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Price transparency compliance and variation for proton therapy in the United States 美国质子治疗的价格透明度、依从性和变化。
IF 10.1 1区 医学 Q1 ONCOLOGY Pub Date : 2026-01-16 DOI: 10.1016/j.canlet.2026.218260
Kasey R. Cargill , Noah M. Feder , Tyler Wilhite , Walid F. Gellad , Heath D. Skinner , Yvonne M. Mowery , Christopher T. Wilke
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引用次数: 0
Cutting-edge AI technologies in skin cancer applications 皮肤癌应用中的尖端人工智能技术。
IF 10.1 1区 医学 Q1 ONCOLOGY Pub Date : 2026-01-14 DOI: 10.1016/j.canlet.2026.218256
Yueqin Diao , Xiao Chen , Ziyan Huang , Qian Tan , Meng Yang , Hanyi Yu , Yanwu Xu , Xing Hu
The rapid development of multimodal large language models (LLMs) such as GPT and Med-PaLM is reshaping medical practice. Skin cancer, one of the most prevalent malignancies, encompasses diverse subtypes and early signs that often resemble benign lesions, making timely detection and accurate diagnosis challenging. Traditional diagnostic methods are hindered by subjectivity, sampling bias, and low efficiency. Skin cancer diagnosis is largely constrained by strong subjectivity, sampling bias, and low diagnostic efficiency regularly. Although immunotherapy and targeted therapy aimed at the tumor microenvironment have brought new therapeutic possibilities to patients, tumor heterogeneity and immune evasion remain major unresolved challenges. Artificial intelligence techniques based on deep learning and complex neural networks can integrate dermoscopic images, histopathological information, and genetic databases through multimodal fusion strategies, enabling the extraction of richer and complementary features and thereby significantly improving diagnostic accuracy and robustness. Moreover, tailoring treatment strategies according to individual patient characteristics facilitates truly personalized therapy and prognostic assessment. In the field of drug development, artificial intelligence accelerates the screening and simulation of candidate compounds, substantially reducing development time and expenditure. This review summarizes recent advances in AI for skin cancer, with emphasis on early detection, individualized therapy, and patient management. We further discuss challenges related to data quality and model interpretability, emphasizing the importance of dermatology-specific foundation models and collaboration between clinicians and engineers.
GPT和Med-PaLM等多模态大语言模型(llm)的快速发展正在重塑医疗实践。皮肤癌是最常见的恶性肿瘤之一,包括多种亚型和早期症状,通常类似于良性病变,这使得及时发现和准确诊断具有挑战性。传统的诊断方法存在主观性、抽样偏差和效率低等问题。皮肤癌的诊断在很大程度上受主观性强、抽样偏倚、诊断效率低等制约。尽管针对肿瘤微环境的免疫治疗和靶向治疗为患者带来了新的治疗可能性,但肿瘤异质性和免疫逃避仍然是主要的未解决的挑战。基于深度学习和复杂神经网络的人工智能技术可以通过多模态融合策略整合皮肤镜图像、组织病理信息和遗传数据库,从而提取更丰富和互补的特征,从而显著提高诊断的准确性和鲁棒性。此外,根据患者个体特征定制治疗策略有助于真正的个性化治疗和预后评估。在药物开发领域,人工智能加速了候选化合物的筛选和模拟,大大减少了开发时间和支出。本文综述了人工智能治疗皮肤癌的最新进展,重点是早期发现、个体化治疗和患者管理。我们进一步讨论了与数据质量和模型可解释性相关的挑战,强调了皮肤科特定基础模型以及临床医生和工程师之间合作的重要性。
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引用次数: 0
Corrigendum to “DAB2IP suppresses tumor malignancy by inhibiting GRP75-driven p53 ubiquitination in colon cancer” [Cancer Lett. 532 (2022) 215588] “DAB2IP通过抑制结肠癌中grp75驱动的p53泛素化来抑制肿瘤恶性”的更正[癌症杂志]. 532(2022)215588]。
IF 10.1 1区 医学 Q1 ONCOLOGY Pub Date : 2026-01-14 DOI: 10.1016/j.canlet.2026.218251
Shengjie Feng , Qingwen Huang , Jiao Deng , Weiyi Jia , Jianping Gong , Daxing Xie , Jie Shen , Liang Liu
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引用次数: 0
Programmable Smart CAR-T design: A new paradigm in precision immunotherapy driven by logic gates, conditional activation, allogeneic strategies, and artificial intelligence 可编程智能CAR-T设计:由逻辑门、条件激活、同种异体策略和人工智能驱动的精确免疫治疗的新范式
IF 10.1 1区 医学 Q1 ONCOLOGY Pub Date : 2026-01-13 DOI: 10.1016/j.canlet.2026.218257
Peizhen Wen , Qi Ai , Xiang Fan , Zhangyuan Gu , Bo Chen , Hui Qian
Chimeric antigen receptor T-cell (CAR-T) therapy has achieved unprecedented success in hematological malignancies but faces formidable challenges in solid tumors. These limitations include severe “on-target, off-tumor” toxicity, antigen heterogeneity, and the immunosuppressive tumor microenvironment, where the dense extracellular matrix acts as a physical barrier hindering T-cell infiltration. To address these hurdles, this review proposes a comprehensive Efficacy, Safety, and Accessibility (ESA) framework for engineering next-generation “Smart” CAR-T cells. We explore the implementation of programmable Boolean logic gates (AND, OR, NOT) and conditional activation systems (e.g., synNotch, focused ultrasound) that allow T cells to compute antigen patterns and precisely sense tumor-specific cues. Furthermore, we examine the development of off-the-shelf allogeneic platforms that utilize advanced gene editing technologies—such as CRISPR-Cas9 and base editing—to eliminate endogenous receptors and prevent graft-versus-host disease. Crucially, we highlight the transformative potential of Artificial Intelligence/Machine Learning in accelerating the “Design-Build-Test-Learn” cycle, from optimizing single-chain variable fragment (scFv) affinity to predicting clinical toxicity risks. By integrating these multi-dimensional strategies, we outline a new paradigm in precision immunotherapy, aiming to transform CAR-T cells into intelligent, controllable, and universally accessible living drugs capable of eradicating complex solid tumors.
嵌合抗原受体t细胞(CAR-T)治疗在血液系统恶性肿瘤中取得了前所未有的成功,但在实体肿瘤中面临着巨大的挑战。这些限制包括严重的“靶向、非肿瘤”毒性、抗原异质性和免疫抑制肿瘤微环境,其中致密的细胞外基质充当阻碍t细胞浸润的物理屏障。为了解决这些障碍,本综述提出了一个综合的功效、安全性和可及性(ESA)框架,用于设计下一代“智能”CAR-T细胞。我们探索了可编程布尔逻辑门(AND, OR, NOT)和条件激活系统(例如synNotch,聚焦超声)的实现,这些系统允许T细胞计算抗原模式并精确地感知肿瘤特异性线索。此外,我们研究了利用先进的基因编辑技术(如CRISPR-Cas9和碱基编辑)消除内源性受体和预防移植物抗宿主病的现成同种异体平台的发展。至关重要的是,我们强调了人工智能/机器学习在加速“设计-构建-测试-学习”周期方面的变革潜力,从优化单链可变片段(scFv)亲和力到预测临床毒性风险。通过整合这些多维策略,我们概述了精准免疫治疗的新范式,旨在将CAR-T细胞转化为能够根除复杂实体肿瘤的智能、可控和普遍可及的活药物。
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引用次数: 0
ABCG2-mediated SN-38 efflux drives resistance to Sacituzumab govitecan in urothelial carcinoma abcg2介导的SN-38外排驱动尿路上皮癌对Sacituzumab Govitecan的耐药
IF 10.1 1区 医学 Q1 ONCOLOGY Pub Date : 2026-01-13 DOI: 10.1016/j.canlet.2026.218254
Isabella Prantl , Reinhard Grausenburger , Julia Müller , Oliver Baumfried , Iris Elisabeth Ertl , Christoph Nössing , Paula Herek , Christine Pirker , Daniel Valcanover , Yuri Bastos-Moreira , Eszter Borsos , Lena Marie Hauser , Luis Rupp , Ursula Lemberger , Lisa Gabler-Pamer , Ekaterina Laukhtina , Agata Suleja , André Oszwald , Gabriel Wasinger , Eva Compérat , Bernhard Englinger
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引用次数: 0
SUMOylation of SND1 drives mature miRNA degradation and tumor progression SND1的summoylation驱动成熟miRNA降解和肿瘤进展
IF 10.1 1区 医学 Q1 ONCOLOGY Pub Date : 2026-01-12 DOI: 10.1016/j.canlet.2026.218253
Yingting Cao , Yanli Wang , Xindi Zhang , Yixin Zhang , Xintong Zhang , Xiaopeng Tan , Lian Li , Ran Chen , Runhui Lu , Ruiyu Xie , Jianxiu Yu , Xiaojing Zhao
The global downregulation of microRNAs (miRNAs) is a hallmark of many cancers, yet the mechanisms governing mature miRNA degradation remain poorly understood. Post-translational modifications (PTMs) have emerged as key regulators of RNA metabolism. However, the specific role of stress-responsive PTMs in driving miRNA degradation within the complex stress landscape of the tumor microenvironment is a critical unanswered question. We demonstrate that the endonuclease SND1 is SUMOylated at K513 in response to stresses such as oxidative stress and Cisplatin. This inducible modification enhances the miRNA-degrading activity of SND1 by promoting its interaction with AGO2 and UPF1, thereby facilitating mature miRNA decay. A key consequence is the degradation of a novel tumor-suppressive miRNA, miR-chr5_25226, leading to elevated MAPK10 expression that fuels tumor cell proliferation, migration, and Cisplatin resistance. Functional rescue experiments confirmed that restoring miR-chr5_25226 or silencing MAPK10 reverses these oncogenic effects. Furthermore, the SUMOylation inhibitor 2-D08 effectively restored miR-chr5_25226 expression and sensitized tumor cells to Cisplatin. Together, our findings reveal a novel oncogenic axis in which stress-induced SUMOylation of SND1 links tumor microenvironment stress to miRNA degradation. This SUMO1–SND1/miR-chr5_25226/MAPK10 pathway identifies the targeting of SND1 SUMOylation as a potential therapeutic strategy to modulate oncogenic miRNA decay and enhance chemosensitivity.
microrna (miRNA)的全球下调是许多癌症的标志,但控制成熟miRNA降解的机制仍然知之甚少。翻译后修饰(ptm)已成为RNA代谢的关键调控因子。然而,在肿瘤微环境的复杂应激环境中,应激反应性ptm在驱动miRNA降解中的具体作用是一个关键的未解之谜。我们证明了内切酶SND1在K513处被su甲基化,以响应氧化应激和顺铂等应激。这种诱导修饰通过促进SND1与AGO2和UPF1的相互作用来增强其降解miRNA的活性,从而促进成熟miRNA的衰变。一个关键的结果是一种新的肿瘤抑制miRNA miR-chr5_25226的降解,导致MAPK10表达升高,从而促进肿瘤细胞增殖、迁移和顺铂耐药性。功能修复实验证实,恢复miR-chr5_25226或沉默MAPK10可逆转这些致癌作用。此外,SUMOylation抑制剂2-D08有效地恢复了miR-chr5_25226的表达,并使肿瘤细胞对顺铂敏感。总之,我们的研究结果揭示了一个新的致癌轴,其中应激诱导的SND1的SUMOylation将肿瘤微环境应激与miRNA降解联系起来。SUMO1-SND1 /miR-chr5_25226/MAPK10通路确定了SND1 summoylation的靶向性,作为调节致癌miRNA衰减和增强化疗敏感性的潜在治疗策略。
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引用次数: 0
Corrigendum to “LCH-7749944, a novel and potent p21-activated kinase 4 inhibitor, suppresses proliferation and invasion in human gastric cancer cells” [Cancer Lett. 317 (2012) 24–32] “LCH-7749944,一种新型有效的p21活化激酶4抑制剂,抑制人胃癌细胞的增殖和侵袭”的更正[癌症杂志]. 317(2012)24-32]。
IF 10.1 1区 医学 Q1 ONCOLOGY Pub Date : 2026-01-12 DOI: 10.1016/j.canlet.2026.218250
Jian Zhang , Jian Wang , Qiqiang Guo , Yu Wang , Ying Zhou , Huizhi Peng , Maosheng Cheng , Dongmei Zhao , Feng Li
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引用次数: 0
Dysregulation of PCSK9 via m6A-dependent epitranscriptomic programs fosters hepatocellular carcinoma progression 通过m6a依赖的表转录组程序失调PCSK9促进肝细胞癌的进展。
IF 10.1 1区 医学 Q1 ONCOLOGY Pub Date : 2026-01-12 DOI: 10.1016/j.canlet.2026.218255
Wen-Lung Wang , Chih-Chieh Yen , Chia-Sheng Yen , Yu-Hsuan Huang , Hsuan-Yi Huang , Ju-Fei Chen , Yen-Yu Liu , Sih-Ting Wang , Yu-Tzu Liu , Mien-Chie Hung , Chia-Jui Yen
PCSK9, besides its established role in cholesterol metabolism in the liver, has recently emerged as a tumor-promoting gene in various types of cancer including hepatocellular carcinoma (HCC). However, the regulatory pathways governing oncogenic PCSK9 in HCC remain poorly understood, particularly those involving epitranscriptomic modifications. Here, we identify PCSK9 as a novel mRNA target of METTL3 in HCC. Furthermore, METTL3 promotes tumor cell growth by upregulating PCSK9 mRNA through m6A methylation in the 3’ UTR. Additionally, IGF2BP3 exerts its m6A reading function to maintain PCSK9 mRNA stability in an m6A-dependent manner, thereby fostering the capacity of tumor growth. Moreover, ILF3 interacts with IGF2BP3 to collaboratively enhance PCSK9 mRNA stability and ultimately contributes to tumor growth. The METTL3-IGF2BP3-ILF3-PCSK9 signaling pathway is additionally confirmed in HCC patient cohorts. In summary, our findings highlight that PCSK9 is controlled by m6A-dependent METTL3-IGF2BP3-ILF3 epitranscriptomic programs and contributes to HCC progression. The study provides a rationale for repurposing PCSK9-depleting therapeutics into a potential antitumor treatment.
PCSK9,除了其在肝脏胆固醇代谢中的既定作用外,最近在包括肝细胞癌(HCC)在内的各种类型的癌症中作为肿瘤促进基因出现。然而,HCC中致癌PCSK9的调控途径仍然知之甚少,特别是那些涉及表转录组修饰的调控途径。在这里,我们发现PCSK9是HCC中METTL3的一个新的mRNA靶点。此外,METTL3通过3' UTR中的m6A甲基化上调PCSK9 mRNA,从而促进肿瘤细胞的生长。此外,IGF2BP3发挥其m6A读取功能,以m6A依赖的方式维持PCSK9 mRNA的稳定性,从而促进肿瘤的生长能力。此外,ILF3与IGF2BP3相互作用,共同增强PCSK9 mRNA的稳定性,最终促进肿瘤生长。METTL3-IGF2BP3-ILF3-PCSK9信号通路在HCC患者队列中也得到证实。总之,我们的研究结果强调PCSK9是由m6a依赖的METTL3-IGF2BP3-ILF3表转录组程序控制的,并有助于HCC的进展。该研究为将pcsk9耗尽疗法重新用于潜在的抗肿瘤治疗提供了理论依据。
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引用次数: 0
Targeting the stromal-immune barrier: A novel strategy to overcome resistance to CLDN18.2/CD3 bispecific T-cell engager therapy in pancreatic cancer 靶向基质免疫屏障:一种克服胰腺癌CLDN18.2/CD3双特异性t细胞浸润治疗耐药的新策略
IF 10.1 1区 医学 Q1 ONCOLOGY Pub Date : 2026-01-08 DOI: 10.1016/j.canlet.2026.218248
Shiqian Liu , Matthäus Felsenstein , Shaokun Liu , Igor Maximilian Sauer , Muhammad Imtiaz Ashraf
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引用次数: 0
Baseline tumor-informed circulating tumor DNA concentration predicts early chemoimmunotherapy failure in diffuse large B-cell lymphoma 基线肿瘤信息循环肿瘤DNA浓度预测弥漫性大b细胞淋巴瘤早期化疗免疫治疗失败。
IF 10.1 1区 医学 Q1 ONCOLOGY Pub Date : 2026-01-08 DOI: 10.1016/j.canlet.2026.218249
Qing Shi , Muchen Zhang , Yang He , Ronggui Lin , Mingci Cai, Huijuan Zhong, Shu Cheng, Pengpeng Xu, Weili Zhao, Li Wang
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引用次数: 0
期刊
Cancer letters
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