Pub Date : 2026-02-01Epub Date: 2025-12-27DOI: 10.1016/j.jncc.2025.11.001
Viriya Keo , Xiaodong Lu , Jonathan C. Zhao , Jindan Yu
Treatment-induced neuroendocrine prostate cancer (t-NEPC) is a lethal subtype of castration-resistant prostate cancer (CRPC) characterized by unique pathological features and molecular changes, including the loss of androgen receptor (AR) activities and the gain of neuroendocrine gene expression. The incidence of t-NEPC has increased substantially in the last decade, in up to 20 % of CRPC cases, largely due to intensive treatment of advanced prostate cancer (PCa) with AR pathway inhibitors (ARPi). While genomic alterations between CRPC and t-NEPC are largely conserved, their epigenetic programs are markedly distinct. The molecular mechanisms underlying the neuroendocrine transformation (NET) of PCa are rapidly emerging. Here, we first briefly summarize the genetic drivers of t-NEPC and then comprehensively review 2D and 3D chromatin alterations, including changes in DNA methylation, histone modifications, chromatin accessibility, and 3D chromatin organization, during NET of PCa. We then review key molecular regulators, including lineage-specific transcription factors and chromatin modifiers, of such epigenetic programs. Lastly, we discuss evidence that suggests a mixed model of clonal selection and transformation that underlies NEPC progression.
{"title":"Genetic and epigenetic mechanisms underlying treatment-induced neuroendocrine prostate cancer","authors":"Viriya Keo , Xiaodong Lu , Jonathan C. Zhao , Jindan Yu","doi":"10.1016/j.jncc.2025.11.001","DOIUrl":"10.1016/j.jncc.2025.11.001","url":null,"abstract":"<div><div>Treatment-induced neuroendocrine prostate cancer (t-NEPC) is a lethal subtype of castration-resistant prostate cancer (CRPC) characterized by unique pathological features and molecular changes, including the loss of androgen receptor (AR) activities and the gain of neuroendocrine gene expression. The incidence of t-NEPC has increased substantially in the last decade, in up to 20 % of CRPC cases, largely due to intensive treatment of advanced prostate cancer (PCa) with AR pathway inhibitors (ARPi). While genomic alterations between CRPC and t-NEPC are largely conserved, their epigenetic programs are markedly distinct. The molecular mechanisms underlying the neuroendocrine transformation (NET) of PCa are rapidly emerging. Here, we first briefly summarize the genetic drivers of t-NEPC and then comprehensively review 2D and 3D chromatin alterations, including changes in DNA methylation, histone modifications, chromatin accessibility, and 3D chromatin organization, during NET of PCa. We then review key molecular regulators, including lineage-specific transcription factors and chromatin modifiers, of such epigenetic programs. Lastly, we discuss evidence that suggests a mixed model of clonal selection and transformation that underlies NEPC progression.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 88-97"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286448","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 : 2026-02-01Epub Date: 2025-11-25DOI: 10.1016/j.jncc.2025.09.007
Anqi Lin , Xiuhui Fang , Pengpeng Zhang , Nan Zhang , Zaoqu Liu , Quan Cheng , Jian Zhang , Bufu Tang , Peng Luo
The tumor microenvironment (TME) is a highly intricate and dynamic system composed of various cellular and non-cellular components, which plays a crucial role in regulating key biological processes such as tumor initiation, progression, and therapeutic response. Recent studies have uncovered a complex regulatory network between the circadian rhythm system and TME, which significantly impacts the clinical efficacy of immune checkpoint inhibitors (ICIs). This review systematically delineates the multi-level regulatory mechanisms by which circadian rhythms influence key components within the TME, including tumor cell biological characteristics, immune cell functional states, angiogenesis processes, and cancer-associated fibroblast activity. It deeply analyzes the systemic impact of the TME on ICI treatment efficacy via immunosuppressive networks, immune checkpoint molecule expression, T cell functional states, and drug bioavailability. The review underscores the central role and clinical significance of circadian rhythms in regulating immune checkpoint molecule expression, immune cell function, ICI drug pharmacokinetics, and TME homeostasis. Based on these research advancements, this paper systematically presents ICI treatment optimization strategies grounded in circadian rhythm dynamics and TME characteristics, encompassing time-dependent dosing regimens, combination therapies targeting the TME, circadian rhythm modulation methods, and precision personalized treatment approaches. Additionally, it offers a systematic outlook on the research frontiers and clinical translation prospects in this field, encompassing multi-omics integrated analysis of circadian regulatory networks, artificial intelligence (AI)-based precision chronomedicine strategies, novel chronotherapeutic approaches, and standardized clinical translation systems. This review establishes a crucial theoretical foundation for understanding the circadian rhythm-TME-ICI interaction network and optimizing cancer immunotherapy strategies.
{"title":"Temporal dynamics in cancer immunotherapy: the interplay between circadian rhythms, tumor microenvironment, and immune checkpoint blockade","authors":"Anqi Lin , Xiuhui Fang , Pengpeng Zhang , Nan Zhang , Zaoqu Liu , Quan Cheng , Jian Zhang , Bufu Tang , Peng Luo","doi":"10.1016/j.jncc.2025.09.007","DOIUrl":"10.1016/j.jncc.2025.09.007","url":null,"abstract":"<div><div>The tumor microenvironment (TME) is a highly intricate and dynamic system composed of various cellular and non-cellular components, which plays a crucial role in regulating key biological processes such as tumor initiation, progression, and therapeutic response. Recent studies have uncovered a complex regulatory network between the circadian rhythm system and TME, which significantly impacts the clinical efficacy of immune checkpoint inhibitors (ICIs). This review systematically delineates the multi-level regulatory mechanisms by which circadian rhythms influence key components within the TME, including tumor cell biological characteristics, immune cell functional states, angiogenesis processes, and cancer-associated fibroblast activity. It deeply analyzes the systemic impact of the TME on ICI treatment efficacy via immunosuppressive networks, immune checkpoint molecule expression, T cell functional states, and drug bioavailability. The review underscores the central role and clinical significance of circadian rhythms in regulating immune checkpoint molecule expression, immune cell function, ICI drug pharmacokinetics, and TME homeostasis. Based on these research advancements, this paper systematically presents ICI treatment optimization strategies grounded in circadian rhythm dynamics and TME characteristics, encompassing time-dependent dosing regimens, combination therapies targeting the TME, circadian rhythm modulation methods, and precision personalized treatment approaches. Additionally, it offers a systematic outlook on the research frontiers and clinical translation prospects in this field, encompassing multi-omics integrated analysis of circadian regulatory networks, artificial intelligence (AI)-based precision chronomedicine strategies, novel chronotherapeutic approaches, and standardized clinical translation systems. This review establishes a crucial theoretical foundation for understanding the circadian rhythm-TME-ICI interaction network and optimizing cancer immunotherapy strategies.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 98-115"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286464","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 : 2026-02-01Epub Date: 2025-11-03DOI: 10.1016/j.jncc.2025.10.002
Yubo Liang , Xingming Chen , Jin Li , Jinxiang Zuo , Jianbiao Zhang , Shuangxi Li , Yang Ke
{"title":"Experimental approaches to the function of tumor-associated lymphatic vessels","authors":"Yubo Liang , Xingming Chen , Jin Li , Jinxiang Zuo , Jianbiao Zhang , Shuangxi Li , Yang Ke","doi":"10.1016/j.jncc.2025.10.002","DOIUrl":"10.1016/j.jncc.2025.10.002","url":null,"abstract":"","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 3-4"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286419","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 : 2026-02-01Epub Date: 2025-06-13DOI: 10.1016/j.jncc.2025.06.001
Yujun Shuai , Haojie Huang
Prostate cancer is the most commonly diagnosed and the second-leading cause of cancer-related mortality in men worldwide, especially in Western counties. Therapeutic resistance of prostate cancer remains a major challenge in modern oncology, necessitating new scientific understanding of the disease and devising new targeting strategies. This review examines the intricate relationship between transcriptional and epigenetic reprogramming, lineage plasticity, and therapeutic resistance in prostate cancer. Prostate cancer cells can adapt and resist various treatment modalities, including androgen deprivation therapy (ADT) and next-generation androgen receptor (AR) signaling inhibitors (ARSI), through transcriptional reprogramming and epigenetic modifications. Lineage plasticity, the ability of cells to alter their cellular identities, further drives treatment resistance. Moreover, cancer cells can adjust their gene expression profiles to evade therapy by activating key transcription factors and epigenetic regulatory mechanisms such as DNA methylation, histone modification, and non-coding RNA expression. The article concludes by discussing new therapeutic strategies targeting these reprogramming and plasticity mechanisms, emphasizing the importance of combination therapy and precision medicine in developing more effective treatments for advanced prostate cancer.
{"title":"Transcriptional and epigenetic reprogramming, lineage plasticity and therapy resistance in prostate cancer","authors":"Yujun Shuai , Haojie Huang","doi":"10.1016/j.jncc.2025.06.001","DOIUrl":"10.1016/j.jncc.2025.06.001","url":null,"abstract":"<div><div>Prostate cancer is the most commonly diagnosed and the second-leading cause of cancer-related mortality in men worldwide, especially in Western counties. Therapeutic resistance of prostate cancer remains a major challenge in modern oncology, necessitating new scientific understanding of the disease and devising new targeting strategies. This review examines the intricate relationship between transcriptional and epigenetic reprogramming, lineage plasticity, and therapeutic resistance in prostate cancer. Prostate cancer cells can adapt and resist various treatment modalities, including androgen deprivation therapy (ADT) and next-generation androgen receptor (AR) signaling inhibitors (ARSI), through transcriptional reprogramming and epigenetic modifications. Lineage plasticity, the ability of cells to alter their cellular identities, further drives treatment resistance. Moreover, cancer cells can adjust their gene expression profiles to evade therapy by activating key transcription factors and epigenetic regulatory mechanisms such as DNA methylation, histone modification, and non-coding RNA expression. The article concludes by discussing new therapeutic strategies targeting these reprogramming and plasticity mechanisms, emphasizing the importance of combination therapy and precision medicine in developing more effective treatments for advanced prostate cancer.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 73-87"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286288","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 : 2026-02-01Epub Date: 2025-10-02DOI: 10.1016/j.jncc.2025.06.006
Yang An , Jiaolin Zhou , Lan Su , Lin Cong , Xinxin Mao , Bo Chen , Yuhua Gong , Yaping Xu , Han Chen , Chentong Wang , Guole Lin , Huanwen Wu
Objective
We sought to characterize the genomic and immune landscape of signet ring cell carcinoma (SRCC), a rare and aggressive subtype of colorectal cancer (CRC).
Methods
Tissue samples and clinicopathological data were retrospectively analyzed from 37 SRCC and 172 conventional adenocarcinomas (AC) of rectum and sigmoid colon. The genetic and immune profiles were assessed using DNA next-generation sequencing (NGS) and multiplex immunohistochemistry.
Results
Compared to AC, SRCC patients were younger, had higher tumor, node, metastasis (TNM) stages and tumor grades (all P < 0.05), and exhibited significantly worse 3-year disease-free survival (DFS) and overall survival (OS) (both P < 0.0001). SRCC exhibited fewer somatic mutations in well-known CRC driver genes including APC (32 % vs. 74 %), KRAS (16 % vs. 42 %), and FBXW7 (0 vs. 20 %), but showed higher frequencies of genetic alterations in SMAD4, RNF43, BCL2L11 (present only in SRCC), MYC, and ARID2 (all P < 0.05). SRCC showed significantly higher levels of CD8+ tumor-infiltrating lymphocytes (TILs), but lower PD-1+CD8+ TILs in both stroma and intratumoral regions (all P < 0.05). Interestingly, high PD-1+CD8+ TILs in intratumoral regions significantly predicted longer DFS and OS in all SRCC and stage II-III SRCC patients (all P < 0.05), while CD3+ or CD8+ TILs did not. Moreover, the characteristic immune cell infiltration correlated with specific genetic alterations in SRCC.
Conclusions
Colorectal SRCC is a clinically and molecularly distinct and highly malignant subtype compared to AC. It exhibits a “pseudo-T cell-inflamed” tumor microenvironment with increased total CD8+ TILs but reduced PD-1+CD8+ TIL infiltration. Notably, PD-1+CD8+ TIL infiltration is associated with favorable prognosis. These findings provide new insights into tumor-immune interactions in SRCC, with potential implications for prognostic stratification and the development of personalized immunotherapeutic strategies.
{"title":"Clinicopathologic, genetic and immune cell infiltration analysis of colorectal signet ring cell carcinoma with comparison to conventional adenocarcinoma","authors":"Yang An , Jiaolin Zhou , Lan Su , Lin Cong , Xinxin Mao , Bo Chen , Yuhua Gong , Yaping Xu , Han Chen , Chentong Wang , Guole Lin , Huanwen Wu","doi":"10.1016/j.jncc.2025.06.006","DOIUrl":"10.1016/j.jncc.2025.06.006","url":null,"abstract":"<div><h3>Objective</h3><div>We sought to characterize the genomic and immune landscape of signet ring cell carcinoma (SRCC), a rare and aggressive subtype of colorectal cancer (CRC).</div></div><div><h3>Methods</h3><div>Tissue samples and clinicopathological data were retrospectively analyzed from 37 SRCC and 172 conventional adenocarcinomas (AC) of rectum and sigmoid colon. The genetic and immune profiles were assessed using DNA next-generation sequencing (NGS) and multiplex immunohistochemistry.</div></div><div><h3>Results</h3><div>Compared to AC, SRCC patients were younger, had higher tumor, node, metastasis (TNM) stages and tumor grades (all <em>P</em> < 0.05), and exhibited significantly worse 3-year disease-free survival (DFS) and overall survival (OS) (both <em>P</em> < 0.0001). SRCC exhibited fewer somatic mutations in well-known CRC driver genes including <em>APC</em> (32 % vs. 74 %), <em>KRAS</em> (16 % vs. 42 %), and <em>FBXW7</em> (0 vs. 20 %), but showed higher frequencies of genetic alterations in <em>SMAD4, RNF43, BCL2L11</em> (present only in SRCC), <em>MYC</em>, and <em>ARID2</em> (all <em>P</em> < 0.05). SRCC showed significantly higher levels of CD8<sup>+</sup> tumor-infiltrating lymphocytes (TILs), but lower PD-1<sup>+</sup>CD8<sup>+</sup> TILs in both stroma and intratumoral regions (all <em>P</em> < 0.05). Interestingly, high PD-1<sup>+</sup>CD8<sup>+</sup> TILs in intratumoral regions significantly predicted longer DFS and OS in all SRCC and stage II-III SRCC patients (all <em>P</em> < 0.05), while CD3<sup>+</sup> or CD8<sup>+</sup> TILs did not. Moreover, the characteristic immune cell infiltration correlated with specific genetic alterations in SRCC.</div></div><div><h3>Conclusions</h3><div>Colorectal SRCC is a clinically and molecularly distinct and highly malignant subtype compared to AC. It exhibits a “pseudo-T cell-inflamed” tumor microenvironment with increased total CD8<sup>+</sup> TILs but reduced PD-1<sup>+</sup>CD8<sup>+</sup> TIL infiltration. Notably, PD-1<sup>+</sup>CD8<sup>+</sup> TIL infiltration is associated with favorable prognosis. These findings provide new insights into tumor-immune interactions in SRCC, with potential implications for prognostic stratification and the development of personalized immunotherapeutic strategies.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 30-39"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286453","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 : 2026-02-01Epub Date: 2025-05-24DOI: 10.1016/j.jncc.2025.04.004
Furong Huang , Kexin Li , Jeffrey W. Shevach , Qianben Wang
Prostate cancer remains the second most common malignancy among men worldwide, with treatment paradigms evolving dramatically over the last two decades. Despite the longstanding efficacy of androgen deprivation therapy (ADT) and its combination with next-generation androgen receptor (AR) signaling inhibitors or chemotherapy in metastatic hormone-sensitive settings, most tumors ultimately develop resistance and progress to lethal castration-resistant prostate cancer (CRPC). This resistance often stems from a range of molecular alterations, including AR mutations, amplifications, splice variants, and tumor suppressor gene lesions (e.g., TP53, RB1). Recent advances in genomic and translational research underscore the importance of biomarker-guided patient stratification to optimize therapeutic choices. Novel strategies to circumvent resistance include non–ligand-binding-domain AR inhibitors, potent AR degraders (e.g., proteolysis-targeting chimeras [PROTACs]), bipolar androgen therapy, and combination regimens incorporating PARP inhibitors or immunotherapies for selected subsets of patients. Additionally, gene-editing approaches targeting “undruggable” genetic lesions offer promise in preclinical models. Moving forward, clinical development of these emerging agents and personalized treatment approaches, supported by robust genomic profiling, is poised to enhance tumor control, extend survival, and improve quality of life for patients with advanced prostate cancer.
{"title":"Emerging therapies to overcome antiandrogen resistance and beyond in lethal prostate cancer","authors":"Furong Huang , Kexin Li , Jeffrey W. Shevach , Qianben Wang","doi":"10.1016/j.jncc.2025.04.004","DOIUrl":"10.1016/j.jncc.2025.04.004","url":null,"abstract":"<div><div>Prostate cancer remains the second most common malignancy among men worldwide, with treatment paradigms evolving dramatically over the last two decades. Despite the longstanding efficacy of androgen deprivation therapy (ADT) and its combination with next-generation androgen receptor (AR) signaling inhibitors or chemotherapy in metastatic hormone-sensitive settings, most tumors ultimately develop resistance and progress to lethal castration-resistant prostate cancer (CRPC). This resistance often stems from a range of molecular alterations, including AR mutations, amplifications, splice variants, and tumor suppressor gene lesions (e.g., <em>TP53, RB1</em>). Recent advances in genomic and translational research underscore the importance of biomarker-guided patient stratification to optimize therapeutic choices. Novel strategies to circumvent resistance include non–ligand-binding-domain AR inhibitors, potent AR degraders (e.g., proteolysis-targeting chimeras [PROTACs]), bipolar androgen therapy, and combination regimens incorporating PARP inhibitors or immunotherapies for selected subsets of patients. Additionally, gene-editing approaches targeting “undruggable” genetic lesions offer promise in preclinical models. Moving forward, clinical development of these emerging agents and personalized treatment approaches, supported by robust genomic profiling, is poised to enhance tumor control, extend survival, and improve quality of life for patients with advanced prostate cancer.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 42-57"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286451","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 : 2026-02-01Epub Date: 2025-06-18DOI: 10.1016/j.jncc.2025.05.003
Shuai Gao , Nolan D. Patten , Changmeng Cai
The androgen receptor (AR) is instrumental in the onset and progression of prostate cancer (PCa), establishing androgen deprivation therapy (ADT) as the first-line treatment for metastatic disease. However, the effectiveness of ADT is commonly short-lived. Many patients eventually relapse and develop castration-resistant prostate cancer (CRPC), commonly marked by reactivated AR signaling. Although next-generation AR signaling inhibitors (ARSi) provide temporary control, resistance inevitably emerges. While a small subset of CRPC cases may evolve through AR-independent pathways, most regain partial AR function through multiple mechanisms. A key regulator of AR activity is the pioneer transcription factor FOXA1, which governs AR binding to chromatin. The AR-FOXA1 axis is essential for prostate luminal epithelial cell lineage determination and drives the development of prostate adenocarcinoma. Emerging evidence shows profound alterations in this axis in CRPC and in tumors resistant to ARSi therapies. In this review, we highlight the genetic, epigenetic, transcriptional, and posttranscriptional changes within the AR-FOXA1 axis in PCa following ADT and ARSi treatments.
{"title":"Alterations in AR-FOXA1 signaling in prostate cancer progression and therapeutic resistance","authors":"Shuai Gao , Nolan D. Patten , Changmeng Cai","doi":"10.1016/j.jncc.2025.05.003","DOIUrl":"10.1016/j.jncc.2025.05.003","url":null,"abstract":"<div><div>The androgen receptor (AR) is instrumental in the onset and progression of prostate cancer (PCa), establishing androgen deprivation therapy (ADT) as the first-line treatment for metastatic disease. However, the effectiveness of ADT is commonly short-lived. Many patients eventually relapse and develop castration-resistant prostate cancer (CRPC), commonly marked by reactivated AR signaling. Although next-generation AR signaling inhibitors (ARSi) provide temporary control, resistance inevitably emerges. While a small subset of CRPC cases may evolve through AR-independent pathways, most regain partial AR function through multiple mechanisms. A key regulator of AR activity is the pioneer transcription factor FOXA1, which governs AR binding to chromatin. The AR-FOXA1 axis is essential for prostate luminal epithelial cell lineage determination and drives the development of prostate adenocarcinoma. Emerging evidence shows profound alterations in this axis in CRPC and in tumors resistant to ARSi therapies. In this review, we highlight the genetic, epigenetic, transcriptional, and posttranscriptional changes within the AR-FOXA1 axis in PCa following ADT and ARSi treatments.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 58-72"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286502","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 : 2026-02-01Epub Date: 2025-11-15DOI: 10.1016/j.jncc.2025.10.004
Allan Saj Porcacchia , David Gozal , Sergio Tufik , Monica L. Andersen
{"title":"The vicious cycle of circadian disruption and obstructive sleep apnea: implications for cancer risk","authors":"Allan Saj Porcacchia , David Gozal , Sergio Tufik , Monica L. Andersen","doi":"10.1016/j.jncc.2025.10.004","DOIUrl":"10.1016/j.jncc.2025.10.004","url":null,"abstract":"","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 1-2"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286021","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 : 2026-02-01Epub Date: 2025-11-19DOI: 10.1016/j.jncc.2025.07.004
Hong Hui Jing , Mitesh Patel , Mohd Adnan , Sreenivasan Sasidharan
Carbon dots (CDs) have emerged as promising nanomaterials in cancer phototherapy due to their unique optical properties, biocompatibility, and tunability. This review comprehensively examines the role of CDs in photodynamic therapy (PDT) and photothermal therapy (PTT), highlighting their mechanisms of action, including the induction of apoptosis, necrosis, and necroptosis in cancer cells. Key factors influencing the efficacy of cancer phototherapy—such as the tumor microenvironment (TME), nanoparticle stability, and light parameters—are thoroughly analyzed. Advancements in surface modifications, targeted, drug delivery and multifunctional applications, including their integration with chemotherapy and immunotherapy, further expand the clinical potential of CDs. While preclinical studies have demonstrated the efficacy of CDs in selectively targeting cancer cells and inducing therapeutic effects, challenges related to biosafety and regulatory approval hinder clinical translation. By addressing existing challenges and leveraging interdisciplinary innovations, CDs hold great promise for personalized and less invasive cancer treatments. Their future success in clinical application will depend on overcoming biological barriers and optimizing the safety profile to facilitate their seamless integration into oncology.
{"title":"Light-responsive nanotherapeutic carbon dots: a next generation tool for cancer phototherapy","authors":"Hong Hui Jing , Mitesh Patel , Mohd Adnan , Sreenivasan Sasidharan","doi":"10.1016/j.jncc.2025.07.004","DOIUrl":"10.1016/j.jncc.2025.07.004","url":null,"abstract":"<div><div>Carbon dots (CDs) have emerged as promising nanomaterials in cancer phototherapy due to their unique optical properties, biocompatibility, and tunability. This review comprehensively examines the role of CDs in photodynamic therapy (PDT) and photothermal therapy (PTT), highlighting their mechanisms of action, including the induction of apoptosis, necrosis, and necroptosis in cancer cells. Key factors influencing the efficacy of cancer phototherapy—such as the tumor microenvironment (TME), nanoparticle stability, and light parameters—are thoroughly analyzed. Advancements in surface modifications, targeted, drug delivery and multifunctional applications, including their integration with chemotherapy and immunotherapy, further expand the clinical potential of CDs. While preclinical studies have demonstrated the efficacy of CDs in selectively targeting cancer cells and inducing therapeutic effects, challenges related to biosafety and regulatory approval hinder clinical translation. By addressing existing challenges and leveraging interdisciplinary innovations, CDs hold great promise for personalized and less invasive cancer treatments. Their future success in clinical application will depend on overcoming biological barriers and optimizing the safety profile to facilitate their seamless integration into oncology.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 11-29"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286479","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 : 2026-02-01Epub Date: 2026-01-22DOI: 10.1016/j.jncc.2026.01.001
Zhenyan Jiang , Yang Ke , Yong Peng
{"title":"Intranasal circRNA vaccine elicits localized and safer antitumor immunity","authors":"Zhenyan Jiang , Yang Ke , Yong Peng","doi":"10.1016/j.jncc.2026.01.001","DOIUrl":"10.1016/j.jncc.2026.01.001","url":null,"abstract":"","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 5-7"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286461","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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