Pub Date : 2025-01-01DOI: 10.1177/15330338241311136
Jia-Huan Cai, Xun Peng, Jia-Yang Lu
Purpose: To evaluate the impact of patient setup errors on the dosimetry and radiobiological models of intensity-modulated radiotherapy (IMRT) for esophageal cancer.
Methods and materials: This retrospective study with 56 patients in thermoplastic mask (TM) and vacuum bag (VB) groups utilized real setup-error (RSE) data from cone-beam CT scans to generate simulated setup-error (SSE) data following a normal distribution. The SSE data were applied to simulate all treatment fractions per patient by shifting the plan isocenter and recalculating the dose. A simulated plan sum (SPS) was created by accumulating all simulated fraction plans. Comparisons of target dose, improved homogeneity index (iHI), conformity index (CI), tumor control probability (TCP) and normal tissue complication probability (NTCP) were conducted between SPSs and original treatment plans (OTPs). Correlations between RSE and TCP/NTCP were analyzed.
Results: Compared to OTPs in the TM group, the planning target volume (PTV) of SPSs showed reductions in D95%, D98%, iHI, CI and TCP by 1.2%, 2.2%, 2.3%, 7.3% and 1.2%, while D2% increased by 0.3%; D2% of clinical target volume (CTV) increased by 0.2% (P < .05). In the VB group, D95%, D98%, iHI, CI and TCP of PTV decreased by 2.5%, 4.5%, 4.2%, 15.6% and 2.0%, with D2% increasing by 0.5%; D2% of CTV increased by 0.5% while D98% decreased by 0.2% (P < .05). The dose of organs at risk (OARs) changed slightly in both groups. The mean and standard deviation of absolute RSE negatively correlated with the TCP of PTV, while the mean RSE positively correlated with the NTCP of lung and spinal cord.
Conclusions: Setup errors may reduce dose homogeneity and conformity, potentially reducing TCP of PTV and increasing NTCP, especially when mean RSE shifts the isocenter towards OARs. VB immobilization may result in relatively larger impacts of setup errors, but this needs future validation.
{"title":"Dosimetric and Radiobiological Impact of Patient Setup Errors in Intensity-modulated Radiotherapy for Esophageal Cancer.","authors":"Jia-Huan Cai, Xun Peng, Jia-Yang Lu","doi":"10.1177/15330338241311136","DOIUrl":"10.1177/15330338241311136","url":null,"abstract":"<p><strong>Purpose: </strong>To evaluate the impact of patient setup errors on the dosimetry and radiobiological models of intensity-modulated radiotherapy (IMRT) for esophageal cancer.</p><p><strong>Methods and materials: </strong>This retrospective study with 56 patients in thermoplastic mask (TM) and vacuum bag (VB) groups utilized real setup-error (RSE) data from cone-beam CT scans to generate simulated setup-error (SSE) data following a normal distribution. The SSE data were applied to simulate all treatment fractions per patient by shifting the plan isocenter and recalculating the dose. A simulated plan sum (SPS) was created by accumulating all simulated fraction plans. Comparisons of target dose, improved homogeneity index (iHI), conformity index (CI), tumor control probability (TCP) and normal tissue complication probability (NTCP) were conducted between SPSs and original treatment plans (OTPs). Correlations between RSE and TCP/NTCP were analyzed.</p><p><strong>Results: </strong>Compared to OTPs in the TM group, the planning target volume (PTV) of SPSs showed reductions in D<sub>95%</sub>, D<sub>98%</sub>, iHI, CI and TCP by 1.2%, 2.2%, 2.3%, 7.3% and 1.2%, while D<sub>2%</sub> increased by 0.3%; D<sub>2%</sub> of clinical target volume (CTV) increased by 0.2% (<i>P </i>< .05). In the VB group, D<sub>95%</sub>, D<sub>98%</sub>, iHI, CI and TCP of PTV decreased by 2.5%, 4.5%, 4.2%, 15.6% and 2.0%, with D<sub>2%</sub> increasing by 0.5%; D<sub>2%</sub> of CTV increased by 0.5% while D<sub>98%</sub> decreased by 0.2% (<i>P </i>< .05). The dose of organs at risk (OARs) changed slightly in both groups. The mean and standard deviation of absolute RSE negatively correlated with the TCP of PTV, while the mean RSE positively correlated with the NTCP of lung and spinal cord.</p><p><strong>Conclusions: </strong>Setup errors may reduce dose homogeneity and conformity, potentially reducing TCP of PTV and increasing NTCP, especially when mean RSE shifts the isocenter towards OARs. VB immobilization may result in relatively larger impacts of setup errors, but this needs future validation.</p>","PeriodicalId":22203,"journal":{"name":"Technology in Cancer Research & Treatment","volume":"24 ","pages":"15330338241311136"},"PeriodicalIF":2.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755542/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012180","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}
Long non-coding RNAs (lncRNAs) are known to play vital roles in human cancers. LncRNA TRPM2-AS has been found to be upregulated in various types of cancers. The elevated levels of TRPM2-AS are associated with important clinicopathological parameters such as tumor size, tumor stage, and lymph node metastasis, revealing that TRPM2-AS could be a potential target for cancer diagnosis, prognosis and treatment. Moreover, TRPM2-AS is involved in regulating the cell proliferation, migration, invasion, apoptosis, drug or radio resistance by serving as a competing endogenous RNA, directly bounding to proteins and regulating multiple signaling pathways. In this review, we comprehensively summarize the latest knowledge on the aberrant expression of TRPM2-AS, the relationship between TRPM2-AS and clinical features, and the detailed mechanisms of potential functions of TRPM2-AS in various cancer types. The current study highlights the potential of TRPM2-AS as a prognostic and therapeutic target in cancers.
{"title":"Clinical Significance and Pathogenic Mechanisms of Long Non-Coding RNA TRPM2-AS in Cancers.","authors":"Shichen Huang, Bowen Li, Huanyu Chen, Cheng Rong, Zheng Yang, Xianqin Zhang","doi":"10.1177/15330338251315625","DOIUrl":"10.1177/15330338251315625","url":null,"abstract":"<p><p>Long non-coding RNAs (lncRNAs) are known to play vital roles in human cancers. LncRNA TRPM2-AS has been found to be upregulated in various types of cancers. The elevated levels of TRPM2-AS are associated with important clinicopathological parameters such as tumor size, tumor stage, and lymph node metastasis, revealing that TRPM2-AS could be a potential target for cancer diagnosis, prognosis and treatment. Moreover, TRPM2-AS is involved in regulating the cell proliferation, migration, invasion, apoptosis, drug or radio resistance by serving as a competing endogenous RNA, directly bounding to proteins and regulating multiple signaling pathways. In this review, we comprehensively summarize the latest knowledge on the aberrant expression of TRPM2-AS, the relationship between TRPM2-AS and clinical features, and the detailed mechanisms of potential functions of TRPM2-AS in various cancer types. The current study highlights the potential of TRPM2-AS as a prognostic and therapeutic target in cancers.</p>","PeriodicalId":22203,"journal":{"name":"Technology in Cancer Research & Treatment","volume":"24 ","pages":"15330338251315625"},"PeriodicalIF":2.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047972","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}
Introduction: Metastasis remains a major cause of death among patients with malignant tumors. Radiotherapy is one of the main modalities of cancer treatment. The rapid development of radiotherapy technology has enabled the widespread application of hypofractionated radiotherapy (HFRT) in clinical practice. This study aimed to evaluate the effect of HFRT on the survival and safety of patients with oligometastatic tumors.
Methods: We conducted a retrospective study that involved 65 patients with well-controlled primary tumors and 1-5 metastatic foci treated at the study site between January 2020 and December 2022. Patients were aged >18 years and had a ≥ 6-month life expectancy. The patients received standard treatments plus HFRT for all metastatic foci. The dose fractionation regimen was adjusted according to the location and size of the patient's metastatic foci. The planning gross tumor volume of HFRT was 82.93 cm3 (range: 10.12-562.80 cm3), and the radiation dose range was 20 Gy/5 F-60 Gy/15 F. Progression-free survival (PFS), overall survival (OS), local control rates, and incidence of adverse events of the patients were observed.
Results: Among the 65 patients, the median follow-up time, PFS, and OS were 26 months (95% CI: 0.80-37.50), 15 months (95% CI: 9.36-20.64), and 28 months (95% CI: 16.71-39.29), respectively. The 1- and 2-year PFS were 53.8% and 40.0%, respectively, while the 1- and 2-year OS rates were 73.8% and 56.9%, respectively. In total, 13.8%, 55.4%, 20.0%, and 13.8% of patients showed complete response, partial response, stable disease, and progressive disease, respectively. Four patients developed grade 3 or worse adverse events, and no treatment-related deaths occurred.
Conclusions: HFRT showed favorable clinical efficacy and safety in patients with oligometastatic tumors, generally achieving a good OS rate. Further randomized trials should be conducted.
{"title":"Efficacy Analysis of Hypofractionated Radiotherapy for Oligometastatic Tumors: A Retrospective Study.","authors":"Qian Sun, Hanqing Zhao, Xianwen Zhang, Suli Zhang, Zelai He, Gengming Wang, Hao Jiang, Aili Xuan, Xianming Li","doi":"10.1177/15330338241310155","DOIUrl":"10.1177/15330338241310155","url":null,"abstract":"<p><strong>Introduction: </strong>Metastasis remains a major cause of death among patients with malignant tumors. Radiotherapy is one of the main modalities of cancer treatment. The rapid development of radiotherapy technology has enabled the widespread application of hypofractionated radiotherapy (HFRT) in clinical practice. This study aimed to evaluate the effect of HFRT on the survival and safety of patients with oligometastatic tumors.</p><p><strong>Methods: </strong>We conducted a retrospective study that involved 65 patients with well-controlled primary tumors and 1-5 metastatic foci treated at the study site between January 2020 and December 2022. Patients were aged >18 years and had a ≥ 6-month life expectancy. The patients received standard treatments plus HFRT for all metastatic foci. The dose fractionation regimen was adjusted according to the location and size of the patient's metastatic foci. The planning gross tumor volume of HFRT was 82.93 cm<sup>3</sup> (range: 10.12-562.80 cm<sup>3</sup>), and the radiation dose range was 20 Gy/5 F-60 Gy/15 F. Progression-free survival (PFS), overall survival (OS), local control rates, and incidence of adverse events of the patients were observed.</p><p><strong>Results: </strong>Among the 65 patients, the median follow-up time, PFS, and OS were 26 months (95% CI: 0.80-37.50), 15 months (95% CI: 9.36-20.64), and 28 months (95% CI: 16.71-39.29), respectively. The 1- and 2-year PFS were 53.8% and 40.0%, respectively, while the 1- and 2-year OS rates were 73.8% and 56.9%, respectively. In total, 13.8%, 55.4%, 20.0%, and 13.8% of patients showed complete response, partial response, stable disease, and progressive disease, respectively. Four patients developed grade 3 or worse adverse events, and no treatment-related deaths occurred.</p><p><strong>Conclusions: </strong>HFRT showed favorable clinical efficacy and safety in patients with oligometastatic tumors, generally achieving a good OS rate. Further randomized trials should be conducted.</p>","PeriodicalId":22203,"journal":{"name":"Technology in Cancer Research & Treatment","volume":"24 ","pages":"15330338241310155"},"PeriodicalIF":2.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11742154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012182","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}
The contemporary concept of carcinogenesis summarizes the role of hypoxia, neoangiogenesis, and hemostasis, including in the stage of progression and metastasis of the tumor process. Metastatic disease is a serious therapeutic challenge for any oncological condition. The purpose of this study was to evaluate the dynamics of specific indicators of neoangiogenesis and hypoxia as potential biomarkers for therapeutic efficacy or risk of disease progression in patients with brain metastases (BM) undergoing robotic stereotactic radiosurgery. Two groups of patients (lung cancer and other types of cancers) with oligometastatic disease and brain metastases were included. The patients (n = 66) were treated CyberKnife system. Human Angiopoietin-2, Hypoxia inducible factor 1 α (HIF-1α) and human Vascular Endothelial Growth Factor-А (VEGF-А) were measured in this prospective longitudinal study. Analysis of human Angiopoietin-2, HIF-1α, human VEGF-A in the post-treatment period showed a statistically significant decrease between the baseline and the 6 months post-treatment time point in both patient groups. The baseline value of serum VEGF-А in the group with lung cancer decreased by 40%, Аngiopoietin-2-by 48%, HIF-1α -by 43%. In the group with other types of cancers, VEGF-А decreased by 54.75%, Аngiopoietin-2-by 52%, HIF-1α -by 39.5%. Despite the significant reduction, the levels remained significantly higher in both groups than in healthy controls. This study underscores the potential of integrating molecular markers like VEGF-A, Angiopoietin-2, and HIF-1α into clinical decision-making to enhance outcomes for patients with brain metastases undergoing RSRS.
{"title":"Dynamics of VEGF-А, Аngiopoietin-2 and HIF-1α Levels in Patients with Brain Metastases Treated with Cyberknife Radiosurgery.","authors":"Veselin Popov, Gabriela Raycheva, Zhanet Grudeva-Popova","doi":"10.1177/15330338251313945","DOIUrl":"10.1177/15330338251313945","url":null,"abstract":"<p><p>The contemporary concept of carcinogenesis summarizes the role of hypoxia, neoangiogenesis, and hemostasis, including in the stage of progression and metastasis of the tumor process. Metastatic disease is a serious therapeutic challenge for any oncological condition. The purpose of this study was to evaluate the dynamics of specific indicators of neoangiogenesis and hypoxia as potential biomarkers for therapeutic efficacy or risk of disease progression in patients with brain metastases (BM) undergoing robotic stereotactic radiosurgery. Two groups of patients (lung cancer and other types of cancers) with oligometastatic disease and brain metastases were included. The patients (n = 66) were treated CyberKnife system. Human Angiopoietin-2, Hypoxia inducible factor 1 α (HIF-1α) and human Vascular Endothelial Growth Factor-А (VEGF-А) were measured in this prospective longitudinal study. Analysis of human Angiopoietin-2, HIF-1α, human VEGF-A in the post-treatment period showed a statistically significant decrease between the baseline and the 6 months post-treatment time point in both patient groups. The baseline value of serum VEGF-А in the group with lung cancer decreased by 40%, Аngiopoietin-2-by 48%, HIF-1α -by 43%. In the group with other types of cancers, VEGF-А decreased by 54.75%, Аngiopoietin-2-by 52%, HIF-1α -by 39.5%. Despite the significant reduction, the levels remained significantly higher in both groups than in healthy controls. This study underscores the potential of integrating molecular markers like VEGF-A, Angiopoietin-2, and HIF-1α into clinical decision-making to enhance outcomes for patients with brain metastases undergoing RSRS.</p>","PeriodicalId":22203,"journal":{"name":"Technology in Cancer Research & Treatment","volume":"24 ","pages":"15330338251313945"},"PeriodicalIF":2.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726525/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971965","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}
Pub Date : 2025-01-01DOI: 10.1177/15330338241312561
Islam Alfreahat, Hamdi Nsairat, Ibrahim Deeb Aldeeb, Ali Al-Samydai, Walhan Alshaer
Background: Doxorubicin (DOX) is a potent chemotherapeutic agent for breast cancer, but its effectiveness is often diminished by resistance mechanisms, particularly through p-glycoprotein (P-gp) mediated drug efflux. Clarithromycin (CAM), a macrolide antibiotic, inhibits multiple metabolic pathways including CYP3A and P-gp, potentially countering DOX resistance.
Objective: This study aimed to evaluate the potentiation of DOX and its effectiveness against the MCF-7 breast cancer cell line by encapsulating both DOX and CAM in PEGylated liposomes.
Methods: PEGylated liposomes containing DOX and CAM were prepared using the thin film hydration method. The physicochemical properties of the liposomes, including average particle size, polydispersity index (PDI), and zeta potential, were characterized. Encapsulation efficiencies for CAM and DOX were assessed, and stability of the liposomes was evaluated over 9 days at room temperature. Cell viability was measured using an IC50 assay, and P-gp expression levels were determined by ELISA.
Results: The CAM/DOX-PEGylated liposomes exhibited optimal average particle size (238 ± 26.7 nm), PDI (0.29 ± 0.107), and zeta potential (-20.9 ± 2.17 mV). These liposomes maintained good stability regarding size and charge over 9 days. Encapsulation efficiencies were 81.05% for CAM and 78.13% for DOX. The IC50 value for CAM/DOX-PEGylated liposomes was 0.13 µM, representing a significant reduction compared to the physical mixture of CAM and DOX (0.25 µM) and free DOX (0.21 µM) against MCF-7 cells. ELISA analysis showed a reduction in P-gp expression of approximately 5% with CAM/DOX-PEGylated liposomes compared to 1.61% with free DOX.
Conclusion: The results indicate that CAM encapsulated in PEGylated liposomes enhances the effectiveness of DOX against breast cancer cells, likely through the inhibition of p-glycoprotein. This approach may offer a promising strategy to overcome DOX resistance and improve chemotherapy outcomes.
{"title":"<i>In Vitro</i> Potentiation of Doxorubicin Cytotoxicity Utilizing Clarithromycin Loaded-PEGylated Liposomes.","authors":"Islam Alfreahat, Hamdi Nsairat, Ibrahim Deeb Aldeeb, Ali Al-Samydai, Walhan Alshaer","doi":"10.1177/15330338241312561","DOIUrl":"10.1177/15330338241312561","url":null,"abstract":"<p><strong>Background: </strong>Doxorubicin (DOX) is a potent chemotherapeutic agent for breast cancer, but its effectiveness is often diminished by resistance mechanisms, particularly through p-glycoprotein (P-gp) mediated drug efflux. Clarithromycin (CAM), a macrolide antibiotic, inhibits multiple metabolic pathways including CYP3A and P-gp, potentially countering DOX resistance.</p><p><strong>Objective: </strong>This study aimed to evaluate the potentiation of DOX and its effectiveness against the MCF-7 breast cancer cell line by encapsulating both DOX and CAM in PEGylated liposomes.</p><p><strong>Methods: </strong>PEGylated liposomes containing DOX and CAM were prepared using the thin film hydration method. The physicochemical properties of the liposomes, including average particle size, polydispersity index (PDI), and zeta potential, were characterized. Encapsulation efficiencies for CAM and DOX were assessed, and stability of the liposomes was evaluated over 9 days at room temperature. Cell viability was measured using an IC<sub>50</sub> assay, and P-gp expression levels were determined by ELISA.</p><p><strong>Results: </strong>The CAM/DOX-PEGylated liposomes exhibited optimal average particle size (238 ± 26.7 nm), PDI (0.29 ± 0.107), and zeta potential (-20.9 ± 2.17 mV). These liposomes maintained good stability regarding size and charge over 9 days. Encapsulation efficiencies were 81.05% for CAM and 78.13% for DOX. The IC50 value for CAM/DOX-PEGylated liposomes was 0.13 µM, representing a significant reduction compared to the physical mixture of CAM and DOX (0.25 µM) and free DOX (0.21 µM) against MCF-7 cells. ELISA analysis showed a reduction in P-gp expression of approximately 5% with CAM/DOX-PEGylated liposomes compared to 1.61% with free DOX.</p><p><strong>Conclusion: </strong>The results indicate that CAM encapsulated in PEGylated liposomes enhances the effectiveness of DOX against breast cancer cells, likely through the inhibition of p-glycoprotein. This approach may offer a promising strategy to overcome DOX resistance and improve chemotherapy outcomes.</p>","PeriodicalId":22203,"journal":{"name":"Technology in Cancer Research & Treatment","volume":"24 ","pages":"15330338241312561"},"PeriodicalIF":2.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047971","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}
Pub Date : 2025-01-01DOI: 10.1177/15330338241300743
Danielle Ramos Martin Matsumoto, Gil Facina
Objectives: We conducted a systematic review to compile the findings of all published studies on the use of percutaneous laser ablation (PLA) in the treatment of early-stage breast cancer. We aimed to identify appropriate methodology as well as parameters for the selection of suitable patients to optimize outcomes with the use of PLA. Additionally, we aimed to analyze whether this method is a viable alternative to current surgical treatments employed. Methods: The PRISMA 2020 method was applied. The terms "laser ablation" AND "breast cancer" were used to select all articles published up to January 2024 on the PubMed and Embase platforms. Articles in English were included. Only original articles were considered for this systematic review. Review articles, editorials, letters, and studies ex-vivo or not performed in humans were excluded. Results: Seventeen articles, including 308 patients were analyzed. Among the studies describing the complete response rate to assess treatment success, there was no residual tumor after ablation in 74.4% of the patients. MRI was the best exam to evaluate the effectiveness of the ablative procedure with a NPV of 92% to 100%. Skin burn was the most commonly observed complication, occurring in 6% of patients. Other less frequent complications were hematoma/bleeding, pain, nodulation, erythema, seroma, and fat necrosis. Conclusions: The use of PLA remains restricted to cases with specific indications or within the context of research protocols. However, future studies may validate this promising technique for the local treatment of early-stage breast cancer. This study was registered at INPLASY (registration number: INPLASY2024100045).
{"title":"Incorporating Percutaneous Laser Ablation for Early Breast Cancer Treatment: A Systematic Review.","authors":"Danielle Ramos Martin Matsumoto, Gil Facina","doi":"10.1177/15330338241300743","DOIUrl":"https://doi.org/10.1177/15330338241300743","url":null,"abstract":"<p><p><b>Objectives:</b> We conducted a systematic review to compile the findings of all published studies on the use of percutaneous laser ablation (PLA) in the treatment of early-stage breast cancer. We aimed to identify appropriate methodology as well as parameters for the selection of suitable patients to optimize outcomes with the use of PLA. Additionally, we aimed to analyze whether this method is a viable alternative to current surgical treatments employed. <b>Methods:</b> The PRISMA 2020 method was applied. The terms \"laser ablation\" AND \"breast cancer\" were used to select all articles published up to January 2024 on the PubMed and Embase platforms. Articles in English were included. Only original articles were considered for this systematic review. Review articles, editorials, letters, and studies ex-vivo or not performed in humans were excluded. <b>Results:</b> Seventeen articles, including 308 patients were analyzed. Among the studies describing the complete response rate to assess treatment success, there was no residual tumor after ablation in 74.4% of the patients. MRI was the best exam to evaluate the effectiveness of the ablative procedure with a NPV of 92% to 100%. Skin burn was the most commonly observed complication, occurring in 6% of patients. Other less frequent complications were hematoma/bleeding, pain, nodulation, erythema, seroma, and fat necrosis. <b>Conclusions:</b> The use of PLA remains restricted to cases with specific indications or within the context of research protocols. However, future studies may validate this promising technique for the local treatment of early-stage breast cancer. This study was registered at INPLASY (registration number: INPLASY2024100045).</p>","PeriodicalId":22203,"journal":{"name":"Technology in Cancer Research & Treatment","volume":"24 ","pages":"15330338241300743"},"PeriodicalIF":2.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971968","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}
Pub Date : 2025-01-01DOI: 10.1177/15330338241297231
Andrea Gaetano Allegra, Luca Nicosia, Michele Rigo, Nicola Bianchi, Riccardo Filippo Borgese, Antonio De Simone, Niccolò Giaj-Levra, Davide Gurrera, Stefania Naccarato, Edoardo Pastorello, Francesco Ricchetti, Gianluisa Sicignano, Ruggero Ruggieri, Filippo Alongi
MR-guided radiotherapy (MRgRT) is novel treatment modality in Radiation Oncology that could allow a higher precision and tolerability of Radiation Treatments. This modality is possible due to dedicated systems consisting of a MR scanner mounted on a conventional linac and software that permit daily online treatment plan adaptation. Prostate cancer (PC) is one of the most common malignancies in RO clinical practice and currently under investigation with this new technology. The focus of this review is to describe the current state of the art and clinical results of MRgRT in the treatment of PC. The available technology are briefly described, as well as the published literature and possible future applications.
{"title":"MR-Guided Adaptive Radiotherapy in Localized Prostate Cancer.","authors":"Andrea Gaetano Allegra, Luca Nicosia, Michele Rigo, Nicola Bianchi, Riccardo Filippo Borgese, Antonio De Simone, Niccolò Giaj-Levra, Davide Gurrera, Stefania Naccarato, Edoardo Pastorello, Francesco Ricchetti, Gianluisa Sicignano, Ruggero Ruggieri, Filippo Alongi","doi":"10.1177/15330338241297231","DOIUrl":"10.1177/15330338241297231","url":null,"abstract":"<p><p>MR-guided radiotherapy (MRgRT) is novel treatment modality in Radiation Oncology that could allow a higher precision and tolerability of Radiation Treatments. This modality is possible due to dedicated systems consisting of a MR scanner mounted on a conventional linac and software that permit daily online treatment plan adaptation. Prostate cancer (PC) is one of the most common malignancies in RO clinical practice and currently under investigation with this new technology. The focus of this review is to describe the current state of the art and clinical results of MRgRT in the treatment of PC. The available technology are briefly described, as well as the published literature and possible future applications.</p>","PeriodicalId":22203,"journal":{"name":"Technology in Cancer Research & Treatment","volume":"24 ","pages":"15330338241297231"},"PeriodicalIF":2.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047974","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}
Pub Date : 2025-01-01DOI: 10.1177/15330338251317094
Rami Yanes, Turcin Saridogan, Vikram Gorantla, Abigail Overacre, Ronan W Hsieh, James Celebrezze, Tara Magge, Meghana Singhi, Anwaar Saeed, Amer H Zureikat, Arvind N Dasari, Ibrahim Halil Sahin
The management of early-stage colon cancer involves surgical resection of the primary tumor with or without chemotherapy, depending on pathological staging. The benefit of adjuvant chemotherapy for stage II and III colon cancer is approximately 5% and 15%, indicating the need for optimization for risk stratification and patient selection. Several studies have revealed that current clinicopathological factors lack precision. Circulating tumor DNA (ctDNA) is cell-free DNA originating from cancer cells and can be detected even in the absence of radiologically detectable disease among patients with colon cancer. Recent cohort studies revealed that ctDNA is one of the most significant prognostic factors for patients with early-stage colon cancer, surpassing pathological and clinical risk factors. Prospective cohort studies also suggest there may be a predictive role for ctDNA on the decision for consideration of adjuvant therapy. Currently, randomized clinical trials are enrolling to better define this role. In this review article, we review recent literature on ctDNA and its role in patients with colon cancer. We also elaborate on the future clinical utility of ctDNA in clinical practice and the unmet need for research to optimize currently available ctDNA assays.
{"title":"Shedding Light on the Prognostic and Predictive Value of Circulating Tumor DNA for Management of Patients with Early-Stage Colon Cancer.","authors":"Rami Yanes, Turcin Saridogan, Vikram Gorantla, Abigail Overacre, Ronan W Hsieh, James Celebrezze, Tara Magge, Meghana Singhi, Anwaar Saeed, Amer H Zureikat, Arvind N Dasari, Ibrahim Halil Sahin","doi":"10.1177/15330338251317094","DOIUrl":"10.1177/15330338251317094","url":null,"abstract":"<p><p>The management of early-stage colon cancer involves surgical resection of the primary tumor with or without chemotherapy, depending on pathological staging. The benefit of adjuvant chemotherapy for stage II and III colon cancer is approximately 5% and 15%, indicating the need for optimization for risk stratification and patient selection. Several studies have revealed that current clinicopathological factors lack precision. Circulating tumor DNA (ctDNA) is cell-free DNA originating from cancer cells and can be detected even in the absence of radiologically detectable disease among patients with colon cancer. Recent cohort studies revealed that ctDNA is one of the most significant prognostic factors for patients with early-stage colon cancer, surpassing pathological and clinical risk factors. Prospective cohort studies also suggest there may be a predictive role for ctDNA on the decision for consideration of adjuvant therapy. Currently, randomized clinical trials are enrolling to better define this role. In this review article, we review recent literature on ctDNA and its role in patients with colon cancer. We also elaborate on the future clinical utility of ctDNA in clinical practice and the unmet need for research to optimize currently available ctDNA assays.</p>","PeriodicalId":22203,"journal":{"name":"Technology in Cancer Research & Treatment","volume":"24 ","pages":"15330338251317094"},"PeriodicalIF":2.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047976","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}
Pub Date : 2024-09-14DOI: 10.1177/15330338241271998
Hang Lu, Xin Yu, Zhiliang Xu, Jingwen Deng, Master Jingwen Zhang, Yimin Zhang, Shengrong Sun
IGFBP6, a member of the IGF binding protein (IGFBP) family, is a specific inhibitor of insulin-like growth factor II (IGF-II) and can inhibit the growth of malignant tumors overexpressing IGF-II. Type 2 diabetes (T2D) is a basic disorder of glucose metabolism that can be regulated by IGF-related pathways. We performed bioinformatics analysis of the TCGA database to explore the possible mechanism of IGFBP6 in breast cancer (BC) metabolism and prognosis and collected clinical samples from BC patients with and without T2D to compare and verify the prognostic effect of IGFBP6. In our study, the levels of IGFBP1–6 were positively correlated with overall survival (OS) in patients with breast cancer. IGFBP6 was upregulated in estrogen receptor (ER)-positive BC, and ER-positive and progesterone receptor (PR) positive patients had a higher expression level of IGFBP6 than ER-negative and PR-negative patients. IGFBP6 could be used as an independent prognostic factor in BC. The expression of IGFBP6 was decreased in BC tissue, and BC tissue from patients with T2D had lower IGFBP6 expression levels than BC tissue from patients without T2D. IGFBP6 is mainly involved in the PI3K–Akt and TGF-β signaling pathways and tumor microenvironment regulation. In terms of metabolism, the expression of IGFBP6 was negatively correlated with that of most glucose metabolism-related genes. IGFBP6 expression was mainly correlated with mutations in TP53, PIK3CA, CDH1, and MAP3K1. In addition, the upregulation of IGFBP6 in BC increased the drug sensitivity to docetaxel, paclitaxel and gemcitabine. Overall, these results indicated that high expression of IGFBP6 is associated with a good prognosis in BC patients, especially in those without T2D. It is not only involved in the maintenance of the tumor microenvironment in BC but also inhibits the energy metabolism of cancer cells through glucose metabolism-related pathways. These findings may provide a new perspective on IGFBP6 as a potential prognostic marker for BC.
IGFBP6 是 IGF 结合蛋白(IGFBP)家族的成员,是胰岛素样生长因子 II(IGF-II)的特异性抑制剂,可抑制过度表达 IGF-II 的恶性肿瘤的生长。2 型糖尿病(T2D)是一种基本的糖代谢紊乱,可由 IGF 相关通路调控。我们对TCGA数据库进行了生物信息学分析,以探索IGFBP6在乳腺癌(BC)代谢和预后中的可能机制,并收集了有T2D和无T2D的BC患者的临床样本,以比较和验证IGFBP6的预后作用。在我们的研究中,IGFBP1-6的水平与乳腺癌患者的总生存期(OS)呈正相关。IGFBP6在雌激素受体(ER)阳性的乳腺癌患者中上调,ER阳性和孕激素受体(PR)阳性患者的IGFBP6表达水平高于ER阴性和PR阴性患者。IGFBP6可作为BC的一个独立预后因素。IGFBP6在BC组织中的表达降低,T2D患者BC组织的IGFBP6表达水平低于非T2D患者的BC组织。IGFBP6主要参与PI3K-Akt和TGF-β信号通路及肿瘤微环境调控。在代谢方面,IGFBP6 的表达与大多数葡萄糖代谢相关基因的表达呈负相关。IGFBP6的表达主要与TP53、PIK3CA、CDH1和MAP3K1的突变相关。此外,IGFBP6 在 BC 中的上调增加了对多西他赛、紫杉醇和吉西他滨的药物敏感性。总之,这些结果表明,IGFBP6的高表达与BC患者的良好预后有关,尤其是那些没有T2D的患者。它不仅参与了 BC 肿瘤微环境的维持,还通过葡萄糖代谢相关途径抑制了癌细胞的能量代谢。这些发现可能为IGFBP6作为BC潜在预后标志物提供了新的视角。
{"title":"Prognostic Value of IGFBP6 in Breast Cancer: Focus on Glucometabolism","authors":"Hang Lu, Xin Yu, Zhiliang Xu, Jingwen Deng, Master Jingwen Zhang, Yimin Zhang, Shengrong Sun","doi":"10.1177/15330338241271998","DOIUrl":"https://doi.org/10.1177/15330338241271998","url":null,"abstract":"IGFBP6, a member of the IGF binding protein (IGFBP) family, is a specific inhibitor of insulin-like growth factor II (IGF-II) and can inhibit the growth of malignant tumors overexpressing IGF-II. Type 2 diabetes (T2D) is a basic disorder of glucose metabolism that can be regulated by IGF-related pathways. We performed bioinformatics analysis of the TCGA database to explore the possible mechanism of IGFBP6 in breast cancer (BC) metabolism and prognosis and collected clinical samples from BC patients with and without T2D to compare and verify the prognostic effect of IGFBP6. In our study, the levels of IGFBP1–6 were positively correlated with overall survival (OS) in patients with breast cancer. IGFBP6 was upregulated in estrogen receptor (ER)-positive BC, and ER-positive and progesterone receptor (PR) positive patients had a higher expression level of IGFBP6 than ER-negative and PR-negative patients. IGFBP6 could be used as an independent prognostic factor in BC. The expression of IGFBP6 was decreased in BC tissue, and BC tissue from patients with T2D had lower IGFBP6 expression levels than BC tissue from patients without T2D. IGFBP6 is mainly involved in the PI3K–Akt and TGF-β signaling pathways and tumor microenvironment regulation. In terms of metabolism, the expression of IGFBP6 was negatively correlated with that of most glucose metabolism-related genes. IGFBP6 expression was mainly correlated with mutations in TP53, PIK3CA, CDH1, and MAP3K1. In addition, the upregulation of IGFBP6 in BC increased the drug sensitivity to docetaxel, paclitaxel and gemcitabine. Overall, these results indicated that high expression of IGFBP6 is associated with a good prognosis in BC patients, especially in those without T2D. It is not only involved in the maintenance of the tumor microenvironment in BC but also inhibits the energy metabolism of cancer cells through glucose metabolism-related pathways. These findings may provide a new perspective on IGFBP6 as a potential prognostic marker for BC.","PeriodicalId":22203,"journal":{"name":"Technology in Cancer Research & Treatment","volume":"3 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142263447","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}
Pub Date : 2024-09-14DOI: 10.1177/15330338241281310
Fei Ma, Jinxuan Song, Min He, Xiuqing Wang
Purpose: To investigate the inhibitory effect of antimicrobial peptide merecidin on triple-negative breast cancer (TNBC) and the mechanism of inhibiting epithelial-mesenchymal transformation (EMT) by regulating miR-30d-5p/vimentin. Methods: TNBC cell lines (MDA-MB-231, MDA-MB-468) were treated with merecidin to assess proliferation, migration, invasion ability, and EMT. Confocal laser localization was used to examine the role of merecidin and TNBC cells. The relationship between merecidin and miR-30d-5p was determined through RT-qPCR and dual-luciferase reporter gene, and the relationship between merecidin and vimentin was verified through pulling down the experiment. The effects of miR-30d-5p on the migration and invasion ability of TNBC cells were confirmed through scratch and transwell experiments. Vimentin levels, tumor volume, shape, size, and weight were observed in the MDA-MB-231 subcutaneous tumor model in nude mice. Results: merecidin inhibited the proliferation, migration, invasion, and EMT of TNBC cells. merecidin was primarily located in the cytoplasm of TNBC cells, and the expression of miR-30d-5p was low in TNBC cells. merecidin significantly up-regulated the expression of miR-30d-5p. miR-30d-5p negatively regulated vimentin. merecidin could bind to vimentin in vitro. miR-30d-5p inhibited the migration and invasion ability of TNBC cells, while vimentin promoted their migration and invasion ability. Down-regulation of miR-30d-5p or overexpression of vimentin partially counteracted the inhibitory effects of merecidin on TNBC cell migration, invasion ability, and EMT. In nude mouse tumor models, merecidin significantly suppressed tumor growth. Conclusion: Merecidin effectively blocks the EMT process and inhibits the migration and invasion of TNBC cells by regulating miR-30d-5p/vimentin.
{"title":"The Antimicrobial Peptide Merecidin Inhibit the Metastasis of Triple-Negative Breast Cancer by Obstructing EMT via miR-30d-5p/Vimentin","authors":"Fei Ma, Jinxuan Song, Min He, Xiuqing Wang","doi":"10.1177/15330338241281310","DOIUrl":"https://doi.org/10.1177/15330338241281310","url":null,"abstract":"Purpose: To investigate the inhibitory effect of antimicrobial peptide merecidin on triple-negative breast cancer (TNBC) and the mechanism of inhibiting epithelial-mesenchymal transformation (EMT) by regulating miR-30d-5p/vimentin. Methods: TNBC cell lines (MDA-MB-231, MDA-MB-468) were treated with merecidin to assess proliferation, migration, invasion ability, and EMT. Confocal laser localization was used to examine the role of merecidin and TNBC cells. The relationship between merecidin and miR-30d-5p was determined through RT-qPCR and dual-luciferase reporter gene, and the relationship between merecidin and vimentin was verified through pulling down the experiment. The effects of miR-30d-5p on the migration and invasion ability of TNBC cells were confirmed through scratch and transwell experiments. Vimentin levels, tumor volume, shape, size, and weight were observed in the MDA-MB-231 subcutaneous tumor model in nude mice. Results: merecidin inhibited the proliferation, migration, invasion, and EMT of TNBC cells. merecidin was primarily located in the cytoplasm of TNBC cells, and the expression of miR-30d-5p was low in TNBC cells. merecidin significantly up-regulated the expression of miR-30d-5p. miR-30d-5p negatively regulated vimentin. merecidin could bind to vimentin in vitro. miR-30d-5p inhibited the migration and invasion ability of TNBC cells, while vimentin promoted their migration and invasion ability. Down-regulation of miR-30d-5p or overexpression of vimentin partially counteracted the inhibitory effects of merecidin on TNBC cell migration, invasion ability, and EMT. In nude mouse tumor models, merecidin significantly suppressed tumor growth. Conclusion: Merecidin effectively blocks the EMT process and inhibits the migration and invasion of TNBC cells by regulating miR-30d-5p/vimentin.","PeriodicalId":22203,"journal":{"name":"Technology in Cancer Research & Treatment","volume":"31 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142263448","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}