Clinical & Experimental Metastasis最新文献_第5页

Pembrolizumab in patients with advanced upper tract urothelial carcinoma: a real-world study from ARON-2 project. Pembrolizumab在晚期上尿路上皮癌患者中的应用：来自ARON-2项目的真实世界研究。

IF 4.2 3区医学

Clinical & Experimental Metastasis Pub Date : 2024-10-01 Epub Date: 2024-06-08 DOI: 10.1007/s10585-024-10296-0

Alessandro Rizzo, Sebastiano Buti, Patrizia Giannatempo, Samer Salah, Javier Molina-Cerrillo, Francesco Massari, Ray Manneh Kopp, Ondřej Fiala, Luca Galli, Zin W Myint, Deniz Tural, Andrey Soares, Renate Pichler, Alessia Mennitto, Halima Abahssain, Fabio Calabrò, Fernando Sabino M Monteiro, Anna Albano, Veronica Mollica, Giulia Claire Giudice, Hideki Takeshita, Matteo Santoni

{"title":"Pembrolizumab in patients with advanced upper tract urothelial carcinoma: a real-world study from ARON-2 project.","authors":"Alessandro Rizzo, Sebastiano Buti, Patrizia Giannatempo, Samer Salah, Javier Molina-Cerrillo, Francesco Massari, Ray Manneh Kopp, Ondřej Fiala, Luca Galli, Zin W Myint, Deniz Tural, Andrey Soares, Renate Pichler, Alessia Mennitto, Halima Abahssain, Fabio Calabrò, Fernando Sabino M Monteiro, Anna Albano, Veronica Mollica, Giulia Claire Giudice, Hideki Takeshita, Matteo Santoni","doi":"10.1007/s10585-024-10296-0","DOIUrl":"10.1007/s10585-024-10296-0","url":null,"abstract":"Upper tract urothelial carcinoma (UTUC) accounts for the 5-10% of all urothelial carcinomas (UCs). In this analysis, we reported the real-world data from the ARON-2 study (NCT05290038) on the efficacy of pembrolizumab in patients with UTUC who recurred or progressed after platinum-based chemotherapy. Medical records of patients with metastatic UTUC treated with pembrolizumab as second-line therapy were reviewed from 34 institutions in 14 countries. Patients were assessed for overall survival (OS), progression-free survival (PFS), and overall response rate (ORR). Univariate and multivariate analyses were used to explore the association of variables of interest with OS and PFS. 235 patients were included in our analysis. Median OS was 8.6 months (95% CI 6.6-12.1), the 1 year OS rate was 43% while the 2 years OS rate 29%. The median PFS was 5.1 months (95% CI 3.9-6.9); 46% of patients were alive at 6 months, 34% at 12 months and 25% at 24 months. According to RECIST 1.1, 18 patients (8%) experienced complete response (CR), 57 (24%) partial response (PR), 44 (19%) stable disease (SD), and 116 (49%) progressive disease (PD), with an ORR of 32%. Our study confirms the effectiveness of pembrolizumab in patients pretreated with a platinum-based combination, irrespective of their sensitivity to the first-line treatment and of their histology. In addition, we emphasized the limited benefit of the treatment with pembrolizumab in patients with hepatic metastases and poor ECOG performance status.","PeriodicalId":10267,"journal":{"name":"Clinical & Experimental Metastasis","volume":" ","pages":"655-665"},"PeriodicalIF":4.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141293221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

GFPT2 expression is induced by gemcitabine administration and enhances invasion by activating the hexosamine biosynthetic pathway in pancreatic cancer. 胰腺癌患者服用吉西他滨会诱导 GFPT2 的表达，并通过激活己胺生物合成途径增强侵袭能力。

IF 4.2 3区医学

Clinical & Experimental Metastasis Pub Date : 2024-10-01 Epub Date: 2024-06-18 DOI: 10.1007/s10585-024-10298-y

Kent Miyazaki, Kyohei Ariake, Satoko Sato, Takayuki Miura, Jingyu Xun, Daisuke Douchi, Masaharu Ishida, Hideo Ohtsuka, Masamichi Mizuma, Kei Nakagawa, Takashi Kamei, Michiaki Unno

{"title":"GFPT2 expression is induced by gemcitabine administration and enhances invasion by activating the hexosamine biosynthetic pathway in pancreatic cancer.","authors":"Kent Miyazaki, Kyohei Ariake, Satoko Sato, Takayuki Miura, Jingyu Xun, Daisuke Douchi, Masaharu Ishida, Hideo Ohtsuka, Masamichi Mizuma, Kei Nakagawa, Takashi Kamei, Michiaki Unno","doi":"10.1007/s10585-024-10298-y","DOIUrl":"10.1007/s10585-024-10298-y","url":null,"abstract":"Our previous studies revealed a novel link between gemcitabine (GEM) chemotherapy and elevated glutamine-fructose-6-phosphate transaminase 2 (GFPT2) expression in pancreatic cancer (PaCa) cells. GFPT2 is a rate-limiting enzyme in the hexosamine biosynthesis pathway (HBP). HBP can enhance metastatic potential by regulating epithelial-mesenchymal transition (EMT). The aim of this study was to further evaluate the effect of chemotherapy-induced GFPT2 expression on metastatic potential. GFPT2 expression was evaluated in a mouse xenograft model following GEM exposure and in clinical specimens of patients after chemotherapy using immunohistochemical analysis. The roles of GFPT2 in HBP activation, downstream pathways, and cellular functions in PaCa cells with regulated GFPT2 expression were investigated. GEM exposure increased GFPT2 expression in tumors resected from a mouse xenograft model and in patients treated with neoadjuvant chemotherapy (NAC). GFPT2 expression was correlated with post-operative liver metastasis after NAC. Its expression activated the HBP, promoting migration and invasion. Treatment with HBP inhibitors reversed these effects. Additionally, GFPT2 upregulated ZEB1 and vimentin expression and downregulated E-cadherin expression. GEM induction upregulated GFPT2 expression. Elevated GFPT2 levels promoted invasion by activating the HBP, suggesting the potential role of this mechanism in promoting chemotherapy-induced metastasis.","PeriodicalId":10267,"journal":{"name":"Clinical & Experimental Metastasis","volume":" ","pages":"777-789"},"PeriodicalIF":4.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11499537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141418154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

UBTF mediates activation of L3MBTL2 to suppress NISCH expression through histone H2AK119 monoubiquitination modification in breast cancer. UBTF 在乳腺癌中通过组蛋白 H2AK119 单泛素化修饰介导 L3MBTL2 的激活以抑制 NISCH 的表达。

IF 4.2 3区医学

Clinical & Experimental Metastasis Pub Date : 2024-10-01 Epub Date: 2024-06-27 DOI: 10.1007/s10585-024-10299-x

Kun Chen, Yun Dong, Gaojian He, Xuefeng He, Meitong Pan, Xuemei Huang, Xiaolan Yu, Jiyi Xia

{"title":"UBTF mediates activation of L3MBTL2 to suppress NISCH expression through histone H2AK119 monoubiquitination modification in breast cancer.","authors":"Kun Chen, Yun Dong, Gaojian He, Xuefeng He, Meitong Pan, Xuemei Huang, Xiaolan Yu, Jiyi Xia","doi":"10.1007/s10585-024-10299-x","DOIUrl":"10.1007/s10585-024-10299-x","url":null,"abstract":"Lethal(3)malignant brain tumor-like protein 2 (L3MBTL2) has been related to transcriptional inhibition and chromatin compaction. Nevertheless, the biological functions and mechanisms of L3MBTL2 are undefined in breast cancer (BRCA). Here, we revealed that L3MBTL2 is responsible for the decline of Nischarin (NISCH), a well-known tumor suppressor, in BRCA, and explored the detailed mechanism. Knockdown of L3MBTL2 reduced monoubiquitination of histone H2A at lysine-119 (H2AK119ub), leading to reduced binding to the NISCH promoter and increased expression of NISCH. Meanwhile, the knockdown of L3MBTL2 decreased proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of BRCA cells, and increased apoptosis, which were abated by NISCH knockdown. Nucleolar transcription factor 1 (UBTF) induced the transcription of L3MBTL2 in BRCA, and the suppressing effects of UBTF silencing on EMT in BRCA cells were also reversed by NISCH knockdown. Knockdown of UBTF slowed tumor progression and attenuated lung tumor infiltration, whereas simultaneous knockdown of NISCH accelerated EMT and increased tumor lung metastasis. Taken together, our results show that L3MBTL2, transcriptionally activated by UBTF, exerts oncogenic functions in BRCA, by catalyzing H2AK119Ub and reducing expression of NISCH.","PeriodicalId":10267,"journal":{"name":"Clinical & Experimental Metastasis","volume":" ","pages":"791-805"},"PeriodicalIF":4.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141455629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction: SETBP1 activation upon MDM4-enhanced ubiquitination of NR3C1 triggers dissemination of colorectal cancer cells. 更正：SETBP1 在 MDM4 增强的 NR3C1 泛素化作用下被激活，从而引发结直肠癌细胞扩散。

IF 4.2 3区医学

Clinical & Experimental Metastasis Pub Date : 2024-10-01 DOI: 10.1007/s10585-024-10303-4

Peng Zhai, Heng Zhang, Qiang Li, Zhifeng Hu, Huaguo Zhang, Ming Yang, Chungen Xing, Yunhu Guo

引用次数: 0

The movement of mitochondria in breast cancer: internal motility and intercellular transfer of mitochondria. 乳腺癌线粒体的移动：线粒体的内部移动和细胞间转移。

IF 4.2 3区医学

Clinical & Experimental Metastasis Pub Date : 2024-10-01 Epub Date: 2024-03-15 DOI: 10.1007/s10585-024-10269-3

Sarah Libring, Emily D Berestesky, Cynthia A Reinhart-King

{"title":"The movement of mitochondria in breast cancer: internal motility and intercellular transfer of mitochondria.","authors":"Sarah Libring, Emily D Berestesky, Cynthia A Reinhart-King","doi":"10.1007/s10585-024-10269-3","DOIUrl":"10.1007/s10585-024-10269-3","url":null,"abstract":"As a major energy source for cells, mitochondria are involved in cell growth and proliferation, as well as migration, cell fate decisions, and many other aspects of cellular function. Once thought to be irreparably defective, mitochondrial function in cancer cells has found renewed interest, from suggested potential clinical biomarkers to mitochondria-targeting therapies. Here, we will focus on the effect of mitochondria movement on breast cancer progression. Mitochondria move both within the cell, such as to localize to areas of high energetic need, and between cells, where cells within the stroma have been shown to donate their mitochondria to breast cancer cells via multiple methods including tunneling nanotubes. The donation of mitochondria has been seen to increase the aggressiveness and chemoresistance of breast cancer cells, which has increased recent efforts to uncover the mechanisms of mitochondrial transfer. As metabolism and energetics are gaining attention as clinical targets, a better understanding of mitochondrial function and implications in cancer are required for developing effective, targeted therapeutics for cancer patients.","PeriodicalId":10267,"journal":{"name":"Clinical & Experimental Metastasis","volume":" ","pages":"567-587"},"PeriodicalIF":4.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11499424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140136571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Isolated hyperthermic perfusions for cutaneous melanoma in-transit metastasis of the limb and uveal melanoma metastasis to the liver. 孤立的高温灌注治疗肢体转移中的皮肤黑色素瘤和肝脏转移的葡萄膜黑色素瘤。

IF 4.2 3区医学

Clinical & Experimental Metastasis Pub Date : 2024-08-01 Epub Date: 2023-10-16 DOI: 10.1007/s10585-023-10234-6

Anne Huibers, Danielle K DePalo, Matthew C Perez, Jonathan S Zager, Roger Olofsson Bagge

引用次数: 0

Personalized therapy in oncology: melanoma as a paradigm for molecular-targeted treatment approaches. 肿瘤学中的个性化疗法：黑色素瘤是分子靶向治疗方法的典范。

IF 4.2 3区医学

Clinical & Experimental Metastasis Pub Date : 2024-08-01 Epub Date: 2024-06-27 DOI: 10.1007/s10585-024-10291-5

Kevin B Kim

引用次数: 0

Immune responses and immunotherapeutic approaches in the treatment against cancer. 治疗癌症的免疫反应和免疫疗法。

IF 4.2 3区医学

Clinical & Experimental Metastasis Pub Date : 2024-08-01 Epub Date: 2024-08-18 DOI: 10.1007/s10585-024-10300-7

Stanley P Leong

引用次数: 0

Cancer metastasis through the lymphatic versus blood vessels. 癌症通过淋巴和血管转移。

IF 4.2 3区医学

Clinical & Experimental Metastasis Pub Date : 2024-08-01 Epub Date: 2024-06-28 DOI: 10.1007/s10585-024-10288-0

Stanley P Leong, Marlys H Witte

引用次数: 0

The role of host response to chemotherapy: resistance, metastasis and clinical implications. 宿主对化疗反应的作用:耐药、转移和临床意义。

IF 4.2 3区医学

Clinical & Experimental Metastasis Pub Date : 2024-08-01 Epub Date: 2023-11-24 DOI: 10.1007/s10585-023-10243-5

Abhilash Deo, Jonathan P Sleeman, Yuval Shaked

{"title":"The role of host response to chemotherapy: resistance, metastasis and clinical implications.","authors":"Abhilash Deo, Jonathan P Sleeman, Yuval Shaked","doi":"10.1007/s10585-023-10243-5","DOIUrl":"10.1007/s10585-023-10243-5","url":null,"abstract":"Chemotherapy remains the primary treatment for most metastatic cancers. However, the response to chemotherapy and targeted agents is often transient, and concurrent development of resistance is the primary impediment to effective cancer therapy. Strategies to overcome resistance to treatment have focused on cancer cell intrinsic factors and the tumor microenvironment (TME). Recent evidence indicates that systemic chemotherapy has a significant impact on the host that either facilitates tumor growth, allowing metastatic spread, or renders treatment ineffective. These host responses include the release of bone marrow-derived cells, activation of stromal cells in the TME, and induction of different molecular effectors. Here, we provide an overview of chemotherapy-induced systemic host responses that support tumor aggressiveness and metastasis, and which contribute to therapy resistance. Studying host responses to chemotherapy provides a solid basis for the development of adjuvant strategies to improve treatment outcomes and delay resistance to chemotherapy. This review discusses the emerging field of host response to cancer therapy, and its preclinical and potential clinical implications, explaining how under certain circumstances, these host effects contribute to metastasis and resistance to chemotherapy.","PeriodicalId":10267,"journal":{"name":"Clinical & Experimental Metastasis","volume":" ","pages":"495-507"},"PeriodicalIF":4.2,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138298565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0