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Biomedicines
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Advanced Research in Anticancer Inhibitors and Targeted Therapy
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Advanced Research in Anticancer Inhibitors and Targeted Therapy

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Drug Discovery, Development and Delivery".

Deadline for manuscript submissions: 31 May 2026 | Viewed by 2632

Special Issue Editors

Dr. Changmin Peng

E-Mail Website
Guest Editor
School of Medicine and Health Sciences, The George Washington University, Washington, DC, USA
Interests: histone deacetylases (HDACs); YAP signaling; drug resistance in cancer; protein O-GlcNAcylation
Dr. Hassan Ebrahim

E-Mail Website
Guest Editor
Department of Biomedical Sciences, Edward Via College of Osteopathic Medicine, Louisiana Campus, Monroe, LA 71203, USA
Interests: drug discovery; cancer pharmacology; novel molecular targets; herbal medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Rapidly advancing targeted cancer therapy has significantly improved treatment efficacy by selectively inhibiting oncogenic signaling pathways. Among these, histone deacetylase (HDAC) inhibitors, kinase inhibitors, and immune checkpoint inhibitors have demonstrated remarkable potential in both preclinical and clinical studies. However, the emergence of drug resistance, tumor heterogeneity, and adverse side effects pose substantial challenges to their clinical application.

This Special Issue aims to explore novel anticancer inhibitors, their molecular mechanisms, and potential combination strategies to overcome resistance, seeking to provide novel insights into improving the effectiveness and durability of targeted cancer therapies. We welcome original research and review articles focusing on epigenetic therapy, small-molecule inhibitors, immune-based treatments, and new therapeutic targets. Studies employing biochemical, molecular, and cellular approaches to investigate drug efficacy, biomarker discovery, and resistance mechanisms are highly encouraged.

Dr. Changmin Peng
Dr. Hassan Ebrahim
Guest Editors

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 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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • histone deacetylases (HDACs)
  • YAP signaling
  • targeted therapy
  • oncogenic signaling
  • biomarker discovery
  • small-molecule inhibitors
  • cancer drug resistance
  • epigenetic therapy

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Published Papers (2 papers)

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Research

19 pages, 7292 KB  
Article
Association of HTR1F with Prognosis, Tumor Immune Microenvironment, and Drug Sensitivity in Cancer: A Multi-Omics Perspective
by Yanjun Gao, Ziyue Zhang, Dafu Ye, Qingqing Li, Yingmei Wen, Shaowen Ma, Bo Zheng, Lei Chen and Yi Yao
Biomedicines 2025, 13(9), 2238; https://doi.org/10.3390/biomedicines13092238 - 11 Sep 2025
Viewed by 671
Abstract
Background: HTR1F (5-Hydroxytryptamine Receptor 1F) encodes a G protein-coupled receptor involved in serotonin signaling. Although dysregulated HTR1F expression has been implicated in certain malignancies, its biological functions and clinical significance across cancer types remain largely unexplored. Methods: We performed an integrative pan-cancer [...] Read more.
Background: HTR1F (5-Hydroxytryptamine Receptor 1F) encodes a G protein-coupled receptor involved in serotonin signaling. Although dysregulated HTR1F expression has been implicated in certain malignancies, its biological functions and clinical significance across cancer types remain largely unexplored. Methods: We performed an integrative pan-cancer analysis of transcriptomic and pharmacogenomic datasets covering 34 cancer types (PAN-CAN cohort, N = 19,131; normal tissues, G = 60,499). Drug sensitivity and molecular docking analyses were conducted using the GSCALite database. The protein–protein interaction (PPI) network of HTR1F was constructed via the STRING database. Additionally, we evaluated the effects of HTR1F overexpression on proliferation and invasion in human lung squamous cell carcinoma (LUSC) cell lines NCI-H520 and NCI-H226. Results: HTR1F expression was significantly upregulated in 17 cancer types and was associated with poor prognosis, with LUSC showing an AUC of 0.912 for 1-year survival prediction. In LUSC, 695 genes were upregulated and 67 downregulated in response to HTR1F overexpression. HTR1F expression correlated with immune-related genes, immune checkpoints, tumor-infiltrating immune cells, tumor mutation burden (TMB), microsatellite instability (MSI), and drug responses. Genomic alterations, including amplification and deletion, were positively associated with HTR1F expression. Drug sensitivity analysis identified compounds such as sotrastaurin (−10.2 kcal/mol), austocystin D (−9.7 kcal/mol), and tivozanib (−9.3 kcal/mol) as potentially effective inhibitors based on predicted binding affinity. Functional enrichment analyses (GO, KEGG) and GSEA revealed that HTR1F is primarily involved in cell cycle regulation, DNA replication, cellular senescence, and immune-related pathways. Functional validation showed that HTR1F overexpression promotes proliferation of LUSC cells via the MAPK signaling pathway. Conclusions: Our integrative analysis highlights HTR1F as a potential biomarker associated with prognosis, immune modulation, and drug sensitivity across multiple cancer types. These findings provide a foundation for future experimental and clinical studies to explore HTR1F-targeted therapies. Full article
(This article belongs to the Special Issue Advanced Research in Anticancer Inhibitors and Targeted Therapy)
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12 pages, 693 KB  
Article
Efficacy and Safety of the Combination of Durvalumab Plus Gemcitabine and Cisplatin in Patients with Advanced Biliary Tract Cancer: A Real-World Retrospective Cohort Study
by Eishin Kurihara, Satoru Kakizaki, Masashi Ijima, Takeshi Hatanaka, Norio Kubo, Yuhei Suzuki, Hidetoshi Yasuoka, Takashi Hoshino, Atsushi Naganuma, Noriyuki Tani, Yuichi Yamazaki and Toshio Uraoka
Biomedicines 2025, 13(8), 1915; https://doi.org/10.3390/biomedicines13081915 - 6 Aug 2025
Cited by 1 | Viewed by 1640
Abstract
Background/Objectives: The TOPAZ-1 phase III trial reported a survival benefit of using durvalumab, an anti-programmed death ligand 1 (anti-PD-L1) antibody, in combination with gemcitabine and cisplatin (GCD) treatment in patients with advanced biliary tract cancer. This retrospective study investigated the efficacy and [...] Read more.
Background/Objectives: The TOPAZ-1 phase III trial reported a survival benefit of using durvalumab, an anti-programmed death ligand 1 (anti-PD-L1) antibody, in combination with gemcitabine and cisplatin (GCD) treatment in patients with advanced biliary tract cancer. This retrospective study investigated the efficacy and safety of GCD treatment for advanced biliary tract cancer in real-world conditions. Methods: The study subjects were 52 patients with biliary tract cancer who received GCD therapy between January 2023 and May 2024. The observation parameters included the modified Glasgow Prognostic Score (mGPS), neutrophil–lymphocyte ratio (NLR), platelet–lymphocyte ratio (PLR), tumor markers (CEA, CA19-9), overall response rate (ORR), disease control rate (DCR), progression-free survival (PFS), overall survival (OS), and adverse events. Results: The cohort included 36 men and 16 women, with a median age of 73.0 years. There were 36 cases of cholangiocarcinoma (distal: 10, perihilar: 19, intrahepatic: 7), 13 cases of gallbladder cancer, and 3 cases of ampullary carcinoma. The stages were locally advanced in 30 cases and metastatic in 22 cases. Biliary drainage was performed in 30 cases. There were 38 cases receiving first-line therapy and 14 cases receiving second-line or later treatments. The median values at the start of GCD therapy were ALB 3.7 g/dL, CRP 0.39 mg/dL, NLR 2.4, PLR 162.5, CEA 4.8 ng/mL, and CA19-9 255.9 U/mL. The mGPS distribution was 0:23 cases, 1:18 cases, and 2:11 cases. The treatment outcomes were ORR 25.0% (CR 2 cases, PR 11 cases), DCR 78.8% (SD 28 cases, PD 10 cases, NE 1 case), median PFS 8.6 months, and median OS 13.9 months. The PLR was suggested to be useful for predicting PFS. A decrease in CEA at six weeks after the start of treatment was a significant predictor of PFS and OS. Gallbladder cancer had a significantly poorer prognosis compared to other cancers. The immune-related adverse events included hypothyroidism in two cases, cholangitis in one case, and colitis in one case. Conclusions: The ORR, DCR, and PFS were comparable to those in the TOPAZ-1 trial. Although limited by its retrospective design and small sample size, this study suggests that GCD therapy is an effective treatment regimen for unresectable biliary tract cancer in real-world clinical practice. Full article
(This article belongs to the Special Issue Advanced Research in Anticancer Inhibitors and Targeted Therapy)
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