Cancer Biotherapy and Radiopharmaceuticals最新文献

Background: Colon cancer is a prevalent malignant tumor of digestive tract occurring in the colon. Colon cancer is the third leading cause of deaths in the world. Basic research on colon cancer is of great importance to patients with the disease. Methods: In this article, the authors observed the expression of KIAA0101 in different types of cancers in public database (GEPIA2), found a gene network associated with KIAA0101 in STRING database, and explored the correlation of these genes with KIAA0101 at the expression level and the immune cells associated with the expression of KIAA0101. Then the authors detected the affection of KIAA0101 to the proliferation and apoptosis of cancer cells and verified the consistency of KIAA0101 expression in 31 tumor patient tissues using the database. Results: KIAA0101 is differentially expressed in all kinds of tumor cells, and it shows high expression in colorectal cancer tissues. The authors found 10 genes related to KIAA0101, including CDC20, TOP2A, CCNB2, CCNA2, and so on, all of which show positive correlation with KIAA0101 expression. In addition, the result of this study showed that KIAA0101 expression had a positive correlation with the infiltration of Th1 and Th2 cells, with correlation coefficients of 0.371 and 0.627, respectively. KIAA0101 gene shows high expression in both HCT15 and SW480 cell lines. Inhibition of KIAA0101 expression can increase caspase 3/7 activity in both HCT15 and SW480 cell lines, inhibit the proliferation ability of the two cell lines, and inhibit Bcl-2 gene expression. KIAA0101 also has tumor-suppressing effects in mice. The expression of KIAA0101 gene also shows a significant increase in the tissues collected from 31 patients with tumor. Conclusions: Inhibition of KIAA0101 expression can regulate cell proliferation and apoptosis in colorectal cancer.

Context: Hepatocellular carcinoma (HCC) poses a serious threat to human health due to its high incidence and mortality rates. In recent years, the application of traditional Chinese medicine (TCM) in the comprehensive treatment of liver cancer has gained increasing attention. Clinical practices have demonstrated the efficacy of Chai Hu Hua Ji Tang (CHHJT) in liver cancer treatment, yet its underlying mechanism remains unexplored. Objective: This article reveals the underlying mechanism of CHHJT in the context of hepatic malignancies. Materials and Methods: CHHJT and HCC-related targets were screened through network pharmacology. PLC/PRF/5 and MHCC97L cells were treated with CHHJT as the experimental group, and those without CHHJT as the control group. After 24 and 48 h, IC₅₀, cloning, scratch, invasion, and Western blot/quantitative real-time PCR were assayed. Subsequently, a model of orthotopic liver cancer was developed in BALB/c nude mice. A volume of 0.2 mL of PBS served as the control group, while the experimental group received 0.2 mL of a 3.55 g/mL CHHJT solution. After 4 weeks, the in vivo effect of CHHJT was evaluated. Results: According to our results of IC₅₀, a concentration of 1600 μg/mL was the most effective dosage for CHHJT to suppress growth of HCC cells. Additionally, CHHJT was found to curb cellular proliferation, migration, and invasiveness. Transcription and protein levels of FLT3, PIK3CA, and AKT1 targets reduced following CHHJT treatment. In the nude mouse model, CHHJT treatment greatly reduced tumor cell volume, integrated tumor cell structure, markedly reduced nodules, well-grown cells, and substantially increased apoptosis. Discussion and Conclusion: CHHJT is likely to impede the PI3K/AKT signaling pathway by downregulating FLT3 protein expression, ending up with suppression of HCC cell differentiation and proliferation, as well as their viability. Future research could stratify patients based on their likelihood of responding to PI3K/AKT pathway-targeted therapies. This could aid in patient selection and optimize treatment outcomes.

Objective: This study analyzed the effectiveness of proactive nursing interventions in patients undergoing ultrasound-guided radiofrequency ablation for uterine fibroids. Materials and Methods: A retrospective analysis included 50 patients who received routine postoperative care from April 2022 to April 2023 as control group (CG) and 54 patients who received proactive nursing from May 2023 to May 2024 as intervention group (IG). Eligible participants were adult women with confirmed uterine fibroids and complete medical records, including preoperative, intraoperative, and postoperative data. Exclusion criteria included individuals with severe comorbidities such as uncontrolled diabetes or hypertension, those who were pregnant or breastfeeding during the study period, and patients with significant gaps in medical records or cognitive impairments that hindered participation in the study. Surgical outcomes, ovarian function markers, immune function markers, oxidative stress indicators, and complications were compared between the two groups. Results: In IG, intraoperative blood loss (15.83 ± 4.35 mL vs. 49.75 ± 7.62 mL), surgical duration (27.64 ± 8.04 min vs. 55.08 ± 6.67 min), hospital stay (3.17 ± 0.65 d vs. 5.48 ± 0.83 d), and time to ambulation (1.43 ± 0.27 d vs. 2.56 ± 0.34 d) were significantly lower versus CG (p < 0.05, Cohen's d = 0.72∼0.89). Levels of luteinizing hormone, follicle-stimulating hormone, estradiol, reactive oxygen species, malondialdehyde, and advanced oxidation protein products at 1 d and 30 d postoperatively were significantly lower in IG versus CG (p < 0.05, Cohen's d = 0.6∼0.80). CD3 and CD8 levels at 1 d and 30 d postoperatively were significantly lower in IG, whereas CD4 and CD4/CD8 (2.45 ± 0.56 vs. 1.58 ± 0.44) were significantly higher versus CG (p < 0.05, Cohen's d = 0.65). The incidence of postoperative complications in IG (14.81%) was significantly inferior to that in CG (22%) (p < 0.05, Cohen's d = 0.52∼0.87). Conclusions: Proactive nursing interventions applied in the management of patients after ultrasound-guided radiofrequency ablation for uterine fibroids demonstrate significant clinical advantages. Specifically, they reduce intraoperative bleeding, shorten surgical and hospitalization durations, and potentially benefit ovarian and immune functions of patients.

Malignant brain tumors remain a major therapeutic challenge due to poor intracellular delivery of therapeutics. Radiopharmaceuticals such as Technetium-99m (^^99mTc) are valuable for imaging and therapy but suffer from limited tumor uptake caused by cellular and membrane barriers. Focused ultrasound (FUS) offers a noninvasive strategy to transiently enhance membrane permeability through sonoporation. Unlike prior studies largely focused on blood-brain barrier disruption, this work specifically investigates direct tumor cell sonoporation as an independent uptake mechanism. This study evaluates FUS-mediated enhancement of ^^99mTc radiopharmaceutical uptake in brain tumor cells and determines optimal acoustic parameters balancing efficacy and safety. Human glioblastoma (U87-MG) and astrocytoma (A172) cells were cultured and exposed to FUS at intensities of 0.3, 0.5, and 0.7 W/cm² for 30-120 s. Radiopharmaceutical uptake was quantified using γ-scintillation counting. Membrane integrity was assessed by live/dead fluorescence microscopy and lactate dehydrogenase release, while cell viability was evaluated via medical training therapy (MTT) assays. U87-MG cells exhibited up to a 3.1-fold increase at 0.7 W/cm² for 120 s, with a 2.3-fold enhancement at the clinically relevant 0.5 W/cm² for 60 s while maintaining >92% viability. A172 cells showed similar trends with slightly lower magnitudes. Safety assays confirmed reversible membrane permeabilization at ≤0.5 W/cm². The temporal uptake kinetics aligned with established membrane pore resealing dynamics, supporting reversible sonoporation as the uptake mechanism. Importantly, while ^^99mTc complexes are primarily diagnostic, enhanced intracellular delivery achieved by optimized FUS may also support future theranostic strategies, including radionuclide therapy. These findings underscore the translational potential of FUS in neuro-oncology, where tumor heterogeneity necessitates parameter optimization to maximize radiopharmaceutical delivery, improve imaging contrast, and overcome therapeutic resistance.

Background: Response to neoadjuvant chemotherapy (NACT) in locally advanced gastric cancer varies. This study compares tumor response to NACT across anatomical locations, considering clinicopathological differences. Materials and Methods: This retrospective study included 212 patients with gastric adenocarcinoma who received NACT followed by surgery. Tumors were classified by location (antrum-pylorus, corpus-fundus, cardia). Treatment response was assessed using the Modified Ryan Scoring System (0 = complete, 1 = near complete, 2 = partial, 3 = minimal/none). Results: Tumor locations were antrum-pylorus (30.2%), corpus-fundus (28.3%), and cardia (41.5%). Localization showed no statistically significant differences in response (p = 0.337). However, cardia tumors were more frequent in Groups 3 (40.9%) and 4 (48.1%), which showed poorer pathological responses, whereas antrum (34.6%) and corpus (38.5%) tumors were more common in Group 1, representing patients with a pathological complete response. These findings suggest that cardia tumors may have a lower response to NACT, although definitive conclusions cannot be drawn. In multivariate analysis, only advanced T stage (T3-4) was independently associated with poor tumor regression grade response (odds ratio 14.3, 95% confidence interval 5.4-37.5, p < 0.001). Conclusions: Tumor response to NACT varied by anatomical location, although differences were not statistically significant. Cardia tumors showed a trend toward lower response rates. To the authors' knowledge, this is the first study evaluating gastric anatomical subgroups in this context. While not conclusive, the findings suggest that tumor location may influence treatment strategies, warranting validation in larger studies.

Ocular malignancies provide a unique therapeutic challenge because of their anatomical intricacy, limited accessibility, and vision-critical nature. Recent developments in radiopharmaceutical design have been paired with ultrasound-mediated medicine administration to create highly targeted, less invasive therapies for intraocular cancers. This research looks at the emerging topic of ultrasound-responsive radiopharmaceutical devices built specifically for ocular oncology. These methods enhance tumor selectivity, decrease off-target effects, and enable real-time imaging-guided therapy by utilizing targeted ultrasound to induce localized medication release or radiotherapeutic agent activation. Microbubble-assisted delivery, thermosensitive liposomes, and phase-transition nanodroplets carrying radionuclides have all been designed to optimize ocular pharmacokinetics and tissue penetration. Preclinical studies reveal promising results in increasing radiotherapeutic efficacy against retinoblastoma and uveal melanoma while sparing healthy ocular tissues.

Recent research has significantly altered the understanding of the immunogenic profile of certain processes of cancer cell death, leading to the recognition of a new subclass of apoptosis called "immunogenic apoptosis." This form of cell death, induced by specific chemotherapeutic agents, has been shown to elicit a "chemotherapy vaccine effect" in vivo, effectively stimulating an antitumor immune response. At the molecular level, "a collection of molecules" known as "damage-associated molecular patterns (DAMPs)" have been identified as key contributors to the immunogenicity of various cell death pathways. Intracellular molecules, such as heat-shock proteins, high-mobility group box 1 protein, and calreticulin, act as DAMPs when exposed or secreted in response to specific certain stressors, stimuli, and modes of cell death. These discoveries have fueled ongoing research focused on the identification of novel DAMPs, uncovering new mechanisms of their exposure or secretion and developing therapeutic agents capable of inducing immunogenic cell death (ICD). In addition, there is growing interest in addressing the current challenges and limitations within this emerging paradigm. The authors believe that this integrated strategy-combining DAMPs, ICD, and anticancer therapies-may hold the key to significantly reducing cancer-related mortality in the near future.

To properly target tumors during preoperative chemoradiotherapy, differentiated thyroid carcinoma (DTC) must be careful. This method increases treatment success and decreases recurrence. Ultrasound coupled with SPECT/CT may provide novel localization and dose planning possibilities. Many systems solely use anatomical or functional imaging. This may result in insufficient dosage delivery and wasted radiation exposure to healthy tissues. These issues are addressed by Dual-Modality Imaging-Guided Adaptive Chemoradiotherapy Planning (DMI-ACP). This innovative approach combines real-time ultrasound imaging with 6 Å SPECT/CT imaging for precise tumor delineation and tailored dosimetry. This system enables clinicians to adjust chemoradiotherapy regimens by seamlessly integrating functional iodine absorption data with anatomical characteristics, thereby targeting therapy to cancerous areas. The outcomes of this method for patients with DTC were promising, including better lesion targeting, reduced radiation exposure to healthy tissues, and improved chemotherapeutic dose distribution. In clinical evaluations, the DMI-ACP framework demonstrated a sensitivity of 94% and a specificity of 89% in identifying malignant lesions compared with traditional imaging techniques. Furthermore, the integration of adaptive planning resulted in a 20% improvement in tumor control probability and a 15% reduction in exposure to surrounding healthy tissue, as assessed through dosimetric analysis. 2023075 Nanjing Drum Tower Hospital Group Suqian Hospital/The Affiliated Suqian Hospital of Xuzhou Medical University.