewed by 1625

Abstract

Background and Aims: Hepatoblastoma (HBL), a deadly malignancy in children, is the most common type of pediatric liver cancer. We recently demonstrated that β-catenin, phosphorylated at S675 (ph-S675-β-catenin), causes pathological alterations in fibrolamellar hepatocellular carcinoma (FLC), by activating oncogenes and fibrotic genes via human genomic regions, known as cancer-enhancing genomic regions or aggressive liver cancer domains (CEGRs/ALCDs). The aim of this study was to determine the role of the ph-S675-β-catenin-TCF4-CEGRs/ALCDs pathway in HBL. Methods: The ph-S675-β-catenin-TCF4-CEGRs/ALCDs pathway was examined in a large cohort of HBL specimens, in HBL cell lines HepG2 and Huh6, and in patient-derived xenografts (PDXs). Results: β-catenin is phosphorylated at S675 in a large portion of tested HBL patients. In these patients, ph-S675-β-catenin forms complexes with TCF4 and opens CEGRs/ALCDs-dependent oncogenes for transcription, leading to a massive overexpression of the oncogenes. The inhibition of the β-catenin-TCF4-CEGRs/ALCDs axis inhibits the proliferation of cancer cells and tumor growth in HBL cell lines and HBL-PDXs. The ph-S675-β-catenin is abundant in mitotic cells. We found that markers of HBL Glypican 3 (GPC3) and Alpha Fetoprotein (AFP) are increased in HBL patients by β-catenin-TCF4-p300 complexes. Conclusions: The phosphorylation-mediated activation of the β-catenin-TCF4-p300-CEGRs/ALCDs pathway increases oncogene expression in patients with aggressive liver cancer and promotes the development of hepatoblastoma. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers)

► Show Figures

Graphical abstract

19 pages, 3429 KiB

Open AccessArticle

DNA Methylation Regulates a Set of Long Non-Coding RNAs Compromising Hepatic Identity during Hepatocarcinogenesis

by Miriam Recalde, María Gárate-Rascón, José María Herranz, María Elizalde, María Azkona, Juan P. Unfried, Loreto Boix, María Reig, Bruno Sangro, Maite G. Fernández-Barrena, Puri Fortes, Matías A. Ávila, Carmen Berasain and María Arechederra

Cancers 2022, 14(9), 2048; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14092048 - 19 Apr 2022

Cited by 6 | Viewed by 2129

Abstract

Background: Long noncoding RNAs (lncRNAs) are emerging as key players in cancer, including hepatocellular carcinoma (HCC). Here we identify the mechanism implicated in the HCC inhibition of a set of lncRNAs, and their contribution to the process of hepatocarcinogenesis. Methods and Results: The top-ranked 35 lncRNAs downregulated in HCC (Top35 LNDH) were validated in several human HCC cohorts. We demonstrate that their inhibition is associated with promoter hypermethylation in HCC compared to control tissue, and in HCC human cell lines compared to primary hepatocytes. Moreover, demethylating treatment of HCC human cell lines induced the expression of these lncRNAs. The Top35 LNDH were preferentially expressed in the adult healthy liver compared to other tissues and fetal liver and were induced in well-differentiated HepaRG cells. Remarkably, their knockdown compromised the expression of other hepato-specific genes. Finally, the expression of the Top35 LNDH positively correlates with the grade of tumor differentiation and, more importantly, with a better patient prognosis. Conclusions: Our results demonstrate that the selected Top35 LNDH are not only part of the genes that compose the hepatic differentiated signature but participate in its establishment. Moreover, their downregulation through DNA methylation occurs during the process of hepatocarcinogenesis compromising hepatocellular differentiation and HCC patients’ prognosis. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers)

► Show Figures

Graphical abstract

13 pages, 5064 KiB

Open AccessArticle

A Minimal Subset of Seven Genes Associated with Tumor Hepatocyte Differentiation Predicts a Poor Prognosis in Human Hepatocellular Carcinoma

by Matthis Desoteux, Corentin Louis, Kevin Bévant, Denise Glaise and Cédric Coulouarn

Cancers 2021, 13(22), 5624; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13225624 - 10 Nov 2021

Cited by 6 | Viewed by 2122

Abstract

Hepatocellular carcinoma (HCC) is a deadly cancer worldwide as a result of a frequent late diagnosis which limits the therapeutic options. Tumor progression in HCC is closely correlated with the dedifferentiation of hepatocytes, the main parenchymal cells in the liver. Here, we hypothesized that the expression level of genes reflecting the differentiation status of tumor hepatocytes could be clinically relevant in defining subsets of patients with different clinical outcomes. To test this hypothesis, an integrative transcriptomics approach was used to stratify a cohort of 139 HCC patients based on a gene expression signature established in vitro in the HepaRG cell line using well-controlled culture conditions recapitulating tumor hepatocyte differentiation. The HepaRG model was first validated by identifying a robust gene expression signature associated with hepatocyte differentiation and liver metabolism. In addition, the signature was able to distinguish specific developmental stages in mice. More importantly, the signature identified a subset of human HCC associated with a poor prognosis and cancer stem cell features. By using an independent HCC dataset (TCGA consortium), a minimal subset of seven differentiation-related genes was shown to predict a reduced overall survival, not only in patients with HCC but also in other types of cancers (e.g., kidney, pancreas, skin). In conclusion, the study identified a minimal subset of seven genes reflecting the differentiation status of tumor hepatocytes and clinically relevant for predicting the prognosis of HCC patients. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers)

► Show Figures

Figure 1

23 pages, 3891 KiB

Open AccessArticle

Tetraspanin 5 (TSPAN5), a Novel Gatekeeper of the Tumor Suppressor DLC1 and Myocardin-Related Transcription Factors (MRTFs), Controls HCC Growth and Senescence

by Laura Schreyer, Constanze Mittermeier, Miriam J. Franz, Melanie A. Meier, Dietmar E. Martin, Kerstin C. Maier, Kerstin Huebner, Regine Schneider-Stock, Stephan Singer, Kerstin Holzer, Dagmar Fischer, Silvia Ribback, Bernhard Liebl, Thomas Gudermann, Achim Aigner and Susanne Muehlich

Cancers 2021, 13(21), 5373; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13215373 - 26 Oct 2021

Cited by 5 | Viewed by 2886

Abstract

Human hepatocellular carcinoma (HCC) is among the most lethal and common cancers in the human population, and new molecular targets for therapeutic intervention are urgently needed. Deleted in liver cancer 1 (DLC1) was originally identified as a tumor suppressor gene in human HCC. DLC1 is a Rho-GTPase-activating protein (RhoGAP) which accelerates the return of RhoGTPases to an inactive state. We recently described that the restoration of DLC1 expression induces cellular senescence. However, this principle is not amenable to direct therapeutic targeting. We therefore performed gene expression profiling for HepG2 cells depleted of DLC1 to identify druggable gene targets mediating the effects of DLC1 on senescence induction. This approach revealed that versican (VCAN), tetraspanin 5 (TSPAN5) and N-cadherin (CDH2) were strongly upregulated upon DLC1 depletion in HCC cells, but only TSPAN5 affected the proliferation of HCC cells and human HCC. The depletion of TSPAN5 induced oncogene-induced senescence (OIS), mediated by the p16^INK4a/pRb pathways. Mechanistically, silencing TSPAN5 reduced actin polymerization and thereby myocardin-related transcription factor A- filamin A (MRTF-A-FLNA) complex formation, resulting in decreased expression of MRTF/SRF-dependent target genes and senescence induction in vitro and in vivo. Our results identify TSPAN5 as a novel druggable target for HCC. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers)

► Show Figures

Figure 1

0 pages, 4618 KiB

Open AccessArticle

RANBP2 Activates O-GlcNAcylation through Inducing CEBPα-Dependent OGA Downregulation to Promote Hepatocellular Carcinoma Malignant Phenotypes

by Xiaoming Liu, Xingyu Chen, Mengqing Xiao, Yuxing Zhu, Renjie Gong, Jianye Liu, Qinghai Zeng, Canxia Xu, Xiong Chen, Fen Wang and Ke Cao

Cancers 2021, 13(14), 3475; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13143475 - 12 Jul 2021

Cited by 12 | Viewed by 2815 | Correction

Abstract

O-GlcNAcylation is an important post-translational modification (PTM) jointly controlled by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). Aberrant hyper-O-GlcNAcylation is reported to yield hepatocellular carcinoma (HCC) malignancy, but the underlying mechanisms of the OGT/OGA imbalance responsible for HCC tumorigenesis remain largely unknown. Here, we report that RAN-binding protein 2 (RANBP2), one of the small ubiquitin-like modifier (SUMO) E3 ligases, contributed to malignant phenotypes in HCC. RANBP2 was found to facilitate CCAAT/enhancer-binding protein alpha (CEBPα) SUMOylation and degradation by direct interplay with CEBPα. As a transcriptional factor, CEBPα was verified to augment OGA transcription, and further experiments demonstrated that RANBP2 enhanced the O-GlcNAc level by downregulating OGA transcription while not affecting OGT expression. Importantly, we provided in vitro and in vivo evidence of HCC malignant phenotypes that RANBP2 triggered through an imbalance of OGT/OGA and subsequent higher O-GlcNAcylation events for oncogenic proteins such as peroxisome proliferative-activated receptor gamma coactivator 1 alpha (PGC1α) in a CEBPα-dependent manner. Altogether, our results show a novel molecular mechanism whereby RANBP2 regulates its function through CEBPα-dependent OGA downregulation to induce a global change in the hyper-O-GlcNAcylation of genes, such as PGC1α, encouraging the further study of promising implications for HCC therapy. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers)

► Show Figures

Graphical abstract

24 pages, 2766 KiB

Open AccessArticle

Estrogen Receptor-α Suppresses Liver Carcinogenesis and Establishes Sex-Specific Gene Expression

by Mara H. O’Brien, Henry C. Pitot, Sang-Hyuk Chung, Paul F. Lambert, Norman R. Drinkwater and Andrea Bilger

Cancers 2021, 13(10), 2355; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13102355 - 13 May 2021

Cited by 17 | Viewed by 2555

Abstract

Estrogen protects females from hepatocellular carcinoma (HCC). To determine whether this protection is mediated by classic estrogen receptors, we tested HCC susceptibility in estrogen receptor-deficient mice. In contrast to a previous study, we found that diethylnitrosamine induces hepatocarcinogenesis to a significantly greater extent when females lack Esr1, which encodes Estrogen Receptor-α. Relative to wild-type littermates, Esr1 knockout females developed 9-fold more tumors. Deficiency of Esr2, which encodes Estrogen Receptor-β, did not affect liver carcinogenesis in females. Using microarrays and QPCR to examine estrogen receptor effects on hepatic gene expression patterns, we found that germline Esr1 deficiency resulted in the masculinization of gene expression in the female liver. Six of the most dysregulated genes have previously been implicated in HCC. In contrast, Esr1 deletion specifically in hepatocytes of Esr1 conditional null female mice (in which Cre was expressed from the albumin promoter) resulted in the maintenance of female-specific liver gene expression. Wild-type adult females lacking ovarian estrogen due to ovariectomy, which is known to make females susceptible to HCC, also maintained female-specific expression in the liver of females. These studies indicate that Esr1 mediates liver cancer risk, and its control of sex-specific liver gene expression involves cells other than hepatocytes. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers)

► Show Figures

Figure 1

Review

Jump to: Editorial, Research, Other

21 pages, 406 KiB

Open AccessReview

Impact of Alternative Splicing Variants on Liver Cancer Biology

by Jose J. G. Marin, Maria Reviejo, Meraris Soto, Elisa Lozano, Maitane Asensio, Sara Ortiz-Rivero, Carmen Berasain, Matias A. Avila and Elisa Herraez

Cancers 2022, 14(1), 18; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14010018 - 21 Dec 2021

Cited by 11 | Viewed by 3488

Abstract

The two most frequent primary cancers affecting the liver, whose incidence is growing worldwide, are hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (iCCA), which are among the five most lethal solid tumors with meager 5-year survival rates. The common difficulty in most cases to reach an early diagnosis, the aggressive invasiveness of both tumors, and the lack of favorable response to pharmacotherapy, either classical chemotherapy or modern targeted therapy, account for the poor outcome of these patients. Alternative splicing (AS) during pre-mRNA maturation results in changes that might affect proteins involved in different aspects of cancer biology, such as cell cycle dysregulation, cytoskeleton disorganization, migration, and adhesion, which favors carcinogenesis, tumor promotion, and progression, allowing cancer cells to escape from pharmacological treatments. Reasons accounting for cancer-associated aberrant splicing include mutations that create or disrupt splicing sites or splicing enhancers or silencers, abnormal expression of splicing factors, and impaired signaling pathways affecting the activity of the splicing machinery. Here we have reviewed the available information regarding the impact of AS on liver carcinogenesis and the development of malignant characteristics of HCC and iCCA, whose understanding is required to develop novel therapeutical approaches aimed at manipulating the phenotype of cancer cells. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers)

17 pages, 1737 KiB

Open AccessReview

The Role of Protein SUMOylation in Human Hepatocellular Carcinoma: A Potential Target of New Drug Discovery and Development

by Hongchao Yuan, Yuanjun Lu, Yau-Tuen Chan, Cheng Zhang, Ning Wang and Yibin Feng

Cancers 2021, 13(22), 5700; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13225700 - 14 Nov 2021

Cited by 10 | Viewed by 2842

Abstract

Small ubiquitin-like modifier (SUMO) is a highly conserved post-translational modification protein, mainly found in eukaryotes. They are widely expressed in different tissues, including the liver. As an essential post-translational modification, SUMOylation is involved in many necessary regulations in cells. It plays a vital role in DNA repair, transcription regulation, protein stability and cell cycle progression. Increasing shreds of evidence show that SUMOylation is closely related to Hepatocellular carcinoma (HCC). The high expression of SUMOs in the inflammatory hepatic tissue may lead to the carcinogenesis of HCC. At the same time, SUMOs will upregulate the proliferation and survival of HCC, migration, invasion and metastasis of HCC, tumour microenvironment as well as drug resistance. This study reviewed the role of SUMOylation in liver cancer. In addition, it also discussed natural compounds that modulate SUMO and target SUMO drugs in clinical trials. Considering the critical role of SUMO protein in the occurrence of HCC, the drug regulation of SUMOylation may become a potential target for treatment, prognostic monitoring and adjuvant chemotherapy of HCC. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers)

► Show Figures

Figure 1

22 pages, 1727 KiB

Open AccessReview

Intrinsic and Extrinsic Control of Hepatocellular Carcinoma by TAM Receptors

by Viola Hedrich, Kristina Breitenecker, Leila Djerlek, Gregor Ortmayr and Wolfgang Mikulits

Cancers 2021, 13(21), 5448; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13215448 - 29 Oct 2021

Cited by 7 | Viewed by 3570

Abstract

Hepatocellular carcinoma (HCC) is the major subtype of liver cancer, showing high mortality of patients due to limited therapeutic options at advanced stages of disease. The receptor tyrosine kinases Tyro3, Axl and MerTK—belonging to the TAM family—exert a large impact on various aspects of cancer biology. Binding of the ligands Gas6 or Protein S activates TAM receptors causing homophilic dimerization and heterophilic interactions with other receptors to modulate effector functions. In this context, TAM receptors are major regulators of anti-inflammatory responses and vessel integrity, including platelet aggregation as well as resistance to chemotherapy. In this review, we discuss the relevance of TAM receptors in the intrinsic control of HCC progression by modulating epithelial cell plasticity and by promoting metastatic traits of neoplastic hepatocytes. Depending on different etiologies of HCC, we further describe the overt role of TAM receptors in the extrinsic control of HCC progression by focusing on immune cell infiltration and fibrogenesis. Additionally, we assess TAM receptor functions in the chemoresistance against clinically used tyrosine kinase inhibitors and immune checkpoint blockade in HCC progression. We finally address the question of whether inhibition of TAM receptors can be envisaged for novel therapeutic strategies in HCC. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers)

► Show Figures

Graphical abstract

21 pages, 1214 KiB

Open AccessReview

The Emerging Factors and Treatment Options for NAFLD-Related Hepatocellular Carcinoma

by Chunye Zhang and Ming Yang

Cancers 2021, 13(15), 3740; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13153740 - 26 Jul 2021

Cited by 23 | Viewed by 4459

Abstract

Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer, followed by cholangiocarcinoma (CCA). HCC is the third most common cause of cancer death worldwide, and its incidence is rising, associated with an increased prevalence of obesity and nonalcoholic fatty liver disease (NAFLD). However, current treatment options are limited. Genetic factors and epigenetic factors, influenced by age and environment, significantly impact the initiation and progression of NAFLD-related HCC. In addition, both transcriptional factors and post-transcriptional modification are critically important for the development of HCC in the fatty liver under inflammatory and fibrotic conditions. The early diagnosis of liver cancer predicts curative treatment and longer survival. However, clinical HCC cases are commonly found in a very late stage due to the asymptomatic nature of the early stage of NAFLD-related HCC. The development of diagnostic methods and novel biomarkers, as well as the combined evaluation algorithm and artificial intelligence, support the early and precise diagnosis of NAFLD-related HCC, and timely monitoring during its progression. Treatment options for HCC and NAFLD-related HCC include immunotherapy, CAR T cell therapy, peptide treatment, bariatric surgery, anti-fibrotic treatment, and so on. Overall, the incidence of NAFLD-related HCC is increasing, and a better understanding of the underlying mechanism implicated in the progression of NAFLD-related HCC is essential for improving treatment and prognosis. Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers)

► Show Figures

Figure 1

Other

Jump to: Editorial, Research, Review

2 pages, 925 KiB

Open AccessCorrection

Correction: Liu et al. RANBP2 Activates O-GlcNAcylation through Inducing CEBPα-Dependent OGA Downregulation to Promote Hepatocellular Carcinoma Malignant Phenotypes. Cancers 2021, 13, 3475

by Xiaoming Liu, Xingyu Chen, Mengqing Xiao, Yuxing Zhu, Renjie Gong, Jianye Liu, Qinghai Zeng, Canxia Xu, Xiong Chen, Fen Wang and Ke Cao

Cancers 2024, 16(5), 1018; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers16051018 - 29 Feb 2024

Viewed by 471

Abstract

In the original publication [...] Full article

(This article belongs to the Special Issue Molecular Mechanisms Underlying Tumor Onset and Progression in Liver Cancers)

► Show Figures