Cancer Science最新文献

{"title":"Permeable Lung Vasculature Creates Chemoresistant Endothelial Niche by Producing SERPINE1 at Breast Cancer Metastatic Sites","authors":"Tsunaki Hongu,&nbsp; Sarenqiqige,&nbsp; Shandan,&nbsp;Hirokazu Kusunoki,&nbsp;Akihiko Ishimura,&nbsp;Takeshi Suzuki,&nbsp;Thordur Oskarsson,&nbsp;Noriko Gotoh","doi":"10.1111/cas.70050","DOIUrl":"10.1111/cas.70050","url":null,"abstract":"<p>Chemotherapy resistance remains a major obstacle for eradicating metastatic cancer cells in distant organs. We identified that endothelial cells (ECs) in the lungs, where breast cancer cells often metastasize, form a chemoresistant perivascular niche for disseminated breast cancer cells. By investigating the lung EC secretome activated by metastasis, we found that serine protease inhibitor family E member 1 (SERPINE1), encoded by <i>Serpine1</i>, is upregulated in metastasis-associated lung ECs. This upregulation shields cancer cells from paclitaxel-induced apoptosis and promotes cancer stem cell properties. <i>Serpine1</i> expression appears to be driven by YAP-TEAD activation in lung ECs that lose cell–cell contact, a phenomenon associated with increased vascular permeability in lungs affected by metastasis. Crucially, pharmacological inhibition of SERPINE1 enhances the chemotherapy sensitivity of metastatic breast cancer cells in the lung. Overall, our findings underscore the pivotal role of the vascular niche, which produces SERPINE1, in conferring chemoresistance to breast cancer cells during metastatic progression in the lungs.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 6","pages":"1604-1615"},"PeriodicalIF":4.5,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70050","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144041247","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":"Association of Intratumoral Bacterial Abundance With Lung Cancer Prognosis in Chiba University Hospital Cohort","authors":"Takahiro Ochi,&nbsp;Ryoji Fujiki,&nbsp;Masaki Fukuyo,&nbsp;Bahityar Rahmutulla,&nbsp;Takuya Nakagawa,&nbsp;Masayuki Ota,&nbsp;Jun-ichiro Ikeda,&nbsp;Yukiko Matsui,&nbsp;Ichiro Yoshino,&nbsp;Hidemi Suzuki,&nbsp;Atsushi Kaneda","doi":"10.1111/cas.70080","DOIUrl":"10.1111/cas.70080","url":null,"abstract":"<p>The relationship between cancer prognosis and intratumoral microbiome has recently gained attention. Regarding lung cancer, most studies have focused on bacteria outside tumors, such as sputum or lavage fluid, with few examining intratumoral bacteria and their impact on prognosis. In this study, we extracted DNA from lung tumor samples of 507 patients undergoing surgery at Chiba University Hospital and quantified intratumoral bacterial abundance using bacteria-specific PCR primers. Bacteria were detected in 77.1% of cases, and bacterial abundance was significantly higher in lung adenocarcinoma than in squamous cell carcinoma. Patients were categorized into three groups (High, Low, and Very-Low) based on bacterial abundance, and associations with clinicopathological factors were analyzed. In lung squamous cell carcinoma, higher bacterial abundance was significantly associated with worse recurrent-free survival and overall survival and was found to be a poor prognostic factor independent of pathological tumor stage. In conclusion, intratumoral bacterial abundance was found in the majority of lung cancer tissues, with variations based on pathology. This abundance may serve as a useful marker for stratifying lung squamous cell carcinoma with distinct prognoses.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 7","pages":"2040-2046"},"PeriodicalIF":4.5,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70080","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043328","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":"First-Line Genomic Profiling in Previously Untreated Advanced Solid Tumors: 1-Year Follow-Up of the FIRST-Dx Study","authors":"Junichi Matsubara,&nbsp;Kumi Mukai,&nbsp;Tomohiro Kondo,&nbsp;Masahiro Yoshioka,&nbsp;Hidenori Kage,&nbsp;Katsutoshi Oda,&nbsp;Sadakatsu Ikeda,&nbsp;Hiromichi Ebi,&nbsp;Kei Muro,&nbsp;Shinya Kajiura,&nbsp;Ryuji Hayashi,&nbsp;Reiko Ashida,&nbsp;Masayuki Kitano,&nbsp;Manabu Muto","doi":"10.1111/cas.70077","DOIUrl":"10.1111/cas.70077","url":null,"abstract":"<p>The FIRST-Dx study prospectively evaluated the clinical utility of the comprehensive genomic profiling (CGP) test (FoundationOne CDx) in the first-line setting for patients with chemotherapy-naïve advanced solid tumors (gastrointestinal, biliary, pancreatic, lung, breast, gynecologic, melanoma) in six hospitals in Japan. Here, we report the results of the 1-year interim analysis of the follow-up study about the clinical benefits provided by the upfront CGP test. The primary endpoint was overall survival (OS), and secondary endpoints were the proportion of patients who actually received molecular-based recommended therapy (MBRT) determined by the molecular tumor board, best overall response rate (ORR) in each line of therapy, and progression-free survival (PFS) ratio (PFS on MBRT/PFS on the first-line therapy). Data from 172 patients with a median follow-up of 15.1 months (range: 0.1–21.5 months) were available. The median OS was not reached. Thirty-nine patients (22.7%) received MBRT during this follow-up period. ORR in first-line therapy was 56.3% in the MBRT group (<i>n</i> = 16) vs. 42.3% in the non-MBRT group (<i>n</i> = 137), and in the second-line was 26.3% in the MBRT group (<i>n</i> = 19) vs. 17.1% in the non-MBRT group (<i>n</i> = 82). Regarding the PFS ratio of second-line MBRT (<i>n</i> = 12), the median PFS ratio was 1.1, and four patients (33.3%) had a ratio ≥ 1.3, indicating that MBRT might be effective in changing the clinical outcome. The findings of this study imply that CGP testing before the standard of care for patients with advanced solid tumors could prove to be a clinically beneficial strategy for guiding subsequent precision anticancer treatments.</p><p><b>Trial Registration:</b> Japan Registry of Clinical Trials (jRCT) ID: jRCT1050220041</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 7","pages":"1908-1919"},"PeriodicalIF":4.5,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70077","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144056520","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":"Novel TEAD1 Inhibitor VT103 Enhances Dabrafenib Efficacy in BRAF V600E Mutated Lung Adenocarcinoma via Survivin Downregulation","authors":"Kazutaka Hosoya,&nbsp;Hiroaki Ozasa,&nbsp;Hironori Yoshida,&nbsp;Hitomi Ajimizu,&nbsp;Takahiro Tsuji,&nbsp;Masatoshi Yamazoe,&nbsp;Tatsuya Ogimoto,&nbsp;Kentaro Hashimoto,&nbsp;Tomoko Funazo (Yamamoto),&nbsp;Keiichiro Suminaga,&nbsp;Yusuke Shima,&nbsp;Hiroshi Yoshida,&nbsp;Takashi Nomizo,&nbsp;Hiroaki Ito,&nbsp;Kazuhiro Terada,&nbsp;Shigeto Nishikawa,&nbsp;Toshi Menju,&nbsp;Akihiko Yoshizawa,&nbsp;Hiroshi Date,&nbsp;Toyohiro Hirai","doi":"10.1111/cas.70075","DOIUrl":"10.1111/cas.70075","url":null,"abstract":"<p>The <i>BRAF</i> V600E mutation is observed in 2% of the patients with lung adenocarcinoma (LUAD), and combination therapy targeting BRAF and mitogen-activated protein kinase (MEK) is the standard treatment for this population. However, acquired resistance inevitably develops, which highlights the need for novel therapeutic strategies. In this study, we established a patient-derived <i>BRAF</i> V600E-mutated LUAD cell line, KTOR81, and investigated the potential of targeting the Yes-associated protein 1 (YAP1)/transcriptional enhanced associate domain 1 (TEAD1) pathway in combination with BRAF inhibition. We observed that the novel TEAD1 inhibitor VT103 enhanced the efficacy of the BRAF inhibitor dabrafenib in KTOR81 cells and xenograft models. The combination of dabrafenib and VT103 downregulated the expression of the antiapoptotic protein survivin, which is transcriptionally regulated by the YAP1/TEAD1 complex, leading to increased apoptosis. Moreover, we used a LUAD tissue microarray to compare the staining patterns of YAP1, TEAD1, and survivin, and examined their association with prognosis. These analyses revealed a strong correlation between YAP1, TEAD1, and survivin expression in LUAD, suggesting the relevance of the YAP1/TEAD1-survivin axis beyond <i>BRAF</i> V600E-mutated cases. While no statistically significant association was observed between survivin expression and prognosis, when limited to driver oncogene-positive patients, high survivin expression was suggested to be associated with poor prognosis. These findings provide preclinical evidence for the efficacy of combining TEAD1 inhibition with BRAF-targeted therapy in BRAF V600E-mutated LUAD and highlight the YAP1/TEAD1-survivin axis as a potential therapeutic target especially in the driver oncogene-positive LUAD patients.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 7","pages":"1883-1896"},"PeriodicalIF":4.5,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143812759","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":"BRCA1 Promoter Methylation in Ovarian Cancer: Clinical Relevance and a Novel Diagnostic Approach Using Fragment Analysis","authors":"Saki Tsuchimochi,&nbsp;Yoko Yamamoto,&nbsp;Ayumi Taguchi,&nbsp;Masahito Kawazu,&nbsp;Kenbun Sone,&nbsp;Masako Ikemura,&nbsp;Kana Tamai,&nbsp;Shuhei Kitamura,&nbsp;Daisuke Yoshimoto,&nbsp;Sayuri Fukaya,&nbsp;Aya Ishizaka,&nbsp;Anh Duong Quynh,&nbsp;Akira Nishijima,&nbsp;Yuichiro Miyamoto,&nbsp;Mayuyo Mori,&nbsp;Osamu Hiraike,&nbsp;Kosei Hasegawa,&nbsp;Tetsuo Ushiku,&nbsp;Katsutoshi Oda,&nbsp;Yasushi Hirota,&nbsp;Yutaka Osuga","doi":"10.1111/cas.70078","DOIUrl":"10.1111/cas.70078","url":null,"abstract":"<p>Homologous recombination deficiency (HRD) tests, including MyChoice CDx, are companion diagnostics for poly (ADP-ribose) polymerase (PARP) inhibitors. <i>BRCA1</i> promoter hypermethylation, a major HRD cause, may correlate with poorer prognosis. This study aimed to develop a simple, accurate method for detecting <i>BRCA1</i> promoter hypermethylation and elucidate the characteristics of such cases. <i>BRCA1</i> promoter methylation was analyzed using bisulfite sequencing (BIS-seq) in high-grade serous ovarian carcinoma specimens. We developed a newly developed <i>BRCA1</i> methylation assay, <i>BRCA1</i>-Fragment Analysis of Methylation (<i>BRCA1</i>-FAM), which combines restriction enzyme digestion with fragment analysis. The accuracy of this assay was compared to the results of BIS-seq. We evaluated the relationship between <i>BRCA1</i> promoter hypermethylation and prognosis and examined its association with <i>BRCA1</i> expression and loss of heterozygosity. <i>BRCA1</i> mutations and promoter methylation were mutually exclusive in the analyzed cases, with methylation observed in 28.9% (22/76) of primary debulking surgery cases. The <i>BRCA1</i>-FAM showed high sensitivity (91.3%) and specificity (100%) for detecting <i>BRCA1</i> promoter hypermethylation, comparable to BIS-seq. Cases with <i>BRCA1</i> promoter hypermethylation had significantly poorer progression-free survival (log-rank test, <i>p</i> = 0.048). Among these cases, 86.4% displayed abnormal <i>BRCA1</i> immunostaining, with lower frequencies of <i>BRCA1</i> loss of heterozygosity compared to those of other groups. <i>BRCA1</i> promoter hypermethylation is associated with poor prognosis, underscoring the importance of its identification for HRD stratification. <i>BRCA1</i>-FAM is a simple and highly accurate method for evaluating <i>BRCA1</i> promoter methylation. This approach may potentially enhance the precision of personalized therapies for ovarian cancer.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 7","pages":"1996-2007"},"PeriodicalIF":4.5,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70078","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143812758","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":"Evans Blue Acts as a Selective Inhibitor of CaMKII-α to Impede the Progression of TCL Identified by HTS","authors":"Jianru Tian,&nbsp;Aiqin Zhang,&nbsp;Lansong Li,&nbsp;Hong Liu,&nbsp;Hui Jiang,&nbsp;Ruqi Liang","doi":"10.1111/cas.70051","DOIUrl":"10.1111/cas.70051","url":null,"abstract":"<p>T-cell lymphoma (TCL) poses a significant challenge in clinical oncology, characterized by its aggressive behavior and resistance to conventional therapies. Despite considerable research efforts, the prognosis for TCL patients remains poor, primarily due to the lack of effective therapeutic strategies that can inhibit tumor progression and metastasis. In this study, we identified CaMKII-α as a potential therapeutic target for TCL. To explore its role in TCL pathogenesis, we investigated its effects on TCL cell lines. Protein expression levels within the PI3K-AKT signaling pathway were assessed using western blot analysis. Through siRNA-mediated gene silencing, we downregulated CaMKII-α expression and monitored TCL cell proliferation. Furthermore, we identified Evans Blue (IC₅₀ = 197.1 nM) as a selective small-molecule inhibitor of CaMKII-α through high-throughput screening (HTS). Evans Blue demonstrated significant tumor-suppressive effects, potentially inhibiting TCL cell proliferation via regulation of the PI3K-AKT signaling pathway. Notably, the antitumor effect of Evans Blue was comparable to that observed with genetic CaMKII-α ablation, highlighting its potential as a novel therapeutic strategy for the treatment of TCL.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 7","pages":"1941-1951"},"PeriodicalIF":4.5,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70051","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143781464","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":"Exploring Long Noncoding RNAs as Regulators of Tumor Ferroptosis: Advances and Challenges","authors":"Gang Li,&nbsp;Bing Wang,&nbsp;Lisha Ye,&nbsp;Guohua Wang","doi":"10.1111/cas.70074","DOIUrl":"10.1111/cas.70074","url":null,"abstract":"<p>Long noncoding RNAs (lncRNAs), a class of noncoding RNAs exceeding 200 nucleotides in length, play critical roles in regulating diverse biological processes and gene expression. Emerging evidence highlights their significant association with cancer occurrence, progression, prognosis, and therapeutic resistance, positioning lncRNAs as promising molecular targets for tumor detection and treatment. Ferroptosis, a regulated form of cell death characterized by the accumulation of iron-dependent lipid peroxides, has gained attention as a potential therapeutic strategy for cancer, complementing existing modalities such as surgery, chemotherapy, radiotherapy, hormone therapy, and targeted molecular therapy. Recent research demonstrates that lncRNAs modulate ferroptosis in solid tumors, thereby influencing tumor cell invasion, metastasis, and proliferation. Inducing ferroptosis has been shown to inhibit tumor growth, reduce chemoresistance, and enhance radiotherapy efficacy. This review explores recent advancements in understanding the role of lncRNAs in tumor ferroptosis, with a focus on their involvement in iron metabolism and their potential as therapeutic targets in cancer combination therapies.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 7","pages":"1795-1806"},"PeriodicalIF":4.5,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70074","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143774816","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":"Geographical Discrepancy in Medical Care Access Among Children, Adolescents, and Young Adults With Cancer in Japan, 2016–2019","authors":"Anna Tsutsui,&nbsp;Yoshitaka Murakami,&nbsp;Takako Fujimaki,&nbsp;Masayuki Endo,&nbsp;Yuko Ohno","doi":"10.1111/cas.70069","DOIUrl":"10.1111/cas.70069","url":null,"abstract":"<p>In Japan, cancer control measures have been developed in specialized hospitals for children (0–14 years), and adolescents and young adults (15–39 years) patients with cancer. We investigated geographical discrepancies between residential addresses and cancer treatment hospitals in patients aged 0–39 in Japan between 2016 and 2019. Using Japan's National Population-Based Cancer Registry data (<i>n</i> = 99,968), we classified the cases into 10 diagnostic groups and four age groups: 0–14, 15–19, 20–29, and 30–39. Using five types of hospital groups, we examined the origin–destination relationships between patients' residences and hospitals at the prefecture and Secondary Medical Area (SMA) levels via cross-tabulation, summarizing the results using descriptive statistics and heat maps. Generalized Estimating Equation analysis was performed to investigate the factors associated with receiving treatment outside the residential prefecture based on individual data. The median percentage of patients receiving treatment within their residential prefecture was 81.82% or higher across age groups and hospital groups. At the SMA level, the percentage ranged from 0% to 57.00% (median)—minimum 0.0% and maximum 100.0%. Model analysis revealed that patients with retinoblastoma (adjusted risk ratio: 5.45) and those living in metropolitan (Tokyo: 3.73, Osaka: 2.00) and non-metropolitan and depopulated (1.67) areas were significantly more likely to travel outside their residential prefectures. These findings reveal that Japan faces geographical discrepancies in access to cancer care, particularly for specific cancer types and areas. These findings can inform targeted interventions to support equitable access to specialized cancer care for young Japanese patients.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 7","pages":"1972-1983"},"PeriodicalIF":4.5,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70069","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143765506","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":"Pimitespib, an HSP90 Inhibitor, Enhances the Efficacy of PARP Inhibitors in PARP Inhibitor-Insensitive Breast Cancer Cells","authors":"Hiromi Muraoka,&nbsp;Hiromi Kazuno,&nbsp;Akihiro Hashimoto,&nbsp;Hiroshi Sootome,&nbsp;Shuichi Ohkubo","doi":"10.1111/cas.70058","DOIUrl":"10.1111/cas.70058","url":null,"abstract":"<p>Heat shock protein 90 (HSP90) plays a crucial role in the maintenance of protein homeostasis in cancer cells. Inhibition of HSP90 is anticipated to exert anticancer activities by reducing levels of HSP90 client proteins. Pimitespib (TAS-116) has emerged as a potent ATP-competitive inhibitor of both HSP90α and β, demonstrating favorable therapeutic properties in preclinical models. Notably, pimitespib is the first HSP90 inhibitor approved for the treatment of advanced gastrointestinal stromal tumors in Japan. Poly(ADP-ribose) polymerase (PARP) inhibitors target cancers susceptible to the homologous recombination (HR) pathway and are used for treating various types of tumors, particularly those harboring defects in HR repair pathways within DNA damage repair (DDR) such as mutations in breast cancer genes 1 and 2 (BRCA1 and BRCA2, respectively). However, PARP inhibitors have shown limited efficacy in HR-proficient tumors, and the development of resistance to PARP inhibitors via restoration of DDR systems poses a significant challenge. In this study, we explored the potential of pimitespib to enhance PARP inhibitor activity. In PARP inhibitor-insensitive breast cancer cell lines, pimitespib impaired HR pathway function by promoting the proteasome-mediated degradation of proteins involved in HR, such as BRCA1, BRCA2, and Rad51 homologous 1 (RAD51). Consequently, pimitespib enhanced antitumor activity and DNA damage induced by PARP inhibitors in vitro. In human breast cancer xenograft mouse models, pimitespib downregulated RAD51 proteins and augmented the antitumor effects of PARP inhibitors. These findings highlight the potential of pimitespib as a therapeutic agent in combination with PARP inhibitors to treat PARP inhibitor-insensitive cancers.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 6","pages":"1745-1757"},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70058","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755376","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 “Loss of Polarity Protein Par3, via Transcription Factor Snail, Promotes Bladder Cancer Metastasis”","authors":"","doi":"10.1111/cas.70073","DOIUrl":"10.1111/cas.70073","url":null,"abstract":"<p>Wang S, Cai J, Zhang S, et al. Loss of Polarity Protein Par3, via Transcription Factor Snail, Promotes Bladder Cancer Metastasis. <i>Cancer Science</i> 2021;112:2625–2641, https://doi.org/10.1111/cas.14920.</p><p>Some figures in the above article are incorrect.</p><p>The corrected Figures 2C, 2E, 5B, 5C, 5D, 5E, 6F and 6G are as follows:</p><p>We apologize for this error.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 6","pages":"1786-1788"},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.70073","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143765459","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}