Cancer Biology & TherapyPub Date : 2026-12-31Epub Date: 2026-06-04DOI: 10.1080/15384047.2026.2683171
Xing Liu, Hejin Zhang, Renchun Du, Zixu Liu, Yunyun Ren, Xiao Yang
{"title":"Leveraging the bacteria for enhanced cancer immunotherapy: from a perspective of synthetic biology.","authors":"Xing Liu, Hejin Zhang, Renchun Du, Zixu Liu, Yunyun Ren, Xiao Yang","doi":"10.1080/15384047.2026.2683171","DOIUrl":"10.1080/15384047.2026.2683171","url":null,"abstract":"<p><p>In recent years, synthetic biology has been widely applied to engineer and program cellular behaviors. Using this approach, bacteria can be designed to express immunotherapeutic agents, improve tumor targeting, and deliver therapeutic payloads directly to tumor sites. To further improve efficacy, strategies such as hypoxia-responsive promoters, bacterial swarming, and extracellular vesicles (EVs) have been investigated, along with the synergistic effects of combining bacterial therapy with other treatments (e.g., photodynamic therapy, chemotherapy, immune checkpoint inhibitors). This review summarizes recent advances in synthetic biology for bacteria-based cancer immunotherapies, focusing on how bacterial agents activate the immune system and the engineering strategies used to achieve tumor targeting.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2683171"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13240942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148155412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer Biology & TherapyPub Date : 2026-12-31Epub Date: 2026-07-28DOI: 10.1080/15384047.2026.2703892
Bo Zhou, Zhixin Wang, Jun Qi, Fengke Liang, Haohui Liu, Yunqi Li
{"title":"DNA polymerase theta (Polθ): a novel candidate for targeted cancer therapy.","authors":"Bo Zhou, Zhixin Wang, Jun Qi, Fengke Liang, Haohui Liu, Yunqi Li","doi":"10.1080/15384047.2026.2703892","DOIUrl":"10.1080/15384047.2026.2703892","url":null,"abstract":"<p><p>DNA double-strand breaks (DSBs) are the most severe DNA damage, and defective repair can lead to apoptosis or malignant transformation. DSBs are mainly repaired by nonhomologous end joining (NHEJ) and homologous recombination (HR), while microhomology-mediated end joining (MMEJ) serves as a backup pathway. Since DNA polymerase theta (Polθ) is essential for MMEJ, this pathway is also named Polθ-mediated end joining. Polθ is barely expressed in normal tissues but overexpressed in many cancers, making it a promising therapeutic target. In recent years, Polθ inhibitors and related therapeutic strategies have emerged rapidly, with clinical trials underway. This review summarizes the structure, function and expression of Polθ in tumorigenesis, highlights synthetic lethal strategies, drug development and clinical translation, and discusses current limitations and future directions for cancer research.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2703892"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13432876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148599384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer Biology & TherapyPub Date : 2026-12-31Epub Date: 2026-06-05DOI: 10.1080/15384047.2026.2683942
Ritvik Illindala, Yunpeng Yang, Tyler Mandt, Nicholas Webster, Nicole Steinmetz, Isabel Newton
{"title":"The tumor microenvironment in triple negative breast cancer and a strategy to improve responses to immunotherapy using cryoablation and immunostimulants.","authors":"Ritvik Illindala, Yunpeng Yang, Tyler Mandt, Nicholas Webster, Nicole Steinmetz, Isabel Newton","doi":"10.1080/15384047.2026.2683942","DOIUrl":"10.1080/15384047.2026.2683942","url":null,"abstract":"<p><p>One in eight women will develop breast cancer (BC) over their lifetime. Triple-negative breast cancer (TNBC) accounts for up to 20% of BC cases and has fewer treatment options, greater metastatic potential, a higher risk of recurrence, and a poorer prognosis compared to other BC subtypes. Compared to hormone receptor-positive BCs, TNBC has more tumor-infiltrating lymphocytes, a higher tumor mutational burden, and greater programmed death ligand-1 (PD-L1) expression. While these features suggest greater immunogenicity, the balance of the complex TNBC tumor microenvironment (TME) is immunosuppressive. The TME leads to modest and variable effects of immune checkpoint inhibitors (ICI) for TNBC. This review explores the dysfunctional immunological state of TNBC and proposes a multi-modal strategy integrating cryoablation as a source of tumor-associated antigens (TAAs) and immunostimulatory agents to reprogram antitumor immunity. It specifically explores the strategy of combining ICI and immunostimulants with cryoablation as a source of TAAs.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2683942"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13245102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148175523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer Biology & TherapyPub Date : 2026-12-31Epub Date: 2026-06-25DOI: 10.1080/15384047.2026.2694136
Yu-Nan Man, Mao-Lin He
{"title":"Advances in SEC61G research: from ER translocon subunit to emerging pan-cancer oncogenic roles.","authors":"Yu-Nan Man, Mao-Lin He","doi":"10.1080/15384047.2026.2694136","DOIUrl":"10.1080/15384047.2026.2694136","url":null,"abstract":"<p><p>SEC61G, the <i>γ</i> subunit of the Sec61 translocon, has long been regarded as a passenger co-amplification target of EGFR on chromosome 7p11.2. Recent studies have revealed its independent oncogenic functions across multiple cancers. This review proposes a mechanism-based classification of SEC61G oncogenic activities: (1) immune checkpoint regulation via canonical translocation; (2) aberrant calcium signaling; and (3) non-canonical mechanisms independent of channel functions. We further delineate the pan-cancer expression and CRISPR-Cas9 dependency landscape, highlighting a dual \"high expression, high dependency\" profile in cervical squamous cell carcinoma. We distinguish current pore-targeting Sec61 inhibitors from subunit-specific strategies and propose future directions including PROTAC degraders and PPI inhibitors. Our review identifies SEC61G as a pan‑cancer prognostic biomarker and immunotherapy response predictor, with mechanistic evidence supporting its driver roles in glioblastoma, non‑small cell lung cancer, and colorectal cancer, whereas associations in other cancers remain correlative and require further validation.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2694136"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13313179/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148315940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer Biology & TherapyPub Date : 2026-12-31Epub Date: 2026-03-11DOI: 10.1080/15384047.2026.2641263
Gongcheng Wang, Zhenzhen Li, Siyu Tan, Jing Ma, Zhiyong Yin, Juan Du, Linni Fan
{"title":"Research progress on the compositional characteristics of the tumor immune microenvironment and immunopredictive models in esophageal squamous cell carcinoma.","authors":"Gongcheng Wang, Zhenzhen Li, Siyu Tan, Jing Ma, Zhiyong Yin, Juan Du, Linni Fan","doi":"10.1080/15384047.2026.2641263","DOIUrl":"10.1080/15384047.2026.2641263","url":null,"abstract":"<p><p>Esophageal cancer is one of the most prevalent malignant tumors of the digestive tract, with esophageal squamous cell carcinoma (ESCC) as its main histological type. In recent years, immunotherapeutic regimens centered on immune checkpoint inhibitors (ICIs) have achieved remarkable efficacy in patients with advanced ESCC. However, due to the heterogeneity of the tumor immune microenvironment (TIME), the degree of clinical benefit varies among patients. This heterogeneity not only affects the biological behavior of tumors but also determines the efficacy and prognosis of immunotherapy. Therefore, exploring the interactions between tumor cells and diverse immunological components inside the TIME in ESCC, as well as how to use ICIs to reshape the TIME, may bring new therapeutic opportunities for ESCC patients. This review looks at the important aspects of TIME and immunological prediction models and explores potential therapeutic strategies targeting both, providing a theoretical basis for improving immunotherapy outcomes in ESCC.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2641263"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12987515/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer Biology & TherapyPub Date : 2026-12-31Epub Date: 2026-03-25DOI: 10.1080/15384047.2026.2644667
Junlin Liu, Junhua Xie, Yunyu Ding
{"title":"Molecular mechanisms and therapeutic strategies: DNA methylation in pancreatic cancer.","authors":"Junlin Liu, Junhua Xie, Yunyu Ding","doi":"10.1080/15384047.2026.2644667","DOIUrl":"10.1080/15384047.2026.2644667","url":null,"abstract":"<p><strong>Objective: </strong>This narrative review examines DNA methylation dysregulation in pancreatic cancer, focusing on its mechanistic roles in tumorigenesis and applications in biomarkers and therapies.</p><p><strong>Methods: </strong>We analyzed experimental and clinical studies on aberrant DNA methylation patterns, emphasizing their links to invasion, metastasis, therapy resistance, and immune modulation.</p><p><strong>Results: </strong>Pancreatic cancer exhibits recurrent tumor suppressor gene hypermethylation and locus-specific hypomethylation, driving progression and resistance. Methylation-based biomarkers (tissue/cfDNA) show promise for early detection and prognostication, though evidence remains largely retrospective or preclinical.</p><p><strong>Discussion: </strong>DNA methyltransferase inhibitors, alone or combined with immunotherapy/targeted agents, demonstrate preclinical and early clinical efficacy. Key challenges include mechanistic gaps, tumor heterogeneity, and assay standardization.</p><p><strong>Conclusion: </strong>DNA methylation is a actionable regulatory layer in pancreatic cancer, but further mechanistic and clinical validation is needed for translational impact.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2644667"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13020873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer Biology & TherapyPub Date : 2026-12-31Epub Date: 2026-09-29DOI: 10.1080/15384047.2026.2740303
{"title":"Statement of Retraction: STAT3-induced upregulation of long noncoding RNA HNF1A-AS1 promotes the progression of oral squamous cell carcinoma via activating Notch signaling pathway.","authors":"","doi":"10.1080/15384047.2026.2740303","DOIUrl":"10.1080/15384047.2026.2740303","url":null,"abstract":"","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2740303"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer Biology & TherapyPub Date : 2026-12-31Epub Date: 2026-01-14DOI: 10.1080/15384047.2026.2615418
Meng Zhu, Yuepeng Liu, Yumin Jia, Lixin Ren, Shuhui An, Yaxuan Wang
{"title":"Jujuboside A induces bladder cancer cell apoptosis by inhibiting ATP1A2-mediated mitochondrial energy metabolism regulation.","authors":"Meng Zhu, Yuepeng Liu, Yumin Jia, Lixin Ren, Shuhui An, Yaxuan Wang","doi":"10.1080/15384047.2026.2615418","DOIUrl":"10.1080/15384047.2026.2615418","url":null,"abstract":"<p><strong>Background: </strong>Conventional treatments for bladder cancer exhibit various limitations. Therefore, natural products, such as jujuboside A (JuA), have been explored for their multi-target effects and low toxicity. However, the specific effects of JuA in bladder cancer remain unclear.</p><p><strong>Objective: </strong>To determine whether JuA affects mitochondrial energy metabolism and apoptosis in bladder cancer cells by regulating the ATPase Na+/K+ transporting subunit alpha 2 (ATP1A2) expression.</p><p><strong>Methods: </strong>Differentially expressed genes (DEGs) in bladder cancer were analyzed using the GSE133624 dataset. ATP1A2 overexpression and knockdown bladder cancer cell models were constructed. Cell phenotypes and markers related to apoptosis and mitochondrial energy metabolism were assessed. Moreover, targeting effects of JuA were investigated.</p><p><strong>Results: </strong>Interleukin (IL)-6, ATP1A2, and hydroxysteroid 11-beta dehydrogenase 1 were identified as potential JuA targets, with ATP1A2 being the main target. ATP1A2 overexpression enhanced the viability and inhibited the apoptosis of bladder cancer cells and promoted mitochondrial energy metabolism in vitro, whereas ATP1A2 knockdown had the opposite effects. JuA decreased cell viability, inhibited ATP1A2 expression, and disrupted mitochondrial energy metabolism. These anticancer effects of JuA were reversed by ATP1A2 overexpression.</p><p><strong>Conclusion: </strong>This study elucidated the molecular mechanism by which JuA regulates mitochondrial energy metabolism and induces apoptosis in bladder cancer cells through targeted inhibition of ATP1A2. These findings reveal the crucial role of ATP1A2 in the energy metabolism and survival of bladder cancer cells, providing a new molecular perspective for a deeper understanding of the pathological mechanisms of bladder cancer.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2615418"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12818801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer Biology & TherapyPub Date : 2026-12-31Epub Date: 2026-04-21DOI: 10.1080/15384047.2026.2662031
Li-Wei Lyu, Na Yao, Zi-Xian Liu, Yan-Ying Wang, Jie Li, He-Bing Zhou, Li-Hong Li, Zhen-Ling Li, Liang Wang
{"title":"Real-world efficacy of Bruton tyrosine kinase inhibitor based maintenance therapy in diffuse large B-cell lymphoma: a multicenter retrospective cohort study with external historical control.","authors":"Li-Wei Lyu, Na Yao, Zi-Xian Liu, Yan-Ying Wang, Jie Li, He-Bing Zhou, Li-Hong Li, Zhen-Ling Li, Liang Wang","doi":"10.1080/15384047.2026.2662031","DOIUrl":"10.1080/15384047.2026.2662031","url":null,"abstract":"<p><strong>Introduction: </strong>The selection of an optimal maintenance agent in diffuse large B-cell lymphoma (DLBCL) continues to pose a significant clinical challenge. This study aims to evaluate the prognostic impact of maintenance therapy (MT) in DLBCL.</p><p><strong>Methods: </strong>We conducted a retrospective analysis of data from DLBCL patients undergoing first-line MT at four hospitals in Beijing between January 2019 and August 2024. The REMoDL-B trial database was selected as the control group.</p><p><strong>Results: </strong>The MT group comprised 106 cases and a median follow-up duration of 25.4 months. The rates of progression and death were 11.32% (12/106) and 1.89% (2/106), respectively. The 2-y progression-free survival (PFS) and overall survival (OS) rates were 90% and 98%, respectively. The MT group demonstrated significantly superior PFS and OS compared to the control group (<i>p</i> = 0.024, <i>p</i> = 0.008). Furthermore, multivariate analysis indicated that MT (<i>p</i> = 0.021, OR = 0.037, 95% CI, 0.002-0.605) was an independent prognostic factor associated with improved PFS. For patients receiving Bruton tyrosine kinase inhibitors (BTKi), the 2-y PFS and OS rates were 87.6% and 97.2%, respectively, both significantly better than those of the control group (<i>p</i> = 0.048, <i>p</i> = 0.024). Despite 43.6% of patients being at high risk for central nervous system (CNS), no CNS recurrences were observed. The PFS of the MCD subtype is better than that of the A53 subtype.</p><p><strong>Conclusions: </strong>While limited by the retrospective study, our analysis raises the hypothesis that MT may correlate with improved DLBCL outcomes. A similar trend suggesting potential benefit from BTKi maintenance was noted, meriting further investigation in controlled settings.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2662031"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13108342/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cancer Biology & TherapyPub Date : 2026-12-31Epub Date: 2026-09-29DOI: 10.1080/15384047.2026.2740300
{"title":"Statement of Retraction: Long non-coding RNA MEG3 suppresses the development of bladder urothelial carcinoma by regulating miR-96 and TPM1.","authors":"","doi":"10.1080/15384047.2026.2740300","DOIUrl":"10.1080/15384047.2026.2740300","url":null,"abstract":"","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2740300"},"PeriodicalIF":5.7,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13625714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}