Cancer pathogenesis and therapy最新文献

{"title":"The latest research on advanced gynecological oncology: A therapeutic perspective","authors":"Bohao Zheng , Jinlu Ma , Shengtao Zhou","doi":"10.1016/j.cpt.2024.08.003","DOIUrl":"10.1016/j.cpt.2024.08.003","url":null,"abstract":"","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 3","pages":"Pages 179-180"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143887141","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":"Epithelial–mesenchymal transition (EMT) and its role in acquired epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) chemoresistance in non-small cell lung cancer (NSCLC)","authors":"Ma. Carmela P. Dela Cruz,&nbsp;Paul Mark B. Medina","doi":"10.1016/j.cpt.2024.07.001","DOIUrl":"10.1016/j.cpt.2024.07.001","url":null,"abstract":"<div><div>Epithelial–mesenchymal transition (EMT) is a biological process that involves the transformation of epithelial cells into cells with a mesenchymal phenotype, enhancing their migratory and invasive capabilities. EMT is crucial in embryonic development, tissue healing, and wound repair, and aids in forming diverse cell types and structures. However, aberrant EMT is involved in pathogenic processes, including fibrosis, cancer development, and progression. Recent studies show that EMT contributes to resistance to cancer treatment, including epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) therapy in non-small cell lung cancer (NSCLC). This review discusses the intricate relationship between EMT and acquired chemoresistance to EGFR-TKIs. It details evidence on how EGFR-TKIs might induce EMT and how EMT may cause EGFR-TKI resistance. Understanding these pathways is crucial for developing effective prognostic and therapeutic strategies to predict and combat acquired chemoresistance in NSCLC, advancing the field toward more targeted and personalized treatment approaches.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 3","pages":"Pages 215-225"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141713967","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":"Spices and culinary herbs for the prevention and treatment of breast cancer: A comprehensive review with mechanistic insights","authors":"Md. Liakot Ali,&nbsp;Fabiha Noushin,&nbsp;Qurratul Ain Sadia,&nbsp;Afroz Fathema Metu,&nbsp;Jannatul Naima Meem,&nbsp;Md. Tanvir Chowdhury,&nbsp;Md. Hossain Rasel,&nbsp;Khurshida Jahan Suma,&nbsp;Md. Abdul Alim,&nbsp;Muhammad Abdul Jalil,&nbsp;Md. Jahirul Islam Mamun,&nbsp;Md. Mahmudul Hasan,&nbsp;Neamul Hoque,&nbsp;Eva Azme","doi":"10.1016/j.cpt.2024.07.003","DOIUrl":"10.1016/j.cpt.2024.07.003","url":null,"abstract":"<div><div>Breast cancer (BC) continues to be the primary malignant neoplasm affecting women. For many years, traditional approaches such as chemotherapy, hormone therapy, radiation, and surgical interventions have been employed to treat BC. However, these therapies often fall short due to considerable adverse effects and the development of multidrug resistance or tolerance. Spices and culinary herbs that have been utilized in culinary practices for millennia have also demonstrated therapeutic effects in traditional medicinal practices serving to both prevent and treat BC. This review aims to comprehensively explore the roles and underlying mechanisms through which spices and culinary herbs exert anti-BC properties. These natural ingredients exhibit diverse anti-BC effects that encompass diverse mechanisms, including the inhibition of BC cell proliferation, migration, metastasis, and angiogenesis, as well as the induction of cell cycle arrest and apoptosis. These actions are achieved by targeting signaling pathways such as phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR), notch signaling, Hedgehog signaling, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and Wingless/int (Wnt)/β-catenin signaling pathways that are predominantly overexpressed in breast tumors or are exploited by them to promote cancer progression. Additionally, compounds such as curcumin, allicin, gingerol, zerumbone, diosgenin, capsaicin, piperine, quercetin, malabaricone C, eugenol, cardamomin, carnosol, cinnamaldehyde, sinigrin present in these spices and herbs may be more effective with reduced side effects against BC compared to conventional chemotherapeutic drugs. This review presents a concise overview of the potential contributions of spices, culinary herbs, and their potent bioactive constituents against BC, with particular emphasis on elucidating their mechanisms of action.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 3","pages":"Pages 197-214"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141707282","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":"Tumor-associated macrophages (TAMs): Constructing an immunosuppressive microenvironment bridge for pancreatic ductal adenocarcinoma (PDAC)","authors":"Runjie Liu ,&nbsp;Jianang Li ,&nbsp;Liang Liu ,&nbsp;Wenquan Wang ,&nbsp;Jinbin Jia","doi":"10.1016/j.cpt.2024.07.004","DOIUrl":"10.1016/j.cpt.2024.07.004","url":null,"abstract":"<div><div>Pancreatic ductal adenocarcinoma (PDAC) is a fatal disease with increasing incidences worldwide. The overall 5-year survival rate remains low, underscoring the urgent need for effective therapies. Despite the promising efficacy of immunotherapy for various solid tumors, its benefits for pancreatic cancer have been disappointing. This is largely because of the complex and unique mechanisms of immune evasion inherent in PDAC. Emerging evidence has highlighted the pivotal role of tumor-associated macrophages (TAMs) in facilitating the immune escape of PDAC. TAMs significantly contribute to forming an immunosuppressive microenvironment, which hinders the effectiveness of immunotherapeutic approaches. They achieve this through multiple pathways, including the secretion of cytokines and the promotion or inhibition of multiple immune cells. In this review, we summarized the main pathways through which TAMs form an immunosuppressive microenvironment in PDAC. We also examined the current status and recent progress of immunotherapy strategies that specifically target macrophages. By understanding these mechanisms and exploring targeted therapies, we aimed to shed light on potential avenues for improving the treatment outcomes of this devastating disease.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 3","pages":"Pages 183-196"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141845627","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":"ACSM2B rs73530508 polymorphism affects susceptibility to esophageal cancer by regulating indolepropionic acid levels","authors":"Yun Chen ,&nbsp;Ruijun Lin ,&nbsp;Qianhua Luo ,&nbsp;Tao Liu ,&nbsp;Xiaoyan Li ,&nbsp;Danling Zheng ,&nbsp;Siman Su ,&nbsp;Meini Chen ,&nbsp;Jianxiang Huang ,&nbsp;Yihui Huang ,&nbsp;Shuyao Zhang","doi":"10.1016/j.cpt.2024.09.003","DOIUrl":"10.1016/j.cpt.2024.09.003","url":null,"abstract":"<div><h3>Background</h3><div>Tryptophan metabolism is involved in esophageal carcinogenesis. However, its genetic mechanisms remain unclear. This study aimed to investigate the effect of genetic variants that encode tryptophan metabolism on susceptibility to esophageal cancer (EC) and elucidate the mechanisms underlying genetic variation in EC progression.</div></div><div><h3>Methods</h3><div>Age- and sex-matched cohorts of 167 patients with EC and 236 healthy controls were enrolled in this study. The concentrations of tryptophan and its metabolites were determined by self-assembled high-performance liquid chromatography-tandem mass spectrometry. High-throughput sequencing techniques were utilized to detect candidate coding genetic variants, and dominant genetic models were used to elucidate the genotypic associations.</div></div><div><h3>Results</h3><div>Tryptophan metabolism was significantly imbalanced in patients with EC, with elevated indolepropionic acid (IPA) levels reducing the risk of EC susceptibility. <em>ACSM2B</em> rs73530508 (A &gt; G) mutation was associated with higher IPA levels <em>in vivo</em> (<em>P</em> = 0.0004, false discovery rate [FDR] = 0.0092) and significantly reduced the risk of EC susceptibility (odds ratio [OR]: 0.576, <em>P</em>_adj = 0.0161). Mediation effect analysis indicated that single-nucleotide polymorphism may inhibit carcinogenesis by reducing IPA metabolism and excretion with a mediation effect of 45.54%.</div></div><div><h3>Conclusions</h3><div>This study identifies the potential mechanism of <em>ACSM2B</em> rs73530508 (A &gt; G) in esophageal carcinogenesis and its role in driving increased IPA levels, thereby suppressing the risk of development.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 3","pages":"Pages 244-252"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143887013","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":"Targeting cuproptosis for cancer therapy: Focus on the anti-tumor immune system","authors":"Xuan Zhang,&nbsp;Xiaohong Han","doi":"10.1016/j.cpt.2024.07.005","DOIUrl":"10.1016/j.cpt.2024.07.005","url":null,"abstract":"<div><div>Copper (Cu) is an indispensable micronutrient that maintains signaling pathways and biological homeostasis in almost all cell types; however, its excess affects the tricarboxylic acid cycle, causes the accumulation of fatty acylated proteins, destabilization of iron–sulfur cluster proteins, and increases the levels of intracellular reactive oxygen species, leading to proteotoxic stress and cell death. Cuproptosis, a form of Cu-dependent cell death, differs from other types of regulated cell death (RCD) and was first reported in <em>Science</em> in 2022. Recently, the RCD pathways have been targeted in cancer therapy. However, the escape of apoptosis in tumor cells causes resistance to treatment and tumor recurrence. Therefore, there is an urgent need to study the alternative mechanisms of cancer cell mortality. Compared to normal patients, a significant increase in serum Cu ion levels has been observed in patients with tumors. Moreover, tumor cell proliferation, angiogenesis, and metastasis are associated with cuproptosis. Thus, exploring cancer signaling pathways related to cuproptosis will provide a new perspective for the development of anti-cancer drugs. Importantly, cuproptosis is closely associated with the modulation of anti-tumor immunity. The expression of cuproptosis-related genes (CRGs) is significantly correlated with immune cell infiltration and the immune checkpoint programmed cell death protein 1 (<em>PD-1</em>)/programmed death-ligand 1 (<em>PD-L1</em>). Based on these findings, a series of cuproptosis-related drugs have been used in tumor-targeted combination therapy or as immune synergists. Therefore, elucidating the role of cuproptosis per cancer stage and in the tumor immune microenvironment (TIME) is helpful in clarifying the potential value of Cu in the treatment of specific cancers. In this review, we summarize specific cancer signaling pathways related to cuproptosis and cancer treatment based on the regulation of Cu concentration. The combination of these two approaches may help researchers develop more therapies targeting cuproptosis-related pathways. Importantly, we focused on the effect of cuproptosis on the TIME and systematically discussed the role of CRGs in tumor immunity considering CRG-related anti-tumor immune signaling pathways, tumor prognosis scoring system, anti-tumor immunotherapy, and biological experiments and bioinformatics prediction models, to provide new ideas for the development of anticancer therapy targeting cuproptosis-related pathways.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 3","pages":"Pages 226-243"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141853812","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":"Insights on the prognostic value of visceral obesity in stage IVB cervical cancer treatment","authors":"Raghul Murugan","doi":"10.1016/j.cpt.2025.02.001","DOIUrl":"10.1016/j.cpt.2025.02.001","url":null,"abstract":"","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 3","pages":"Pages 267-268"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143887011","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":"Role of Candida albicans in chronic inflammation and the development of oral squamous cell carcinoma","authors":"Malavika G,&nbsp;Sujith Sri Surya Ravi,&nbsp;Datchanamoorthy Maheswary,&nbsp;Kakithakara Vajravelu Leela,&nbsp;Rahul Harikumar Lathakumari,&nbsp;Lekshmi Priya K S","doi":"10.1016/j.cpt.2025.03.002","DOIUrl":"10.1016/j.cpt.2025.03.002","url":null,"abstract":"<div><div>Oral cancer pathogenesis is significantly influenced by <em>Candida</em> species, especially <em>C. albicans</em>, through chronic inflammation and cellular dysregulation. Epidemiological studies highlight a strong correlation between persistent <em>Candida</em> infections and oral carcinogenesis. Experimental evidence has identified key biomolecular mechanisms, including biofilm formation, epithelial invasion, and immune evasion. Chronic inflammation induced by <em>Candida</em> fosters a pro-tumorigenic environment characterized by oxidative stress, cytokine imbalance, and genomic instability. Animal models of <em>Candida</em>-induced oral lesions offer insights into premalignant conditions, and case series studies further support the association between fungal infections and oral cancer. This review critically examines the role of <em>Candida</em>, particularly <em>C. albicans</em>, in oral squamous cell carcinoma (OSCC) pathogenesis by analyzing epidemiological, experimental, and mechanistic data. We emphasize the importance of early detection and therapeutic strategies, including antifungal prophylaxis, to manage <em>Candida</em> colonization in cancer patients. A comprehensive literature search of studies published between 2015 and 2025 was conducted using Pub Med, Scopus, and Web of Science. Key findings were synthesized to understand the relationship between <em>Candida</em> infections and OSCC. The persistent <em>Candida</em> infections create a pro-tumorigenic microenvironment that accelerates dysplastic changes and malignant progression, particularly in high-risk individuals. While the direct causative relationship is complex, the combined effects of <em>Candida</em>, tobacco, alcohol use, and immunosuppression are significant in oral carcinogenesis. Early detection, antifungal treatments, and personalized therapies are essential to improving patient outcomes. A multidisciplinary approach involving oncologists, microbiologists, and immunologists is crucial for developing integrated strategies to manage both <em>Candida</em> infections and cancer. Future research should focus on dual-action therapies targeting both <em>Candida</em>-induced inflammation and tumor progression.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 5","pages":"Pages 402-410"},"PeriodicalIF":2.8,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144913337","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":"Exploring the significance of extracellular vesicles: Key players in advancing cancer and possible theranostic tools","authors":"Bhaumik Patel ,&nbsp;Shreyas Gaikwad ,&nbsp;Sahdeo Prasad","doi":"10.1016/j.cpt.2024.04.005","DOIUrl":"10.1016/j.cpt.2024.04.005","url":null,"abstract":"<div><div>Metastasis remains a critical challenge in cancer treatment and the leading cause of cancer-related mortality. Ongoing research has demonstrated the key role of extracellular vesicles (EVs) in facilitating communication between distant organs. Cancer cells release a substantial number of EVs that carry distinct cargo molecules, including oncogenic proteins, DNA fragments, and various RNA species. Upon uptake, these cargo molecules profoundly influence the biology of both normal and cancerous cells. This review consolidates the understanding of how EVs promote tumorigenesis by regulating processes such as proliferation, migration, metastasis, angiogenesis, stemness, and immunity. The exploration of EVs as a non-invasive method for cancer detection holds great promise, given that different cancer types exhibit unique protein and RNA signatures that can serve as valuable biomarkers for early diagnosis. Furthermore, growing interest exists in the potential bioengineering EVs for use as prospective therapeutic tools for cancer treatment.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 2","pages":"Pages 109-119"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140794287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Breast cancer risk associated with BRCA1 and BRCA2 pathogenic variants in the Eastern Chinese population","authors":"Sanjian Yu ,&nbsp;Xia Qiu ,&nbsp;Zezhou Wang ,&nbsp;Jialong Xiao ,&nbsp;Hui Ji ,&nbsp;Hailin Shan ,&nbsp;Qing Shao ,&nbsp;Heng Xia ,&nbsp;Feng Cao ,&nbsp;Jun Li ,&nbsp;Cuixia Fu ,&nbsp;Liqin Chen ,&nbsp;Xiaofang Lu ,&nbsp;Tingting Su ,&nbsp;Qianqian Yu ,&nbsp;Shengqun Hou ,&nbsp;Honglian Wang ,&nbsp;Ying Zheng ,&nbsp;Zhimin Shao ,&nbsp;Yun Liu ,&nbsp;Zhen Hu","doi":"10.1016/j.cpt.2024.04.002","DOIUrl":"10.1016/j.cpt.2024.04.002","url":null,"abstract":"<div><h3>Background</h3><div>Population-based penetrance studies of breast cancer gene 1/2 (<em>BRCA1/2)</em> pathogenic or likely pathogenic (P/LP) variants in the Eastern Chinese population are currently lacking; thus, we aimed to investigate the penetrance of breast cancer and other malignant tumors among BRCA1/2 P/LP variant carriers using a population-based breast cancer cohort from communities in Eastern China.</div></div><div><h3>Methods</h3><div>Between July 2019 and March 2021, we tested 2216 breast cancer probands from Chinese communities for <em>BRCA1/2</em> mutations and collected detailed information on the age, survival status, and malignancy history of first-degree relatives. The kin-cohort method was used to calculate the penetrance of breast cancer and other malignant tumors.</div></div><div><h3>Results</h3><div>Of the 2216 breast cancer probands, 109 (4.90%) carried <em>BRCA1/2</em> P/LP variants, 49 in the <em>BRCA1</em> gene and 60 in the <em>BRCA2</em> gene. The penetrance of female breast cancer by 85 years of age was 22.50% and 18.20% in <em>BRCA1</em> and <em>BRCA2</em> P/LP variant carriers, respectively. The penetrance of ovarian cancer by 85 years of age was 26.00% in <em>BRCA1</em> P/LP variant carriers. The penetrance of other malignancies did not reach statistical significance owing to the small number of events.</div></div><div><h3>Conclusions</h3><div>Our findings showed that breast cancer penetrance among <em>BRCA1</em> and <em>BRCA2</em> P/LP variant carriers was 22.50% and 18.20%, respectively, which suggests that prophylactic mastectomy may not be necessary for such Chinese individuals.</div></div><div><h3>Trial registration</h3><div>ClinicalTrials.gov; <span><span>https://clinicaltrials.gov/ct2/show/NCT04265937</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":93920,"journal":{"name":"Cancer pathogenesis and therapy","volume":"3 2","pages":"Pages 147-153"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140758642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}