Cancer Biotherapy and Radiopharmaceuticals最新文献

{"title":"Value of Semi-Quantitative Parameters of ⁶⁸Ga-FAPI-04 PET/CT in Primary Malignant and Benign Diseases: A Comparison with ¹⁸F-FDG.","authors":"Tianyue Li, Yunuan Liu, Meng Dai, Xiujuan Zhao, Jingya Han, Zhaoqi Zhang, Fenglian Jing, Weiwei Tian, Jingmian Zhang, Xinming Zhao, Jianfang Wang, Tiancheng Hao, Tingting Wang","doi":"10.1089/cbr.2024.0026","DOIUrl":"10.1089/cbr.2024.0026","url":null,"abstract":"<p><p><b><i>Objectives:</i></b> We compared the value of the semiquantitative parameters of ⁶⁸Ga-labeled FAP inhibitor (⁶⁸Ga-FAPI)-04 positron emission tomography/computed tomography (PET/CT) and ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) in diagnosing primary malignant and benign diseases. <b><i>Materials and Methods:</i></b> ¹⁸F-FDG and ⁶⁸Ga-FAPI-04 PET/CT images of 80 patients were compared. Semiquantitative parameters, including maximum standardized uptake value (SUV_max), mean SUV (SUV_mean), peak SUV (SUV_peak), peak SUV by lean body mass (SUL_peak), metabolic tumor volume (or tumor volume of FAPI; FAPI-TV), and TLG (or total lesion activity of FAPI; FAPI-TLA), were automatically obtained using the IntelliSpace Portal image processing workstation with a threshold of 40% SUV_max. The liver blood pool was measured as the background, and the tumor-to-background ratio (TBRliver) was calculated. <b><i>Results:</i></b> In all malignant lesions, FAPI-TV and FAPI-TLA were higher in ⁶⁸Ga-FAPI-04 PET/CT than in ¹⁸F-FDG. In the subgroup analysis, ⁶⁸Ga-FAPI-04 had higher FAPI-TV and FAPI-TLA and lower SUV_max than ¹⁸F-FDG had in group A, including gynecological tumor, esophageal, and colorectal cancers. However, six semiquantitative parameters were higher in group B (the other malignant tumors). For the benign diseases, SUV_max, SUV_mean, SUV_peak, and SUL_peak were lower in ⁶⁸Ga-FAPI-04 PET/CT than in ¹⁸F-FDG. ⁶⁸Ga-FAPI-04 PET/CT showed a lower liver background and a higher TBRliver than ¹⁸F-FDG did. ⁶⁸Ga-FAPI-04 PET/CT had higher accuracy, sensitivity, and specificity than ¹⁸F-FDG had. <b><i>Conclusion:</i></b> More accurate semiquantitative parameters and lower abdominal background in ⁶⁸Ga-FAPI-04 PET/CT make it more competitive in the differential diagnosis of malignant and benign diseases than in ¹⁸F-FDG.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"654-663"},"PeriodicalIF":2.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141163030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing Cancer Theranostics Through Integrin αVβ3-Targeted Peptidomimetic IAC: From Bench to Bedside.","authors":"Somit Pandey, Gurvinder Kaur, Nivedita Rana, Sejal Chopra, Imran Rather, Rajender Kumar, Ishita Laroiya, Vijayta D Chadha, Stanley Satz, Micheal G Stabin, Bhagwant Rai Mittal, Jaya Shukla","doi":"10.1089/cbr.2023.0140","DOIUrl":"10.1089/cbr.2023.0140","url":null,"abstract":"<p><p><b><i>Introduction:</i></b> The expression of alpha-five beta-three (αVβ3) integrins is upregulated in various malignancies undergoing angiogenesis. The development of integrin antagonists as diagnostic probes makes the αVβ3 integrin a suitable candidate for targeting tumor angiogenesis. The goal of this study was to optimize the radiolabeling and evaluate the potential of conjugated integrin antagonist carbamate (IAC), a peptidomimetic, as a theranostic radiopharmaceutical for targeting tumor angiogenesis. <b><i>Methodology:</i></b> Radiolabeling of DOTAGA [2,2',2\"-{10-(2,6-dioxotetrahydro-2H-pyran-3-yl)-1,4,7,10-tetraazacyclododecane-1,4,7-triyl} triacetic-acid]-IAC with [⁶⁸Ga]Ga, [¹⁷⁷Lu]Lu, and [²²⁵Ac]Ac was optimized. The binding affinity (K_d) of DOTAGA-IAC for the αVβ3 receptor and cancer cell lines was quantified. The biodistribution studies were conducted in healthy Wistar rats. Dosimetry analysis was performed on [¹⁷⁷Lu]Lu-DOTAGA-IAC distribution data. A pilot study of [⁶⁸Ga]Ga-DOTAGA-IAC and [¹⁸F]FDG Positron Emission Tomography (PET/CT) imaging was performed in five patients with histopathologically confirmed breast cancer. PET/CT findings were compared between [⁶⁸Ga]Ga-DOTAGA-IAC and [¹⁸F]FDG in these patients. <b><i>Results:</i></b> Radiopharmaceuticals were prepared with high radiochemical purity (>99.9%). K_d and B_max measurements were 15.02 nM and 417 fmol for αVβ3 receptor protein: 115.7 nM and 295.3 fmol for C6 glioma cells. Biodistribution studies in rats suggested the excretion via kidneys and partially through the hepatobiliary route. The effective dose of [¹⁷⁷Lu]Lu-DOTAGA-IAC was found to be 0.17 mSv/MBq. The dynamic study in patients revealed the optimal imaging time to be 30-35 mins postadministration. Out of the cohort, [⁶⁸Ga]Ga-DOTAGA-IAC detected the primary lesions in all five patients with a mean standard uptake value (SUV_max) of 3.94 ± 0.58 compared with [¹⁸F]FDG (SUV_max 13.8 ± 6.53). <b><i>Conclusion:</i></b> The study demonstrates that DOTAGA-IAC exhibits strong binding to αVβ3 integrin, positioning it as a promising PET agent for assessing primary and metastatic cancers. The outcomes from the pilot study suggest the potential of [⁶⁸Ga]Ga-DOTAGA-IAC PET/CT in breast carcinoma diagnosis. While recognizing the theranostic potential of DOTAGA-IAC for αVβ3 integrin-expressing tumors, further clinical investigations are warranted to comprehensively assess therapeutic efficacy.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"632-643"},"PeriodicalIF":2.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141560427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Theranostics: Timing is Everything.","authors":"J Harvey Turner","doi":"10.1089/cbr.2024.0088","DOIUrl":"10.1089/cbr.2024.0088","url":null,"abstract":"<p><p>On stage, and in real life, timing is critical for success. Theranostic cancer care epitomizes the central role of timing in the evolution of efficacious molecular targeted radioligand therapy and its incorporation into routine clinical practice of oncology. Nuclear medicine has returned to its therapeutic roots, having been founded as a medical specialty, over three-quarters of a century ago, with radioiodine therapy of thyroid cancer. The very recent oncologist acceptance of ⁶⁸Ga/¹⁷⁷Lu/²²⁵Ac-PSMA effectiveness in treating prostate cancer has re-established the role of the physician in nuclear medicine. This article addresses various important issues in respect of timing related to this resurgence. Training of the required new workforce in technical -omics expertise and physicianly virtues is an urgent priority. Precision in radioligand therapy requires definition of individual radiation absorbed dose (Gy) to tumor and to critical normal organs, preferably prospectively. It is time to abandon one-size-fits-all administration of fixed activities (GBq) in arbitrary cycle intervals and duration. The time has also come to design combination sequenced theranostic-immuno-chemotherapeutic approaches to metastatic cancer to address unmet needs, particularly in pancreatic carcinoma; exploiting the potential of new fibroblast activation protein inhibitor radioligands targeting the tumor microenvironment. Public perception of all things \"nuclear,\" including nuclear medicine, has recently recovered from the general opprobrium and radiophobia of the last half-century. Nuclear is the new green. At last, there have arisen propitious circumstances for the future development of theranostics: The timing is right, now.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"611-618"},"PeriodicalIF":2.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140961037","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A New Perspective on the Effectiveness of FDG PET/CT in Predicting KRAS Mutation in Colon Cancer Cases.","authors":"Fatih Tamer, Ulkem Yararbas","doi":"10.1089/cbr.2024.0028","DOIUrl":"10.1089/cbr.2024.0028","url":null,"abstract":"<p><p><b><i>Aim:</i></b> The main aim of this study was to evaluate the effectiveness of ¹⁸F-fluorodeoxyglucose (¹⁸FDG) positron emission tomography/computerized tomography (PET/CT) parameters in predicting the Kristen rat sarcoma viral oncogene(<i>KRAS</i>) mutation status of patients with colon cancer. <b><i>Materials and Methods:</i></b> Between April 2013 and December 2020, 79 patients who were diagnosed with colon cancer by colonoscopy underwent staging ¹⁸FDG PET/CT with this diagnosis and met all the inclusion criteria were included in this study. Clinical and prognostic features and also imaging (¹⁸FDG PET/CT and magnetic resonance imaging) reports of the patients were collected and analyzed retrospectively. <b><i>Results:</i></b> <i>KRAS</i> mutation was seen in 32 of patients (40.5%). No significant difference was observed between <i>KRAS</i> mutant and wild-type patients in terms of clinical features (tumor location, findings regarding metastasis, T stage, and tumor differentiation grade in patients who underwent surgery) and overall survival. Progression-free survival was significantly shorter in <i>KRAS</i> mutant patients (<i>p</i> = 0.018). Primary tumor standardized uptake value (SUV_mean) was significantly higher in <i>KRAS</i> mutant cases in the whole group (<i>p</i> = 0.024) and in patients in whom <i>KRAS</i> analysis was performed only in the primary lesion (<i>p</i> = 0.036). The cutoff value for predicting <i>KRAS</i> mutation status was 7.01 g/mL (area under the curve [AUC]: 0.650, confidence interval [CI] 95%, 0.56-0.74). <b><i>Conclusions:</i></b> When colon and rectal cancer cases were evaluated separately, the primary tumor SUV_mean value was significantly higher in <i>KRAS</i> mutant colon cancer cases. However, its effectiveness in predicting <i>KRAS</i> mutation status was low, similar to other parameters in the literature.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"664-672"},"PeriodicalIF":2.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nomogram for Predicting Survival in Locally Advanced Cervical Cancer with Concurrent Chemoradiotherapy plus or Not Adjuvant Chemotherapy: A Retrospective Analysis Based on 2018 FIGO Staging.","authors":"Li Hua, Mengzhuan Wei, Chengjun Feng, Shiting Li, Xiaomin Wen, Shaojun Chen","doi":"10.1089/cbr.2023.0199","DOIUrl":"10.1089/cbr.2023.0199","url":null,"abstract":"<p><p><b><i>Background:</i></b> The comprehensive treatment mode of combining concurrent chemoradiotherapy (CCRT) with adjuvant chemotherapy (AC) is a commonly used mainstream model in the clinical practice of locally advanced cervical cancer (LACC). However, the necessity for AC after CCRT lacks sufficient evidence-based medical support. This study constructs a predictive model for the survival time dependence of CCRT ± AC for LACC based on the 2018 International Federation of Gynecology and Obstetrics (FIGO) staging with internal validation, the prognosis was assessed with intensity-modulated radiotherapy (IMRT) and concurrent cisplatin, and provides guidance for future stratified treatment. <b><i>Materials and Methods:</i></b> The retrospective analysis included 482 patients with LACC who CCRT from January 2016 to January 2023. Patients who used the 2009 FIGO staging were all standardized for the 2018 FIGO staging. The 482 patients with LACC were divided into a training set (<i>n</i> = 290) and a validation set (<i>n</i> = 192) at a ratio of 6:4. COX multivariate regression model and LASSO regression were used to screen for independent prognostic factors affecting progression-free survival (PFS) and overall survival (OS), and a nomogram clinical prediction model was constructed based on these factors. Evaluate the effectiveness of the model through the receiver operating characteristic curve, calibration curve, decision curve, risk heat map, and survival curves for risk stratification. <b><i>Results:</i></b> The PFS and OS independent prognostic risk factors affecting the 2018 FIGO staging of LACC during CCRT were validated to be similar to the 2009 FIGO staging prediction model reported in previous literature. In the training cohort, area under the curve (AUC) values at 1, 3, and 5 years were 0.941, 0.882, and 0.885 for PFS, and 0.946, 0.946, and 0.969 for OS, respectively. When applied to a test cohort, the model also showed accurate prediction result (AUC at 1, 3, and 5 years were 0.869, 0.891, and 0.899 for PFS, and 0.891, 0.941 and 0.878 for OS, respectively). Subgroup analysis suggests that patients with LACC, adenocarcinoma, stage IVA, pelvic lymph node metastasis, pretreatment hemoglobin ≤100 g/l and residual tumor diameter >2 cm, who received CCRT in the 2018 FIGO stage, may benefit more from adjuvant chemtherapy. <b><i>Conclusions:</i></b> Based on the 2018 FIGO staging, a nomogram prediction model for PFS and OS in patients with LACC undergoing CCRT was developed. The model, established by combining weighted clinical and pathological factors, can provide more personalized treatment predictions in clinical practice. For patients with high-risk factors such as residual tumor diameter > 2 cm after CCRT for LACC, AC may bring benefits.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"690-705"},"PeriodicalIF":2.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TGF-β Promotes Hepatocellular Carcinoma Metastasis Through Through m6A Modification of PCDHGA9.","authors":"Huamin Wang, Wen Guan, Xianzhou Zhang, Yanting Wu, Yanghui Ou, Yali Zhang, Zhijun Zeng, Hongliang Yao","doi":"10.1089/cbr.2023.0144","DOIUrl":"10.1089/cbr.2023.0144","url":null,"abstract":"<p><p><b><i>Objective:</i></b> Hepatocellular carcinoma (HCC) is a highly lethal cancer with significant mortality, primarily attributed to metastasis. Although Protocadherin Gamma Subfamily A, 9 (PCDHGA9) has been identified as a tumor suppressor gene in cancer metastasis, its role in HCC remains ambiguous. This study clarifies the role of PCDHGA9 in HCC by examining its expression, clinical significance, and molecular activities. <b><i>Methods:</i></b> Tissue microarray immunofluorescence analysis evaluated the expression of PCDHGA9 and its clinical relevance. <i>In vitro</i> experiments involved manipulating PCDHGA9 levels in SK-HEP-1 cells to assess migration through wound-healing and transwell assays. <i>In vivo</i>, shPCDHGA9 cell injections were utilized to observe effects on tumor growth and metastasis. Protein analysis and Western Blot validated epithelial-mesenchymal transition (EMT)-related proteins. Subsequent to TGF-β treatment, cell proliferation and apoptosis were quantified using cell counting kit-8 and flow cytometry, respectively, followed by investigation of TGF-β effects on PCDHGA9 N6-methyladenosine (m6A) modification via Methylated RNA immunoprecipitation, RT-qPCR, and Western blot analysis. <b><i>Results:</i></b> Downregulation of PCDHGA9 expression in HCC tissues is correlated with poor prognosis. <i>In vitro</i> experiments demonstrated that modulating PCDHGA9 expression influenced HCC cell migration. <i>In vivo</i>, PCDHGA9 knockdown is correlated with increased metastasis. Furthermore, TGF-β stimulation promoted cell proliferation and inhibited apoptosis. Mechanistically, TGF-β-mediated m6A modification led to PCDHGA9 decay, promoting EMT in HCC cells. <b><i>Conclusion:</i></b> PCDHGA9 serves as a potential tumor suppressor in HCC by inhibiting EMT. During this process, TGF-β is observed to exert regulatory control over m6A modifications of PCDHGA9.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"644-653"},"PeriodicalIF":2.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GSK-3: An \"Ace\" Among Kinases.","authors":"Theodore Lemuel Mathuram","doi":"10.1089/cbr.2024.0025","DOIUrl":"10.1089/cbr.2024.0025","url":null,"abstract":"<p><p><b><i>Background:</i></b> Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase known to participate in the regulation of β-catenin signaling (<i>Wnt</i> signaling). This aids in the establishment of a multicomponent destruction complex that stimulates phosphorylation, leading to the destruction of β-catenin. Evidence about the role of increasingly active β-catenin signaling is involved in many forms of human cancer. The understanding of GSK-3 remains elusive as recent research aims to focus on developing potent GSK-3 inhibitors to target this kinase. <b><i>Objective:</i></b> This short review aims to highlight the regulation of GSK-3 with emphasis on <i>Wnt</i> signaling while highlighting its interaction with miRNAs corresponding to pluripotency and epithelial mesenchymal transition substantiating this kinase as an \"Ace\" among kinases in regulation of cellular processes. <b><i>Result:</i></b> Significant findings of miRNA regulation by GSK-3 exemplify the underpinnings of kinase-mediated transcriptional regulation in cancers. <b><i>Conclusion:</i></b> The review provides evidence on the role of GSK-3 as a possible master regulator of proteins and noncoding RNA, thereby implicating the fate of a cell.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"619-631"},"PeriodicalIF":2.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140923913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Comprehensive Analysis of LYAR in Colorectal Cancer: Prognostic Marker and Therapeutic Target.","authors":"Jia-Ying Wen, Ye-Ying Fang, Dong-Ming Li, Yu-Lu Tang, He-Qing Huang, Li-Min Liu, Jiang-Hui Zeng, Yi-Wu Dang, Yan-Fang Pan, Da-Tong Zeng, Wei-Jian Huang, Gang Chen, Hui Li","doi":"10.1089/cbr.2023.0181","DOIUrl":"10.1089/cbr.2023.0181","url":null,"abstract":"<p><p><b><i>Background:</i></b> Colorectal cancer (CRC) is a major global health challenge with a need for new biomarkers and therapeutic targets. This work investigated the biological mechanisms and clinical value of Ly1 antibody reactive (LYAR) in CRC. <b><i>Methods:</i></b> We analyzed LYAR mRNA expression across multiple public databases, including genotype-tissue expression, gene expression omnibus, Oncomine, and the cancer genome atlas, alongside in-house immunohistochemical data to evaluate LYAR protein expression in CRC and non-CRC colorectal tissues. Gene set enrichment analysis (GSEA) was used to elucidate LYAR's biological functions, and its impact on the tumor immune microenvironment was assessed using CIBERSORT, ESTIMATE, and single-cell RNA sequencing techniques. In addition, LYAR's association with clinicopathological features and patient prognosis was explored, and its influence on drug sensitivity was investigated using the Connectivity Map database. <b><i>Results:</i></b> LYAR was significantly upregulated in CRC tissues compared with non-CRC colorectal counterparts, associated with altered immune cell composition and enhanced RNA processing, splicing, and cell cycle regulation. High LYAR expression correlated with poor disease-free and overall survival, underscoring its prognostic value. GSEA revealed LYAR's involvement in critical cellular processes and pathways, including DNA repair, cell cycle, and mTORC1 signaling. Correlation analysis identified genes positively and negatively associated with LYAR, leading to the discovery of temsirolimus and WYE-354, mTOR inhibitors, as potential therapeutic agents for CRC. Furthermore, LYAR expression predicted increased sensitivity to cetuximab in RAS wild-type metastatic CRC, indicating its utility as a biomarker for treatment responsiveness. <b><i>Conclusions:</i></b> LYAR's upregulation in CRC highlights its potential as a biomarker for prognosis and therapeutic targeting, offering insights into CRC pathology and suggesting new avenues for treatment optimization.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"673-689"},"PeriodicalIF":2.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142005928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ-PGAM1 Enhances Matrine Resistance of Non-Small Cell Lung Cancer via the miR-326/CXCR5 Axis.","authors":"Caijun Dong, Liangwei Yang, Guofang Zhao","doi":"10.1089/cbr.2022.0039","DOIUrl":"10.1089/cbr.2022.0039","url":null,"abstract":"<p><p><b><i>Background:</i></b> Circular RNAs (circ-RNAs) have been demonstrated to influence initiation, drug resistance, and metastasis of tumors. However, the effects of circular-phosphoglycerate mutase 1 (circ-PGAM1) on matrine resistance in nonsmall cell lung cancer (NSCLC) remain unknown. <b><i>Materials and Methods:</i></b> The reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to determine gene expression. The terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and cell colony formation assays were used to evaluate NSCLC apoptosis and cell proliferation after indicated treatments, respectively. <b><i>Results:</i></b> circ-PGAM1 was upregulated in human NSCLC cell lines (H1299 and A549) compared with the human normal lung epithelial (BEAS-2B) cells. circ-PGAM1 overexpression reversed the matrine treatment-induced inhibition on proliferation of NSCLC cells (A549 and H1299) and rescued the matrine treatment-stimulated apoptosis of these cells. miR-326 was demonstrated to interact with circ-PGAM1. circ-PGAM1 knockdown enhanced the antitumor effect of matrine on NSCLC cell proliferation and apoptosis, which was reversed by miR-326 inhibition. The authors also identified CXCR5 as a key downstream target of miR-326 in A549 cells. <b><i>Conclusions:</i></b> circ-PGAM1 enhances matrine resistance of NSCLC cells through the miR-326/CXCR5 axis. The authors' findings provide new insights into NSCLC-targeted therapy.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"593-599"},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10433558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development in the Study of Natural Killer Cells for Malignant Peritoneal Mesothelioma Treatment.","authors":"Yi-Tong Liu, He-Liang Wu, Yan-Dong Su, Yi Wang, Yan Li","doi":"10.1089/cbr.2024.0078","DOIUrl":"10.1089/cbr.2024.0078","url":null,"abstract":"<p><p>Malignant peritoneal mesothelioma (MPeM) is a rare primary malignant tumor originating from peritoneal mesothelial cells. Insufficient specificity of the symptoms and their frequent reappearance following surgery make it challenging to diagnose, creating a need for more efficient treatment options. Natural killer cells (NK cells) are part of the innate immune system and are classified as lymphoid cells. Under the regulation of activating and inhibiting receptors, NK cells secrete various cytokines to exert cytotoxic effects and participate in antiforeign body, antiviral, and antitumor activities. This review provides a comprehensive summary of the specific alterations observed in NK cells following MPeM treatment, including changes in cell number, subpopulation distribution, active receptors, and cytotoxicity. In addition, we summarize the impact of various therapeutic interventions, such as chemotherapy, immunotherapy, and targeted therapy, on NK cell function post-MPeM treatment.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"551-561"},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141879866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}