Pub Date : 2025-11-06DOI: 10.1016/j.cpt.2025.11.001
Jiaen You , Zebing Liu , Kang He
Primary cardiac tumors are rare and often present diagnostic challenges due to their non-specific symptoms and imaging characteristics. In this report, we present a case of right atrial intimal sarcoma (IS) with liver metastasis. A 49-year-old woman presented to the emergency department with acute dyspnea, cyanosis, nausea, vomiting, and upper abdominal pain. Echocardiography revealed a large pericardial effusion and a mass in the right atrium. Contrast-enhanced computed tomography (CT) and positron emission tomography/CT (PET/CT) confirmed the presence of multiple nodules in the right atrium and hepatic masses, suggesting metastatic disease. Laboratory tests indicated liver dysfunction, with elevated carbohydrate antigen 125 (CA125) and normal alpha-fetoprotein (AFP) levels. These clinical features initially suggested a diagnosis of hepatocellular carcinoma with isolated cardiac metastasis. However, the final pathological examination and gene sequencing results were unexpected, leading to the diagnosis of right atrial IS with liver metastasis. The patient was managed conservatively and remained alive for 8 months at the time of manuscript submission.
{"title":"Right atrial intimal sarcoma with liver metastasis: A case report and literature review","authors":"Jiaen You , Zebing Liu , Kang He","doi":"10.1016/j.cpt.2025.11.001","DOIUrl":"10.1016/j.cpt.2025.11.001","url":null,"abstract":"<div><div>Primary cardiac tumors are rare and often present diagnostic challenges due to their non-specific symptoms and imaging characteristics. In this report, we present a case of right atrial intimal sarcoma (IS) with liver metastasis. A 49-year-old woman presented to the emergency department with acute dyspnea, cyanosis, nausea, vomiting, and upper abdominal pain. Echocardiography revealed a large pericardial effusion and a mass in the right atrium. Contrast-enhanced computed tomography (CT) and positron emission tomography/CT (PET/CT) confirmed the presence of multiple nodules in the right atrium and hepatic masses, suggesting metastatic disease. Laboratory tests indicated liver dysfunction, with elevated carbohydrate antigen 125 (CA125) and normal alpha-fetoprotein (AFP) levels. These clinical features initially suggested a diagnosis of hepatocellular carcinoma with isolated cardiac metastasis. However, the final pathological examination and gene sequencing results were unexpected, leading to the diagnosis of right atrial IS with liver metastasis. The patient was managed conservatively and remained alive for 8 months at the time of manuscript submission.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"4 2","pages":"Pages 158-161"},"PeriodicalIF":2.8,"publicationDate":"2025-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146078480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-29DOI: 10.1016/j.cpt.2025.08.005
Haitao Tao , Yining Liu , Lijie Wang , Jinliang Wang , Junxun Ma , Guoqing Zhang , Zhefeng Liu , Yi Hu
Background
Immune checkpoint inhibitors combined with PARP inhibitors and chemotherapy can enhance anti-tumor activity. This phase Ib clinical study was designed to evaluate the safety and efficacy of cisplatin in combination with sintilimab and niraparib in patients with advanced solid tumors.
Methods
Patients with advanced solid tumors who had progressed after one or more lines of standard therapy were enrolled in the study, and received cisplatin and sintilimab on day 1 and niraparib from days 1–21 every 3 weeks for up to 4 cycles, followed by maintenance therapy with sintilimab and niraparib (the same doses and schedules as before), until disease progression, death, or intolerable toxicities. During the dose-escalation phase, patients were divided into three dose groups on the basis of a 3 + 3 dose-escalation regimen, and a dose-expansion phase was conducted based on the determined maximum tolerated dose (MTD). The primary endpoint was safety, including treatment-related adverse events (TRAEs), dose-limiting toxicity (DLT), and the recommended phase 2 dose (RP2D), and the secondary endpoint was efficacy. In addition, exploratory endpoints were prespecified to analyze potential biomarkers.
Results
From July 31, 2019, to July 1, 2022, a total of 26 patients were enrolled, and no DLTs were observed in the dose-escalation phase. The recommended RP2Ds of cisplatin, sintilimab, and niraparib were 60 mg/m2, 200 mg, and 100 mg every 3 weeks, respectively. All patients experienced TRAEs of varying severity, and a 19.23% (5 patients) incidence of immune-related adverse events (irAEs). With the median follow-up time of 47.9 months (95% CI: 38.8–NA), objective response rate was 26.92% (7 patients, 95% confidence interval [CI], 11.57–47.79), disease control rate was 57.69% (15 patients, 95% CI: 36.92–76.65), the median progression-free survival (PFS) was 3.30 months (95% CI: 2.14–4.46) and the median overall survival (OS) was 8.03 months (95% CI: 3.41–12.66), with PFS rates of 26.92% (seven patients) and 11.54% (three patients) at 6 and 12 months, and OS rates of 69.23%, 34.62% and 11.54% at 6, 12 and 24 months, respectively. Patients with programmed cell death ligand 1 (PD-L1) expression ≥ 1% showed significantly longer PFS (3.93 months, P = 0.032) and OS (14.97 months, P = 0.036) compared to those with PD-L1 expression < 1%.
Conclusion
The combination of cisplatin with sintilimab and niraparib showed a manageable safety profile and modest anti-tumor activity in patients with advanced solid tumors. Further validation in larger, histology-specific patients is needed to confirm clinical benefit.
{"title":"Safety and efficacy of Cisplatin in combination with Sintilimab and Niraparib in patients with advanced solid tumors: A phase Ib study","authors":"Haitao Tao , Yining Liu , Lijie Wang , Jinliang Wang , Junxun Ma , Guoqing Zhang , Zhefeng Liu , Yi Hu","doi":"10.1016/j.cpt.2025.08.005","DOIUrl":"10.1016/j.cpt.2025.08.005","url":null,"abstract":"<div><h3>Background</h3><div>Immune checkpoint inhibitors combined with PARP inhibitors and chemotherapy can enhance anti-tumor activity. This phase Ib clinical study was designed to evaluate the safety and efficacy of cisplatin in combination with sintilimab and niraparib in patients with advanced solid tumors.</div></div><div><h3>Methods</h3><div>Patients with advanced solid tumors who had progressed after one or more lines of standard therapy were enrolled in the study, and received cisplatin and sintilimab on day 1 and niraparib from days 1–21 every 3 weeks for up to 4 cycles, followed by maintenance therapy with sintilimab and niraparib (the same doses and schedules as before), until disease progression, death, or intolerable toxicities. During the dose-escalation phase, patients were divided into three dose groups on the basis of a 3 + 3 dose-escalation regimen, and a dose-expansion phase was conducted based on the determined maximum tolerated dose (MTD). The primary endpoint was safety, including treatment-related adverse events (TRAEs), dose-limiting toxicity (DLT), and the recommended phase 2 dose (RP2D), and the secondary endpoint was efficacy. In addition, exploratory endpoints were prespecified to analyze potential biomarkers.</div></div><div><h3>Results</h3><div>From July 31, 2019, to July 1, 2022, a total of 26 patients were enrolled, and no DLTs were observed in the dose-escalation phase. The recommended RP2Ds of cisplatin, sintilimab, and niraparib were 60 mg/m<sup>2</sup>, 200 mg, and 100 mg every 3 weeks, respectively. All patients experienced TRAEs of varying severity, and a 19.23% (5 patients) incidence of immune-related adverse events (irAEs). With the median follow-up time of 47.9 months (95% CI: 38.8–NA), objective response rate was 26.92% (7 patients, 95% confidence interval [CI], 11.57–47.79), disease control rate was 57.69% (15 patients, 95% CI: 36.92–76.65), the median progression-free survival (PFS) was 3.30 months (95% CI: 2.14–4.46) and the median overall survival (OS) was 8.03 months (95% CI: 3.41–12.66), with PFS rates of 26.92% (seven patients) and 11.54% (three patients) at 6 and 12 months, and OS rates of 69.23%, 34.62% and 11.54% at 6, 12 and 24 months, respectively. Patients with programmed cell death ligand 1 (PD-L1) expression ≥ 1% showed significantly longer PFS (3.93 months, <em>P</em> = 0.032) and OS (14.97 months, <em>P</em> = 0.036) compared to those with PD-L1 expression < 1%.</div></div><div><h3>Conclusion</h3><div>The combination of cisplatin with sintilimab and niraparib showed a manageable safety profile and modest anti-tumor activity in patients with advanced solid tumors. Further validation in larger, histology-specific patients is needed to confirm clinical benefit.</div></div><div><h3>Trial registration</h3><div><span><span>https://www.chictr.org.cn/</span><svg><path></path></svg></span>; ID: ChiCTR1900024488.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"4 1","pages":"Pages 41-50"},"PeriodicalIF":2.8,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145618290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-08DOI: 10.1016/j.cpt.2025.07.002
Yaguang Peng , Peng Lyu , Xiaoxia Peng
{"title":"Improving research transparency: An interpretation of the updated consolidated standards of reporting trials 2025 guideline from the perspective of clinical trials in oncology","authors":"Yaguang Peng , Peng Lyu , Xiaoxia Peng","doi":"10.1016/j.cpt.2025.07.002","DOIUrl":"10.1016/j.cpt.2025.07.002","url":null,"abstract":"","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"4 1","pages":"Pages 75-80"},"PeriodicalIF":2.8,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145790124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-05DOI: 10.1016/j.cpt.2025.06.008
Zhuocheng Lai , Chenxi Hu , Jirong Jie , Yongyuan Xiao , Yuanchao Zhu , Xueni Guo , Yintong Liu , Yiwei Wang , Shiyu Pang , Xiangbo Zeng , Wanlong Tan , Qiong Wang
Neuroendocrine prostate cancer (NEPC) is an aggressive subtype of castration-resistant prostate cancer (CRPC) that is typically resistant to nearly all current therapies. In this study, single-cell RNA sequencing (scRNA-seq) and dataset analyses identified Centrosomal Protein 55 (CEP55) as a critical factor in the transformation from hormone-sensitive prostate cancer (HSPC) to CRPC and, ultimately to, NEPC. Subsequent bioinformatics analyses and validation with clinical samples demonstrated that CEP55 is significantly upregulated in NEPC tissues compared to HSPC and CRPC. Furthermore, while CEP55 show no significant association with the immune microenvironment or cancer-associated fibroblasts (CAFs), our findings indicate that it directly mediates the plasticity of prostate cancer cells, thereby driving NEPC progression. Specifically, in vivo and in vitro experiments confirmed that CEP55 enhances cell proliferation, migration, invasion and the expression of NEPC biomarkers in prostate cancer. Importantly, although cisplatin is the primary treatment for NEPC clinically, CEP55 has been shown to regulate cisplatin resistance through the phosphorylation of CDK1 at the tyrosine 15 (Tyr15) site. In summary, our study identifies a key gene that influences the neuroendocrine differentiation process in prostate cancer, suggesting its potential as an important therapeutic target.
{"title":"Neuroendocrine prostate cancer (NEPC)-associated CEP55 promotes cisplatin resistance in prostate cancer by regulating CDK1 phosphorylation","authors":"Zhuocheng Lai , Chenxi Hu , Jirong Jie , Yongyuan Xiao , Yuanchao Zhu , Xueni Guo , Yintong Liu , Yiwei Wang , Shiyu Pang , Xiangbo Zeng , Wanlong Tan , Qiong Wang","doi":"10.1016/j.cpt.2025.06.008","DOIUrl":"10.1016/j.cpt.2025.06.008","url":null,"abstract":"<div><div>Neuroendocrine prostate cancer (NEPC) is an aggressive subtype of castration-resistant prostate cancer (CRPC) that is typically resistant to nearly all current therapies. In this study, single-cell RNA sequencing (scRNA-seq) and dataset analyses identified Centrosomal Protein 55 (<em>CEP55</em>) as a critical factor in the transformation from hormone-sensitive prostate cancer (HSPC) to CRPC and, ultimately to, NEPC. Subsequent bioinformatics analyses and validation with clinical samples demonstrated that <em>CEP55</em> is significantly upregulated in NEPC tissues compared to HSPC and CRPC. Furthermore, while <em>CEP55</em> show no significant association with the immune microenvironment or cancer-associated fibroblasts (CAFs), our findings indicate that it directly mediates the plasticity of prostate cancer cells, thereby driving NEPC progression. Specifically, <em>in vivo</em> and <em>in vitro</em> experiments confirmed that <em>CEP55</em> enhances cell proliferation, migration, invasion and the expression of NEPC biomarkers in prostate cancer. Importantly, although cisplatin is the primary treatment for NEPC clinically, <em>CEP55</em> has been shown to regulate cisplatin resistance through the phosphorylation of CDK1 at the tyrosine 15 (Tyr15) site. In summary, our study identifies a key gene that influences the neuroendocrine differentiation process in prostate cancer, suggesting its potential as an important therapeutic target.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"4 1","pages":"Pages 51-63"},"PeriodicalIF":2.8,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145618291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The pathophysiology of many ailments, including neurological, gastrointestinal, and metabolic problems, is well known to be influenced by intestinal dysbiosis. Clinical research has provided evidence suggesting a strong correlation between dysbiosis of the gut microbiome and colorectal cancer (CRC) development. The active reprogramming of metabolic pathways to boost glycolysis, fatty acid production, lipogenesis, and glutaminolysis constitutes a major metabolic shift in cancer development, including CRC. The complex combination of different factors leads to CRC, making it an environmental disease. These factors include food and lifestyle choices, genetics and family history, age, underlying intestinal diseases, and dysbiosis of the gut microbiota. One of the primary risk factors for carcinoma development is diet, which impacts an individual’s gut microbiome. In addition to impacting CRC formation, the gut microbiome also has immunomodulatory effects, including various immunological interactions and the underlying mechanisms governing them. Microbial interactions in CRC have been extensively studied, yet numerous unresolved queries exist on how gut bacteria can influence treatment. It is possible to perform microbiome-driven immunotherapies focusing on probiotics, prebiotics, and synbiotics. However, large-scale treatment utilization in CRC patients is limited by several issues, including variations in the microbial makeup of each patient’s gut and a lack of established methods. The study highlights the impact of several risk factors, including dysbiosis of the gut microbiome and different approaches to halting and treating CRC progression with a focus on diet changes and modulation of the gut flora. Given the foregoing, we propose that if research gaps are addressed and immunotherapy is paired with microbial interventions, microbiota-based therapeutics could potentially impede the growth of tumors and treat CRC.
{"title":"Emerging risk factors and the role of gut microbiota in immunomodulation and therapeutic implications in colorectal cancer","authors":"Sonakshi Modeel , Sneha Siwach , Padma Dolkar , Meenu Chaurasia , Pankaj Yadav , Apoorva Atri , Aarzoo Yadav , Tarana Negi , Ram Krishan Negi","doi":"10.1016/j.cpt.2025.06.007","DOIUrl":"10.1016/j.cpt.2025.06.007","url":null,"abstract":"<div><div>The pathophysiology of many ailments, including neurological, gastrointestinal, and metabolic problems, is well known to be influenced by intestinal dysbiosis. Clinical research has provided evidence suggesting a strong correlation between dysbiosis of the gut microbiome and colorectal cancer (CRC) development. The active reprogramming of metabolic pathways to boost glycolysis, fatty acid production, lipogenesis, and glutaminolysis constitutes a major metabolic shift in cancer development, including CRC. The complex combination of different factors leads to CRC, making it an environmental disease. These factors include food and lifestyle choices, genetics and family history, age, underlying intestinal diseases, and dysbiosis of the gut microbiota. One of the primary risk factors for carcinoma development is diet, which impacts an individual’s gut microbiome. In addition to impacting CRC formation, the gut microbiome also has immunomodulatory effects, including various immunological interactions and the underlying mechanisms governing them. Microbial interactions in CRC have been extensively studied, yet numerous unresolved queries exist on how gut bacteria can influence treatment. It is possible to perform microbiome-driven immunotherapies focusing on probiotics, prebiotics, and synbiotics. However, large-scale treatment utilization in CRC patients is limited by several issues, including variations in the microbial makeup of each patient’s gut and a lack of established methods. The study highlights the impact of several risk factors, including dysbiosis of the gut microbiome and different approaches to halting and treating CRC progression with a focus on diet changes and modulation of the gut flora. Given the foregoing, we propose that if research gaps are addressed and immunotherapy is paired with microbial interventions, microbiota-based therapeutics could potentially impede the growth of tumors and treat CRC.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"4 1","pages":"Pages 14-30"},"PeriodicalIF":2.8,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145521277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Despite significant advances in cancer diagnosis and therapy, the global burden of cancer continues to escalate, characterized by increasing incidence and mortality rates. A problem for successful treatment is chemoresistance, which undermines the effectiveness of traditional and targeted treatments. This review synthesizes emerging therapeutic strategies, including targeted agents, combinatorial regimens, and advances in precision medicine, with a focus on improving clinical outcomes. Integrating the latest understanding from molecular biology, genomics, and pharmacology emphasizes new paths to overcoming resistance. Particular attention is focused on the roles played by exosomes, metabolic reprogramming, and the tumour microenvironment in facilitating drug resistance, as well as promising approaches to counteract these mechanisms and improve therapeutic responsiveness.
{"title":"Chemoresistance: The hidden barrier in cancer treatment","authors":"Vivek Kumar Dhiman , Manju Kumari , Devendra Singh","doi":"10.1016/j.cpt.2025.07.001","DOIUrl":"10.1016/j.cpt.2025.07.001","url":null,"abstract":"<div><div>Despite significant advances in cancer diagnosis and therapy, the global burden of cancer continues to escalate, characterized by increasing incidence and mortality rates. A problem for successful treatment is chemoresistance, which undermines the effectiveness of traditional and targeted treatments. This review synthesizes emerging therapeutic strategies, including targeted agents, combinatorial regimens, and advances in precision medicine, with a focus on improving clinical outcomes. Integrating the latest understanding from molecular biology, genomics, and pharmacology emphasizes new paths to overcoming resistance. Particular attention is focused on the roles played by exosomes, metabolic reprogramming, and the tumour microenvironment in facilitating drug resistance, as well as promising approaches to counteract these mechanisms and improve therapeutic responsiveness.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"4 2","pages":"Pages 98-109"},"PeriodicalIF":2.8,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145885752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Weight management in overweight or obesity: Implications for cancer pathogenesis and prognosis","authors":"Yue Wang , Haitao Niu , Peng Lyu, Bing Liu, Junmin Wei","doi":"10.1016/j.cpt.2025.05.001","DOIUrl":"10.1016/j.cpt.2025.05.001","url":null,"abstract":"","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 4","pages":"Pages 273-275"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144548945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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