Cancer Science最新文献_第9页

RETRACTION: MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway 返回：MicroRNA-16 通过抑制 BCL2 和核因子-κB1/MMP9 信号通路抑制胶质瘤细胞的生长和侵袭。

IF 4.5 2区医学

Cancer Science Pub Date : 2024-07-22 DOI: 10.1111/cas.16269

{"title":"RETRACTION: MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway","authors":"","doi":"10.1111/cas.16269","DOIUrl":"10.1111/cas.16269","url":null,"abstract":"Retraction: T.-Q. Yang, X.-J. Lu, T.-F. Wu, D.-D. Ding, Z.-H. Zhao, G.-L. Chen, X.-S. Xie, B. Li, Y.-X. Wei, L.-C. Guo, Y. Zhang, Y.-L. Huang, Y.-X. Zhou, and Z.-W. Du, “MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway,” Cancer Science 105 no. 3 (2014): 265–271. https://doi.org/10.1111/cas.12351.The above article, published online on 13 January 2014 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Masanori Hatakeyama; the Japanese Cancer Association; and John Wiley and Sons Ltd. The journal had previously published a correction regarding duplicated portions of Figure 4a on 24 May 2022. Following publication of this correction, the journal was made aware that not all duplicated portions of Figure 4a had been replaced. Additionally, concerns were raised of splicing in Figure 2d and image duplications in Figures 2d, 3d, and 4c. The authors did not respond to inquiries from the publisher regarding these concerns. and did not provide the requested original images and data. Therefore, the data reported in this article are considered unreliable and the journal must issue a retraction. The authors did not respond to our notice of retraction.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"115 9","pages":"3200"},"PeriodicalIF":4.5,"publicationDate":"2024-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.16269","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141735376","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}

引用次数: 0

NAT10 inhibition promotes ac4C-dependent ferroptosis to counteract sorafenib resistance in nasopharyngeal carcinoma 抑制NAT10可促进ac4C依赖性铁氧化，从而抵消鼻咽癌患者对索拉非尼的耐药性。

IF 4.5 2区医学

Cancer Science Pub Date : 2024-07-22 DOI: 10.1111/cas.16249

Ziyi Xue, Haijing Xie, Ying Shan, Lin Zhang, Lin Cheng, Wenyue Chen, Rui Zhu, Kaiwen Zhang, Haosheng Ni, Zhenxin Zhang, Yiwen You, Bo You

{"title":"NAT10 inhibition promotes ac4C-dependent ferroptosis to counteract sorafenib resistance in nasopharyngeal carcinoma","authors":"Ziyi Xue, Haijing Xie, Ying Shan, Lin Zhang, Lin Cheng, Wenyue Chen, Rui Zhu, Kaiwen Zhang, Haosheng Ni, Zhenxin Zhang, Yiwen You, Bo You","doi":"10.1111/cas.16249","DOIUrl":"10.1111/cas.16249","url":null,"abstract":"Sorafenib, an anticancer drug, has been shown to induce ferroptosis in cancer cells. However, resistance to sorafenib greatly limits its therapeutic efficacy, and the exact mechanism of resistance is not fully understood. This study investigated the role of N-Acetyltransferase 10 (NAT10) in influencing the anticancer activity of sorafenib in nasopharyngeal carcinoma (NPC) and its molecular mechanism. NAT10 expression was significantly upregulated in NPC. Mechanistically, NAT10 promotes proteins of solute carrier family 7 member 11 (SLC7A11) expression through ac4C acetylation, inhibiting sorafenib-induced ferroptosis in NPC cells. The combined application of sorafenib and the NAT10 inhibitor remodelin significantly inhibits SLC7A11 expression and promotes ferroptosis in NPC cells. In vivo knockout of NAT10 inhibited the growth of sorafenib-resistant NPC. Our findings suggest that NAT10 inhibition might be a promising therapeutic approach to enhance the anticancer activity of sorafenib.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"115 10","pages":"3256-3272"},"PeriodicalIF":4.5,"publicationDate":"2024-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11447888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141749396","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}

引用次数: 0

Which occurs first, ARID1A inactivation or microsatellite instability?: A comment to Yamamoto et al. (2024) ARID1A失活和微卫星不稳定哪个先发生？对 Yamamoto 等人（2024 年）的评论。

IF 4.5 2区医学

Cancer Science Pub Date : 2024-07-21 DOI: 10.1111/cas.16294

Dakeun Lee

引用次数: 0

The role of gastric mucins and mucin-related glycans in gastric cancers 胃粘蛋白和粘蛋白相关聚糖在胃癌中的作用。

IF 4.5 2区医学

Cancer Science Pub Date : 2024-07-19 DOI: 10.1111/cas.16282

Junya Arai, Yoku Hayakawa, Hiroaki Tateno, Hiroaki Fujiwara, Masato Kasuga, Mitsuhiro Fujishiro

引用次数: 0

Discovering cancer stem-like molecule, nuclear factor I X, using spatial transcriptome in gastric cancer 利用胃癌空间转录组发现癌症干样分子--核因子 I X。

IF 4.5 2区医学

Cancer Science Pub Date : 2024-07-17 DOI: 10.1111/cas.16288

Akira Ishikawa, Takafumi Fukui, Aya Kido, Narutaka Katsuya, Kazuya Kuraoka, Naohiro Uraoka, Takahisa Suzuki, Shiro Oka, Takahiro Kotachi, Hassan Ashktorab, Duane Smoot, Wataru Yasui

{"title":"Discovering cancer stem-like molecule, nuclear factor I X, using spatial transcriptome in gastric cancer","authors":"Akira Ishikawa, Takafumi Fukui, Aya Kido, Narutaka Katsuya, Kazuya Kuraoka, Naohiro Uraoka, Takahisa Suzuki, Shiro Oka, Takahiro Kotachi, Hassan Ashktorab, Duane Smoot, Wataru Yasui","doi":"10.1111/cas.16288","DOIUrl":"10.1111/cas.16288","url":null,"abstract":"Gastric cancer (GC) is characterized by significant intratumoral heterogeneity, and stem cells are promising therapeutic targets. Despite advancements in spatial transcriptome analyses, unexplored targets for addressing cancer stemness remain unknown. This study aimed to identify Nuclear Factor IX (NFIX) as a critical regulator of cancer stemness in GC and evaluate its clinicopathological significance and function. Spatial transcriptome analysis of GC was conducted. The correlation between NFIX expression, clinicopathological factors, and prognosis was assessed using immunostaining in 127 GC cases. Functional analyses of cancer cell lines validated these findings. Spatial transcriptome analysis stratified GC tissues based on genetic profiles, identified CSC-like cells, and further refined the classification to identify and highlight the significance of NFIX, as validated by Monocle 3 and CytoTRACE analyses. Knockdown experiments in cancer cell lines have demonstrated the involvement of NFIX in cancer cell proliferation and kinase activity. This study underscores the role of spatial transcriptome analysis in refining GC tissue classification and identifying therapeutic targets, highlighting NFIX as a pivotal factor. NFIX expression is correlated with poor prognosis and drives GC progression, suggesting its potential as a novel therapeutic target for personalized GC therapies.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"115 9","pages":"3180-3193"},"PeriodicalIF":4.5,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.16288","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141635143","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}

引用次数: 0

Ropivacaine synergizes with sorafenib to induce apoptosis of hepatocellular carcinoma cells via the IL-6/STAT3 pathway 罗哌卡因与索拉非尼协同作用，通过IL-6/STAT3途径诱导肝癌细胞凋亡。

IF 4.5 2区医学

Cancer Science Pub Date : 2024-07-16 DOI: 10.1111/cas.16261

Wenting Wang, Hongyun Lin, Desheng Liu, Tao Wang, Zicheng Zhu, Peng Yu, Jing Zhang

{"title":"Ropivacaine synergizes with sorafenib to induce apoptosis of hepatocellular carcinoma cells via the IL-6/STAT3 pathway","authors":"Wenting Wang, Hongyun Lin, Desheng Liu, Tao Wang, Zicheng Zhu, Peng Yu, Jing Zhang","doi":"10.1111/cas.16261","DOIUrl":"10.1111/cas.16261","url":null,"abstract":"The development of resistance in hepatocellular carcinoma (HCC) cells limits the effectiveness of sorafenib, but combination therapy with other drugs may have a positive effect. However, the effect of ropivacaine combined with sorafenib on the treatment of HCC cells and its potential regulatory mechanisms remain unclear. The proliferation and apoptosis of HCC cells treated with ropivacaine, sorafenib, and ropivacaine plus sorafenib were analyzed by cell-counting kit 8 and flow cytometry. The protein levels were measured by Western blot. The antitumor effect of ropivacaine, sorafenib, and their combination was verified by a tumor xenograft model. Ropivacaine and sorafenib markedly impeded the viability of HCC cells in a concentration-dependent manner. Compared with ropivacaine or sorafenib treatment alone, ropivacaine and sorafenib combination treatment impeded HCC cell proliferation, facilitated apoptosis, enhanced cleaved caspase-3, cleaved caspase-9, and cyclin D1 protein expression, while it reduced IL-6 and p-STAT3 expression and inhibited tumor growth in vivo. Importantly, the activation of the IL-6/STAT3 pathway could reverse the repressive or stimulative effects of ropivacaine and sorafenib on the proliferation and apoptosis in HCC cells. In summary, ropivacaine synergistically induces sorafenib-stimulated apoptosis of HCC cells via the IL-6/STAT3 pathway. Ropivacaine is a potential drug for the treatment of HCC when combined with sorafenib.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"115 9","pages":"2923-2930"},"PeriodicalIF":4.5,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.16261","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141628042","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}

引用次数: 0

Protein phosphatase 6 promotes stemness of colorectal cancer cells 蛋白磷酸酶 6 可促进结直肠癌细胞的干性。

IF 4.5 2区医学

Cancer Science Pub Date : 2024-07-16 DOI: 10.1111/cas.16271

Nobuyuki Fujiwara, Ryouichi Tsunedomi, Yuta Kimura, Masao Nakajima, Shinobu Tomochika, Shuhei Enjoji, Takashi Ohama, Koichi Sato, Hiroaki Nagano

{"title":"Protein phosphatase 6 promotes stemness of colorectal cancer cells","authors":"Nobuyuki Fujiwara, Ryouichi Tsunedomi, Yuta Kimura, Masao Nakajima, Shinobu Tomochika, Shuhei Enjoji, Takashi Ohama, Koichi Sato, Hiroaki Nagano","doi":"10.1111/cas.16271","DOIUrl":"10.1111/cas.16271","url":null,"abstract":"Colorectal cancer (CRC) remains a significant global health concern, demanding a more profound comprehension of its molecular foundations for the development of improved therapeutic strategies. This study aimed to elucidate the role of protein phosphatase 6 (PP6), a member of the type 2A protein phosphatase family, in CRC. Protein phosphatase 6 functions as a heterotrimer with a catalytic subunit (PP6c), regulatory subunits (PP6Rs; PP6R1, PP6R2, and PP6R3), and scaffold subunits (ANKRD28, ANKRD44, and ANKRD52). Elevated PP6c expression has been identified in CRC tissues compared to normal mucosa, aligning with its potential involvement in CRC pathogenesis. PP6c knockdown resulted in decreased colony-forming ability and in vivo proliferation of various CRC cell lines. Transcriptome analysis revealed that PP6c knockdown resulted in altered expression of genes associated with cancer stemness. Notably, the PP6c-PP6R3 complex is a key player in regulating cancer stem cell (CSC) markers. Additionally, increased PP6c expression was observed in CSC-like cells induced by sphere formation, implicating the role of PP6c in CSC maintenance. This study highlights the role of PP6c in CRC and suggests that it is a potential therapeutic target disrupting a pathway critical for CRC progression and stem cell maintenance.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"115 9","pages":"3067-3078"},"PeriodicalIF":4.5,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.16271","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141628041","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}

引用次数: 0

UBA2 SUMOylates NQO1 and promotes the proliferation of hepatocellular carcinoma by modulating the MAPK pathway UBA2 SUMOylates NQO1 并通过调节 MAPK 通路促进肝细胞癌的增殖。

IF 4.5 2区医学

Cancer Science Pub Date : 2024-07-16 DOI: 10.1111/cas.16290

Hailong Chen, Huifang Li, Minke He, Zhicheng Lai, Lichang Huang, Dongsheng Wen, Ming Shi, Anna Kan

{"title":"UBA2 SUMOylates NQO1 and promotes the proliferation of hepatocellular carcinoma by modulating the MAPK pathway","authors":"Hailong Chen, Huifang Li, Minke He, Zhicheng Lai, Lichang Huang, Dongsheng Wen, Ming Shi, Anna Kan","doi":"10.1111/cas.16290","DOIUrl":"10.1111/cas.16290","url":null,"abstract":"In our previous study, we found that small ubiquitin-related modifier (SUMO)-activating enzyme ubiquitin-associated-2 domain (UBA2) was upregulated in hepatocellular carcinoma (HCC) patients who were insensitive to chemoembolization. In this study, we aimed to investigate the role of UBA2 in HCC progression. Three cohorts were used to evaluate the efficacy of UBA2 as a prognostic factor for HCC. Our results indicated that UBA2 was associated with aggressive clinical behaviors and was a strong indicator of poor prognosis in HCC. In vitro experiments demonstrated that UBA2 accelerated cell growth, invasion, and migration. These results were further supported by in vivo experiments. RNA-sequencing analysis indicated NQO1 as a target of UBA2, with its levels altering following UBA2 manipulation. The results were verified by western blotting (WB) and quantitative PCR. The SUMOplot Analysis Program predicted lysine residue K240 as a modification target of UBA2, which was confirmed by immunoprecipitation (IP) assays. Subsequent mutation of NQO1 at K240 in HCC cell lines and functional assays revealed the significance of this modification. In addition, the oncogenic effect of UBA2 could be reversed by the SUMO inhibitor ML792 in vivo and in vitro. In conclusion, our study elucidated the regulatory mechanism of UBA2 in HCC and suggested that the SUMO inhibitor ML792 may be an effective combinatory treatment for patients with aberrant UBA2 expression.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"115 9","pages":"2998-3012"},"PeriodicalIF":4.5,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.16290","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141628043","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}

引用次数: 0

Cytochrome P450 2J2 is required for the natural compound austocystin D to elicit cancer cell toxicity 细胞色素 P450 2J2 是天然化合物奥斯特胱氨酸 D 引发癌细胞毒性的必要条件。

IF 4.5 2区医学

Cancer Science Pub Date : 2024-07-15 DOI: 10.1111/cas.16289

Yukiko Kojima, Saki Fujieda, Liya Zhou, Masahiro Takikawa, Kouji Kuramochi, Toshiki Furuya, Ayaka Mizumoto, Noritaka Kagaya, Teppei Kawahara, Kazuo Shin-ya, Shingo Dan, Akihiro Tomida, Fuyuki Ishikawa, Mahito Sadaie

{"title":"Cytochrome P450 2J2 is required for the natural compound austocystin D to elicit cancer cell toxicity","authors":"Yukiko Kojima, Saki Fujieda, Liya Zhou, Masahiro Takikawa, Kouji Kuramochi, Toshiki Furuya, Ayaka Mizumoto, Noritaka Kagaya, Teppei Kawahara, Kazuo Shin-ya, Shingo Dan, Akihiro Tomida, Fuyuki Ishikawa, Mahito Sadaie","doi":"10.1111/cas.16289","DOIUrl":"10.1111/cas.16289","url":null,"abstract":"Austocystin D is a natural compound that induces cytochrome P450 (CYP) monooxygenase-dependent DNA damage and growth inhibition in certain cancer cell lines. Cancer cells exhibiting higher sensitivity to austocystin D often display elevated CYP2J2 expression. However, the essentiality and the role of CYP2J2 for the cytotoxicity of this compound remain unclear. In this study, we demonstrate that CYP2J2 depletion alleviates austocystin D sensitivity and DNA damage induction, while CYP2J2 overexpression enhances them. Moreover, the investigation into genes involved in austocystin D cytotoxicity identified POR and PGRMC1, positive regulators for CYP activity, and KAT7, a histone acetyltransferase. Through genetic manipulation and analysis of multiomics data, we elucidated a role for KAT7 in CYP2J2 transcriptional regulation. These findings strongly suggest that CYP2J2 is crucial for austocystin D metabolism and its subsequent cytotoxic effects. The potential use of austocystin D as a therapeutic prodrug is underscored, particularly in cancers where elevated CYP2J2 expression serves as a biomarker.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"115 9","pages":"3054-3066"},"PeriodicalIF":4.5,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.16289","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141621261","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}

引用次数: 0

Tumor thickness as a novel risk factor for lymph node metastasis by superficial squamous cell carcinoma of head and neck 肿瘤厚度是头颈部浅表鳞状细胞癌淋巴结转移的新风险因素。

IF 4.5 2区医学

Cancer Science Pub Date : 2024-07-15 DOI: 10.1111/cas.16209

Satoshi Fujii, Chikatoshi Katada, Hidenobu Watanabe, Tadakazu Shimoda, Atsushi Ochiai, Tetsuji Yokoyama, Yasutoshi Sakamoto, Koichi Kano, Masaaki Ichinoe, Tetsuo Nemoto, Masahiro Fujita, Yoko Tateishi, Hitoshi Sugiura, Tetuo Mikami, Tomonori Yano, Takakuni Kato, Manabu Muto, Ryuichi Hayashi

{"title":"Tumor thickness as a novel risk factor for lymph node metastasis by superficial squamous cell carcinoma of head and neck","authors":"Satoshi Fujii, Chikatoshi Katada, Hidenobu Watanabe, Tadakazu Shimoda, Atsushi Ochiai, Tetsuji Yokoyama, Yasutoshi Sakamoto, Koichi Kano, Masaaki Ichinoe, Tetsuo Nemoto, Masahiro Fujita, Yoko Tateishi, Hitoshi Sugiura, Tetuo Mikami, Tomonori Yano, Takakuni Kato, Manabu Muto, Ryuichi Hayashi","doi":"10.1111/cas.16209","DOIUrl":"10.1111/cas.16209","url":null,"abstract":"Narrow-band imaging combined with magnified endoscopy has enabled the detection of superficial squamous cell carcinoma of the head and neck (SSCCHN) that has been resected with minimally invasive treatment, preserving vocalization and swallowing functions. However, risk factors of lymph node metastasis (LNM) must be identified, as some patients with LNM have a poor prognosis. From an initial 599 patients with 700 lesions who underwent trans-oral surgery in 27 Japanese hospitals (a nationwide registration survey), we enrolled 541 patients with 633 SSCCHNs, as indicated by central pathological diagnoses. All pathological specimens for each patient were examined using 20 pathological factors that are thought to affect the LNM of SSCCHN. In all, 24 (4.4%) of the 568 SSCCHNs exhibited LNM, and all 24 had at least one solitary nest of epithelial neoplastic cells present in the stroma, clearly separated from the intraepithelial carcinoma. Multivariate analysis also showed that tumor thickness (p = 0.0132, RR: 7.85, 95% confidence interval [CI]: 1.54–40.02), and an INFc pattern classified as infiltrating growth (INF) with unclear boundaries between tumor and non-tumor tissues (p = 0.0003, RR: 14.47, 3.46–60.46), and tumor budding (p = 0.0019, RR: 4.35, CI: 1.72–11.01) were significantly associated with LNM. Solitary nests may be indicative of LNM. In addition, tumor thickness was revealed to be a risk factor for LNM in SSCCHNs using pT factors that do not include an invasion depth element because of the anatomical absence of the muscularis mucosae.","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"115 9","pages":"3169-3179"},"PeriodicalIF":4.5,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cas.16209","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141621262","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}

引用次数: 0