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The Biology of Hepatocellular Carcinoma: Implications for Genomic and Immune Therapies (2nd Edition)

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

Deadline for manuscript submissions: 31 January 2026 | Viewed by 536

Special Issue Editor


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Guest Editor
Department of Gastroenterology and Hepatology, Faculty of Medicine, Kindai University, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511, Japan
Interests: hepatocellular carcinoma; molecular classification; tumor microenvironment; genome; epigenome; transcriptome; diagnosis; treatment; molecular targeted agent; multikinase inhibitor; immune checkpoint inhibitor; artificial intelligence
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Special Issue Information

Dear Colleagues,

This Special Issue is the second edition of “The Biology of Hepatocellular Carcinoma: Implications for Genomic and Immune Therapies”.

Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide, with a high recurrence rate and mortality. Although the biological behavior of HCC is complex, where a variety of oncogenic pathways are involved, recent analyses of the genome, epigenome, and transcriptome indicate a sophisticated molecular classification of this type of cancer that reflects HCC biology. Such “omics” analyses allow us to show a responsible cancer pathway and help to develop specific molecular targeted agents as well as understand cancer biology in each case. In addition, it is known that omics-based classifications are also associated with the immune phenotype of HCC, which should affect the efficacy of immune-based treatment, including immune checkpoint inhibitors in addition to molecular targeted agents. From these points of view, understanding biology in each HCC is required to establish the personalized medicine expected for the effective treatment of cancer.

From this point of view, this Special Issue will highlight the current state of the art in genetic and immune therapies based on the biological understanding of HCC from both basic and clinical aspects.

In addition, recent technology in artificial intelligence (AI) is playing a critical role in applying omics data to understanding the biology in each HCC; AI-based analyses of precision medicine are also welcome.

Prof. Dr. Naoshi Nishida
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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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
  • diagnosis
  • treatment
  • molecular targeted agent
  • immune checkpoint inhibitor
  • artificial intelligence

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Published Papers (1 paper)

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Research

14 pages, 1104 KB  
Article
No Correlation Between Proteinuria and Renal Function in Patients with Unresectable Hepatocellular Carcinoma Treated with Atezolizumab Plus Bevacizumab: ARISE Study
by Kazuomi Ueshima, Naoshi Nishida, Satoru Hagiwara, Yasunori Minami, Hiroshi Ida, Masahiro Takita, Hirokazu Chishina, Masahiro Morita, Tomoko Aoki, Tetsutaro Hamano, Ryosuke Take, Chizuko Watanabe, Kohsuke Asoh, Ai Tanaka and Masatoshi Kudo
Cancers 2025, 17(23), 3826; https://doi.org/10.3390/cancers17233826 - 28 Nov 2025
Viewed by 337
Abstract
Background: Atezolizumab plus bevacizumab (Atezo + Bev) is the standard of care for treatment-naïve patients with unresectable hepatocellular carcinoma (uHCC). Proteinuria is a treatment-emergent adverse event that often leads to Bev interruption. However, the relationship between Bev-related proteinuria and renal dysfunction is unclear. [...] Read more.
Background: Atezolizumab plus bevacizumab (Atezo + Bev) is the standard of care for treatment-naïve patients with unresectable hepatocellular carcinoma (uHCC). Proteinuria is a treatment-emergent adverse event that often leads to Bev interruption. However, the relationship between Bev-related proteinuria and renal dysfunction is unclear. We retrospectively investigated the impact of proteinuria after starting Atezo + Bev on renal function in patients with uHCC. Methods: We performed a single-arm retrospective study of patients with uHCC treated with Atezo + Bev between 25 September 2020 and 31 May 2022, at Kindai University Hospital, Japan. The impact of proteinuria on renal function during Atezo + Bev treatment was analyzed in terms of the correlation between changes in urine protein creatinine ratio (UPCR) and estimated glomerular filtration rate (eGFR) relative to baseline. Results: We analyzed data from 100 patients (median age 74 years; range 41–89; 75% male). During Atezo + Bev treatment, the median (interquartile range) maximum increase from baseline in UPCR was 0.39 (0.08 to 2.05) and the median maximum decline from baseline in eGFR was −7.5 (−20.5 to −3.0) mL/min/1.73 m2. The Pearson and Spearman correlation coefficients (95% confidence intervals) between these variables were −0.16 (−0.34 to 0.04) and −0.13 (−0.32 to 0.07), respectively. Conclusions: We found no correlation between the changes in UPCR and eGFR during Atezo + Bev treatment. Bev interruption criteria are based on the degree of proteinuria; however, our results suggest that proteinuria does not necessarily impair renal function. Physicians should consider the risk–benefit profile when deciding whether to discontinue Bev in patients who develop proteinuria during Atezo + Bev treatment. Full article
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