비타민B3 (나이아시나마이드)
Vitamin B3 (Niacinamide)
📖 핵심 요약
📖 75편 · 38분 읽기비타민B3 (나이아시나마이드)은(는) 비타민 계열 보충제입니다. 주로 항암, 근육 분야에서 연구되었으며, PubMed에 75편의 관련 논문이 있습니다.
🔍 연구 분야별 근거
* 제목에 해당 키워드가 포함된 논문 수 (PubMed 근거)
📊 효과 크기 분포 (Forest plot)
각 연구의 효과 추정치와 95% 신뢰구간. 개별 연구를 통합(pooling)하지 않고 그대로 표시합니다.
📚 관련 논문 (75편) · 📊 정량 근거 3건
1. Int J Mol Sci. 2025 Apr 18;26(8):3840. doi: 10.3390/ijms26083840. Updated Meta-Analysis on Vitamin Supplementation for Chronic Pruritus: Expanding Evidence Beyond Vitamin D. Kuo WH(1), Chang KS(2), Chang MH(3), Hsiao Y(4), Tsai RY(5)(6). Author information: (1)Department of Gastroenterology a
2. J Cachexia Sarcopenia Muscle. 2025 Jun;16(3):e13799. doi: 10.1002/jcsm.13799. The Effect of Nicotinamide Mononucleotide and Riboside on Skeletal Muscle Mass and Function: A Systematic Review and Meta-Analysis. Prokopidis K(1), Moriarty F(2), Bahat G(3), McLean J(4), Church DD(5), Patel HP(6)(
3. Nutrients. 2023 Dec 27;16(1):100. doi: 10.3390/nu16010100. The Role of Nicotinamide as Chemo-Preventive Agent in NMSCs: A Systematic Review and Meta-Analysis. Tosti G(1), Pepe F(1), Gnagnarella P(2), Silvestri F(1), Gaeta A(3)(4), Queirolo P(5), Gandini S(3). Author information: (1)Dermato-O
4. J Cancer Res Ther. 2018 Dec;14(Supplement):S948-S956. doi: 10.4103/0973-1482.188430. Bleeding risk in cancer patients treated with sorafenib: A meta-analysis of randomized controlled trials. Dai C(1), Zhou F(2), Shao JH(2), Wu LQ(2), Yu X(1), Yin XB(1). Author information: (1)Department of H
5. Nutr Rev. 2017 Jun 1;75(6):471-490. doi: 10.1093/nutrit/nux011. Definition of a tolerable upper intake level of niacin: a systematic review and meta-analysis of the dose-dependent effects of nicotinamide and nicotinic acid supplementation. Minto C(1), Vecchio MG(2), Lamprecht M(2), Gregori D(
6. Lancet Neurol. 2026 May;25(5):469-481. doi: 10.1016/S1474-4422(26)00082-7. Safety and efficacy of individualised exercise and NAD(+) precursor supplementation in patients with Friedreich's ataxia in the USA: a single-centre, 2 × 2 factorial, randomised controlled trial. Lin KY(1), Bucha A(1),
7. Nat Metab. 2026 Jan;8(1):62-73. doi: 10.1038/s42255-025-01421-8. Epub 2026 Jan 15. The differential impact of three different NAD(+) boosters on circulatory NAD and microbial metabolism in humans. Christen S(1), Redeuil K(1), Goulet L(1), Giner MP(1), Breton I(1), Rota R(1), Frézal A(1), Naz
8. Ter Arkh. 2025 Dec 20;97(11):933-939. doi: 10.26442/00403660.2025.11.203483. [Pathogenetic and therapeutic approaches to the correction of neurocognitive disorders in patients with chronic brucellosis]. [Article in Russian; Abstract available in Russian from the publisher] Shuldyakov AA(1), S
9. J Peripher Nerv Syst. 2026 Mar;31(1):e70101. doi: 10.1111/jns.70101. Evaluation of Nicotinamide Riboside in Prevention of Small Nerve Fiber Axon Degeneration and Promotion of Nerve Regeneration. Thomas S(1), Ben-Davies R(1), Cetinkaya-Fisgin A(1), Hu X(1)(2), Li X(1), Stewart S(1), Pan B(1),
10. J Cosmet Dermatol. 2026 Jan;25(1):e70641. doi: 10.1111/jocd.70641. Rapid and Visible Efficacy of a Dermocosmetic in Acne Patients With Fair Skin Phototypes: Results of a Randomized Split-Face Study. Queille-Roussel C(1), Odeimi J(2), Broallier M(2), Kerob D(2), Tan J(3). Author information:
11. Blood. 2026 Mar 26;147(13):1433-1446. doi: 10.1182/blood.2025029210. Asciminib demonstrates superior efficacy and safety in newly diagnosed chronic myeloid leukemia in the ASC4FIRST trial. Cortes JE(1), Hughes TP(2), Wang J(3), Kim DW(4), Kim DDH(5), Mayer J(6), Goh YT(7), le Coutre P(8), Et
12. ESMO Open. 2025 Dec;10(12):105848. doi: 10.1016/j.esmoop.2025.105848. Epub 2025 Dec 2. Radiomic signatures to estimate survival in patients with advanced hepatocellular carcinoma treated with sorafenib: Cancer and Leukemia Group B 80802 (Alliance). Dercle L(1), Geyer S(2), Nixon AB(3), Inno
13. Sci Rep. 2025 Nov 28;15(1):42739. doi: 10.1038/s41598-025-26693-8. Safety and efficacy of niosomal and conventional tranexamic acid/niacinamide vs. hydroquinone creams in melasma: A randomized, double-blind, case-controlled clinical trial. Ghasemiyeh P(1), Haghighi NF(2)(3), Dastgheib L(2)(3
14. J Cosmet Dermatol. 2025 Dec;24(12):e70555. doi: 10.1111/jocd.70555. Enhancing Facial Rejuvenation Outcomes With a Novel Retinaldehyde-Based Cream: A Comparative Randomized Intra-Individual Study. Monteil C(1), Barreto-Campos V(2), Lain E(3), Guillou E(4), Doat G(4), Nocera T(1). Author info
15. Lancet Oncol. 2025 Dec;26(12):1598-1611. doi: 10.1016/S1470-2045(25)00543-1. Camrelizumab plus rivoceranib versus sorafenib as first-line therapy for unresectable hepatocellular carcinoma (CARES-310): final analysis of a randomised, open-label, international, phase 3 study. Qin S(1), Gu S(2)
42. Int J Pharm. 2026 May 5;696:126853. doi: 10.1016/j.ijpharm.2026.126853. Epub 2026 Apr 5. Self-assembled nanoparticles overcoming hypoxic and acidic microenvironment to synergistically potentiate ferroptosis in triple-negative breast cancer. Xu S(1), Gao W(1), Lin S(2), Xu S(3), Shi X(1), Zhe
27. Phytomedicine. 2026 Jun;155:158086. doi: 10.1016/j.phymed.2026.158086. Epub 2026 Mar 14. Usenamine a potentiates anti-CRC activity of sorafenib by inducing autophagy and inhibiting YAP pathway through targeting SOD2. Zhuge W(1), Kuang J(2), Kuang K(2), Rao M(2), Jian D(2), Lin H(2), Li Z(3),
8. J Colloid Interface Sci. 2026 May 15;710:140048. doi: 10.1016/j.jcis.2026.140048. Epub 2026 Feb 3. Ferroptosis-sensitizing nanoprodrug system for synergistic therapy of triple-negative breast cancer. Huang Y(1), Quan T(1), Li B(2), Zhen C(1), Zhang H(1), Li Z(3), Wu C(3), Liang R(4), Sun L(5
4. Int J Biol Sci. 2026 Jan 1;22(3):1082-1102. doi: 10.7150/ijbs.118753. eCollection 2026. Combining sorafenib with spermine and sphingosine synergistically enhances anticancer efficacy by modulating metabolic pathways and gut microbiome in hepatocellular carcinoma. Jang HR(1), Kim HJ(1), Kim B
6. Pest Manag Sci. 2026 May;82(5):4194-4205. doi: 10.1002/ps.70532. Epub 2026 Jan 16. Plasma-activated water as a potential synergist to enhance the insecticidal activity of imidacloprid and flonicamid against cotton aphids. Xu C(#)(1)(2), Han J(#)(1), Chen X(#)(1), Feng J(3), Xu H(1)(2)(4), Cui
48. Biochem Pharmacol. 2026 Feb;244:117585. doi: 10.1016/j.bcp.2025.117585. Epub 2025 Dec 3. Nicotinamide riboside enhances the efficacy of gemcitabine and suppresses PDAC premalignant lesions via SIRT3 activation. Wu Z(1), Wan Y(1), Liu H(1), Liu J(2), Hu X(3), Meng W(1), Yang X(4), Pu B(5), L
8. Int J Cosmet Sci. 2026 Apr;48(2):445-455. doi: 10.1111/ics.70044. Epub 2025 Nov 30. Synergistic effects of niacinamide and low pH on melanin synthesis, melanocyte function and hyperpigmentation: In vitro and clinical insights. Hakozaki T(1), Laughlin T(1), Zhao W(1), Deng G(2), Wang J(1), Mou
34. Cell Death Dis. 2025 Nov 17;16(1):839. doi: 10.1038/s41419-025-08178-8. Synergistic antitumor activity of sorafenib and the NUPR1 inhibitor LZX-2-73 in multiple cancer models. Liu X(#)(1)(2), Estaras M(#)(1), Cosialls E(1), Peng L(2), Santofimia-Castaño P(3), Iovanna J(4)(5)(6). Author info
18. Int J Biol Macromol. 2025 Dec;334(Pt 1):148778. doi: 10.1016/j.ijbiomac.2025.148778. Epub 2025 Nov 5. Structural characterisation of a polysaccharide from Sanghuangporus vaninii and its synergistic anti-hepatocellular carcinoma activity in combination with sorafenib. Li J(1), Shi M(1), Jia
13. Invest New Drugs. 2025 Oct;43(5):1166-1176. doi: 10.1007/s10637-025-01587-8. Epub 2025 Oct 18. Synergistic combination of the adrenergic antagonist SR59230A with common chemotherapeutic drugs and target therapies in cancer and endothelial cells. Bandini A(#)(1), Biso L(#)(1), Viaggi C(1), Pa
30. Int J Hematol. 2025 Nov;122(5):647-659. doi: 10.1007/s12185-025-04014-z. Epub 2025 May 26. Asciminib in patients with newly diagnosed chronic myeloid leukemia: results from the Japanese subgroup of ASC4FIRST. Takahashi N(1), Kikushige Y(2), Nakamae H(3), Goto T(4), Tomita A(5), Ichii M(6),
32. Lancet Oncol. 2025 Jun;26(6):719-731. doi: 10.1016/S1470-2045(25)00190-1. Epub 2025 May 8. Anlotinib plus penpulimab versus sorafenib in the first-line treatment of unresectable hepatocellular carcinoma (APOLLO): a randomised, controlled, phase 3 trial. Zhou J(1), Bai L(2), Luo J(3), Bai Y(
34. Cancer Chemother Pharmacol. 2025 Feb 28;95(1):39. doi: 10.1007/s00280-025-04755-y. Population pharmacokinetic modeling of asciminib in support of exposure-response and ethnic sensitivity analyses in patients with chronic myeloid leukemia. Darstein C(1), Yoon D(2), Yang Y(2), Kapoor S(3), Das
11. Int J Mol Sci. 2024 Aug 27;25(17):9286. doi: 10.3390/ijms25179286. Phase I-IV Drug Trials on Hepatocellular Carcinoma in Asian Populations: A Systematic Review of Ten Years of Studies. Raghav A(1), Jeong GB(1). Author information: (1)Department of Anatomy and Cell Biology, College of Medicin
50. J Hepatol. 2025 Feb;82(2):258-267. doi: 10.1016/j.jhep.2024.07.017. Epub 2024 Jul 31. Outcomes in the Asian subgroup of the phase III randomised HIMALAYA study of tremelimumab plus durvalumab in unresectable hepatocellular carcinoma. Lau G(1), Abou-Alfa GK(2), Cheng AL(3), Sukeepaisarnjaroen
1. Radiol Imaging Cancer. 2026 Jul;8(4):e250732. doi: 10.1148/rycan.250732. Liver Background Uptake of Prostate-specific Membrane Antigen-targeted PET Radiotracers: A Systematic Review and Meta-Analysis. Ulaner GA(1)(2), Parihar AS(3)(4), Calais J(5), Sutcliffe S(6), Schoones JW(7). Author information: (1)Molecular Imaging and Therapy, Hoag Family Cancer Institute, 16105 Sand Canyon, Irvine, CA. (2)Radiology and Cancer Biology, University of Southern California, Los Angeles, Calif. (3)Division of Nuclear Medicine, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St Louis, Mo. (4)Siteman Cancer Center, Washington University School of Medicine, St Louis, Mo. (5)Ahmanson Translational Theranostics Division, Department of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, Calif. (6)Division of Public Health Sciences, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St Louis, Mo. (7)Directorate of Research and Valorisation, Leiden University Medical Center, Leiden, the Netherlands. Purpose To perform a systematic review and meta-analysis of liver background uptake across four prostate-specific membrane antigen (PSMA)-targeting PET radiotracers (fluorine 18 [18F]-piflufolastat, gallium 68 [68Ga]-PSMA-11, 18F-flotufolastat, and 18F-PSMA-1007) and evaluate the potential impact on patient selection for PSMA-targeted therapy. Materials and Methods A comprehensive literat
2. PeerJ. 2026 Jun 9;14:e21300. doi: 10.7717/peerj.21300. eCollection 2026. Nicotinamide metabolism-related signature and lncRNA regulatory network in kidney renal clear cell carcinoma. Dong P(#)(1), Zhao L(#)(1), Shi P(1), Ma M(1), Huang B(1), Wang Z(1), Zhang S(1), Liu H(1). Author information: (1)The Fourth Hospital of Hebei Medical University, State Grid Hebei Information & Telecommunication Company, Shijiazhuang, Hebei, China. (#)Contributed equally Renal carcinoma ranks among the most lethal cancers, primarily attributed to its atypical symptoms and high metastatic potential. The metabolism of nicotinamide (NAM) plays a significant role in the progression of various tumors. However, investigations into the impact of the NAM metabolism-related signature (NMRS) in kidney renal clear cell carcinoma (KIRC) remain insufficient. Clinical and RNA sequencing data (RNA-seq) from 541 KIRC tissues and 72 adjacent normal tissues were extracted from TCGA. NAM metabolism-related genes (NMRGs) were identified through the Molecular Signatures Database. Cox regression analyses (univariate/multivariate) were conducted to develop NMRS. Time-dependent ROC curve analysis showed that this method had good accuracy in predicting 1-year (AUC = 0.691), 3-year (AUC = 0.749), and 5-year (AUC = 0.764) survival. The Receiver Operating Characteristic (ROC) curve from the external RECA-EU dataset (AUC = 0.682) highlights the accurate prognostic assessment of the NMRS. Overall survi
3. Int J Mol Sci. 2026 May 30;27(11):4989. doi: 10.3390/ijms27114989. Molecular and Functional Interactions Between Cisplatin and Nicotinamide: A Combined Computational, Spectroscopic, and Biological Study. Szefler B(1), Wujak M(2), Skotnicka A(3), Skowron K(4), Czuba J(4), Czeleń P(1), Szupryczyński K(5), Cysewski P(1). Author information: (1)Department of Physical Chemistry, Faculty of Pharmacy, Collegium Medicum, Nicolaus Copernicus University, Kurpińskiego 5, 85-096 Bydgoszcz, Poland. (2)Department of Medicinal Chemistry, Faculty of Pharmacy, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University, Jurasza 2, 85-089 Bydgoszcz, Poland. (3)Faculty of Chemical Technology and Engineering, Bydgoszcz University of Science and Technology, Seminaryjna 3, 85-326 Bydgoszcz, Poland. (4)Department of Microbiology, Faculty of Pharmacy, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University, M. Curie Skłodowskiej 9, 85-094 Bydgoszcz, Poland. (5)Faculty of Pharmacy, Doctoral School of Medical and Health Sciences, Collegium Medicum, Nicolaus Copernicus University, Jagiellońska 13, 85-067 Bydgoszcz, Poland. Cisplatin remains a widely used anticancer agent; however, its effectiveness can be influenced by systemic toxicity, resistance mechanisms, and interactions with exogenous compounds. Nicotinamide (vitamin B3), an NAD+ precursor and a commonly used dietary supplement, is involved in cellular metabolism, redox homeostasis, and DNA repair pathways, which ma
4. Int J Mol Sci. 2026 May 29;27(11):4918. doi: 10.3390/ijms27114918. Skin Cancer Prevention and Antiaging: Role of Nicotinamide. Moro F(1)(2), Panebianco ASI(1), Bartolocci V(3), Capone A(3), Di Guardo A(1), Hyeraci M(4), Gemma GPA(2), Di Lella G(1), Colonna L(1), Ricci F(1)(5), Dellambra E(3), Fania L(1)(5). Author information: (1)Dermatology Unit, IDI-IRCCS, 00167 Rome, Italy. (2)Dermatology Clinic, Department of Medical and Cardiovascular Sciences, Sapienza University of Rome, 00161 Rome, Italy. (3)Molecular and Cell Biology Laboratory, IDI-IRCCS, 00167 Rome, Italy. (4)Department of Molecular Medicine, University of Padua, 35122 Padua, Italy. (5)Department of Life Science, Health, and Health Professions, Link University of Rome, 00165 Rome, Italy. Nicotinamide (NAM), the amide form of vitamin B3, has gained increasing attention in dermatology due to its potential role in both skin aging and non-melanoma skin cancer (NMSC) prevention. This review summarizes the biological rationale and current clinical evidence supporting the use of NAM and other NAD+ precursors in photoaging and cutaneous carcinogenesis. Chronic ultraviolet exposure induces DNA damage, oxidative stress, inflammation, immune dysregulation, and extracellular matrix remodeling, linking photoaged skin to increased susceptibility to actinic keratoses (AKs), squamous cell carcinoma (SCCs), and basal cell carcinoma (BCCs). Through the NAD+ salvage pathway, NAM contributes to the maintenance of i
5. Cells. 2026 May 22;15(11):961. doi: 10.3390/cells15110961. Pharmacological Inhibition of SP1 Reverses Cancer Stemness and Enhances Sorafenib Efficacy in Hepatocellular Carcinoma. Padelli M(1)(2), Desterke C(3), Devocelle A(1), Clay D(4), Bourillon A(2), Uzan G(1), Lemoine A(1)(2), Giron-Michel J(1). Author information: (1)INSERM UMR-S 1193, Université Paris-Saclay, 94800 Villejuif, France. (2)Department of Biochemistry and Oncogenetics, Paul Brousse Hospital, AP-HP, 94800 Villejuif, France. (3)INSERM UMR1310, Université Paris-Saclay, 94800 Villejuif, France. (4)INSERM UMS-44, Hôpital Paul Brousse, Université Paris-Saclay, 94807 Villejuif, France. Hepatocellular carcinoma (HCC) is a highly heterogeneous malignancy characterized by poor prognosis and limited therapeutic response. Cancer stem cells (CSCs) contribute to tumor progression, therapeutic resistance, and tumor recurrence. Among transcriptional regulators potentially involved in these processes, Specificity Protein 1 (SP1) has emerged as a candidate integrator of oncogenic and epigenetic signaling networks. However, its contribution to CSC-associated phenotypes and drug resistance in HCC remains incompletely defined. In this study, we combined transcriptomic analyses of TCGA datasets with functional experiments in HCC cell lines (Huh7 and HepG2). SP1-associated transcriptional programs were targeted pharmacologically using mithramycin A (MIT-A) and genetically using siRNA-mediated knockdown. The ef
6. J Enzyme Inhib Med Chem. 2026 Dec;41(1):2678755. doi: 10.1080/14756366.2026.2678755. Epub 2026 Jun 8. Lidocaine enhances antitumor effects of sorafenib and GW5074 in colorectal cancer cells. Lin TC(1), Wu ZS(2), Huang SM(2), Liu CW(2), Hu JM(1), Wen CC(1). Author information: (1)Division of Colon and Rectal Surgery, Department of Surgery, School of Medicine, College of Medicine, Tri-Service General Hospital, National Defense Medical University, Taipei, Taiwan Republic of China. (2)Graduate Institute of Biochemistry, College of Biomedical Sciences, National Defense Medical University, Taipei City, Taiwan, Republic of China. Targeted therapies have broadened the treatment landscape for colorectal cancer (CRC), highlighting the need for rational combination strategies. Although sorafenib and GW5074 show therapeutic promise and lidocaine may sensitise cancer cells to treatment, the mechanisms underlying these combinations remain poorly understood. Here, we systematically evaluated the effects of combining lidocaine with sorafenib and/or GW5074 in CRC cell lines. Combination index analysis showed that sorafenib increased responsiveness to GW5074 by 19.5- and 1.7 × 107-fold in HT29 and SW480 cells, respectively, while lidocaine enhanced this response by 45- and 3 × 107-fold. Ropivacaine, bupivacaine, and levobupivacaine also showed synergistic interactions with GW5074 by 14- and 1.03 × 107-fold, 15.1- and 6.5 × 106-fold, and 33.6- and 3.8 × 107-fold in HT29 a
7. J Cell Mol Med. 2026 Jun;30(11):e71226. doi: 10.1111/jcmm.71226. AFP Stimulates Glucose Metabolic Reprogramming Contributing to Hepatocellular Carcinoma Resist Sorafenib Through Activating PI3K/AKT Signalling Pathway. Zhou Y(1), Feng S(1), Chen Y(1), Lin B(1), Li W(1), Dong X(1), Liu K(1), Yin Q(1), Li M(1)(2), Zhu M(1). Author information: (1)Key Laboratory of Tropical Translational Medicine, Ministry of Education, and Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, School of Basic Medical Sciences, Hainan Medical University, Haikou, Hainan Province, P.R. China. (2)Department of Medical Oncology, Second Affiliated Hospital, Hainan Medical University, Haikou, Hainan Province, P.R. China. Alpha fetoprotein (AFP) regulates glucose metabolism reprogramming (GMR) related to drug resistance of hepatocellular carcinoma (HCC) and remains unclear. This study explores the effect of AFP regulating GMR (Glucose metabolic reprogramming) on the tolerance of HCC cells to sorafenib. Thirty clinical liver cancer samples and multi-omics databases were collected; the expression of AFP, GMR-related proteins, pyruvate kinase M2 (PKM2), and the PI3K/AKT signalling pathway-associated proteins were assessed using immunohistochemistry (IHC) or Western blotting. MTT, cloning assays, flow cytometry, and TUNEL were performed to evaluate the effects of AFP on HCC resistance to sorafenib. Alterations in glucose consumption, lactate dehydrogenase activity, and AT
8. Funct Integr Genomics. 2026 Jun 4;26(1):124. doi: 10.1007/s10142-026-01914-z. 3D chromatin architecture-related genes orchestrate LUAD evolution and therapy resistance: insights from integrative machine learning and spatial single-cell mapping. Jing Y(#)(1), Xing Y(#)(1), Liu Y(1), Zhang N(1), Pan Y(1), Zhang W(1), Zhu C(1), Zhong Z(1), Zhang G(2)(3), Li JC(4)(5), Dong X(6)(7)(8)(9). Author information: (1)Laboratory of Receptor Gene Regulation and Drug Discovery, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China. (2)Department of Thoracic Surgery, The First Affiliated Hospital of Henan University, Kaifeng, 475000, Henan, China. kfzgy315@163.com. (3)Kaifeng Key Laboratory of Translational Medicine for Thoracic Diseases, Kaifeng, 475000, Henan, China. kfzgy315@163.com. (4)Laboratory of Receptor Gene Regulation and Drug Discovery, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China. zjulijicheng@163.com. (5)Institute of Cell Biology, Zhejiang University, Hangzhou, 310030, China. zjulijicheng@163.com. (6)Laboratory of Receptor Gene Regulation and Drug Discovery, School of Basic Medical Sciences, Henan University, Kaifeng, 475004, Henan, China. dongxiaotao@henu.edu.cn. (7)Department of Thoracic Surgery, The First Affiliated Hospital of Henan University, Kaifeng, 475000, Henan, China. dongxiaotao@henu.edu.cn. (8)Kaifeng Key Laboratory of Translational Medicine for Thoracic Diseases, Kaifeng, 475000, H
9. Cancer Chemother Pharmacol. 2026 Jun 4;96(1):61. doi: 10.1007/s00280-026-04908-7. Evaluation of anticancer activity of beta glucan in non-alcoholic steatohepatitis associated hepatocellular carcinoma in rats. Bisht S(1), Gupta S(2). Author information: (1)Amity Institute of Pharmacy (AIP), Amity University Uttar Pradesh, Noida Campus, Noida, India. (2)Amity Institute of Pharmacy (AIP), Amity University Uttar Pradesh, Noida Campus, Noida, India. sgupta23@amity.edu. BACKGROUND: Hepatocellular carcinoma (HCC) arising from non-alcoholic steatohepatitis (NASH) represents a growing clinical challenge with limited therapeutic options. Despite known antioxidant and immunomodulatory properties, the role of beta-glucan in NASH-associated HCC remains insufficiently explored. METHODS: HCC was experimentally induced in rats via a single intraperitoneal (i.p.) injection of diethylnitrosamine (DEN; 200 mg/kg), followed by repeated intraperitoneal administrations of thioacetamide (TAA; 300 mg/kg) thrice weekly for four weeks. Upon establishment of hepatic tumors, beta-glucan was administered orally (p.o.) at doses of 25, 50, and 75 mg/kg/day for eight consecutive weeks. Sorafenib (30 mg/kg/day; p.o.) was used as the reference standard. Key parameters, including serum biochemical markers, oxidative stress indicators, insulin-like growth factor-1 (IGF-1) levels, and histopathological alterations, were evaluated to assess therapeutic efficacy. RESULTS: Administration of hi
10. J Med Chem. 2026 Jun 11;69(11):13141-13164. doi: 10.1021/acs.jmedchem.6c00096. Epub 2026 May 30. Discovery of a Biased Kelch-like ECH-Associated Protein 1-p62 (Keap1-p62) Protein-Protein Interaction (PPI) Inhibitor for the Management of p62 Aberrant Hepatocellular Carcinoma. Zhao Z(1), Lu H(1), Zhang J(1), Zhao J(1), Wang J(1), Zhu T(1), Xu S(1), You Q(1), Lu M(2), Jiang Z(1). Author information: (1)Jiang Su Key Laboratory of Drug Design and Optimization and Department of Medicinal Chemistry, School of Pharmacy, China Pharmaceutical University, Nanjing 210009, China. (2)Department of Medicinal Chemistry, College of Pharmaceutical Sciences, Soochow University Medical College, Suzhou 215123, China. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a pleiotropic transcription factor essential for cellular defense. Extensive research has demonstrated its oncogenic role, positioning Nrf2 as a promising target for cancer therapy. However, achieving tumor-specific Nrf2 inhibition remains a challenge. Herein, we report the discovery of 13, a biased inhibitor of Kelch-like ECH-associated protein 1-phosphorylated p62 (Keap1-p-p62) interaction, as a selective and effective Nrf2 inhibitor. In fluorescence polarization assays, 13 showed potent Keap1-p-p62 inhibitory activity (IC50 = 0.11 μM) and high selectivity over the inhibition of Keap1-Nrf2 interaction. Notably, 13 specifically inhibited Nrf2 activity in p62 aberrant hepatocellular carcinoma (HCC) cells b
11. AAPS PharmSciTech. 2026 May 27;27(5):221. doi: 10.1208/s12249-026-03461-z. Exploring Synergistic Potential of Sorafenib and Atorvastatin to Launch Apoptosis and Ferroptosis-driven Mixed Cell Death Mechanism in Colorectal Cancer. Yadav V(1), Dighe S(1), Dhake P(1), Jain S(2). Author information: (1)Centre for Pharmaceutical Nanotechnology, Department of Pharmaceutics, National Institute of Pharmaceutical Education and Research (NIPER), S.A.S. Nagar (Mohali), Sector 67, Punjab, 160062, India. (2)Centre for Pharmaceutical Nanotechnology, Department of Pharmaceutics, National Institute of Pharmaceutical Education and Research (NIPER), S.A.S. Nagar (Mohali), Sector 67, Punjab, 160062, India. sanyogjain@niper.ac.in. Colorectal cancer (CRC) is a third leading cause of death and is often recognised by a higher mutation burden. The standard clinical regimen for CRC chiefly focuses on targeting a single-cell death mechanism, which encounters constraints such as resistance, chronic toxicity, and suboptimal efficacy. Thus, triggering a hybrid cell death mechanism that acts through distinct pathways offers a promising avenue in CRC management. The present investigation explores the combined therapy of Sorafenib (SOR) and Atorvastatin (ATST) to induce a dual cell death mechanism, specifically ferroptosis and classic apoptosis, in colon cancer cells. The combination of ATST + SOR at a 1:1 ratio showed a combination index value of < 1 and a dose reduction index > 1 in
12. Molecules. 2026 May 20;31(10):1757. doi: 10.3390/molecules31101757. (E)-4-(4-Acrylamidophenoxy)-N-Methylpicolinamides as b-Raf/VEGFR-2 Inhibitors with Antiangiogenic Activity in HUVEC and Zebrafish Model. Velma GR(1)(2)(3), Telukutla SR(1)(4), Vankudoth J(5), Grewal AS(6), Privér S(1), Yedla P(3), Akunuri R(3), Wlodkowic D(7), Pabbaraja S(2)(3), Bhargava SK(1), Plebanski M(4), Kamal A(2)(3)(8). Author information: (1)Centre for Advanced Materials & Industrial Chemistry (CAMIC), School of Science, RMIT University, GPO BOX 2476, Melbourne, VIC 3001, Australia. (2)Academy of Scientific and Innovative Research (AcSIR), Anusandhan Bhawan, 2-Rafi Marg, New Delhi 110 001, India. (3)Department of Organic Synthesis & Process Chemistry, CSIR-Indian Institute of Chemical Technology (IICT), Hyderabad 500 007, India. (4)Accelerator for Translational Research in Clinical Trials (ATRACT) Centre, School of Health and Biomedical Sciences, STEM College, RMIT University, Melbourne, VIC 3083, Australia. (5)Department of Biochemistry, Chemical Synthesis Core Facility, Albert Einstein College of Medicine, Gruss MRRC-314, Bronx, NY 10461, USA. (6)Department of Pharmaceutical Sciences, Guru Gobind Singh College of Pharmacy, Yamuna Nagar 135 001, India. (7)Phenomics Laboratory, School of Science, RMIT University, Plenty Road, P.O. Box 71, Bundoora, VIC 3083, Australia. (8)Department of Chemistry, Osmania University, Hyderabad 500 007, India. Pharmacophore hybridization is a well-es
13. Int J Mol Sci. 2026 May 13;27(10):4342. doi: 10.3390/ijms27104342. Identification of Changes in the Transcriptome Profile of Human Hepatoma HepG2 Cells Exposed to Combined Sorafenib and Cannabis Treatment. Udomkritayachai K(1), Thiamsuk T(1), Jarujamrat T(1), Kudikhong P(1), Raksakhom S(1), Suphattana P(2), Khankham N(2), Thanawong P(3), Khacha-Ananda S(2). Author information: (1)Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand. (2)Department of Forensic Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand. (3)Multidisciplinary and Interdisciplinary School, Chiang Mai University, Chiang Mai 50200, Thailand. Cannabis-derived compounds are increasingly used as adjuncts in cancer therapy due to their reported antiproliferative and pro-apoptotic effects. However, potential drug-herb interactions with standard anticancer agents-namely sorafenib-remain unclear. This study investigated the interaction between cannabis and sorafenib, together with transcriptomic alterations in human hepatoma HepG2 cells. Cell viability was assessed using the MTT assay, and drug interactions were evaluated using the Combenefit program. RNA sequencing was performed to characterize gene expression changes across treatment groups. Combination analysis demonstrated concentration-dependent synergistic effects at intermediate doses. Transcriptomic profiling revealed that the combination treatment induced a broader and more distinct set
14. Mol Cell. 2026 Jun 4;86(11):2106-2123.e8. doi: 10.1016/j.molcel.2026.04.026. Epub 2026 May 22. Hypoxia-driven lncRNA SHIELD promotes GPX4 translation and protects against ferroptosis in hepatocellular carcinoma. Liu K(1), Liu Y(1), Thorne RF(2), Meng F(3), Liu Y(4), Wu M(5), Liu L(6). Author information: (1)Department of Hepatobiliary Surgery, State Key Laboratory of Immune Response and Immunotherapy, Centre for Leading Medicine and Advanced Technologies of IHM, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, China; Anhui Provincial Key Laboratory of Hepatopancreatobiliary Surgery, Hefei 230001, China; Anhui Provincial Clinical Research Center for Hepatobiliary Diseases, Hefei 230001, China. (2)Translational Research Institute, Henan Provincial People's Hospital, Zhengzhou 450053, China. (3)Department of Hepatobiliary Surgery, State Key Laboratory of Immune Response and Immunotherapy, Centre for Leading Medicine and Advanced Technologies of IHM, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, China; Anhui Provincial Key Laboratory of Hepatopancreatobiliary Surgery, Hefei 230001, China; Anhui Provincial Clinical Research Center for Hepatobiliary Diseases, Hefei 230001, China. Electronic address: mengfz@ustc.edu.cn. (4)Department of Hepatobiliary Surgery, State Key Laboratory
15. Curr Oncol Rep. 2026 May 22;28(1):57. doi: 10.1007/s11912-026-01792-5. Advancing Systemic Treatment beyond First Line for Advanced Hepatocellular Carcinoma. Wysocki PT(1), Chmiel P(2), Jassem J(1), Kraj L(3). Author information: (1)Department of Oncology and Radiotherapy, Medical University of Gdańsk, Gdańsk, Poland. (2)Department of Soft Tissue/Bone Sarcoma and Melanoma, Maria Sklodowska-Curie National Research Institute of Oncology, 02-781, Warsaw, Poland. (3)Department of Oncology, Medical University of Warsaw, 02-091, Warsaw, Poland. leszek.kraj@wum.edu.pl. PURPOSE OF REVIEW: Hepatocellular carcinoma (HCC) ranks among the most prevalent solid malignancies worldwide. A substantial proportion of patients are diagnosed at advanced stages, making systemic therapies the primary treatment option. In recent years, treatment strategies have shifted from single-agent targeted therapies, such as sorafenib and lenvatinib, to combination regimens incorporating immune checkpoint inhibitors, with or without antiangiogenic agents. This evolving treatment paradigm has led to an increasing number of patients receiving second-line and subsequent therapies. However, clinical guidelines for treatment selection remain lacking. RECENT FINDINGS: Currently, available salvage therapies include various molecularly targeted agents, immune checkpoint inhibitors, and combination regimens. Nonetheless, evidence supporting their efficacy and patient selection for specific strateg
1. Cancer Chemother Pharmacol. 2026 Aug 12;96(1):87. doi: 10.1007/s00280-026-04934-5. Pharmacological inhibition of store-operated calcium entry enhances sorafenib-induced antitumor effects in Huh7 hepatocellular carcinoma cells. Yasar BY(1), Yilmaz E(2), Erac Y(3). Author information: (1)Department of Pharmacology, Faculty of Pharmacy, Istinye University, Istanbul, Turkey. (2)Department of Biotechnology, The Institute of Natural and Applied Sciences, Ege University, Izmir, Turkey. (3)Department of Pharmacology, Faculty of Pharmacy, Ege University, Izmir, Turkey. yasemin.erac@ege.edu.tr. PURPOSE: Sorafenib remains a systemic treatment option for advanced hepatocellular carcinoma (HCC), but its clinical efficacy is limited by rapid development of adaptive cellular responses that promote cell survival and phenotypic plasticity. Store-operated calcium entry (SOCE) is a key regulator of intracellular calcium signaling and has been implicated in proliferation, apoptosis, migration, and epithelial-mesenchymal plasticity in cancer. This study investigated the association between SOCE and early adaptive responses to sorafenib in Huh7 HCC cells. METHODS: Huh7 cells were treated with sorafenib, the SOCE inhibitor SKF-96365, or their combination. Functional effects were evaluated using real-time proliferation assays, intracellular calcium measurements, apoptosis analysis, and wound-healing assays. Findings were complemented by integrated bioinformatic analyses of TCG
2. Langmuir. 2026 Aug 11;42(31):22678-22685. doi: 10.1021/acs.langmuir.6c02044. IGFIIR Aptamer-Functionalized Liposomes for Targeted Delivery of Sorafenib to Ameliorate Liver Fibrosis. Cai T(1)(2), Qin R(3), Li D(1), Yao Y(1)(2), Li Y(1), Fan Z(1), Wang M(1), Chen P(3), Zhang J(3), Guo Z(3), Xu L(4), Li P(1), Yang Q(1). Author information: (1)State Key Laboratory of Metabolic Dysregulation & Prevention and Treatment of Esophageal Cancer, Innovation Center for Basic Medical Research of Metabolic Associated Fatty Liver Disease, Ministry of Education, Tianjian Laboratory of Advanced Biomedical Sciences, School of Convergence Medicine, Zhengzhou University, Zhengzhou450052, China. (2)School of Life Sciences, Zhengzhou University, Zhengzhou450001, China. (3)School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou450001, China. (4)Department of Respiratory and Critical Care, Quzhou Affiliated Hospital of Wenzhou Medical University, Quzhou324000, China. Liver fibrosis, a major cause of morbidity in chronic liver diseases, lacks effective therapies. Activated hepatic stellate cells (HSCs) are a promising therapeutic target for liver fibrosis, as their transformation into myofibroblasts drives disease progression by excessively depositing an extracellular matrix. Despite its antifibrotic potential, sorafenib faces clinical challenges due to poor aqueous solubility and lack of HSC specificity. To overcome these challenges, we developed IGFIIR aptamer-functio
3. Int J Urol. 2026 Aug;33(8):e70587. doi: 10.1111/iju.70587. [(18)F]PSMA-1007 PET-Based Recurrence Site Distribution and Predictors of Metastatic Disease in Patients With Biochemical Recurrence of Prostate Cancer. Hatano K(1), Watabe T(2)(3), Hirata T(4), Konishi M(1), Kanaki T(1), Tani M(1), Oka T(1), Ishizuya Y(1), Hayashi T(1), Yamamoto Y(1), Kato T(1), Kawashima A(1), Fujita K(1)(5), Uemura M(1)(6)(7), Giesel FL(2)(8), Nonomura N(1). Author information: (1)Department of Urology, The University of Osaka Graduate School of Medicine, Suita, Japan. (2)Department of Radiology, The University of Osaka Graduate School of Medicine, Suita, Japan. (3)Institute for Radiation Sciences, The University of Osaka, Suita, Japan. (4)Department of Radiation Oncology, The University of Osaka Graduate School of Medicine, Suita, Japan. (5)Department of Urology, Kindai University Faculty of Medicine, Sakai, Japan. (6)Department of Urology, Fukushima Medical University School of Medicine, Fukushima, Japan. (7)Department of Urology, Iwase General Hospital, Sukagawa, Japan. (8)Department of Nuclear Medicine, Medical Faculty and University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, Germany. OBJECTIVES: Prostate-specific membrane antigen positron emission tomography (PSMA-PET) is a sensitive imaging modality for detecting recurrent prostate cancer following definitive local therapy. However, evidence on 18F-labeled PSMA tracers in Japanese patients with biochemical re
4. Clin Nucl Med. 2026 Sep 1;51(9):815-817. doi: 10.1097/RLU.0000000000006510. Epub 2026 Jul 8. Benign Hyperplastic Nodule in the Peripheral Zone of the Prostate Mimicking Prostate Cancer on 18 F-PSMA-1007 PET/CT. Man X(1)(2), Dong C(3), Dong A(4), Song X(1)(2)(5). Author information: (1)Department of Urology, The First Hospital of China Medical University. (2)Institute of Urology, China Medical University, Shenyang, Liaoning Province. (3)Department of Urology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong. (4)Department of Nuclear Medicine, Changhai Hospital, Naval Medical University, Shanghai. (5)Department of Urology, Shenyang Fifth People's Hospital, Shenyang, Liaoning Province, China. Benign prostatic hyperplasia mainly arises within the para-urethral transition zone and is rarely seen in the peripheral zone. We describe MRI and 18 F-PSMA-1007 PET/CT findings in a patient with a large benign hyperplastic nodule in the peripheral zone. The benign prostatic hyperplastic nodule appeared as a well-defined mass with heterogeneous signal intensity at T2-weighted images and increased 18 F-PSMA-1007 with SUV max of 7.3. This case indicates that a large benign prostatic hyperplastic nodule can arise from the peripheral zone and shows increased 18 F-PSMA-1007 uptake mimicking prostate cancer. Copyright © 2026 Wolters Kluwer Health, LLC. All rights reserved. DOI: 10.1097/RLU.0000000000006510 PMID: 42530276 [Indexed for MEDLINE]
5. Front Public Health. 2026 Jul 6;14:1781790. doi: 10.3389/fpubh.2026.1781790. eCollection 2026. Economic value of finotonlimab plus bevacizumab versus sorafenib for first-line treatment of unresectable hepatocellular carcinoma in China and the United States. He Y(1), Jiang Q(1), Pan X(1), Deng L(1), Hu X(1), Yang Z(2), Lang W(3). Author information: (1)Department of Oncology, Nanxishan Hospital of Guangxi Zhuang Autonomous Region, Guilin, China. (2)Department of Hepatobiliary Surgery, Nanxishan Hospital of Guangxi Zhuang Autonomous Region, Guilin, China. (3)Department of Pharmacy, Nanxishan Hospital of Guangxi Zhuang Autonomous Region, Guilin, China. BACKGROUND: Finotonlimab combined with bevacizumab demonstrated superior progression-free survival and overall survival compared with sorafenib in patients with unresectable hepatocellular carcinoma. However, its economic value in different healthcare systems has not been fully characterized. This study evaluated the cost-effectiveness of finotonlimab plus bevacizumab from the perspectives of U.S. payers and the Chinese healthcare system. A Markov state-transition model was constructed using clinical efficacy data from a phase 3 randomized controlled trial. METHODS: Health state utilities were obtained directly from trial data, and cost inputs were derived from published sources and country-specific charge databases. The outcomes included quality-adjusted life years (QALYs), incremental cost-effectiveness ra
6. J Vis Exp. 2026 Jul 7;(233). doi: 10.3791/71295. Development and Internal Validation of a Prediction Model For Biochemical Recurrence Following Radical Prostatectomy. Li Y(1), Zhang Q(1), Li X(2). Author information: (1)Department of Nuclear Medicine, First Affiliated Hospital of Xinjiang Medical University. (2)Department of Nuclear Medicine, First Affiliated Hospital of Xinjiang Medical University; LYB67915@hotmail.com. This study aimed to develop and validate a predictive model for biochemical recurrence (BCR) after radical prostatectomy in patients with prostate cancer, incorporating clinical, pathological, inflammatory, and 18F-PSMA-1007 positron emission tomography/computed tomography (PET/CT) imaging parameters. This retrospective study included 240 patients with histopathologically confirmed prostate adenocarcinoma who underwent radical prostatectomy between June 2022 and July 2025. BCR was defined as a postoperative serum prostate-specific antigen (≥0.2 ng/mL). Preoperative clinical variables, systemic immune-inflammation index (SII), PET/CT lesion status, and maximum standardized uptake value (SUVmax) were collected along with postoperative pathological staging. Patients were divided into BCR (n = 64) and non-BCR (n = 176) groups. Univariate and multivariate logistic regression analyses identified independent predictors of BCR. A multivariable predictive model was developed and internally validated using a 70/30 training-validation split. Model
7. Hum Vaccin Immunother. 2026 Dec 31;22(1):2707849. doi: 10.1080/21645515.2026.2707849. Epub 2026 Jul 27. Cost-effectiveness of finotonlimab plus bevacizumab versus sorafenib as first-line therapy in unresectable hepatocellular carcinoma in China. Xu H(1), Yu S(2), Yang Y(3), Bian H(4), Wu Z(1), Xuan F(2). Author information: (1)Department of Infectious Diseases, Cixi People's Hospital, Wenzhou Medical University, Ningbo, China. (2)Department of Radiation Oncology, Zhuji Affiliated Hospital of Wenzhou Medical University, Shaoxing, China. (3)Department of Medical Oncology, Zhuji Affiliated Hospital of Wenzhou Medical University, Shaoxing, China. (4)Department of Pharmacy, Zhuji Affiliated Hospital of Wenzhou Medical University, Shaoxing, China. Hepatocellular carcinoma (HCC) imposes a substantial health burden in China. Finotonlimab plus bevacizumab recently prolonged progression-free survival (PFS) and overall survival (OS) vs. sorafenib, but its economic value remains unknown. Here we evaluated the cost-effectiveness of finotonlimab plus bevacizumab vs. sorafenib from the Chinese healthcare system perspective. Parametric survival models were fitted to extrapolate PFS and OS. Total costs, life-years (LYs), quality-adjusted life-years (QALYs), incremental cost-effectiveness ratios (ICERs), incremental net monetary benefit (INMB), and incremental net health benefit (INHB) were estimated at a willingness-to-pay (WTP) threshold of $27,906 per QALY. Uncertainty
8. Drug Resist Updat. 2026 Sep;88:101451. doi: 10.1016/j.drup.2026.101451. Epub 2026 Jul 16. Protein SUMOylation confers sorafenib resistance in human hepatocellular carcinoma via the induction of PKM2-mediated glycolysis. Yuan H(1), Lu Y(2), Jiang Z(1), Chan YT(1), Wu J(1), Feng Z(1), Xu L(1), Li Q(1), Lu P(3), Kwok CF(1), Fong TL(1), Huang Q(4), Wei L(5), Feng Y(1), Chen ZS(6), Wang N(7). Author information: (1)School of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, 3 Sassoon Road, Pokfulam, Hong Kong. (2)School of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, 3 Sassoon Road, Pokfulam, Hong Kong; Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, China. (3)School of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, 3 Sassoon Road, Pokfulam, Hong Kong; Laboratory for Synthetic Chemistry and Chemical Biology Limited, Hong Kong Science Park, Hong Kong. (4)School of Chinese Medicine, LKS Faculty of Medicine, The University of Hong Kong, 3 Sassoon Road, Pokfulam, Hong Kong; Department of Neurosurgery, The Second Affiliated Hospital, Shantou University Medical College, Shantou, China. (5)School of Pharmacy, Shandong Second Medical University, Weifang, Shandong, China. (6)Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University,
9. J Biochem Mol Toxicol. 2026 Jul;40(7):e71017. doi: 10.1002/jbt.71017. Caffeine in the Context of Sorafenib Chemotherapy: Insights From Experimental Hepatocarcinogenesis. Valente LC(1), Silva JSD(1), Riechelmann-Casarin L(1), Romeiro FG(2), Barbisan LF(3), Romualdo GR(1). Author information: (1)Experimental Research Unit (UNIPEX), Botucatu Medical School, São Paulo State University (UNESP), Botucatu, SP, Brazil. (2)Botucatu Medical School, São Paulo State University (UNESP), Botucatu, SP, Brazil. (3)Department of Structural and Functional Biology, Botucatu Biosciences Institute, São Paulo State University (UNESP), Botucatu, SP, Brazil. Hepatocellular carcinoma (HCC) features a high mortality burden worldwide, highlighting the need for improved therapeutic strategies. Caffeine (CAF), a widely consumed bioactive compound, has been reported to exert chemopreventive effects in HCC, but its interaction with standard therapies remains poorly explored. We investigated whether CAF enhances the antitumor effects of sorafenib (SOR) chemotherapy in preclinical HCC models. C3H/HeJ mice were submitted to diethylnitrosamine (DEN)-induced hepatocarcinogenesis and treated with CAF (50 mg/kg), SOR (30 mg/kg), or their combination for 3 weeks. C3A+LX2 spheroids and transwell co-cultures were also exposed to CAF, SOR, or their combination at 1/5 or 1/10 of the half-maximal effective concentration. The combination of CAF and SOR produced a synergistic reduction in tumor sphe
10. Biochem Biophys Res Commun. 2026 Sep 10;830:154242. doi: 10.1016/j.bbrc.2026.154242. Epub 2026 Jul 4. SMURF1-mediated EFEMP1 ubiquitination reverses the resistance of HCC cells to sorafenib by promoting ferroptosis. Zhou T(1), Shen L(2), Ma Y(3), Mo S(4), Lan H(5), Gao S(6). Author information: (1)Department of General Surgery, The First People's Hospital of Linping District, Hangzhou, 311100, China. Electronic address: zhouti_fmmu@163.com. (2)Department of General Surgery, The First People's Hospital of Linping District, Hangzhou, 311100, China. Electronic address: shenlianqiang@126.com. (3)Department of General Surgery, The First People's Hospital of Linping District, Hangzhou, 311100, China. Electronic address: 709762180@qq.com. (4)Department of General Surgery, The First People's Hospital of Linping District, Hangzhou, 311100, China. Electronic address: 201811112511317@zcmu.edu.cn. (5)Department of General Surgery, The First People's Hospital of Linping District, Hangzhou, 311100, China. Electronic address: haibinbule@163.com. (6)Department of General Surgery, The First People's Hospital of Linping District, Hangzhou, 311100, China. Electronic address: drgaoshan@126.com. BACKGROUND: Acquired resistance to sorafenib remains a major obstacle to effectively treating advanced hepatocellular carcinoma (HCC). Ferroptosis has emerged as a key mechanism influencing therapeutic response. EGF-containing fibulin extracellular matrix protein 1 (EFEMP1) contributes
11. Drug Dev Res. 2026 Aug;87(5):e70339. doi: 10.1002/ddr.70339. Benzimidazole-Based VEGFR-2 Inhibitors Inspired by Sorafenib: Synthesis, Biological Evaluation, and Mechanistic Insights. Dewidar MA(1)(2), Allam HA(3), Abdel-Aziz HA(4), Elnagar MR(5)(6), Ibrahim NM(3). Author information: (1)Postgraduate Program in Pharmaceutical Chemistry, Faculty of Pharmacy, Cairo University, Cairo, Egypt. (2)National Cancer Institute, Cairo University, Cairo, Egypt. (3)Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Cairo University, Cairo, Egypt. (4)Department of Applied Organic Chemistry, National Research Centre, Dokki, Giza, Egypt. (5)Department of Pharmacology and Toxicology, Faculty of Pharmacy, Al-Azhar University, Cairo, Egypt. (6)Department of Pharmacology, College of Pharmacy, The Islamic University, Najaf, Iraq. Vascular endothelial growth factor receptor-2 (VEGFR-2) plays a central role in tumor angiogenesis and remains a well-established therapeutic target in cancer treatment. In this study, twenty-six benzimidazole-based derivatives (3a-k, 5a-d, 8a-g, and 10a-d) were rationally designed to incorporate the essential structural and pharmacophoric features required for effective VEGFR-2 inhibition, followed by their synthesis and biological evaluation. In vitro kinase assays demonstrated that the synthesized derivatives inhibited VEGFR-2 with IC50 values ranging from 0.061 to 1.895 µM. Based on their enzymatic potency, the most active compounds (3
12. Mol Biol Rep. 2026 Jun 30;53(1):1050. doi: 10.1007/s11033-026-12152-8. Clomipramine potentiates sorafenib efficacy in experimental hepatocellular carcinoma by targeting lysosomal sequestration and modulating the cathepsin B/Bcl-2/Beclin-1 axis. Abass SA(1), Abdelrafea R(2), Eldomany RA(3), Elsisy RA(4), Zakaria S(5). Author information: (1)Faculty of Pharmacy, Biochemistry Department, Kafrelsheikh University, Kafrelsheikh, 33516, Egypt. (2)Faculty of Pharmacy, Biochemistry Department, Kafrelsheikh University, Kafrelsheikh, 33516, Egypt. rania.gad@pharm.kfs.edu.eg. (3)Faculty of Pharmacy, Department of Microbiology and Immunology, Kafrelsheikh University, Kafrelsheikh, 33516, Egypt. (4)Faculty of Medicine, Department of Anatomy and Embryology, Kafrelsheikh University, Kafrelsheikh, 33516, Egypt. (5)Faculty of Pharmacy, Department of Pharmacology and Toxicology, Kafrelsheikh University, Kafrelsheikh, 33516, Egypt. BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common causes of death around the world, and it is commonly diagnosed late, so systemic chemotherapy is commonly used. Lysosomal sequestration of chemotherapy drugs such as sorafenib [1] decreases the effective concentration of chemotherapy at the target sites and leads to chemoresistance, also chemoresistance may arise from autophagy activation. We aimed to find a new therapeutic regimen for HCC through enhancing the chemosensitivity of SB by combining it with the lysosomotropic drug
13. Genome Med. 2026 Jun 27;18(1):114. doi: 10.1186/s13073-026-01679-x. Dual functional genomics reveals a broad and convergent landscape of asciminib resistance in BCR::ABL1. Sokirniy I(1), Yang Z(2), Pritchard J(3)(4). Author information: (1)Huck Institute for the Life Sciences, The Pennsylvania State University, University Park, PA, 16802, USA. (2)Department of Biomedical Engineering, The Pennsylvania State University, University Park, PA, 16802, USA. (3)Huck Institute for the Life Sciences, The Pennsylvania State University, University Park, PA, 16802, USA. jrp94@psu.edu. (4)Department of Biomedical Engineering, The Pennsylvania State University, University Park, PA, 16802, USA. jrp94@psu.edu. BACKGROUND: Drug resistance is a constantly evolving challenge. The allosteric inhibitor asciminib is a novel therapy for chronic myelogenous leukemia (CML) that targets the myristoyl pocket of the BCR::ABL1 kinase. While it can overcome resistance to active-site inhibitors like imatinib, new resistance mutations to asciminib are emerging. The complete landscape of these mutations, particularly those outside the kinase domain or those arising from epistatic interactions between mutations, are not well understood. METHODS: This study employed a dual functional genomics approach in CML cell line models. A high-throughput adenosine base editing (ABE) screen was used to identify broad hotspots of asciminib resistance across the entire BCR::ABL1 protein. Deep mutational
14. Cell Signal. 2026 Oct;146:112699. doi: 10.1016/j.cellsig.2026.112699. Epub 2026 Jun 27. SHC4 suppresses ferroptosis and promotes sorafenib resistance in hepatocellular carcinoma by disrupting the interaction between NCOA4 and FTH1. Chai D(1), Zhang J(2), Dong K(1), Yu J(1), Zhang X(1), Kuang T(1), Feng J(3), Li M(4), Wang W(5). Author information: (1)Department of Hepatobiliary Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 40060, People's Republic of China; Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 40060, People's Republic of China. (2)Department of Hepatobiliary Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 40060, People's Republic of China; Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan Province 610041, People's Republic of China. (3)Department of Hepatobiliary Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 40060, People's Republic of China. (4)Department of Hepatobiliary Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 40060, People's Republic of China. Electronic address: liman192@whu.edu.cn. (5)Department of Hepatobiliary Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei Province 40060, People's Republic of China. Electronic address: wangwx@whu.edu.cn. Ferroptosis, an iron-dependent form of regulated cell death, plays a pivotal role in hepatocellu
15. Int J Oncol. 2026 Aug;69(2):92. doi: 10.3892/ijo.2026.5905. Epub 2026 Jun 26. Stress‑induced catecholamines attenuate sorafenib efficacy by inhibiting ferroptosis in β2‑adrenergic receptor positive renal cell carcinoma. Ushijima M(1), Naito S(1), Ito H(1), Narisawa T(1), Ichiyanagi O(1), Kanno H(1), Fukuhara H(1), Takai Y(1), Yagi M(1), Yamagishi A(1), Nishida H(1), Obara Y(2), Tsuchiya N(1). Author information: (1)Department of Urology, Yamagata University Faculty of Medicine, Yamagata 990‑9585, Japan. (2)Department of Pharmacology, Yamagata University Faculty of Medicine, Yamagata 990‑9585, Japan. Ferroptosis, an iron‑dependent form of non‑apoptotic cell death, is a potential target for cancer therapy. Sorafenib, a molecular targeted agent for renal cell carcinoma (RCC), is involved in ferroptosis induction. Chronic stress, mediated by catecholamines via β2‑adrenergic receptors (ADRB2), promotes cancer progression, yet its influence on drug resistance and ferroptosis remains elusive. To investigate ADRB expression in RCC, immunohistochemistry of surgical specimens was performed and assessed ADRB mRNA and protein levels were assessed by RT‑qPCR and western blotting in RCC cell lines. To determine whether β‑adrenergic signaling modulates sorafenib sensitivity, we used ADRB2‑expresing ACHN cells and conducted MTS cell viability assays following β‑adrenergic agonist isoproterenol (ISO) stimulation, ADRB2 knockdown by siRNA, as well as a restraint‑stress
1. J Skin Cancer. 2026 Oct 5;2026:8756577. doi: 10.1155/jskc/8756577. eCollection 2026. Oral Nicotinamide for the Secondary Prevention of Cutaneous Squamous Cell Carcinoma and Other Keratinocyte Carcinomas: A Systematic Review. Guerra Jiménez AL(1), Ortegón Garciaherreros JC(2), Suárez Escobar LP(3), Vargas Monroy LV(4), Madariaga Estupiñán MC(5). Author information: (1)Faculty of Health Sciences Fundación Universitaria San Martín Bogotá D.C. Colombia. (2)School of Medicine and Health Sciences Universidad del Rosario Bogotá D.C. Colombia urosario.edu.co. (3)Faculty of Medicine Fundación Universitaria de Ciencias de la Salud Bogotá D.C. Colombia fucsalud.edu.co. (4)Faculty of Medicine Universidad Nacional de Colombia Bogotá D.C. Colombia unal.edu.co. (5)Department of Public Health Universidad del Norte Barranquilla Atlántico Colombia uninorte.edu.co. BACKGROUND: Oral nicotinamide has been proposed as a chemoprevention strategy to reduce new keratinocyte carcinomas in people with a history of skin cancer, but its effect may differ between immunocompetent patients and transplant recipients. OBJECTIVE: To evaluate the effectiveness and safety of oral nicotinamide for the secondary prevention of cutaneous squamous cell carcinoma and other keratinocyte carcinoma-related outcomes in adults with a history of skin cancer. METHODS: We conducted a systematic review following PRISMA 2020. We searched PubMed/MEDLINE, Embase, and LILACS through the Virtual Health Library
2. Neurochem Res. 2026 Oct 5;51(5):282. doi: 10.1007/s11064-026-04904-6. Desflurane Increases Hippocampal RAF-MAPK-MSK1 Protein Levels and Reduces CLOCK Expression: Sorafenib Attenuates Cognitive Impairment in Aged Mice. Chou C(#)(1), Jia Y(#)(1)(2), Zhang X(1)(2), Bai J(1)(2), Shang X(3), Duan X(4). Author information: (1)Department of Anesthesiology, Inner Mongolia Baogang Hospital, No. 20 Shaoxian Road, Kundulun District, Baotou, 014010, Inner Mongolia, China. (2)Baotou Medical College, No. 31 Jianshe Road, Donghe District, Baotou, 014040, Inner Mongolia, China. (3)Department of Anesthesiology, Baotou Cancer Hospital, No. 18 Tuanjie Street, Qingshan District, Baotou, 014030, Inner Mongolia, China. shangxuying1989@163.com. (4)Department of Anesthesiology, Inner Mongolia Baogang Hospital, No. 20 Shaoxian Road, Kundulun District, Baotou, 014010, Inner Mongolia, China. alonlord2023@gmail.com. (#)Contributed equally Postoperative cognitive dysfunction (POCD) is common after anesthesia and surgery in older adults, yet no targeted therapy exists, and the mechanism linking volatile anesthetic exposure to circadian dysregulation in the aged hippocampus is undefined. Here we show that RAF manipulation bidirectionally alters CLOCK protein levels in HT22 hippocampal neurons, and that RAF-MAPK-MSK1 protein abundance is inversely related to CLOCK levels in the aged hippocampus after desflurane exposure. Aged C57BL/6 mice (18 months, both sexes) were exposed to 2% desfl
3. AAPS PharmSciTech. 2026 Oct 2;27(7):322. doi: 10.1208/s12249-026-03546-9. Glutamine-tagged Sorafenib and Atorvastatin Coloaded Polymeric Nanoparticles for Hybrid Cell Death Induction in Colorectal Cancer: Part I Formulation, Characterization, In-vitro/In-vivo Safety and Efficacy Evaluation. Yadav V(1), Dighe S(1), Dhake P(1), Jain S(2). Author information: (1)Centre for Pharmaceutical Nanotechnology, Department of Pharmaceutics, National Institute of Pharmaceutical Education and Research (NIPER), Mohali, Sector 67, S.A.S., Nagar, Punjab, 160062, India. (2)Centre for Pharmaceutical Nanotechnology, Department of Pharmaceutics, National Institute of Pharmaceutical Education and Research (NIPER), Mohali, Sector 67, S.A.S., Nagar, Punjab, 160062, India. sanyogjain@niper.ac.in. The present study explores the potential of sorafenib (SOR) and atorvastatin (ATST) to induce a ferroptosis and apoptosis-based hybrid cell death mechanism. The synergistic ATST + SOR combination was delivered through Glutamine-tagged PLGA nanoparticles (ATST + SOR/G-PLGA NPs) to promote intratumoral specificity. The formulation was optimized using DesignExpert® software by adopting Box-Behnken design (BBD). The optimized ATST + SOR/G-PLGA NPs had a spherical particle size of ~ 178.3 ± 12.6 nm, a PDI of 0.151 ± 0.08, and a Z-potential of -24.8 ± 5.8 mV. The formulation revealed a biphasic sustained release with higher release at acidic pH. In-vitro biological assessment showed a dose-de
4. Crit Rev Oncol Hematol. 2026 Sep 26;227:105622. doi: 10.1016/j.critrevonc.2026.105622. Online ahead of print. Targeting nicotinamide metabolism to reprogram the tumor microenvironment: Mechanisms and novel therapeutic strategies. Sun WD(1), Bi SZ(1), Zhu XJ(1), Lai SY(1), Zhang CY(1), Liu A(1), Li JH(2). Author information: (1)Physical Education College, Jiangxi Normal University, Nanchang, China. (2)Physical Education College, Jiangxi Normal University, Nanchang, China. Electronic address: lijianghua8@jxnu.edu.cn. The tumor microenvironment (TME) is characterized by heightened metabolic activity, dysfunctional vasculature, and chronic inflammation. Together, these features create an ecosystem that supports tumor progression. This review examines how nicotinamide (NAM) metabolism, mediated through its key enzymes Nicotinamide phosphoribosyl transferase (NAMPT) and Nicotinamide N‑methyltransferase (NNMT), may contribute to malignant remodeling of the TME at three interconnected levels: (1) fueling the hypermetabolic state of cancer cells and contributing to TME acidification; (2) modulating tumor angiogenesis; and (3) establishing and sustaining an immunosuppressive, chronic inflammatory milieu. Building on this framework, we further discuss the therapeutic potential of targeting NAM metabolism-such as via NAM supplementation or inhibition of NAMPT/NNMT-while also addressing challenges like metabolic plasticity. Future research should aim to unravel the d
5. Drug Dev Res. 2026 Nov;87(7):e70390. doi: 10.1002/ddr.70390. Comparative Evaluation of Plumbagin and Sorafenib in NDEA-TAA-Induced Hepatocellular Carcinoma: Effects on Hepatic Function, Redox Homeostasis and Histopathology. Adetola AK(1), Ugbaja RN(2), Adeyi OE(2), Thomas FC(3), Adeyemo JA(1), Odesola OA(4). Author information: (1)Department of Biochemistry, KolaDaisi University, Ibadan, Oyo, Nigeria. (2)Department of Biochemistry, Federal University of Agriculture Abeokuta, Abeokuta, Nigeria. (3)Department of Veterinary Medicine, Federal University of Agriculture Abeokuta, Abeokuta, Nigeria. (4)Department of Biological Sciences, KolaDaisi University, Ibadan, Oyo, Nigeria. Hepatocellular carcinoma (HCC) is a major contributor to cancer-related mortality worldwide and is closely linked to oxidative stress and progressive hepatic dysfunction. This study investigated the effects of plumbagin on antioxidant defense systems and hepatic function markers in an N-nitrosodiethylamine-thioacetamide (NDEA-TAA)-induced experimental model of HCC and compared its efficacy with that of sorafenib. Male Wistar rats were assigned to five groups: normal control, plumbagin-only, HCC control, HCC treated with plumbagin, and HCC treated with sorafenib. Hepatocarcinogenesis was induced using NDEA-TAA, after which antioxidant parameters including reduced glutathione (GSH), glutathione-S-transferase (GST), glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD)
6. Mol Biol Rep. 2026 Sep 18;53(1):1591. doi: 10.1007/s11033-026-12760-4. NHSL3 knockout modulates sorafenib response, growth, and motility in hepatocellular carcinoma cell models. Yıldız G(1)(2), Karabulut S(3), Dinçer T(4)(3). Author information: (1)Department of Medical Biology, Faculty of Medicine, Karadeniz Technical University, 61080, Trabzon, Türkiye. gokhanyildiz@ktu.edu.tr. (2)Department of Medical Biology, Graduate School of Health Sciences, Karadeniz Technical University, 61080, Trabzon, Türkiye. gokhanyildiz@ktu.edu.tr. (3)Department of Medical Biology, Graduate School of Health Sciences, Karadeniz Technical University, 61080, Trabzon, Türkiye. (4)Department of Medical Biology, Faculty of Medicine, Karadeniz Technical University, 61080, Trabzon, Türkiye. BACKGROUND: Nance-Horan syndrome-like protein 3 (NHSL3) has been implicated in hepatocellular carcinoma (HCC) progression, but its role in sorafenib response and related growth and motility phenotypes remains unclear. In this study, we examined NHSL3 loss in Huh-7 cells and selected phenotypes in Hep3B cells. METHODS AND RESULTS: NHSL3 knockout clones were generated in both cell lines by paired Cas9 nickase editing. Data were obtained from three independent biological experiments. In Huh-7 cells, NHSL3 loss increased sorafenib sensitivity, lowering the 24 h half-maximal inhibitory concentration from 13.4 µM to 5.8 µM. NHSL3 loss was associated with G1 enrichment, reduced S-phase fraction, and impa
7. Drug Dev Res. 2026 Nov;87(7):e70385. doi: 10.1002/ddr.70385. Design, Synthesis, In Vitro Biological Evaluation, and In Silico Studies of Novel Imidazo[4,5-b]Pyridine-Acrylonitrile-Based Derivatives as VEGFR-2 Inhibitors Against Breast Cancer and Hepatocellular Carcinoma. Mohamed LW(1), Saadeldin AA(1)(2), Farag AB(2)(3). Author information: (1)Pharmaceutical Organic Chemistry Department, Faculty of Pharmacy, Cairo University, Cairo, Egypt. (2)Pharmaceutical Chemistry Department, Faculty of Pharmacy, Ahram Canadian University, Giza, Egypt. (3)Department of Cardiology, Sarver Heart Center, University of Arizona, Tucson, Arizona, USA. Vascular endothelial growth factor receptor-2 (VEGFR-2) is a vital mediator of angiogenesis. Therefore, VEGFR-2 inhibition is considered a promising therapeutic target to combat cancer. In the present study, a series of 22 imidazo[4,5-b]pyridine-acrylonitrile-based derivatives was designed and synthesized. All compounds were evaluated for their VEGFR-2 inhibitory activity. Seven of the tested compounds showed high inhibitory activity against VEGFR-2 with IC50 (0.029-0.087 µM) compared to reference drug sorafenib IC50 = 0.091 µM. Four of these derivatives were selected for in vitro cytotoxic activity against breast cancer (MCF-7) and hepatocellular (HepG2) carcinoma cell lines, showing IC50 (0.073-0.196 µM) and (0.20-0.21 µM), respectively, relative to sorafenib IC50 0.16 and 0.19 µM, respectively. Compound 2f exhibiting a supe
8. Signal Transduct Target Ther. 2026 Sep 16;11(1):383. doi: 10.1038/s41392-026-02971-3. HIF1α-KLF4 signaling dictates extra-erythrocyte expression of hemoglobin conferring sorafenib resistance in hepatocellular carcinoma. Zhang B(#)(1)(2), Liu F(#)(3), Gao X(#)(4), Zhu Y(#)(1), Chen T(1)(5), Hao J(1), Wei Y(6), Sun Z(4), Yang R(1), Yang Y(2), Ren H(2), Li Y(1), Yu C(6), Ren T(2), Huang Y(2), Jiang H(6), Melino G(7), Ma L(8)(9)(10), Huang H(11), Sun Q(12)(13)(14). Author information: (1)Laboratory for Major Disease Control, Academy of Military Medical Sciences; Research Unit of Cell Death Mechanism, 2021RU008, Chinese Academy of Medical Science, Beijing, China. (2)Department of Oncology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China. (3)Institute of Molecular Immunology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, China. (4)National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. (5)School of Medicine, Nanjing University, Nanjing, China. (6)College of Life Science and Bioengineering, School of Science, Beijing Jiaotong University, Beijing, China. (7)Department of Experimental Medicine, TOR, University of Rome "Tor Vergata", Rome, Italy. melino@uniroma2.it. (8)Institute of Molecular Immunology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou
9. Mol Biol Rep. 2026 Sep 12;53(1):1566. doi: 10.1007/s11033-026-12715-9. Hepatic stellate cells promote structural and functional remodeling of three-dimensional hepatocellular carcinoma coculture spheroids. Obelar J(1)(2), Vasconcellos JG(3), do Nascimento NB(3)(4), de Sousa AC(3)(4), Giehl M(3), Simões Fischer B(3), de Souza Ferreira J(3)(4), de Oliveira J(3)(4), Trindade VMT(3)(4), Guma FTCR(3)(4). Author information: (1)Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Rio Grande Do Sul, Brazil. jessica.obelar@ufrgs.br. (2)Programa de Pós-Graduação Em Ciências Biológicas: Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Rio Grande Do Sul, Brazil. jessica.obelar@ufrgs.br. (3)Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Rio Grande Do Sul, Brazil. (4)Programa de Pós-Graduação Em Ciências Biológicas: Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Rio Grande Do Sul, Brazil. BACKGROUND: Hepatic stellate cells (HSCs) are major regulators of the hepatocellular carcinoma (HCC) tumor microenvironment, contributing to extracellular matrix remodeling, tumor progression, and therapeutic resistance. Although three-dimensional (3D) coculture spheroid models better represent tumor-stroma interact
10. Front Public Health. 2026 Aug 27;14:1918118. doi: 10.3389/fpubh.2026.1918118. eCollection 2026. Cost-effectiveness of tremelimumab plus durvalumab versus sorafenib for unresectable hepatocellular carcinoma in China: an economic evaluation based on five-year overall survival data from the HIMALAYA trial. Feng R(#)(1)(2), Liang P(#)(2), Wang Y(2), Li D(2), Jia H(2), Zheng Y(2), Huo L(#)(2), Lv Q(#)(1). Author information: (1)School of Disaster and Emergency Medicine, Tianjin University, Tianjin, China. (2)Department of Pharmacy, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China. (#)Contributed equally OBJECTIVE: To assess the cost-effectiveness of tremelimumab plus durvalumab [the Single Tremelimumab Regular Interval Durvalumab (STRIDE) regimen] versus sorafenib as first-line treatment for unresectable hepatocellular carcinoma in China using 5-year follow-up data from the HIMALAYA trial. METHODS: A three-state partitioned survival model comprising progression-free survival, progressed disease, and death was developed from the perspective of the Chinese healthcare system. Individual patient data were reconstructed from the published Kaplan-Meier curves from the HIMALAYA trial and used to estimate and extrapolate progression-free and overall survival. The model used 28-day cycles, a 10-year base-case time horizon, and an annual discount rate of 4.5%. Only direct medical costs were included and expressed in 2025 United States dollars. The
11. Exp Cell Res. 2026 Oct 1;462(2):115170. doi: 10.1016/j.yexcr.2026.115170. Epub 2026 Sep 9. Cuproptosis and copper metabolism regulate hepatocellular carcinoma progression and therapeutic response to sorafenib. Elkateb AS(1), Taha H(2), Atya HB(2), Ali SA(2). Author information: (1)Biochemistry and Molecular Biology Department, Faculty of Pharmacy, Capital University (Former Helwan), P.O. Box 11795, Cairo, Egypt. Electronic address: ahmed.salemali@pharm.helwan.edu.eg. (2)Biochemistry and Molecular Biology Department, Faculty of Pharmacy, Capital University (Former Helwan), P.O. Box 11795, Cairo, Egypt. Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related death, and systemic therapy with sorafenib is limited by primary and acquired resistance. Copper is now recognized both as a growth-promoting cofactor in HCC and as the trigger of cuproptosis, a copper-dependent form of regulated cell death executed through ferredoxin-1 (FDX1)-mediated reduction of Cu2+, aggregation of lipoylated tricarboxylic acid (TCA) cycle proteins such as dihydrolipoamide S-acetyltransferase (DLAT), loss of Fe-S cluster proteins and proteotoxic mitochondrial stress. This review is deliberately restricted to a single mechanistic axis - copper handling, cuproptosis competence and sorafenib response in HCC - and grades the evidence supporting it. We distinguish direct experimental demonstrations of cuproptosis from copper overload, oxidative stress and mitochondria
12. J Am Acad Dermatol. 2026 Sep 7:S0190-9622(26)03468-7. doi: 10.1016/j.jaad.2026.05.146. Online ahead of print. Comment on "Decreased risk of cardiovascular disease in dermatology patients taking niacinamide: A TriNetX cohort study". Li C(1), Pan L(2). Author information: (1)Department of Dermatology, University Hospital Erlangen, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany. (2)Department of Plastic and Hand Surgery, Klinikum Rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Electronic address: lingfeng.pan@tum.de. DOI: 10.1016/j.jaad.2026.05.146 PMID: 42705349 Conflict of interest statement: Conflicts of interest None disclosed.
13. Drug Deliv. 2026 Dec 31;33(1):2726824. doi: 10.1080/10717544.2026.2726824. Epub 2026 Sep 3. Synergistic epigenetic modulation and ferroptosis induction via codelivery of Decitabine and Sorafenib for potent anti-tumor therapy. Xing Y(1)(2), Zhang X(1), Wang R(1), Zhou Y(1), Sun K(1)(2), Yu F(2), Zheng X(3), Zhao W(1)(2). Author information: (1)State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy, Key Laboratory of Molecular Drug Research and KLMDASR of Tianjin, Nankai University, Tianjin, China. (2)Qingdao Central Hospital, NHC Key Laboratory of Cardiopulmonary Rehabilitation and Functional Recovery, Shandong Provincial University Industry-Academia-Research Collaborative and Innovation Center of Intelligent Rehabilitation Drug R&D, Qingdao Key Laboratory of Precision Drug Research for Chronic Disease Rehabilitation, School of Medicine, University of Health and Rehabilitation Sciences, Qingdao, China. (3)Department of Pathology, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China. Despite considerable advances in cancer therapy, the intrinsic heterogeneity of malignant cells continues to compromise therapeutic efficacy with conventional monotherapies, driving the need for combination treatments to achieve more durable and complete responses. The limited efficacy of conventional chemotherapy is largely attributable to the immunosuppressive tumor micr
14. Sci Rep. 2026 Sep 1;16(1):24028. doi: 10.1038/s41598-026-64955-1. Sorafenib/piroxicam therapy with biomarker-defined survival benefit in canine muscle-invasive urothelial carcinoma. Maeda S(1), Yokota S(2), Komori M(2), Goto-Koshino Y(3), Chambers JK(4), Uchida K(4), Yonezawa T(2), Momoi Y(2). Author information: (1)Laboratory of Veterinary Clinical Pathobiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1, Yayoi, Bunkyo-ku, Tokyo, 113-8657, Japan. amaeda@g.ecc.u-tokyo.ac.jp. (2)Laboratory of Veterinary Clinical Pathobiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1, Yayoi, Bunkyo-ku, Tokyo, 113-8657, Japan. (3)Molecular Diagnostic Laboratory, Veterinary Medical Center, The University of Tokyo, Tokyo, Japan. (4)Laboratory of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan. Molecular-targeted therapies require biomarker-driven evaluation to optimize precision oncology strategies; however, translational models integrating clinical outcomes with mechanistic biomarkers are limited. Canine urothelial carcinoma shares molecular features with human muscle-invasive bladder cancer, including activation of VEGFR signaling, providing a valuable comparative oncology platform. Sorafenib is a multi-kinase inhibitor targeting VEGFRs, PDGFRβ, BRAF, and related pathways, but its therapeutic mechanisms and clinical benefit in uroth
15. Cureus. 2026 Jul 30;18(7):e113666. doi: 10.7759/cureus.113666. eCollection 2026 Jul. Beyond Melanin: A Literature Review of Photoprotection Mechanisms and Gaps in Skin of Color. Leybengrub P(1), Eyob W(2), Petrossian L(3), Shetty S(4), Scott BA(5), Kebbe MB(6), Vo K(7). Author information: (1)Renaissance School of Medicine, Stony Brook University, Stony Brook, USA. (2)College of Medicine, University of Cincinnati, Cincinnati, USA. (3)School of Medicine, California University of Science and Medicine, Colton, USA. (4)School of Osteopathic Medicine, Rowan-Virtua School of Osteopathic Medicine, Stratford, USA. (5)School of Medicine, University College Dublin, Dublin, IRL. (6)Department of Dermatology, Istanbul Okan University, Istanbul, TUR. (7)Transitional Year Residency Program, Desert Regional Medical Center, Palm Springs, USA. There is a critical need for tailored photoprotection in skin of color (SOC) populations. SOC has higher eumelanin-to-phenomelanin ratios, more mature melanosomes, and enhanced DNA repair capacity compared with lighter skin. The quantity and distribution of melanin in darker skin provide natural photoprotection. This leads to a misconception that SOC populations are inherently protected from all photodamage and serves as a barrier to proper photoprotection for these populations. Although the skin cancer incidence is lower in dark skin, mortality is higher, perhaps as a result of late diagnosis or misdiagnosis. These populations are
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