Cancer Science最新文献

{"title":"Projection of future gastric cancer incidence and health-care service demand by geographic area in Kanagawa, Japan","authors":"Choy-Lye Chei,&nbsp;Sho Nakamura,&nbsp;Kaname Watanabe,&nbsp;Ryo Watanabe,&nbsp;Akio Kurokawa,&nbsp;Taizo Iwane,&nbsp;Sayaka Itoh,&nbsp;Hiroto Narimatsu","doi":"10.1111/cas.16415","DOIUrl":"10.1111/cas.16415","url":null,"abstract":"<p>Projections of future gastric cancer incidence and the demand for health-care services for gastric cancer patients by geographic area will assist local authorities in determining health-care needs, allocating medical resources, and planning services. This study aims to project the future incidence of gastric cancer, estimate the number of patients per medical institution, and decompose the net changes in cases to assess the impact of population aging by geographic area. Our projections are based on population-based cancer registry data, census data from 2000 to 2020, and the projected population for 2025–2045 in Kanagawa, Japan. We classified Kanagawa into urban, town, outer city, and rural areas based on geographic and population features. The number of medical institutions providing gastric cancer treatment was used to estimate the number of patients per medical institution. We projected a decrease of 25%, 52%, and 5% in gastric cancer cases in towns, outer cities, and rural areas from 2020 to 2045, respectively. However, cases are expected to increase by 9% in urban areas, primarily due to population aging. The annual number of gastric cancer patients per medical institution in urban areas is expected to increase from 54 to 59, while numbers in other areas are predicted to decline from 2020 to 2045. Our long-term projections indicate that the number of older gastric cancer patients will continue to increase in urban areas. While current measures effectively reduce gastric cancer risk, they need to be revised to address the impact of population aging.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 2","pages":"488-499"},"PeriodicalIF":4.5,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786317/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142752196","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":"PD-1 blockade treatment in melanoma: Mechanism of response and tumor-intrinsic resistance","authors":"Tong Wang,&nbsp;Wenjie Ma,&nbsp;Zijian Zou,&nbsp;Jingqin Zhong,&nbsp;Xinyi Lin,&nbsp;Wanlin Liu,&nbsp;Wei Sun,&nbsp;Tu Hu,&nbsp;Yu Xu,&nbsp;Yong Chen","doi":"10.1111/cas.16398","DOIUrl":"10.1111/cas.16398","url":null,"abstract":"<p>Malignant melanoma is characterized by high immunogenicity, genetic heterogeneity, and diverse pathological manifestations, affecting both skin and mucosa over the body. Pembrolizumab and nivolumab, both anti-PD-1 monoclonal antibodies, were approved by the US FDA for unresectable or metastatic melanoma in 2011 and 2014, respectively, with enduring and transformative outcomes. Despite marked clinical achievements, only a subset of patients manifested a complete response. Approximately 55% of melanoma patients exhibited primary resistance to PD-1 antibodies, with nearly 25% developing secondary resistance within 2 years of treatment. Thus, there is a critical need to comprehensively elucidate the mechanisms underlying the efficacy and resistance to PD-1 blockade. This review discusses the fundamental mechanisms of PD-1 blockade, encompassing insights from T cells and B cells, and presents resistance to anti-PD-1 with a particular focus on tumoral-intrinsic mechanisms in melanoma.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 2","pages":"329-337"},"PeriodicalIF":4.5,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142733775","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":"Fibrous corona is reduced in cancer cell lines that attenuate microtubule nucleation from kinetochores","authors":"Yudai Ishikawa,&nbsp;Hirotaka Fukue,&nbsp;Runa Iwakami,&nbsp;Masanori Ikeda,&nbsp;Kenji Iemura,&nbsp;Kozo Tanaka","doi":"10.1111/cas.16406","DOIUrl":"10.1111/cas.16406","url":null,"abstract":"<p>Most cancer cells show increased chromosome missegregation, known as chromosomal instability (CIN), which promotes cancer progression and drug resistance. The underlying causes of CIN in cancer cells are not fully understood. Here we found that breast cancer cell lines show a reduced kinetochore localization of ROD, ZW10, and Zwilch, components of the fibrous corona, compared with non-transformed breast epithelial cell lines. The fibrous corona is a structure formed on kinetochores before their end-on attachment to microtubules and plays a role in efficient kinetochore capture and the spindle assembly checkpoint. The reduction in the fibrous corona was not due to reduced expression levels of the fibrous corona components or to a reduction in outer kinetochore components. Kinetochore localization of Bub1 and CENP-E, which play a role in the recruitment of the fibrous corona to kinetochores, was reduced in cancer cell lines, presumably due to reduced activity of Mps1, which is required for their recruitment to kinetochores through phosphorylating KNL1. Increasing kinetochore localization of Bub1 and CENP-E in cancer cells restored the level of the fibrous corona. Cancer cell lines showed a reduced capacity to nucleate microtubules from kinetochores, which was recently shown to be dependent on the fibrous corona, and increasing kinetochore localization of Bub1 and CENP-E restored the microtubule nucleation capacity on kinetochores. Our study revealed a distinct feature of cancer cell lines that may be related to CIN.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 2","pages":"420-431"},"PeriodicalIF":4.5,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142741076","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":"Pan-immune-inflammation value predicts immunotherapy response and reflects local antitumor immune response in rectal cancer","authors":"Qianyu Wang,&nbsp;Wentao Zhong,&nbsp;Yi Xiao,&nbsp;Guole Lin,&nbsp;Junyang Lu,&nbsp;Lai Xu,&nbsp;Guannan Zhang,&nbsp;Aijun Liu,&nbsp;Junfeng Du,&nbsp;Bin Wu","doi":"10.1111/cas.16400","DOIUrl":"10.1111/cas.16400","url":null,"abstract":"<p>The pan-immune-inflammation value reflects the systemic inflammatory response, and tumor-infiltrating lymphocytes indicate a local immune response in rectal cancer. However, the association between systemic inflammatory response, as indicated by the pan-immune-inflammation value, and local immune responses in rectal cancer remains unclear. This study analyzed 915 treatment-naïve rectal cancer patients from the Peking Union Medical College Hospital and PLA General Hospital (PLAGH) cohorts who underwent radical surgery to investigate the relationship between the pan-immune-inflammation value and immune responses. Lower pan-immune-inflammation value was significantly associated with improved disease-free survival and cancer-specific survival. Multivariate Cox regression models identified the pan-immune-inflammation value as an independent prognostic factor. In the PLAGH cohort, patients with low pan-immune-inflammation values had higher immune cell levels, activated immune pathways, and increased expression of immune checkpoint genes according to RNA sequencing. Hematoxylin and eosin staining and immunohistochemical analysis revealed that lower pan-immune-inflammation value was associated with higher tumor-infiltrating lymphocyte density, more mature tertiary lymphoid structures, increased CD8⁺ T cells, and elevated human lymphocyte antigen class I expression. Conversely, patients with high pan-immune-inflammation values exhibited pathways linked to tumor progression, such as angiogenesis, epithelial–mesenchymal transition, hypoxia, KRAS signaling, and TGF-ß signaling. Among patients receiving anti-PD-1 therapy, responders had low pre- and post-treatment pan-immune-inflammation values. The pan-immune-inflammation value is a reliable marker associated with distinct immune microenvironment characteristics and can effectively predict disease-free survival, cancer-specific survival, and response to immunotherapy.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 2","pages":"350-366"},"PeriodicalIF":4.5,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142733772","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":"TRIM47 promotes hypopharyngeal and laryngeal cancers progression through promoting K63-linked ubiquitination of vimentin","authors":"Shichao Qin,&nbsp;Fen Chang,&nbsp;Xiangkai Sun,&nbsp;Zinan Li,&nbsp;Yin Wang,&nbsp;Dapeng Lei","doi":"10.1111/cas.16397","DOIUrl":"10.1111/cas.16397","url":null,"abstract":"<p>Hypopharyngeal and laryngeal cancers which belong to head and neck squamous cell carcinoma (HNSCC) are the two most malignant types of head and neck cancer, characterized by a low 5-year survival rate, high recurrence and metastasis rate. It is vital to explore strategies to suppress metastasis and improve prognosis for patients with these cancers. In this research, we analyzed the clinical data and found that E3 ubiquitin ligase TRIM47 was upregulated in cancer tissues of hypopharyngeal cancer and was closely associated with poor survival outcomes. In terms of mechanism, we performed tandem affinity chromatography and denatured Ni-NTA Agarose pulldown. As a result, TRIM47 was found to interact with vimentin and control vimentin stabilization through ubiquitination, specifically in the form of K63 chains. Importantly, through experiments of cancer cell viability and migration, we found that TRIM47 could enhance the proliferation and metastasis abilities of cancer cells in a vimentin-dependent manner, thus promoting the advancement of hypopharyngeal and laryngeal cancers. TRIM47 was verified to regulate cancer cells metastasis in vivo using metastasis models. All these results imply that TRIM47 emerges as a potential biomarker for early diagnosis and metastasis prediction of hypopharyngeal and laryngeal cancers and represents a promising therapeutic target.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 2","pages":"367-380"},"PeriodicalIF":4.5,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786321/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711648","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":"S100A8 as a potential therapeutic target for cancer metastasis","authors":"Atsuko Deguchi,&nbsp;Yoshiro Maru","doi":"10.1111/cas.16407","DOIUrl":"10.1111/cas.16407","url":null,"abstract":"<p>Metastasis is a major cause of cancer-related deaths. Similar to the tumor microenvironment formation, the premetastatic niche develops in distant organs before the arrival of tumor cells. Elucidating the mechanism(s) underlying premetastatic niche formation could contribute to the establishment of effective therapeutic targets for metastasis. Our research indicates that primary tumors hijack Toll-like receptor 4 (TLR4) signaling to establish a premetastatic niche in the lungs by utilizing an endogenous ligand S100A8. S100A8 is expressed not only in immune cells but also in various types of tumor cells. By focusing on S100A8 as a therapeutic target, we identified at least three multivalent S100A8 inhibitory peptides. Here, we review the tumor-promoting role of S100A8-mediated TLR4 signaling and propose S100A8 as a potential therapeutic target for aggressive cancer.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 2","pages":"322-328"},"PeriodicalIF":4.5,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786323/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711644","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":"Integrin-α5 expression and its role in non-small cell lung cancer progression","authors":"Mirei Ka,&nbsp;Yoko Matsumoto,&nbsp;Takahiro Ando,&nbsp;Munetoshi Hinata,&nbsp;Qian Xi,&nbsp;Yuriko Sugiura,&nbsp;Takahiro Iida,&nbsp;Natsuki Nakagawa,&nbsp;Masakatsu Tokunaga,&nbsp;Kousuke Watanabe,&nbsp;Masanori Kawakami,&nbsp;Tetsuo Ushiku,&nbsp;Masaaki Sato,&nbsp;Katsutoshi Oda,&nbsp;Hidenori Kage","doi":"10.1111/cas.16416","DOIUrl":"10.1111/cas.16416","url":null,"abstract":"<p>Integrins are transmembrane receptors that facilitate cell adhesion to the extracellular matrix and neighboring cells. Aberrant expression of integrins has been associated with tumor progression and metastasis in various cancer types. Integrin alpha-5 (ITGA5) is an integrin subtype that serves as a receptor for fibronectin, fibrinogen, and fibrillin-1. The purpose of this study was to elucidate how ITGA5 expression plays a role in human non-small cell lung cancer (NSCLC). Our clinical data, along with data retrieved from The Cancer Genome Database (TCGA), revealed that high ITGA5 expression in NSCLC patients was associated with a lower recurrence-free survival and overall survival. In our in vitro functional assays, ITGA5 overexpression in human NSCLC cell lines resulted in increased cell size, adhesion, and migration properties, while knockdown of ITGA5 restored the phenotypes. Correspondingly, knockdown and inhibition of ITGA5 in endogenously high-expressing NSCLC cell lines resulted in decreased cell size, adhesion, migration, and proliferation. The antiproliferative effect was also confirmed by a reduction in Ki-67 without discernible changes in apoptosis. Collectively, these findings reveal the significant role of ITGA5 in various functional behaviors in NSCLC, providing a potential therapeutic target for NSCLC patients with high ITGA5 expression.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 2","pages":"406-419"},"PeriodicalIF":4.5,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786322/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711641","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":"LINC02154 promotes cell cycle and mitochondrial function in oral squamous cell carcinoma","authors":"Takeshi Niinuma,&nbsp;Hiroshi Kitajima,&nbsp;Tatsuya Sato,&nbsp;Toshifumi Ogawa,&nbsp;Kazuya Ishiguro,&nbsp;Masahiro Kai,&nbsp;Eiichiro Yamamoto,&nbsp;Yui Hatanaka,&nbsp;Iyori Nojima,&nbsp;Mutsumi Toyota,&nbsp;Akira Yorozu,&nbsp;Shohei Sekiguchi,&nbsp;Noritsugu Tohse,&nbsp;Masato Furuhashi,&nbsp;Hiroshi Ohguro,&nbsp;Akihiro Miyazaki,&nbsp;Hiromu Suzuki","doi":"10.1111/cas.16379","DOIUrl":"10.1111/cas.16379","url":null,"abstract":"<p>Long noncoding RNAs (lncRNAs) play pivotal roles in the development of human malignancies, though their involvement in oral squamous cell carcinoma (OSCC) remains incompletely understood. Using The Cancer Genome Atlas (TCGA) dataset, we analyzed expression of 7840 lncRNAs in primary head and neck squamous cell carcinoma (HNSCC) and found that upregulation of LINC02154 is associated with a poorer prognosis. LINC02154 knockdown in OSCC cell lines induced cell cycle arrest and apoptosis, and significantly attenuated tumor growth in vitro and in vivo. Notably, depletion of LINC02154 downregulated FOXM1, a master regulator of cell cycle-related genes. RNA pulldown and mass spectrometry analyses identified a series of proteins that could potentially interact with LINC02154, including HNRNPK and LRPPRC. HNRNPK stabilizes FOXM1 expression by interacting with the 3′-UTR of FOXM1 mRNA, which suggests LINC02154 and HNRNPK promote cell cycling by regulating FOXM1 expression. Additionally, LINC02154 positively regulates HNRNPK expression by inhibiting microRNAs targeting HNRPNK. Moreover, LINC02154 affects mitochondrial function by interacting with LRPPRC. Depletion of LINC02154 suppressed expression of mitochondrial genes, including MTCO1 and MTCO2, and inhibited mitochondrial respiratory function in OSCC cells. These results suggest that LINC02154 exerts its oncogenic effects by modulating the cell cycle and oxidative phosphorylation in OSCC, highlighting LINC02154 as a potential therapeutic target.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 2","pages":"393-405"},"PeriodicalIF":4.5,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786299/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693844","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":"Nelarabine-combined chemotherapy improves outcome of T-cell acute lymphoblastic leukemia but shows more severe neurotoxicity: JALSG T-ALL213-O","authors":"Fumihiko Hayakawa,&nbsp;Naoki Mori,&nbsp;Kiyotoshi Imai,&nbsp;Yasuhisa Yokoyama,&nbsp;Yuna Katsuoka,&nbsp;Takeshi Saito,&nbsp;Tohru Murayama,&nbsp;Etsuko Yamazaki,&nbsp;Shinya Sato,&nbsp;Yoshiko Atsuta,&nbsp;Yuichi Ishikawa,&nbsp;Emiko Sakaida,&nbsp;Yoshihiro Hatta,&nbsp;Itaru Matsumura,&nbsp;Yasushi Miyazaki,&nbsp;Hitoshi Kiyoi,&nbsp;Japan Adult Leukemia Study Group (JALSG)","doi":"10.1111/cas.16405","DOIUrl":"10.1111/cas.16405","url":null,"abstract":"<p>We investigated the effectiveness and safety of nelarabine (NEL)-combined chemotherapy for newly diagnosed adult T-cell acute lymphoblastic leukemia (T-ALL) patients. We conducted a phase II trial, T-ALL213-O, where adult T-ALL patients aged 25 to 64 were treated by a regimen based on that used in our previous study, ALL202-O. The main modifications from ALL202-O to T-ALL213-O were as follows: (1) NEL-combined chemotherapy, instead of consolidation (C)1, was used for non-complete remission (CR) patients after induction therapy (IND)1 as IND2; (2) NEL treatments were inserted into C3 and C5 on day 29. Twenty-four patients were analyzed. Ten patients did not receive NEL treatment due to therapy termination prior to C3. Three-year event-free survival (EFS) was 70%, with 52% as the lower limit of its 90% confidence interval, which exceeded the threshold of 25%; thus, the study treatment was considered effective. The CR rates by IND1, IND2, and both were 75%, 100%, and 88%, respectively. The 5-year EFS and 5-year overall survival rates were 66% and 70%, respectively, with median follow-ups of 7.7 and 7.8 years. The addition of NEL improved the CR rate but not survival, compared with T-ALL patients in ALL202-O. Severe neuropathy after NEL administration was observed at a high frequency. Seven (50%) of 14 patients treated with NEL showed grade 3 peripheral neuropathy and/or gait disturbance. The neurotoxicity was considered stronger than that previously reported. Combination therapy of NEL at this dose and intensive multidrug chemotherapy is associated with a high risk of severe neurotoxicity (JALSG T-ALL213-O, UMIN000010642).</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 2","pages":"453-461"},"PeriodicalIF":4.5,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142688861","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":"Micropapillary structure: A natural tumor collective invasion model with enhanced stem-like properties","authors":"Sisi Li,&nbsp;Shuangshu Gao,&nbsp;Ling Qin,&nbsp;Caixia Ding,&nbsp;Jinghui Qu,&nbsp;Yifei Cui,&nbsp;Lixia Qiang,&nbsp;Shengjie Yin,&nbsp;Xiaoyu Zheng,&nbsp;Hongxue Meng","doi":"10.1111/cas.16396","DOIUrl":"10.1111/cas.16396","url":null,"abstract":"<p>Cancer stem cells aggregate to form clusters, which have enhanced stem-like properties and metastasis potential. However, the molecular mechanisms underlying the formation of cancer stem cell cluster-like structures with acquisition of stronger invasion and metastasis abilities remain unclear. Micropapillary carcinoma (MPC) is a subpopulation of small, merulioid, inverted, nonfibrous vascular clusters floating in the stroma present in a range of solid malignant tumors and characterized by frequent vascular/lymphatic vessel invasion and lymph node metastasis. Our results showed that these cell clusters exhibit a stem cell phenotype, supporting the premise that MPC may serve as a promising solid tumor model for studying invasion and metastasis of cancer stem cell clusters. In this review, we discuss the latest advances in MPC research and targeted therapy, focusing on analysis of their stem-like characteristics, mapping their multiomics characteristics, and elucidating the vascular and immune microenvironment of MPC. The existing MPC organoid model was employed to explore potential breakthroughs in targeted therapy and immunotherapy for cancer stem cell clusters.</p>","PeriodicalId":9580,"journal":{"name":"Cancer Science","volume":"116 2","pages":"308-321"},"PeriodicalIF":4.5,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142683228","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}