Cancer Science最新文献

{"title":"Expression of the CXCR4 S338X Variant Improves Anti-Leukemia Efficacy of Anti-CD19 CAR-T Cells","authors":"Yushu Mao,&nbsp;Xiaodan Wang,&nbsp;Chun-Hui Jin,&nbsp;Zhifeng Wei,&nbsp;Qinghao Ding,&nbsp;Ke-Ke Zhang,&nbsp;Bo-Wen Dong,&nbsp;Kai-Wen Zheng,&nbsp;Yufei Hou,&nbsp;Tao Zhang,&nbsp;Wen-Jie Zhao,&nbsp;Zheng Hu,&nbsp;Yong-Guang Yang","doi":"10.1111/cas.70313","DOIUrl":"10.1111/cas.70313","url":null,"abstract":"<p>Chimeric antigen receptor T (CAR-T) cell therapy has demonstrated remarkable success in treating hematological malignancies; however, antigen-positive relapse remains a significant obstacle to achieving sustained remission in B-cell acute lymphoblastic leukemia (B-ALL). To enhance the therapeutic efficacy of anti-CD19 CAR (CAR19)-T cells, we overexpressed CXCR4 in CAR19-T cells to improve their trafficking to bone marrow (BM), a key sanctuary for minimal residual disease. We engineered CAR19-T cells with overexpression of wild-type CXCR4 (CAR19/CXCR4^WT-T) or gain-of-function CXCR4 S338X mutant (CAR19/CXCR4^S338X-T). Both CAR19/CXCR4^WT-T and CAR19/CXCR4^S338X-T cells exhibited enhanced CXCR4 surface expression in vitro and in vivo compared to control CAR19-T cells, with the latter showing significantly superior improvements under all tested conditions, including engagement with CAR-specific antigens or CXCR4 ligand CXCL12. Upon engagement with CXCL12, CAR19/CXCR4^S338X-T cells, but not CAR19/CXCR4^WT-T cells, displayed significantly increased activation of ERK1/2 and AKT signaling pathways, as well as elevated transcription of TNF-α, IFN-γ, granzyme B, CDK6, and BCL2A1, along with strengthened effector functions, chemotaxis, and activation of anti-apoptotic pathways. Furthermore, CAR19/CXCR4^S338X-T cells demonstrated significantly improved migration to and retention in the BM accompanied by increased CD45RA⁺CCR7⁺ memory T cell populations, which correlated with enhanced anti-leukemic effects following injection into B-ALL-bearing mice. This study offers a potentially effective strategy to improve the functionality and durability of CAR-T cell responses in hematological malignancies.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 3","pages":"613-630"},"PeriodicalIF":4.3,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12951118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145858776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol as a Novel YAP Inhibitor Targeting Glioblastoma Progression and Sensitizing to Chemotherapy","authors":"Wannawat Khotchawan,&nbsp;Chanchao Lorthongpanich,&nbsp;Pakpoom Kheolamai,&nbsp;Sith Sathornsumetee,&nbsp;Surapol Issaragrisil","doi":"10.1111/cas.70317","DOIUrl":"10.1111/cas.70317","url":null,"abstract":"<p>Dysregulation of YAP, the terminal effector of the Hippo pathway, contributes to cancer progression and drug resistance. Its role in glioblastoma (GBM), the most aggressive brain cancer, remains incompletely understood. Single-cell RNA sequencing data from a published GBM dataset were reanalyzed to assess YAP expression across cell populations. YAP was silenced via shRNA in GBM cell lines (U-251 MG, U-87 MG) and patient-derived GBM cells. Resveratrol (RV), a natural blood–brain barrier–permeable compound, was evaluated for growth inhibition and YAP-targeted effects. Functional assays measured proliferation, spheroid formation, migration, invasion, and drug sensitivity. YAP and its cofactor TEAD were highly upregulated in GBM cells compared with normal brain and stromal cells. YAP depletion by shRNA suppressed proliferation, spheroid formation, migration, and invasion. RV treatment similarly inhibited YAP expression, reducing proliferation and viability in monolayer and 3D spheroid cultures, and impairing migration and invasion via epithelial–mesenchymal transition (EMT) inhibition. RV-mediated YAP suppression also enhanced sensitivity to temozolomide (TMZ) and carmustine (BCNU), increasing their cytotoxicity in GBM cells. RV acts as a novel YAP inhibitor in GBM, impairing malignant phenotypes and potentiating the effects of standard chemotherapy. These findings support RV as a potential adjunct in YAP-targeted GBM therapy, warranting further in vivo validation for clinical translation.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 3","pages":"695-710"},"PeriodicalIF":4.3,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12951108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145946669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SUSD2 Promotes Metastasis and Primary Tumor Growth in Pancreatic Cancer Cells via Integrin–FAK Signaling Activation","authors":"Junjiro Yoshida,&nbsp;Tomokazu Ohishi,&nbsp;Isao Momose,&nbsp;Shun-ichi Ohba,&nbsp;Kyohei Kurosawa,&nbsp;Akiko Harakawa,&nbsp;Hiroyuki Inoue,&nbsp;Minori Senoo,&nbsp;Daisuke Tatsuda,&nbsp;Hikaru Abe,&nbsp;Atsushi Masamune,&nbsp;Manabu Kawada","doi":"10.1111/cas.70318","DOIUrl":"10.1111/cas.70318","url":null,"abstract":"<p>Tumor tissues in pancreatic cancer develop with abundant cancer-associated fibroblasts (CAFs), promoting tumor progression. CAF-conditioned medium induces the expression of sushi domain-containing 2 (SUSD2) and enhances the invasive potential of pancreatic cancer cells. We showed that SUSD2 binds to integrin β1 and promotes pancreatic cancer cell motility by inducing phosphorylation of focal adhesion kinase (FAK), facilitating the formation of focal adhesion complexes in cells adhered to collagen 1 or fibronectin. Orthotopic transplantation of SUSD2-overexpressing human pancreatic cancer cell lines into the mouse pancreas enhanced liver metastasis in Panc-1 cells, whereas in KP2 cells, it increased primary tumor growth without promoting metastasis. In spheroid cultures of KP2 cells, forced SUSD2 expression elevated FAK phosphorylation independently of cell adhesion, suggesting that SUSD2 promotes cell proliferation even in non-metastatic cells. High SUSD2 expression in cancer cells contributes to tumor growth and metastasis, identifying SUSD2 as a potential therapeutic target in pancreatic cancer.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 3","pages":"711-726"},"PeriodicalIF":4.3,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12951126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145946653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-Cell and Multiomic Analysis Reveals Neutrophil Heterogeneity and Prognostic Value in Cervical Lesions","authors":"Ze Wang,&nbsp;Liang Zhuang,&nbsp;Shiyi Liu,&nbsp;Canhui Cao,&nbsp;Shimin Chen,&nbsp;Nan Yu,&nbsp;Xiaoyuan Huang,&nbsp;Tao Zhang","doi":"10.1111/cas.70294","DOIUrl":"10.1111/cas.70294","url":null,"abstract":"<p>Cervical cancer is a prevalent malignancy among women, yet the involvement of neutrophils in its tumor microenvironment remains insufficiently explored. This study utilized single-cell RNA sequencing (scRNA-seq) to delineate neutrophil subsets and elucidate their roles in disease progression and prognosis. Analysis of 20 cervical biopsy samples across different disease stages identified five neutrophil subsets (N0–N4), among which the N4 subset exhibited a marked increase during disease advancement. Spatial transcriptomics and tissue microarray analyses revealed that N4 neutrophils are enriched in tumor regions and are associated with genes implicated in proliferation, metastasis, and immune evasion. Functional characterization demonstrated that N4 promotes tumor progression via activation of the Wnt signaling pathway and extracellular matrix remodeling. A neutrophil infiltration-based risk model was established and validated through multi-omics approaches, highlighting its potential in prognostic prediction. These findings underscore the pivotal role of N4 neutrophils in cervical cancer and provide valuable insights for the development of targeted immunotherapies and personalized treatment strategies.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 3","pages":"597-612"},"PeriodicalIF":4.3,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12951127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Perioperative Nivolumab in Resectable Non-Small Cell Lung Cancer: A Subanalysis of Japanese Patients From CheckMate 77T","authors":"Fumihiro Tanaka,&nbsp;Yasutaka Watanabe,&nbsp;Shunichi Sugawara,&nbsp;Jiro Okami,&nbsp;Satoshi Muto,&nbsp;Morihito Okada,&nbsp;Yoshitsugu Horio,&nbsp;Masahiro Tsuboi,&nbsp;Yuki Sato,&nbsp;Kazuya Takamochi,&nbsp;Hidehito Horinouchi,&nbsp;Yuichi Tambo,&nbsp;Masahiro Seike,&nbsp;Kyoichi Okishio,&nbsp;Cinthya Coronado Erdmann,&nbsp;Padma Sathyanarayana,&nbsp;Stephanie Meadows-Shropshire,&nbsp;Hiroyuki Ito","doi":"10.1111/cas.70300","DOIUrl":"10.1111/cas.70300","url":null,"abstract":"<p>In the randomized phase III CheckMate 77T study, perioperative nivolumab showed statistically significant and clinically meaningful improvement in event-free survival (EFS) vs. placebo in patients with resectable, non-metastatic non-small cell lung cancer (NSCLC). Here, we report efficacy and safety outcomes in the Japanese subpopulation. Adults with resectable stage IIA–IIIB NSCLC were randomized 1:1 to neoadjuvant nivolumab plus chemotherapy or chemotherapy plus placebo every 3 weeks for ≤ 4 cycles, followed by surgery and adjuvant nivolumab or placebo every 4 weeks for ≤ 13 cycles. Assessments included EFS (primary endpoint), pathological complete response (pCR), major pathological response (MPR), and safety. A total of 68 Japanese patients were randomized to perioperative nivolumab (<i>n</i> = 40) or placebo (<i>n</i> = 28). At 24.9 months' median follow-up, median EFS was not reached (NR; 95% CI: 21.4–NR) with perioperative nivolumab vs. 12.1 (95% CI: 8.1–NR) months with placebo (hazard ratio, 0.46 [95% CI: 0.22–0.95]); 18-month EFS rates were 76.6% vs. 42.9%, respectively. The pCR rate (95% CI) was 42.5% (27.0%–59.1%) with perioperative nivolumab vs. 0% (0%–12.3%) with placebo (odds ratio [OR], not available); MPR rate (95% CI) was 52.5% (36.1%–68.5%) vs. 7.1% (0.9%–23.5%), respectively (OR, 14.37; 95% CI: 3.00–68.82). Grade 3–4 treatment-related and surgery-related adverse events with perioperative nivolumab vs. placebo occurred in 55.0% vs. 39.3% and 16.7% vs. 19.2% of patients. Consistent with the global population, perioperative nivolumab improved EFS, pCR, and MPR vs. placebo in the Japanese subpopulation, with no new safety signals reported, supporting its use in Japanese patients with resectable NSCLC.</p><p>Trial Registration: ClinicalTrials.gov identifier, NCT04025879</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 3","pages":"759-768"},"PeriodicalIF":4.3,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12951114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145811930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hippo Pathway Drives Durable Non-Cell-Autonomous Ferroptosis Resistance in Lung Cancer","authors":"Mohamed Fathi Saleh,&nbsp;Akihiro Nita,&nbsp;Yudai Ohta,&nbsp;Aya Kobayashi,&nbsp;Hao Li,&nbsp;Yasuhisa Sakamoto,&nbsp;Toshiro Moroishi","doi":"10.1111/cas.70299","DOIUrl":"10.1111/cas.70299","url":null,"abstract":"<p>The Hippo pathway effector Yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) play a critical role in promoting lung cancer progression, but paradoxically increase tumor cell sensitivity to ferroptosis, a form of lipid peroxidation-driven cell death. The mechanism through which YAP/TAZ-high cells evade ferroptosis during cancer progression remains unclear. Here, we showed that YAP/TAZ-low lung cancer cells confer durable ferroptosis resistance to neighboring YAP/TAZ-high cells through a non-cell-autonomous mechanism. Using murine lung carcinoma cell coculture models, we demonstrated that transient exposure to YAP/TAZ-deficient cells induces a stable, contact-independent ferroptosis-resistant state in wild-type (WT) cells, enhancing their metastatic seeding capacity in vivo. This adaptation is mediated by the upregulation of <i>Gch1</i>, which encodes GTP cyclohydrolase 1 and suppresses ferroptosis via the synthesis of the antioxidant metabolite tetrahydrobiopterin (BH4). GCH1 overexpression alone was sufficient to confer ferroptosis resistance in WT cells, whereas conditioned medium from YAP/TAZ-deficient cells replicated this effect, indicating that a soluble factor is involved in <i>Gch1</i> induction. Importantly, the genetic deletion of <i>Gch1</i> in YAP/TAZ-deficient cells abolished their ability to protect WT cells, confirming its essential role in this intercellular program. Our findings revealed a Hippo pathway-linked ferroptosis resistance mechanism and suggested that intra-tumoral heterogeneity in YAP/TAZ activity promotes metastatic fitness by enabling the survival of ferroptosis-prone cells via antioxidant signaling.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 3","pages":"683-694"},"PeriodicalIF":4.3,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12951101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145811968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reviewers","authors":"","doi":"10.1111/cas.70314","DOIUrl":"https://doi.org/10.1111/cas.70314","url":null,"abstract":"&lt;p&gt;The publication of invaluable papers in Cancer Science depends on the prompt, careful review of submitted manuscripts. We would like to thank the following experts for reviewing manuscripts submitted between October 1, 2024 to September 30, 2025.&lt;/p&gt;&lt;p&gt;Hiroyuki Abe&lt;/p&gt;&lt;p&gt;Tatsuya Abe&lt;/p&gt;&lt;p&gt;Toshiya Abe&lt;/p&gt;&lt;p&gt;Jun Adachi&lt;/p&gt;&lt;p&gt;Shungo Adachi&lt;/p&gt;&lt;p&gt;Ahmad Adawy&lt;/p&gt;&lt;p&gt;Hisaki Aiba&lt;/p&gt;&lt;p&gt;Masahiko Ajiro&lt;/p&gt;&lt;p&gt;Shusuke Akamatsu&lt;/p&gt;&lt;p&gt;Yoshiki Akatsuka&lt;/p&gt;&lt;p&gt;Jun Akiba&lt;/p&gt;&lt;p&gt;Hirofumi Akita&lt;/p&gt;&lt;p&gt;Toru Akiyama&lt;/p&gt;&lt;p&gt;Yoshimitsu Akiyama&lt;/p&gt;&lt;p&gt;Joseph Amankwaah&lt;/p&gt;&lt;p&gt;Takahiro Ando&lt;/p&gt;&lt;p&gt;Samuel Antwi&lt;/p&gt;&lt;p&gt;Kosuke Aoki&lt;/p&gt;&lt;p&gt;Shigeki Aoki&lt;/p&gt;&lt;p&gt;Shuichi Aoki&lt;/p&gt;&lt;p&gt;Seiji Arai&lt;/p&gt;&lt;p&gt;Hisashi Arase&lt;/p&gt;&lt;p&gt;Tomohiro Arita&lt;/p&gt;&lt;p&gt;Yuki Arita&lt;/p&gt;&lt;p&gt;Ken Asada&lt;/p&gt;&lt;p&gt;Shuhei Asada&lt;/p&gt;&lt;p&gt;Ryutaro Asano&lt;/p&gt;&lt;p&gt;Kotaro Azuma&lt;/p&gt;&lt;p&gt;Masaya Baba&lt;/p&gt;&lt;p&gt;Tsukasa Baba&lt;/p&gt;&lt;p&gt;Hiroko Bando&lt;/p&gt;&lt;p&gt;Narikazu Boku&lt;/p&gt;&lt;p&gt;Eric Bouffet&lt;/p&gt;&lt;p&gt;Horacio Cabral&lt;/p&gt;&lt;p&gt;Junchao Cai&lt;/p&gt;&lt;p&gt;Kun Cai&lt;/p&gt;&lt;p&gt;Luis G. Carvajal-Carmona&lt;/p&gt;&lt;p&gt;Peter H. Cashin&lt;/p&gt;&lt;p&gt;Natsuko Chiba&lt;/p&gt;&lt;p&gt;Shigeru Chiba&lt;/p&gt;&lt;p&gt;Tatsuyuki Chiyoda&lt;/p&gt;&lt;p&gt;Roberto Coppo&lt;/p&gt;&lt;p&gt;Adam P. Cribbs&lt;/p&gt;&lt;p&gt;Kaisa Cui&lt;/p&gt;&lt;p&gt;Haruko Daga&lt;/p&gt;&lt;p&gt;Shipeng Dai&lt;/p&gt;&lt;p&gt;Shingo Dan&lt;/p&gt;&lt;p&gt;Dajun Deng&lt;/p&gt;&lt;p&gt;Hidetoshi Eguchi&lt;/p&gt;&lt;p&gt;Mariko Eguchi&lt;/p&gt;&lt;p&gt;Shogo Ehata&lt;/p&gt;&lt;p&gt;Itaru Endo&lt;/p&gt;&lt;p&gt;Makoto Endo&lt;/p&gt;&lt;p&gt;Motoyoshi Endo&lt;/p&gt;&lt;p&gt;Tomohiro Enokida&lt;/p&gt;&lt;p&gt;Vincent Fradet&lt;/p&gt;&lt;p&gt;Juan Fueyo&lt;/p&gt;&lt;p&gt;Shigeo Fuji&lt;/p&gt;&lt;p&gt;Hiroyuki Fujii&lt;/p&gt;&lt;p&gt;Satoshi Fujii&lt;/p&gt;&lt;p&gt;Shin-Ichiro Fujii&lt;/p&gt;&lt;p&gt;Ayumi Fujimoto&lt;/p&gt;&lt;p&gt;Daichi Fujimoto&lt;/p&gt;&lt;p&gt;Atsushi Fujimura&lt;/p&gt;&lt;p&gt;Takao Fujisawa&lt;/p&gt;&lt;p&gt;Teruaki Fujishita&lt;/p&gt;&lt;p&gt;Hiroaki Fujita&lt;/p&gt;&lt;p&gt;Kazutoshi Fujita&lt;/p&gt;&lt;p&gt;Yukio Fujiwara&lt;/p&gt;&lt;p&gt;Yutaka Fujiwara&lt;/p&gt;&lt;p&gt;Tomohiko Fukuda&lt;/p&gt;&lt;p&gt;Keisuke Fukui&lt;/p&gt;&lt;p&gt;Manabu Fukumoto&lt;/p&gt;&lt;p&gt;Hiroshi Fukushima&lt;/p&gt;&lt;p&gt;Itoh Fumiko&lt;/p&gt;&lt;p&gt;Shinsuke Funakoshi&lt;/p&gt;&lt;p&gt;Yuji Funakoshi&lt;/p&gt;&lt;p&gt;Chikako Funasaka&lt;/p&gt;&lt;p&gt;Michinori Funato&lt;/p&gt;&lt;p&gt;Kyoji Furukawa&lt;/p&gt;&lt;p&gt;Tatsuhiko Furukawa&lt;/p&gt;&lt;p&gt;Toru Furukawa&lt;/p&gt;&lt;p&gt;Mitsuru Futakuchi&lt;/p&gt;&lt;p&gt;Morteza Gholami&lt;/p&gt;&lt;p&gt;John Glod&lt;/p&gt;&lt;p&gt;Akiteru Goto&lt;/p&gt;&lt;p&gt;Hidemasa Goto&lt;/p&gt;&lt;p&gt;Osamu Gotoh&lt;/p&gt;&lt;p&gt;Jichun Gu&lt;/p&gt;&lt;p&gt;Shashi Gujar&lt;/p&gt;&lt;p&gt;Haochen Guo&lt;/p&gt;&lt;p&gt;Zhen Guo&lt;/p&gt;&lt;p&gt;Zhongliang Guo&lt;/p&gt;&lt;p&gt;Hiroshi Haeno&lt;/p&gt;&lt;p&gt;Yoshimi Haga&lt;/p&gt;&lt;p&gt;Shotaro Hagiwara&lt;/p&gt;&lt;p&gt;Akinobu Hamada&lt;/p&gt;&lt;p&gt;Yasuo Hamamoto&lt;/p&gt;&lt;p&gt;Junzo Hamanishi&lt;/p&gt;&lt;p&gt;Hirofumi Hanaoka&lt;/p&gt;&lt;p&gt;Rikinari Hanayama&lt;/p&gt;&lt;p&gt;Hiroshi Handa&lt;/p&gt;&lt;p&gt;Masatoshi Hara&lt;/p&gt;&lt;p&gt;Tomoaki Hara&lt;/p&gt;&lt;p&gt;Hiroshi Harada&lt;/p&gt;&lt;p&gt;Yohei Harada&lt;/p&gt;&lt;p&gt;Daigo Hashimoto&lt;/p&gt;&lt;p&gt;Itaru Hashimoto&lt;/p&gt;&lt;p&gt;Naoya Hashimoto&lt;/p&gt;&lt;p&gt;Shinichi Hashimoto&lt;/p&gt;&lt;p&gt;Taiki Hashimoto&lt;/p&gt;&lt;p&gt;Hisashi Hasumi&lt;/p&gt;&lt;p&gt;Kenji Hata&lt;/p&gt;&lt;p&gt;Shigetsugu Hatakeyama&lt;/p&gt;&lt;p&gt;Shingo Hatakeyama&lt;/p&gt;&lt;p&gt;Koji Hatano&lt;/p&gt;&lt;p&gt;Yoshihiro Hatta&lt;/p&gt;&lt;p&gt;Kazuki Hattori&lt;/p&gt;&lt;p&gt;Naoko Hattori&lt;/p&gt;&lt;p&gt;Fumihiko Hayakawa&lt;/p&gt;&lt;p&gt;Yoku Hayakawa&lt;/p&gt;&lt;p&gt;Shinya Hayami&lt;/p&gt;&lt;p&gt;Koichi Hayano&lt;/p&gt;&lt;p&gt;Hidetoshi Hayashi&lt;/p&gt;&lt;p&gt;Hideyuki Hayashi&lt;/p&gt;&lt;p&gt;Takuo Hayashi&lt;/p&gt;&lt;p&gt;Tsutomu Hayashi&lt;/p&gt;&lt;p&gt;Yoshihiro Hayashi&lt;/p&gt;&lt;p&gt;Eva Hernando&lt;/p&gt;&lt;p&gt;Zoltan Herold&lt;/p&gt;&lt;p&gt;Yoichi Hiasa&lt;/p&gt;&lt;p&gt;Susumu Hijioka&lt;/p&gt;&lt;p&gt;Hayato Hikita&lt;/p&gt;&lt;p&gt;Susumu Hirabayashi&lt;/p&gt;&lt;p&gt;","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 1","pages":"275-279"},"PeriodicalIF":4.3,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70314","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145915818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Mitochondrial Dynamics as a Pathobiological Mediator of Clonal Myeloid Disorders”","authors":"","doi":"10.1111/cas.70295","DOIUrl":"10.1111/cas.70295","url":null,"abstract":"<p>Hayashi Y, Harada H. Mitochondrial Dynamics as a Pathobiological Mediator of Clonal Myeloid Disorders. <i>Cancer Sci</i>. 2023; 114: 2722-2728. doi: 10.1111/cas.15810.</p><p>We apologize for this error.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145688473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MASTL Promotes Hepatocellular Carcinoma Progression and Paclitaxel Resistance Through Mitotic Catastrophe","authors":"Ke Wang,&nbsp;Ziwei Fu,&nbsp;Chuan Xiong,&nbsp;Jing Zhang,&nbsp;Qiang Luo","doi":"10.1111/cas.70287","DOIUrl":"10.1111/cas.70287","url":null,"abstract":"<p>Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with limited therapeutic options. Microtubule-associated serine/threonine kinase-like (<i>MASTL</i>), a pivotal regulator of mitosis, remains poorly characterized in HCC. This study aimed to elucidate the clinical significance, biological functions, and molecular mechanisms of <i>MASTL</i> in HCC progression. Bioinformatics analysis of TCGA and ICGC datasets revealed <i>MASTL</i> overexpression correlated with advanced tumor stage and served as an independent prognostic factor. Functional studies demonstrated that <i>MASTL</i> knockdown significantly disrupts HCC cell proliferation, increases the incidence of abnormal mitotic events, and amplifies DNA damage, collectively driving mitotic catastrophe (MC) and subsequent cell death. Mechanistically, MASTL regulated paclitaxel sensitivity by modulating ENSA phosphorylation and PP2A-B55α activity, with PP2A-B55α knockdown reversing MASTL deficiency-induced MC. Transcriptional regulation analysis identified E2F1 as a direct activator of <i>MASTL</i> expression, confirmed by ChIP-qPCR and dual-luciferase reporter assays. These findings establish <i>MASTL</i> as a critical oncogene in HCC through the E2F1-MASTL-PP2A-B55α axis, suggesting its potential as both a prognostic biomarker and therapeutic target for HCC. Future studies should explore MASTL inhibitors in combination with conventional chemotherapy to overcome drug resistance in HCC patients.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":"377-392"},"PeriodicalIF":4.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145678957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effectiveness and Safety of Radium-223 for Bone-Metastatic Castration-Resistant Prostate Cancer: The KYUCOG-1901 Study","authors":"Masaki Shiota,&nbsp;Shuichi Tatarano,&nbsp;Tomomi Kamba,&nbsp;Toshiyuki Kamoto,&nbsp;Tsukasa Igawa,&nbsp;Naoya Masumori,&nbsp;Hirotsugu Uemura,&nbsp;Kensuke Mitsunari,&nbsp;Takayuki Sumiyoshi,&nbsp;Hiroji Uemura,&nbsp;Katsuyoshi Higashijima,&nbsp;Shoji Tokunaga,&nbsp;Masatoshi Eto","doi":"10.1111/cas.70293","DOIUrl":"10.1111/cas.70293","url":null,"abstract":"<p>Radium-223 dichloride (Ra-223) improves survival in bone-metastatic castration-resistant prostate cancer (mCRPC). However, prospective real-world data are limited, particularly regarding treatment outcomes, predictors of completing six cycles, and integration with subsequent therapies. The KYUCOG-1901 study was a prospective multicenter observational study at 19 Japanese institutions. Patients with mCRPC and ≥ 2 bone metastases received up to six cycles of Ra-223. Effectiveness was assessed by PSA, alkaline phosphatase (ALP), time to visceral metastasis, time to cytotoxic chemotherapy, radiographic progression-free survival (PFS), and overall survival (OS). Safety was evaluated using CTCAE v5.0. Of 101 enrolled, 93 patients were analyzed. Median follow-up was 25.2 months. Early discontinuation was associated with high baseline PSA, ALP, LDH, and symptomatic disease. Subsequent therapies, including taxanes and androgen receptor signaling inhibitors (ARSIs), were administered in most patients. Maximum PSA and ALP declines of ≥ 30% were achieved in 16 (17.2%) and 39 (41.9%) patients, respectively. Median time to visceral metastasis, time to cytotoxic chemotherapy, radiographic PFS (rPFS), and OS were 32.9, 13.7, 8.8, and 23.0 months, respectively. Grade ≥ 3 adverse events occurred in 36.5%. No treatment-related deaths were reported. Ra-223 was effective and well tolerated in Japanese mCRPC patients. Early initiation in less symptomatic patients with lower disease burden may maximize benefit, and integration with subsequent therapies appears feasible.</p><p><b>Trial Registration:</b> University Hospital Medical Information Network Clinical Trials Registry UMIN000040358</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"117 2","pages":"501-510"},"PeriodicalIF":4.3,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12861091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145679050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}