Cancer Communications最新文献

{"title":"Macrophages Drive Ferroptosis Resistance after Radiotherapy.","authors":"Hyewon Chung, Sang Wha Kim, Jae Won Oh, Gyu Mi Park, Yurim Cho, Hae Suk Choi, MinJi Kim, Kwang Pyo Kim, Yi Rang Na, Hye Seung Lee, Hak Jae Kim, Seung Hyeok Seok","doi":"10.34133/cancomm.0039","DOIUrl":"https://doi.org/10.34133/cancomm.0039","url":null,"abstract":"<p><p><b>Background:</b> Radiotherapy eliminates most tumor cells but spares persister tumor cells that evade cell death and drive relapse. Increasing evidence suggests that stromal components of the tumor microenvironment influence treatment responses, yet whether macrophages actively reprogram tumor-intrinsic stress responses to promote radioresistance remains unclear. Here, we investigated the mechanisms by which macrophage-tumor cell interactions regulate ferroptosis and tumor survival after irradiation. <b>Methods:</b> We used macrophage-tumor cell coculture systems, Transwell separation assays, and 3D microfluidic models to examine contact-dependent effects on tumor survival following irradiation. Kinome-wide small interfering RNA screening, RNA sequencing, lipidomic profiling, and quantitative proteomic analysis of secretomes were performed to identify signaling pathways and metabolic changes. Genetic and pharmacological perturbation of Ephrin receptor b4 (Ephb4) signaling were evaluated in vitro and in syngeneic mouse tumor models. Clinical relevance was assessed using transcriptomic analyses and immunohistochemical staining of patient tumor specimens. <b>Results:</b> Macrophage contact reduced lipid peroxidation and cell death in irradiated tumor cells in a contact-dependent manner. Kinome screening identified Ephb4 as a key mediator induced by irradiation in tumor cells. Ephb4 engagement with ephrinb2 on macrophages initiated bidirectional signaling that increased expression of ferroptosis-protective genes (solute carrier family 7 member <i>11</i> [<i>Slc7a11</i>], solute carrier family 3 member 2 [<i>Slc3a2</i>], and glutathione peroxidase 4 [<i>Gpx4</i>]) in tumor cells while activating the toll-like receptor 2- nuclear factor-kappa B pathway and interleukin-6 (IL-6) production in macrophages. Macrophage-derived IL-6 further sustained ferroptosis resistance in tumor cells, and Ephb4-driven secretion of cathepsin S amplified macrophage IL-6 production through a feedforward loop. Genetic or pharmacological inhibition of Ephb4 restored lipid peroxidation and markedly enhanced radiosensitivity in vitro and in vivo. Analysis of patient datasets demonstrated increased EPHB4 expression following radiotherapy and an association between high EPHB4 expression, reduced ferroptosis signatures, and poor treatment response. <b>Conclusions:</b> These findings identify a macrophage-driven ferroptosis evasion program that enables tumor cell survival after irradiation and demonstrate that Ephb4 coordinates bidirectional tumor-macrophage signaling to sustain this resistance. Targeting the Ephb4-ephrinb2 axis represents a potential strategy to enhance ferroptosis and improve radiotherapy efficacy in resistant tumors.</p>","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":"46 ","pages":"0039"},"PeriodicalIF":28.4,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13542434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recruited Monocyte-Derived Macrophages Drive T Cell Inflammation in Immune Checkpoint Inhibitor-Mediated Pneumonitis.","authors":"Xiaoran Cui, Renyong Zhi, Xiaoyan Li, Yinming Ji, Zhisong Hu, Pengfei Cui, Yuhui Qin, Tao Li, Liangliang Wu, Lingxiong Wang, Jinfeng Li, Yibing Bai, Hui Li, Tianyi Liu, Yi Hu","doi":"10.34133/cancomm.0049","DOIUrl":"10.34133/cancomm.0049","url":null,"abstract":"&lt;p&gt;&lt;p&gt;&lt;b&gt;Background:&lt;/b&gt; Immune checkpoint inhibitor-mediated pneumonitis (CIP) constitutes a major toxicity that limits the clinical application of cancer immunotherapy, whereas its underlying mechanisms remain incompletely understood. Current management relies on nonspecific immunosuppressants, lacking precision therapies. Although single-cell RNA sequencing (scRNA-seq) of bronchoalveolar lavage fluid (BALF) has implicated T cell activation and inflammatory myeloid responses in CIP pathogenesis, critical gaps persist regarding interstitial lung immunity and mechanisms governing monocyte/macrophage-T cell co-enrichment and crosstalk. We aimed to delineate the lung immune circuits that drive CIP and to identify targetable monocyte/macrophage-T cell pathways that could be leveraged for precision intervention. &lt;b&gt;Methods:&lt;/b&gt; To elucidate CIP pathogenesis, we performed integrated scRNA-seq analysis of BALF from CIP&lt;sup&gt;+&lt;/sup&gt; and CIP&lt;sup&gt;-&lt;/sup&gt; patients with validation in a prospective cohort using flow cytometry, enzyme-linked immunosorbent assay, Western blotting, and quantitative polymerase chain reaction. Mechanistic studies were performed using an established tumor-bearing forkhead box P3-diphtheria toxin receptor-green fluorescent protein (&lt;i&gt;Foxp3-DTR-GFP&lt;/i&gt;) mouse model of programmed death-1 inhibitor-induced CIP via micro-computed tomography, histopathology, scRNA-seq, flow cytometry, multiplex immunofluorescence, Western blotting, Transwell migration assays, and pharmacologic interventions. &lt;b&gt;Results:&lt;/b&gt; In CIP&lt;sup&gt;+&lt;/sup&gt; patient BALF and mouse lung tissues, CD8&lt;sup&gt;+&lt;/sup&gt; T cells expressing cytotoxic effectors and C-X-C chemokine receptor 3 (CXCR3) expanded concomitantly with distinct C-C chemokine receptor 2 (CCR2)&lt;sup&gt;+&lt;/sup&gt; monocyte-derived macrophages (MoMΦ) exhibiting a highly inflammatory phenotype, while tissue-resident macrophages were markedly reduced. Mouse models revealed that expanded CCR2&lt;sup&gt;+&lt;/sup&gt; MoMΦ originating from circulation replenished the depleted niche of lung-resident interstitial macrophages. Mechanistically, integrated in silico prediction and experimental validation demonstrated that CCR2&lt;sup&gt;+&lt;/sup&gt; MoMΦ recruited CD8&lt;sup&gt;+&lt;/sup&gt; T cells via the C-X-C motif chemokine ligand 9/10 (CXCL9/10)-CXCR3 axis. Conversely, CD8&lt;sup&gt;+&lt;/sup&gt; T cells drove CCR2&lt;sup&gt;+&lt;/sup&gt; MoMΦ expansion and pro-inflammatory phenotype via the interferon-γ (IFN-γ) axis, suggesting the existence of a positive feedback loop between these cell types. Pharmacological targeting of CCR2/CCR5 or CXCR3 signaling attenuated pneumonitis, reduced pulmonary CCR2&lt;sup&gt;+&lt;/sup&gt; MoMΦ infiltration, diminished pathogenic T cell activation and cytotoxicity, and improved survival without compromising antitumor immunity. &lt;b&gt;Conclusions:&lt;/b&gt; Our findings establish CCR2&lt;sup&gt;+&lt;/sup&gt; MoMΦ and the IFN-γ-CXCL9/10-CXCR3 axis as core drivers of CIP pathogenesis and validate their therapeutic targeting potential. This work provides a scientific foundation for de","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":"46 ","pages":"0049"},"PeriodicalIF":28.4,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534810/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic Reprogramming of <i>NSUN2</i>-Mediated m⁵C Modification Promotes the Progression of Hepatocellular Carcinoma by Restricting Natural Killer Cell-Mediated Cytotoxicity.","authors":"Shengwei Mao, Yuan Fang, Jun Gao, Jiafeng Chen, Zhiqi Guan, Xuhui Zhao, Jinglei Wu, Xiaoling Wu, Guiqi Zhu, Xiangyu Zhang, Qianfu Zhao, Rui Yang, Yi Wang, Tianhao Chu, Yichao Bu, Jialu Fu, Hongxu Li, Zheng Tang, Yinghong Shi, Jian Zhou, Jia Fan, Jinling Jiang, Weiren Liu","doi":"10.34133/cancomm.0043","DOIUrl":"10.34133/cancomm.0043","url":null,"abstract":"<p><p><b>Background:</b> Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality, with resistance to immunotherapy posing a major clinical challenge. Natural killer (NK) cells exhibit impaired infiltration and cytotoxicity in HCC; however, the mechanisms underlying NK cell-mediated immune evasion are still poorly understood. This study investigated how NOP2/Sun RNA methyltransferase 2 (NSUN2), a 5-methylcytosine (m⁵C) RNA methyltransferase, induces metabolic reprogramming and immunosuppression to drive HCC progression. <b>Methods:</b> We conducted a genome-wide CRISPR screen in HCC cells cocultured with NK cells. To delineate the downstream mechanisms, we integrated profiling of the m5C epitranscriptome, transcriptome, and chromatin landscape with metabolic characterization. The impact of <i>NSUN2</i> on histone lactylation and programmed cell death 1 ligand 1 (PD-L1) transcription was further investigated. Functional assays in vitro and in vivo using syngeneic murine models and pharmacological inhibition validated these findings. Clinical relevance was assessed using patient tissues, The Cancer Genome Atlas dataset, and immunotherapy cohorts. <b>Results:</b> Genome-wide CRISPR screening in HCC cell-NK cell coculture models identified <i>NSUN2</i> as a key suppressor of NK cell-mediated cytotoxicity. Mechanistically, NSUN2-mediated RNA m⁵C modification enhanced the messenger RNA stability and expression of glycolytic enzymes, including enolase 1 (<i>ENO1</i>), pyruvate kinase M1/2 (<i>PKM</i>), and lactate dehydrogenase A (<i>LDHA</i>), thereby increasing lactate production. Accumulated lactate promoted histone H3 lysine 18 lactylation (H3K18la), which enhanced chromatin accessibility at the <i>CD274</i> (encoding PD-L1) promoter and recruited signal transducer and activator of transcription 3 (STAT3) to drive PD-L1 expression, ultimately inhibiting NK cell-mediated cytotoxicity. Clinically, high NSUN2 expression was associated with elevated PD-L1 levels, poor prognosis, and immunotherapy resistance in patients with HCC. In vivo, <i>NSUN2</i> knockout increased NK cell infiltration and suppressed tumor growth, while the STAT3 inhibitor TTI-101 combined with anti-PD-L1 therapy enhanced NK cell cytotoxicity and inhibited HCC progression. <b>Conclusions:</b> Our data demonstrated that NSUN2 drove immune evasion in HCC by coupling m⁵C-dependent glycolytic reprogramming with H3K18la-mediated epigenetic activation of PD-L1. These findings suggest that NSUN2 could represent a critical nexus between m⁵C RNA methylation and immunosuppression, providing a therapeutic rationale for combination immunotherapy in HCC.</p>","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":"46 ","pages":"0043"},"PeriodicalIF":28.4,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactylation of Mutation-Prone RAS Residues Mimics Oncogenic Mutations and Drives Constitutive Activation.","authors":"Ruocen Liao, Chenglong Ma, Xingyu Chen, Longchang Bai, Qianhua Cao, Yu Zhang, Chenfang Dong","doi":"10.34133/cancomm.0047","DOIUrl":"10.34133/cancomm.0047","url":null,"abstract":"<p><p><b>Background:</b> Elevated expression of wild-type RAS contributes to tumorigenesis, yet the mechanisms underlying its mutation-independent hyperactivity remain unclear. Lactylation, a lactate-derived post-translational modification, has emerged as a regulator in cancer, but its role in RAS activation is unknown. Here, we investigated whether lactylation of RAS at specific residues drives its constitutive activation and the underlying mechanisms. <b>Methods:</b> Lactylation sites on RAS were identified by mass spectrometry. A site-specific lactylation system was employed to introduce lactyl-lysine into RAS at K117 and K147. Structural effects were analyzed via molecular dynamics simulations. RAS activity was assessed through GTP-binding and GTPase assays; protein stability was evaluated using ubiquitination mutants and cycloheximide chase. The responsible enzymes were defined by in vitro lactylation and delactylation assays. Functional impact was tested via colony formation, mammosphere assays, and xenograft models. Clinical relevance was examined in breast cancer tissues and survival databases, and drug synergy was assessed by combining lactate-lowering agents with MEK inhibitors. <b>Results:</b> We reported that RAS was lactylated at K117 and K147, 2 residues mutated in cancers. Mechanistically, RAS lactylation was catalyzed by TIP60 and reversed by SIRT2. Lactylation at these residues recapitulated features of oncogenic mutations by disrupting GTP interaction, impairing intrinsic guanosine triphosphatase (GTPase) activity, and competitively antagonizing K48-linked ubiquitination at K147 to stabilize RAS. Functionally, RAS lactylation promoted malignant transformation and tumorigenesis, phenocopying oncogenic mutations at the same sites. Inhibition of lactate production sensitized lactylated RAS-driven cancer cells to drugs targeting RAS mutations, revealing a therapeutic vulnerability. Clinically, RAS lactylation was elevated in breast cancer tissues and correlated with poor prognosis. Employing a site-specific lactylation system, we further confirmed that lactylation alone phenocopied mutation-driven RAS activation. <b>Conclusions:</b> Our study redefines lactylation as a functional \"mutation mimic\" mechanism, which not only recapitulates the effects of oncogenic mutations but also bridges the gap between genetic and epigenetic drivers in cancer. This suggests that targeting the lactylation pathway alone or in combination with mutation-directed therapies represents a promising strategy for treating wild-type RAS-driven cancers.</p>","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":"46 ","pages":"0047"},"PeriodicalIF":28.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13507527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148825412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Epstein-Barr Virus for Cancer Vaccines: Recent Advances and Future Directions.","authors":"Guibin Lin, Zibei Chen, Qian Zhong, Cong Sun, Mu-Sheng Zeng","doi":"10.34133/cancomm.0044","DOIUrl":"10.34133/cancomm.0044","url":null,"abstract":"","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":"46 ","pages":"0044"},"PeriodicalIF":28.4,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13521305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NSUN2 Promotes Cancer Immune Evasion via Its Moonlighting Function Acting on Metabolic Reprogramming.","authors":"Baoxiang Chen, Yanrong Deng, Xiang Zhai, Peiyun Wang, Kunming Lei, Siyuan Yin, Quanjiao Chen, Qun Qian, Jinfang Zhang, Xianghai Ren, Jianhong Zhao, Congqing Jiang","doi":"10.34133/cancomm.0042","DOIUrl":"https://doi.org/10.34133/cancomm.0042","url":null,"abstract":"<p><p><b>Background:</b> Although cancer immunotherapies have revolutionized cancer treatment, a substantial proportion of patients remain unresponsive. Elucidating the molecular mechanisms underlying tumor immune evasion and identifying key regulators are essential for improving immunotherapy efficacy. NOP2/Sun RNA methyltransferase 2 (NSUN2) exhibits widespread mutations across pan-cancer cohorts. This study aimed to delineate the noncanonical functions of NSUN2 in cancer immune modulation and explore its potential as a therapeutic target for cancer immunotherapy. <b>Methods:</b> Multiple cancer cells expressing catalytically inactive NSUN2 mutants were generated and subjected to in vitro functional assays and in vivo studies in immunocompetent mouse models to evaluate their effects on tumor growth and antitumor immunity. Integrative multi-omics analyses, including transcriptomics, metabolomics, and mass spectrometry, were performed to elucidate the molecular mechanisms underlying NSUN2-mediated immune evasion. A proteolysis-targeting chimera (PROTAC) system was developed to achieve targeted degradation of NSUN2, and the clinical relevance of NSUN2 expression in predicting immunotherapy responses was assessed using institutional and public datasets. <b>Results:</b> The enzymatically inactive NSUN2 mutant had minimal effects on tumor cell proliferation in vitro but markedly promoted tumor immune evasion in vivo. Multi-omics analyses revealed that NSUN2 induced metabolic reprogramming and elevated succinate levels, which suppressed cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling in tumor-associated macrophages (TAMs), thereby remodeling the tumor immune microenvironment and promoting M2-like TAM infiltration. Mechanistically, NSUN2 interacted with GATA-binding protein 3 (GATA3) through its methyltransferase domain, relieving GATA3-mediated transcriptional repression of succinate-CoA ligase GDP/ADP-forming subunit α and β genes (SUCLG1 and SUCLG2), leading to succinate accumulation. A newly developed NSUN2-targeting PROTAC demonstrated therapeutic efficacy and safety in combination with cancer immunotherapy. Clinically, low NSUN2 expression was associated with improved immunotherapy responses and survival. <b>Conclusions:</b> Taken together, these findings revealed a noncanonical role of NSUN2 in reshaping the tumor immunosuppressive microenvironment, positioning NSUN2 as a pivotal repressor of cancer immunity and a promising immunotherapeutic target.</p>","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":"46 ","pages":"0042"},"PeriodicalIF":28.4,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13486727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Short-Course Radiotherapy-Based Total Neoadjuvant Therapy plus Tislelizumab for Locally Advanced Rectal Cancer (Neo-STAR): Early Outcomes of a Randomized Phase II Trial.","authors":"Fengpeng Wu, Xuhua Hu, Baokun Li, Jianfeng Zhang, Guanglin Wang, Haiyan Fan, Guangquan An, Bin Yu, Hongqing Ma, Botian Zhao, Zhihan Li, Bo Gao, Ming Liu, Xuan Wang, Dan Liu, Jitao Hu, Hui Liu, Youqiang Liu, Feifei Wang, Juan Zhang, Jun Feng, Xiaoran Wang, Zesong Meng, Zhenya Zhang, Zheng Li, Jingyi Sun, Shihao Liu, Na Wang, Jing Han, Wenbo Niu, Chaoxi Zhou, Linlin Xiao, Guiying Wang","doi":"10.34133/cancomm.0041","DOIUrl":"10.34133/cancomm.0041","url":null,"abstract":"<p><p><b>Background:</b> Short-course radiotherapy (SCRT)-based total neoadjuvant therapy (TNT) is used for locally advanced rectal cancer (LARC). However, the pathological complete response (pCR) rate still hovers around 30%. Radiotherapy and immune checkpoint inhibitors have been shown to exert synergistic anticancer effects. This phase II randomized clinical trial aimed to evaluate the efficacy and safety of SCRT followed by capecitabine plus oxaliplatin (CAPOX) and tislelizumab versus SCRT followed by CAPOX alone in LARC. <b>Methods:</b> Patients initially diagnosed with clinical tumor stage 1 to 2, with node involvement and no distant metastasis (cT_1-2N₊M₀) or clinical tumor stage 3 to 4, with any node status and no distant metastasis (cT_3-4N_anyM₀) rectal adenocarcinoma were randomly assigned to receive SCRT (25 Gy in 5 fractions [25 Gy/5F]), followed by 4 cycles of CAPOX combined with tislelizumab (SCRT-TNT-ICI) or CAPOX alone (SCRT-TNT). After total mesorectal excision, 2 cycles of postoperative chemotherapy were administered according to the patient's preference. The primary end point was the pCR rate, and secondary end points included major pathological response (tumor regression grade 0 or 1), 3-year progression-free survival, 3-year overall survival, and adverse events. <b>Results:</b> Between September 2021 and March 2024, 118 patients were randomized, of whom 111 started the allocated treatment, with 53 and 58 in SCRT-TNT-ICI and SCRT-TNT groups, respectively. Of those, 89 patients had surgical resection, including 45 in the SCRT-TNT-ICI group and 44 in the SCRT-TNT group. The pCR rate was 45.3% (95% confidence interval [CI], 31.5% to 59.8%) in the SCRT-TNT-ICI group compared to 27.6% (95% CI, 16.6% to 40.8%) in the SCRT-TNT group (odds ratio = 2.17; 95% CI, 0.99 to 4.79; <i>P</i> = 0.052). The major pathological response rates were 50.9% (95% CI, 36.6% to 65.2%) and 31.0% (95% CI, 19.5% to 44.6%), respectively (odds ratio = 2.31; 95% CI, 1.06 to 5.01; <i>P</i> = 0.033). During the neoadjuvant treatment period, the incidence of grade 3 to 4 adverse events was comparable between the SCRT-TNT-ICI and SCRT-TNT groups, with anemia being the most common in both groups. <b>Conclusion:</b> This phase II study provides preliminary evidence of promising tumor regression with SCRT-TNT combined with tislelizumab in LARC, warranting further validation in phase III trials. <b>Trial registration:</b> This trial was registered at clinicaltrials.gov (Identifier: NCT05086627).</p>","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":"46 ","pages":"0041"},"PeriodicalIF":28.4,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13392285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148577043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding the Malignant Potential of Hydatidiform Moles through Fibroblast and LAIR2 Signatures.","authors":"Chen Li, Zhiang Chen, Jiandong Chen, Na Yu, Shuai Zhang, Weiguo Lu, Songfa Zhang, Jiale Qin","doi":"10.34133/cancomm.0038","DOIUrl":"10.34133/cancomm.0038","url":null,"abstract":"","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":"46 ","pages":"0038"},"PeriodicalIF":28.4,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13338560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148403591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Excess Weight May Account for More Than 10% of All Cancers: The Underestimated Impact of the Obesity Epidemic.","authors":"Luna Kiran Adhikari, Fatemeh Safizadeh, Marko Mandic, Hermann Brenner","doi":"10.34133/cancomm.0040","DOIUrl":"10.34133/cancomm.0040","url":null,"abstract":"","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":"46 ","pages":"0040"},"PeriodicalIF":28.4,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13324164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148374721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Albumin-Bound Paclitaxel (SYHX2011) in Patients with Advanced Breast Cancer: A Multicenter, Randomized, Double-Blind, Phase III Study.","authors":"Lina Zhang, Jingxuan Wang, Tao Sun, Fanfan Li, Bing Zhao, Guohui Han, Zhongsheng Tong, Hua Yang, Yongmei Yin, Xiangshun Kong, Ying Wang, Jianyun Nie, Lixia Ma, Yongqiang Zhang, Jing Luo, Changping Shan, Jing Yao, Shisheng Tan, Xiaoling Ling, Hongmei Sun, Huihui Li, Li Ma, Tao Zhou, Yunjiang Liu, Yixin Qi, Zhenchuan Song, Yuntao Li, Chao Yang, Tianli Hui, Meiqi Wang, Haoqi Wang, Xi Zhang, Wenhui Zhao, Yanhui Li, Mengmeng Li, Ying Xin, Xuan Luo, Deliang Yin, Hongmei Luo, Huan Liu, Qianyun Lu, Jing Yuan, Qingyuan Zhang, Cuizhi Geng","doi":"10.34133/cancomm.0037","DOIUrl":"10.34133/cancomm.0037","url":null,"abstract":"<p><p><b>Background:</b> SYHX2011 is a novel albumin-bound paclitaxel, in which most nonparticulate human albumin is replaced with mannitol and sucrose. This study aimed to compare SYHX2011 and paclitaxel for injection (albumin-bound) (PAB) in patients with breast cancer. <b>Methods:</b> Patients with histologically or cytologically confirmed unresectable locally advanced or metastatic breast cancer were randomly assigned to receive SYHX2011 (260 mg/m²) or PAB (260 mg/m²) intravenously once every 3 weeks, stratified by prior taxane use and rash history (prior taxane with rash, prior taxane without rash, or no prior taxane), as well prior lines of chemotherapy for advanced disease (0 or ≥1). The primary endpoint was objective response rate assessed by an independent review committee. Noninferiority was to be declared if the lower bound of the 95% confidence interval (CI) for the rate ratio exceeded 0.75; if the lower bound exceeded 1, superiority would subsequently be tested and considered confirmed. <b>Results:</b> In this multicenter, randomized, double-blind, phase III trial across 56 centers in China, 621 patients were screened between 2023 April 23 and 2024 March 21, of whom 459 patients were randomized to SYHX2011 (<i>n</i> = 229) or PAB (<i>n</i> = 230). The confirmed objective response rate assessed by an independent review committee was 35.8% (95% CI 29.4% to 42.6%) for SYHX2011 and 25.8% (95% CI 20.2% to 32.1%) for PAB (rate ratio = 1.38, 95% CI 1.04 to 1.84; one-sided <i>P</i> = 0.012), indicating that SYHX2011 was noninferior to PAB. The superiority of SYHX2011 over PAB was also confirmed. SYHX2011 showed a lower incidence of rash compared with PAB during the first 2 administration cycles (13.6% vs. 34.3%) and all treatment cycles (16.2% vs. 42.6%). Treatment-related adverse events (TRAEs) occurred in 98.2% of patients receiving SYHX2011 and 98.3% of patients receiving PAB. In the SYHX2011 group, 111 (48.7%) patients experienced grade ≥3 TRAEs, compared with 101 (43.9%) patients in the PAB group. The most common grade ≥3 TRAEs were neutropenia, leukopenia, and peripheral sensory neuropathy. The median investigational drug reconstitution time was 2.0 min for SYHX2011 and 11.0 min for PAB. <b>Conclusions:</b> SYHX2011 demonstrated greater therapeutic benefits than PAB and significantly reduced the incidence of rash. Additionally, it could offer greater convenience in clinical application, providing advanced breast cancer patients with more effective and safer treatment options. <b>Trial registration:</b> ClinicalTrials.gov identifier: NCT05753865. Date of registration: 2023 February 22.</p>","PeriodicalId":9495,"journal":{"name":"Cancer Communications","volume":"46 ","pages":"0037"},"PeriodicalIF":28.4,"publicationDate":"2026-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13305025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148343940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}