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Introduction: Integrating radiopharmaceuticals in anesthesia and orthopedic oncology has revolutionized cancer biotherapy and targeted therapy. This multidisciplinary approach leverages molecular imaging, radioisotopes, and precision medicine to enhance perioperative pain management and improve therapeutic efficacy. Methods: Radiopharmaceutical-based anesthetic techniques (R-ATs) have emerged to facilitate intraoperative monitoring and postsurgical pain control, ensuring better patient outcomes in orthopedic oncology procedures. This article explores combining radiopharmaceuticals with orthopedic cancer management, emphasizing novel theranostic agents, α- and β--emitting radionuclides, in treating metastatic bone disease. Innovations in peptide receptor radionuclide therapy (PRRT) and radiolabeled bisphosphonates have provided a significant leap forward in mitigating skeletal-related events and improving survival rates. Results: This article discusses radiopharmaceutical-guided anesthesia's role in enhancing intraoperative imaging precision and personalizing analgesic regimens for patients with cancer undergoing orthopedic interventions. The article aligns with recent developments in molecular medicine by addressing the translational impact of radiopharmaceuticals on cancer treatment paradigms. In targeted therapy, R-AT attained an effectiveness of up to 96.25%, while PRRT reached 97.45%. Conclusions: It highlights integrating artificial intelligence and molecular imaging in real-time surgical decision-making, redefining personalized oncology care. The synergistic use of radiopharmaceuticals in anesthesia and orthopedic oncology holds immense promise in precision-driven therapeutic strategies for cancer biotherapy.
Lung cancer is the leading cause of cancer‑related mortality worldwide. Current therapies continue to face challenges such as drug resistance and tumour heterogeneity. Radionuclide‑drug conjugates (RDCs) represent an emerging theranostic platform designed to precisely irradiate tumours. This review aims to systematically outline the landscape of advances in RDCs for lung cancer, and provides a forward‑looking perspective on next‑generation RDCs. This analysis was based on preclinical and clinical data retrieved from PubMed and ClinicalTrials.gov, with all records reviewed up to January 2026. Studies were exhaustively surveyed across most radionuclides relevant to RDCs in lung cancer, following the periodic table to ensure comprehensive coverage. In lung cancer, a total of 66 RDCs have been screened, with 30 having entered early‑phase clinical trials. Among completed trials, RDCs underwent a transition from initial 131I/90Y‑labelled antibodies toward 177Lu‑labelled somatostatin receptor (SSTR)‑targeting peptides. SSTR remains the dominant target, with a notable shift from agonists to antagonists. Meanwhile, fibroblast activation protein (FAP), epidermal growth factor receptor (EGFR), and programmed death‑ligand 1 (PD‑L1) are receiving growing attention. Peptides and antibodies are equally employed, with bispecific antibodies (bsAbs), single‑domain antibodies (sdAbs), and cyclic peptides advancing rapidly. Furthermore, nanoparticles (NPs) offer versatile platforms, and pretargeting or dual‑targeting strategies are being developed to improve both efficacy and safety. Crown chelators and bipyridine derivatives provide more stable chelating options. Although 177Lu remains the mainstay, α emitters and emerging mixed‑decay radionuclides like 161Tb are gaining ground. Combination therapies are also being investigated to enable first‑line application. Despite recent progress in RDC development, challenges such as off‑target toxicity, radiation resistance, and radionuclide production remain. Next‑generation RDCs hold promise to overcome these barriers by novel radionuclides, personalised dosimetry, multifunctional delivery platforms, and multidrug combination strategies. Collectively, these innovations will propel RDCs into a personalised, precision theranostic platform for lung cancer.
The oncofetal antigen 5T4 is highly expressed in colorectal cancer (CRC), making it a promising theranostic target. In this study, we developed the diagnostic tracer [89Zr]Zr-DFO-HB5 (5T4 monoclonal antibody) and therapeutic agents [177Lu]Lu/[161Tb]Tb-DOTA-HB5, establishing a novel theranostic strategy for CRC. We selected two 5T4-positive colorectal cancer cell lines and established subcutaneous xenograft models. Immuno-PET imaging revealed specific tumor targeting of [89Zr]Zr-DFO-HB5 in 5T4-positive CRC mouse models. Ex vivo biodistribution studies showed high and sustained tumor uptake of [177Lu]Lu/[161Tb]Tb-DOTA-HB5, with gradually decreasing radioactivity accumulation in normal organs over time. Targeted radionuclide therapy (TRT) further confirmed that [177Lu]Lu/[161 Tb]Tb-DOTA-HB5 significantly inhibited tumor growth in both models. Biosafety evaluation revealed only mild hematological toxicity, without obvious short-term organ damage. In conclusion, [89Zr]Zr-DFO-HB5 enables noninvasive detection of 5T4 expression, while [177Lu]Lu/[161Tb]Tb-DOTA-HB5 exhibits potent antitumor efficacy and favorable biosafety. The study provides a potential theranostic platform for 5T4-positive CRC and related malignancies.
Alterations in the mesenchymal-epithelial transition factor (MET) gene are critical drivers of non-small cell lung cancer (NSCLC). In recent years advances in precision therapies targeting MET alterations have significantly expanded treatment options for NSCLC patients. These alterations include MET exon 14 skipping mutations (MET exon 14 skipping), MET gene amplifications, MET point mutations (primarily kinase domain mutations), and MET protein overexpression. Accurate identification of these alterations and appropriate selection of patient populations and targeted therapies are essential for improving clinical outcomes. The East China Lung Cancer Group, Youth Committee (ECLUNG YOUNG, Yangtze River Delta Lung Cancer Cooperation Group) has synthesized insights from China's innovative drug development landscape and clinical practice to formulate an expert consensus on the diagnosis and treatment of NSCLC patients with MET alterations. This consensus addresses key areas, such as optimal testing timing, testing methods, testing strategies, quality control measures, and treatment approaches. By offering standardized recommendations, this guidance aims to streamline diagnostic and therapeutic processes and enhance clinical decision-making for NSCLC with MET alterations.
Cancer Biotherapy and Radiopharmaceuticals officially retracts the article entitled, "Naringenin Inhibits Cell Migration, Invasion, and Tumor Growth by Regulating circFOXM1/miR-3619-5p/SPAG5 Axis in Lung Cancer" by Zhaofeng Tan, Yuli Sun, Mei Liu, Lei Xia, Fang Cao, Yuanfu Qi, and Yonglei Song, (Cancer Biother Radiopharm; E-pub 27 Jun 2020; doi: 10.1089/cbr.2019.3520) at the authors' request: "...we feel that we have not yet studied our work completely and some new great results are discovered. So after carefully thinking, we are going to rearrange this manuscript and try to give more precise model. Thus we decided to withdraw this manuscript with great pity. We sincerely say sorry for all the staffs involved this manuscript including editors, reviewers etc. because of our action."[sic] After careful consideration, the Editor agreed to retract the paper. The Editor and Publisher of Cancer Biotherapy and Radiopharmaceuticals are committed to preserving the scientific literature and the community it serves.
Pancreatic adenocarcinoma (PAAD) is an extremely lethal cancer, making early detection and precise staging essential for extending survival. Upregulation of 5T4 mRNA was detected in bioinformatics analysis using data from the Cancer Genome Atlas and Genotype-Tissue Expression. In the current work, we confirmed the overexpression of 5T4 protein in tumor samples of PAAD compared with the corresponding paraneoplastic tissue. To visualize 5T4 via positron emission tomography (PET) noninvasively, we successfully developed [18F]AlF-RESCA-H006 based on a single-domain antibody fragment. The radiotracer demonstrated high binding affinity toward 5T4 antigens in vitro and remained stable in the final formulation for up to 4 h storage at room temperature. In two preclinical mouse models of pancreatic cancer, [18F]AlF-RESCA-H006 clearly identified the tumor sites, showing a radioactivity accumulation of 2.43 ± 0.46% ID/g in Balb/C mice with BxPC-3 xenografts and 2.88 ± 1.02% ID/g in NCG mice with PANC-1 xenografts. Taken together, [18F]AlF-RESCA-H006 is a promising PET tracer for detecting 5T4 antigen alteration in PAAD. Further investigations are required to assess its defluorination level in higher species and its permeability through the dense extracellular matrix of pancreatic cancer.
Nuclear protein in testis (NUT) carcinoma (NC) represents a rare, clinically aggressive cancer defined by pathognomonic NUT Midline Carcinoma Family Member 1 (NUTM1) gene fusions, with bromodomain and extraterminal domain (BET) protein 4 (BRD4)-NUTM1 being the predominant oncogenic driver. Since its description in 1991, gradual advances have clarified the pathologic mechanisms of NC and its diagnostic methods; however, NC treatment remains a significant challenge. Moreover, diagnostic and treatment approaches for this cancer require further validation and standardization. These guidelines were developed by the Chinese Alliance of Research for NC (ChARN) based on current evidence in the literature and incorporate consensus-based input from multiple international experts. They provide comprehensive guidance on NC diagnosis and treatment, covering epidemiology, pathogenesis, diagnostic methods, therapeutic strategies, BET-inhibitor toxicity, palliative care, and prognostic assessment during follow-up. They also emphasize the importance of multidisciplinary team collaboration in NC treatment and recommend prioritizing enrollment in prospective clinical trials for patients. Current mainstays of treatment include surgical resection, radiotherapy, and medical treatment (chemotherapy, targeted therapy, and immunotherapy), although no standard treatment protocol exists. Future research directions include improving diagnostic efficiency, exploring new therapeutic strategies (such as highly selective BET inhibitors, BET-inhibitor combinations, and PROTAC technologies), and recommending basket trials as a research approach for patients with NUTM1 gene fusions.
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Radiation therapy (RT), a novel approach to boost the anticancer immune response, has been progressively evaluated in the neoadjuvant setting in breast cancer (BC). We aimed to evaluate immunity-related indicators of response to neoadjuvant chemoradiation therapy (NACRT) in BC for better treatment personalization. We analyzed data of the first 42 patients included in the randomized phase 2 Neo-APBI-01 trial comparing standard neoadjuvant chemotherapy (NACT) and NACRT regimen in locally advanced triple-negative (TN) and luminal B (LB) subtype BC. Clinicopathological parameters, blood counts and the derived parameters, total tumor-infiltrating lymphocytes (TILs) and their subpopulation, as well as TP53 mutation status, were assessed as predictors of response. Twenty-one patients were equally assigned to each group. The pathologic complete response (pCR) was 33% and 38% in the NACT and NACRT groups, respectively, with a dose-response effect. Only one LB tumor reached pCR after NACRT. Numerous parameters associated with response were identified, which differed according to the assigned treatment. In the NACRT group, baseline hemoglobin of ≥13 g/dL and body mass index of <26 were strongly associated with pCR. Higher baseline neutrophils-to-lymphocytes ratio, total TILs, and T-effector cell counts were favorable for pCR. This preliminary analysis identified LB and low-TIL tumors as poor responders to the NACRT protocol, which delivered RT after several cycles of chemotherapy. These findings will allow for amending the selection of patients for the trial and help better design future trials of NACRT in BC.
The article entitled, "lncRNA IGF2-AS Promotes Cell Proliferation, Migration, and Invasion of Gastric Cancer by Modulating miR-937/EZH2 Axis," by Zizi Li, Zhanyu Li, Zhijuan Zhong, Jianhui Zhou, Shenhao Huang, Wenying Zhou, and Jianfeng Xu (Cancer Biother Radiopharm epub 25 May 2020; Doi: 10.1089/cbr.2019.3275) is being officially retracted from the literature. The Editor-in-Chief of Cancer Biotherapy and Radiopharmaceuticals (CBR) received an email from the corresponding author of the article, Wenying Zhou, on September 7, 2020, indicating: "…this manuscript should no longer be published [because of] information from our superior and also after discussion with my research team, we want to repeat our experiment and then revise the [manuscript]. Our team has a lot of controversy about these results. In order to ensure the quality of the data and not to mislead readers, we decided to [retract] the manuscript. We will be more rigorous in our further study." The editor requested further information about precisely which data could not be reproduced, to which Dr. Wenying Zhou responded: "…we found that the results of Figure 4B and 4C, Figure 5A and 5B could not be repeated. Our repeated results of Figure 4B and 4C were as follow[s]: compared with miR-NC group, there was no significant decrease of the luciferase activity in miR-937 group when cells co-transfected with EZH2 3'-UTR-WT. Our repeated results of Figure 5A and 5B were as follow[s]: miR-937 inhibited the proliferation of MNK-28 and SGC-7901 cells, but the cell proliferation had no significant change in miR-937+EZH2 group compared with miR-937+pcDNA group. These findings resulted in the uncertainty of the targeted relationship between miR-937 and EZH2. We also repeated these experiments in different environments, but they all contradict the results in the original data. So, the conclusion is very controversial. In a responsible attitude to the readers, we decide to [retract] the manuscript." The authors have extended their apologies to the Editor and to the readers of CBR. Though in the author's original email, the request was made to "withdraw" the paper, CBR has decided to fully retract it due to irreproducible data, as the journal is committed to preserving the scientific literature and the community it serves.
As an emerging biomarker, tumor mutational burden (TMB) has attracted increasing attention from clinicians in predicting the efficacy of tumor immunotherapy. Currently, TMB is detected primarily by whole-exome sequencing or targeted panel sequencing on high-throughput sequencing platforms. However, the lack of uniformity in detection methods, threshold settings, and reporting formats, as well as the significant differences in TMB values among different cancer types, have hindered the standardized application of this biomarker in clinical practice. This consensus focuses on the definition, standardization of detection, clinical significance, and limitations of TMB, and provides consensus recommendations for the clinical application of TMB in real-world practice in China. This consensus is aimed at helping clinicians and laboratory personnel understand the clinical significance and testing standards of TMB, promoting more accurate interpretation of test results, and improving patient care.
The BRAF gene is an important signaling molecule in human cells that is involved in the regulation of cell growth, differentiation, and survival. When the BRAF gene mutates, it can lead to abnormal activation of the signaling pathway, which promotes cell proliferation, inhibits cell apoptosis, and ultimately contributes to the occurrence and development of cancer. BRAF mutations are widely present in various cancers, including malignant melanoma, thyroid cancer, colorectal cancer, non-small cell lung cancer, and hairy cell leukemia, among others. BRAF is an important target for the treatment of various solid tumors, and targeted combination therapies, represented by BRAF inhibitors, have become one of the main treatment modalities for a variety of BRAF-mutation-positive solid tumors. Dabrafenib plus trametinib, as the first tumor-agnostic therapy, has been approved by the US Food and Drug Administration for the treatment of adult and pediatric patients aged 6 years and older harboring a BRAF V600E mutation with unresectable or metastatic solid tumors that have progressed following prior treatment and who have no satisfactory alternative treatment options. This is also the first time a BRAF/MEK inhibitor combination has been approved for use in pediatric patients. As research into the diagnosis and treatment of BRAF mutations advances, standardizing the detection of BRAF mutations and the clinical application of BRAF inhibitors becomes increasingly important. Therefore, we have established a universal and systematic strategy for diagnosing and treating solid tumors with BRAF mutations. In this expert consensus, we (1) summarize the epidemiology and clinical characteristics of BRAF mutations in different solid tumors, (2) provide recommendations for the selection of genetic testing methods and platforms, and (3) establish a universal strategy for the diagnosis and treatment of patients with solid tumors harboring BRAF mutations.
Fluorine-18-fluorodeoxyglucose positron emission tomography (18F-FDG-PET) is a new technique for identifying different malignant tumors using different uptake values between tumor cells and normal tissues. Here we assessed the diagnostic accuracy of 18F-FDG-PET in patients with testicular cancer by pooling data of existing trials in a meta-analysis. PubMed/MEDLINE, Embase and Cochrane Central Trials databases were searched and studies published in English relating to the diagnostic value of FDG-PET for testicular cancer were collected. The summary receiver operating characteristic (SROC) curve was used to examine the FDG-PET accuracy. A total of 16 studies which included 957 examinations in 807 patients (median age, 31.1 years) were analyzed. A meta-analysis was performed to combine the sensitivity and specificity and their 95% confidence intervals (CIs), from diagnostic odds ratio (DOR), positive likelihood ratios (PLR), negative likelihood ratio (NLR). SROC were derived to demonstrate the diagnostic accuracy of FDG-PET for testicular cancer. The pooled sensitivity and specificity were 0.75 (95% confidence interval (CI), 0.70-0.80) and 0.87 (95% CI, 0.84-0.89), respectively. The pooled DOR was 35.6 (95% CI, 12.9-98.3). The area under the curve (AUC) was 0.88. The pooled PLR and pooled NLR were 7.80 (95% CI, 3.73-16.3) and 0.31 (95% CI, 0.23-0.43), respectively. In patients with testicular cancer, 18F-FDG-PET demonstrated a high SROC area, and could be a potentially useful tool if combined with other imaging methods such as MRI and CT. Nevertheless, the literature focusing on the use of 18F-FDG-PET in this setting still remains limited.
Nitrogen-containing heterocyclic small molecule derivatives have been proved to possess potent affinity with tau aggregates. A series of imidazo[1,2-a]pyridine analogues were designed and synthesized for the screen of potential highly selective tau targeted PET tracers. Structure activity relationship study of these compounds led to the discovery of compound 28, which showed high affinity with tau aggregates (Ki = 0.99 nM). Compound 28 also displayed fast pharmacokinetic properties which are suitable to be developed as PET tracers. Based on the direct SNAr radiofluorination, 18F-28 was successfully produced with high radiochemical yield. In vitro stability tests and log D7.4 measurement indicated 18F-28 hold suitable physicochemical parameters for blood-brain-barrier (BBB) penetration and in vivo PET brain imaging. In micro-PET imaging studies, high initial brain uptake was observed with 18F-28 in normal mice and P301L transgenic mice, as well as a fast clearance from brain. 18F-28 was also evaluated in non-human primates, which also displayed a fast in and fast out accumulation in the brain. According to the autoradiographic analysis of 18F-28 with human brain tissues, positive deposits in temporal lobe can be confirmed, which is well agreed with immunohistochemistry results with tau-antibodies. Therefore, the preclinical results revealed compound 28 holds the potential to be developed as a potent and selective tau aggregate targeted PET tracer, and further optimizations and evaluations may still be needed.
The role of distinct immune cell types in modulating cancer progression has recently gained attention. The immune context is indicated by the abundance of immune infiltration based on quantified lymphocytes in the core of tumors (CT) and invasive tumor margin (IM). Novel immune biomarkers could potentially complement tumor-node-metastasis (TNM) classification for non-small cell lung cancers (NSCLCs), thereby improving prognostic accuracy. This study evaluated the prognostic value of a newly established immunologic score (neo-IS) in patients with NSCLC. We detected 10 immune biomarkers, including CD45RO, CD3, CD8, CD68, CD163, CD66b, FoxP3, PD-1, PD-L1, and TIM-3, in 350 patients with NSCLC from 2 cohorts using immunohistochemistry (IHC). The 3- and 5-year survival and overall survival (OS) rates were evaluated. An immunologic prediction model specifically for NSCLC patients, the neo-immunologic score (neo-ISNSCLC ), was constructed using a Cox proportional hazards regression model. In the discovery cohort (n = 250), the establishment of neo-ISNSCLC was based on 4 immune biomarkers: CD3+IM , CD8+CT , FoxP3+IM , and PD-1+IM . Significant prognostic differences were found upon comparing low-ISNSCLC patients and high-ISNSCLC patients. The OS rate in the high-ISNSCLC group was significantly longer than that in the low-ISNSCLC group (67.5 months vs. 51.2 months, p < 0.001). The neo-ISNSCLC was validated in the validation cohort (n = 100), and the results were confirmed. Multivariate analyses indicated that neo-ISNSCLC was an independent indicator of prognosis in patients with NSCLC. Finally, we combined neo-ISNSCLC with clinicopathologic factors to establish a tumor-node-metastasis-immune (TNM-I) staging system for clinical use, which showed better prediction accuracy than the TNM stage.
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