Pub Date : 2024-01-24DOI: 10.1515/oncologie-2023-0482
Tianfei Ma, Gang Su, Qionghui Wu, Minghui Shen, Xinli Feng, Zhen-chang Zhang
Gliomas are particularly challenging due to their high invasiveness, frequent recurrence, and elevated mortality rates. Despite the availability of treatments like surgery, radiation, and chemotherapy, each of these methods faces significant limitations. This has led to a pressing demand for new strategies against gliomas. In this landscape, mesenchymal stem cells (MSCs) have shown significant potential in recent years. However, the application of MSCs in glioma therapy encounters various challenges. A significant advancement in this field is the utilization of exosomes (Exo), key secretions of MSCs. These exosomes not only carry the benefits inherent in MSCs but also exhibit unique physicochemical properties that make them effective drug carriers. Consequently, MSCs Exo is gaining recognition as a sophisticated drug delivery system, specifically designed for glioma treatment. The scope of MSCs Exo goes beyond being just an innovative drug delivery mechanism; it also shows potential as a standalone therapeutic option. This article aims to provide a detailed summary of the essential role of MSCs Exo in glioma progression and its growing importance as a drug delivery carrier in the fight against this formidable disease.
{"title":"Mesenchymal stem cell exosomes: a promising delivery system for glioma therapy","authors":"Tianfei Ma, Gang Su, Qionghui Wu, Minghui Shen, Xinli Feng, Zhen-chang Zhang","doi":"10.1515/oncologie-2023-0482","DOIUrl":"https://doi.org/10.1515/oncologie-2023-0482","url":null,"abstract":"\u0000 Gliomas are particularly challenging due to their high invasiveness, frequent recurrence, and elevated mortality rates. Despite the availability of treatments like surgery, radiation, and chemotherapy, each of these methods faces significant limitations. This has led to a pressing demand for new strategies against gliomas. In this landscape, mesenchymal stem cells (MSCs) have shown significant potential in recent years. However, the application of MSCs in glioma therapy encounters various challenges. A significant advancement in this field is the utilization of exosomes (Exo), key secretions of MSCs. These exosomes not only carry the benefits inherent in MSCs but also exhibit unique physicochemical properties that make them effective drug carriers. Consequently, MSCs Exo is gaining recognition as a sophisticated drug delivery system, specifically designed for glioma treatment. The scope of MSCs Exo goes beyond being just an innovative drug delivery mechanism; it also shows potential as a standalone therapeutic option. This article aims to provide a detailed summary of the essential role of MSCs Exo in glioma progression and its growing importance as a drug delivery carrier in the fight against this formidable disease.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":0.9,"publicationDate":"2024-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139601570","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 : 2024-01-23DOI: 10.1515/oncologie-2023-0534
Maher Kurdi, Motaz M Fadul, Bassam J. Addas, Eyad Faizo, Ahmed K. Bamaga, Taghreed A. Alsinani, Yousef Katib, Alaa Alkhotani, Amany A Fathaddin, Alaa N. Turkistani, Ahmed A. Najjar, Saleh Baeesa, Fadi A. Toonsi, Majid Almansouri, Shadi Alkhayyat
Protein Arginine Methyltransferase 5 (PRMT5) is an enzyme that regulates gene expression and protein function through arginine methylation. Its association with isocitrate dehydrogenase (IDH) mutation in Grade-4 astrocytoma was rarely investigated. Our aim was to aim to explore the association between IDH mutation and PRMT5 and its effect on tumor recurrence. A retrospective cohort of 34 patients with Grade 4 astrocytoma has been tested for PRMT5 expression using protein and gene expression arrays. The impact of IDH-mutation and PRMT5 expression on tumor recurrence was explored. IDH-wildtype was detected in 13 tumors. PRMT5 protein was highly expressed in 30 tumors and the expression was low in four tumors. PRMT5 gene expression was upregulated in 33 tumors and downregulated in a single tumor case. Tumors with different PRMT5 gene expressions and IDH mutation were found to have a significant statistical difference in recurrence-free interval (RFI) (p-value<0.001). IDH-wildtype glioblastoma with upregulated PRMT5 gene or protein expression showed earlier tumor recurrence compared to IDH-mutant Grade 4 astrocytoma with upregulated PRMT5 expression. The association between IDH mutation and PRMT5 in IDH-mutant Grade 4 astrocytoma or IDH-wildtype glioblastoma is indirectly bidirectional. PRMT5 upregulation in glioblastoma can lead to increased cell proliferation and tumor regrowth.
{"title":"Glioblastoma with PRMT5 gene upregulation is a key target for tumor cell regression","authors":"Maher Kurdi, Motaz M Fadul, Bassam J. Addas, Eyad Faizo, Ahmed K. Bamaga, Taghreed A. Alsinani, Yousef Katib, Alaa Alkhotani, Amany A Fathaddin, Alaa N. Turkistani, Ahmed A. Najjar, Saleh Baeesa, Fadi A. Toonsi, Majid Almansouri, Shadi Alkhayyat","doi":"10.1515/oncologie-2023-0534","DOIUrl":"https://doi.org/10.1515/oncologie-2023-0534","url":null,"abstract":"\u0000 \u0000 \u0000 Protein Arginine Methyltransferase 5 (PRMT5) is an enzyme that regulates gene expression and protein function through arginine methylation. Its association with isocitrate dehydrogenase (IDH) mutation in Grade-4 astrocytoma was rarely investigated. Our aim was to aim to explore the association between IDH mutation and PRMT5 and its effect on tumor recurrence.\u0000 \u0000 \u0000 \u0000 A retrospective cohort of 34 patients with Grade 4 astrocytoma has been tested for PRMT5 expression using protein and gene expression arrays. The impact of IDH-mutation and PRMT5 expression on tumor recurrence was explored.\u0000 \u0000 \u0000 \u0000 IDH-wildtype was detected in 13 tumors. PRMT5 protein was highly expressed in 30 tumors and the expression was low in four tumors. PRMT5 gene expression was upregulated in 33 tumors and downregulated in a single tumor case. Tumors with different PRMT5 gene expressions and IDH mutation were found to have a significant statistical difference in recurrence-free interval (RFI) (p-value<0.001). IDH-wildtype glioblastoma with upregulated PRMT5 gene or protein expression showed earlier tumor recurrence compared to IDH-mutant Grade 4 astrocytoma with upregulated PRMT5 expression.\u0000 \u0000 \u0000 \u0000 The association between IDH mutation and PRMT5 in IDH-mutant Grade 4 astrocytoma or IDH-wildtype glioblastoma is indirectly bidirectional. PRMT5 upregulation in glioblastoma can lead to increased cell proliferation and tumor regrowth.\u0000","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":0.9,"publicationDate":"2024-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139603175","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 : 2024-01-18DOI: 10.1515/oncologie-2023-0406
Quang Hao Nguyen, M. Vu, Tuan Anh Tran, Quoc Chinh Duong, Duc Binh Vu, Ha Thanh Nguyen, Quoc Khanh Bach
Abstract Background Molecular International Prognostic Scoring System (IPSS-M) is a newly developed prognostic model for myelodysplastic neoplasms (MDS), but has not yet been used widely. In this study, we aimed to compare the IPSS-M with the traditional Revised International Prognostic Scoring System (IPSS-R) in predicting the prognosis of decitabine treated-MDS patients. Patients and methods This retrospective cohort study was conducted on 19 newly diagnosed MDS patients who were examined for 51 gene mutations and received decitabine treatment. The survival analysis, including overall survival (OS), progression-free survival (PFS), and leukemia-free survival (LFS), was performed using the Kaplan–Meier method. Comparisons between the risk groups were carried out according to the IPSS-R and IPSS-M models. Results Among the 19 MDS patients, 12 (63.2 %) showed myeloid gene mutations, with the highest frequency of mutations in ASXL1, RUNX1, SRSF2, TET2, and TP53 (15.8 %). Survival analysis found that the OS was significantly different between the risk groups of both IPSS-R and IPSS-M models, but the PFS and LFS showed significant differences between the risk groups in only the IPSS-M model. The PFS of the moderate, high, and very high-risk groups were 34.66, 25.00, and 15.33 months (p=0.031); respectively. The LFS of the moderate, high, and very high-risk groups were 39.20, 25.00, and 18.37 months, (p=0.039); respectively. Conclusions Our results found that IPSS-M was better than IPSS-R in predicting the PFS and LFS of decitabine-treated MDS patients, IPSS-M may be superior to IPSS-R in predicting the prognosis of MDS patients.
{"title":"Comparison of the Molecular International Prognostic Scoring System (IPSS-M) and Revised International Prognostic Scoring System (IPSS-R) in predicting the prognosis of patients with myelodysplastic neoplasms treated with decitabine","authors":"Quang Hao Nguyen, M. Vu, Tuan Anh Tran, Quoc Chinh Duong, Duc Binh Vu, Ha Thanh Nguyen, Quoc Khanh Bach","doi":"10.1515/oncologie-2023-0406","DOIUrl":"https://doi.org/10.1515/oncologie-2023-0406","url":null,"abstract":"Abstract Background Molecular International Prognostic Scoring System (IPSS-M) is a newly developed prognostic model for myelodysplastic neoplasms (MDS), but has not yet been used widely. In this study, we aimed to compare the IPSS-M with the traditional Revised International Prognostic Scoring System (IPSS-R) in predicting the prognosis of decitabine treated-MDS patients. Patients and methods This retrospective cohort study was conducted on 19 newly diagnosed MDS patients who were examined for 51 gene mutations and received decitabine treatment. The survival analysis, including overall survival (OS), progression-free survival (PFS), and leukemia-free survival (LFS), was performed using the Kaplan–Meier method. Comparisons between the risk groups were carried out according to the IPSS-R and IPSS-M models. Results Among the 19 MDS patients, 12 (63.2 %) showed myeloid gene mutations, with the highest frequency of mutations in ASXL1, RUNX1, SRSF2, TET2, and TP53 (15.8 %). Survival analysis found that the OS was significantly different between the risk groups of both IPSS-R and IPSS-M models, but the PFS and LFS showed significant differences between the risk groups in only the IPSS-M model. The PFS of the moderate, high, and very high-risk groups were 34.66, 25.00, and 15.33 months (p=0.031); respectively. The LFS of the moderate, high, and very high-risk groups were 39.20, 25.00, and 18.37 months, (p=0.039); respectively. Conclusions Our results found that IPSS-M was better than IPSS-R in predicting the PFS and LFS of decitabine-treated MDS patients, IPSS-M may be superior to IPSS-R in predicting the prognosis of MDS patients.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":0.9,"publicationDate":"2024-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139525935","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}
Abstract Objectives Integrin subunit beta-like 1 (ITGBL1), a member of the epidermal growth factor (EGF)-like protein family, encodes a beta integrin-related protein that is mainly associated with the development of specific tumours and immune-related signalling pathways. This work aimed to explore the possibility that ITGBL1 functions as a novel target gene for immunotherapy and could be a cancer prognostic molecule. Methods The mRNA data for ITGBL1 were obtained from the public databases The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx) and Gene Expression Omnibus (GEO). Using GEPIA, the differential expression of ITGBL1 in different tumour stages was identified. Cancer prognostic correlations were explored using Kaplan–Meier survival analysis and forest plots. A combination of Gene Set Enrichment Analysis (GSEA), TIMER2.0 and the R package was applied to analyse the ITGBL1-enriched related pathways. The NCI-60 drug database was examined using CellMinerTM. Cytological experiments were conducted to confirm ITGBL1’s impact on cancer cells. Results Our research has shown that ITGBL1 is differentially expressed in 26 cancers, and high ITGBL1 expression predicts a poorer survival prognosis in some specific cancers. Additionally, we found that ITGBL1 is enriched in immune-related pathways, which are closely linked to immunomodulatory molecules, immune-infiltrating cells, and immunomodulatory factors. The results of tumor mutational burden (TMB) and microsatellite instability (MSI) also indicate that the expression of ITGBL1 is beneficial for improving tumor immunotherapy efficacy. Furthermore, a number of antitumor agents associated with ITGBL1 expression have been identified. Finally, knockdown of ITGBL1 restricts the ability of gastric and colorectal cancer cells to proliferate and migrate. Conclusions Our study demonstrates that ITGBL1 can be utilized to accurately prognosticate cancer and has opened up new avenues for the investigation of tumor immune mechanisms and the development of more efficacious immunotherapies.
{"title":"A multi-cancer analysis unveils ITGBL1 as a cancer prognostic molecule and a novel immunotherapy target","authors":"Ziyu Wu, Zhihong Liu, Changji Gu, Yong Wu, Yanan Li, Zeyang Zhou, Xiaodong Yang","doi":"10.1515/oncologie-2023-0455","DOIUrl":"https://doi.org/10.1515/oncologie-2023-0455","url":null,"abstract":"Abstract Objectives Integrin subunit beta-like 1 (ITGBL1), a member of the epidermal growth factor (EGF)-like protein family, encodes a beta integrin-related protein that is mainly associated with the development of specific tumours and immune-related signalling pathways. This work aimed to explore the possibility that ITGBL1 functions as a novel target gene for immunotherapy and could be a cancer prognostic molecule. Methods The mRNA data for ITGBL1 were obtained from the public databases The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx) and Gene Expression Omnibus (GEO). Using GEPIA, the differential expression of ITGBL1 in different tumour stages was identified. Cancer prognostic correlations were explored using Kaplan–Meier survival analysis and forest plots. A combination of Gene Set Enrichment Analysis (GSEA), TIMER2.0 and the R package was applied to analyse the ITGBL1-enriched related pathways. The NCI-60 drug database was examined using CellMinerTM. Cytological experiments were conducted to confirm ITGBL1’s impact on cancer cells. Results Our research has shown that ITGBL1 is differentially expressed in 26 cancers, and high ITGBL1 expression predicts a poorer survival prognosis in some specific cancers. Additionally, we found that ITGBL1 is enriched in immune-related pathways, which are closely linked to immunomodulatory molecules, immune-infiltrating cells, and immunomodulatory factors. The results of tumor mutational burden (TMB) and microsatellite instability (MSI) also indicate that the expression of ITGBL1 is beneficial for improving tumor immunotherapy efficacy. Furthermore, a number of antitumor agents associated with ITGBL1 expression have been identified. Finally, knockdown of ITGBL1 restricts the ability of gastric and colorectal cancer cells to proliferate and migrate. Conclusions Our study demonstrates that ITGBL1 can be utilized to accurately prognosticate cancer and has opened up new avenues for the investigation of tumor immune mechanisms and the development of more efficacious immunotherapies.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":0.9,"publicationDate":"2024-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139437536","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 : 2024-01-09DOI: 10.1515/oncologie-2023-0514
Songül Tezcan, Feyza Nur Yılmaz
Abstract Clinical pharmacy services aim to ensure the rational use of drugs and resolve disease/health conditions with a multidisciplinary approach. Pharmaceutical care plans need to be created to effectively provide clinical pharmacy services in the treatment of hypertension which is one of the common chronic diseases in cancer patients. In this mini-review, we examine which drugs can cause or worsen hypertension in patients receiving cancer treatment, potential drug-drug interactions between drugs used in cancer treatment and antihypertensive drugs, pharmacological and clinical studies for the treatment of hypertension in patients with hypertension before cancer diagnosis or newly diagnosed hypertension due to cancer treatment. Non-pharmacological treatment approaches are presented. We think that our study will be a resource that can be used to solve possible drug-related problems in the practice.
{"title":"Clinical pharmacy services in cancer patients with hypertension","authors":"Songül Tezcan, Feyza Nur Yılmaz","doi":"10.1515/oncologie-2023-0514","DOIUrl":"https://doi.org/10.1515/oncologie-2023-0514","url":null,"abstract":"Abstract Clinical pharmacy services aim to ensure the rational use of drugs and resolve disease/health conditions with a multidisciplinary approach. Pharmaceutical care plans need to be created to effectively provide clinical pharmacy services in the treatment of hypertension which is one of the common chronic diseases in cancer patients. In this mini-review, we examine which drugs can cause or worsen hypertension in patients receiving cancer treatment, potential drug-drug interactions between drugs used in cancer treatment and antihypertensive drugs, pharmacological and clinical studies for the treatment of hypertension in patients with hypertension before cancer diagnosis or newly diagnosed hypertension due to cancer treatment. Non-pharmacological treatment approaches are presented. We think that our study will be a resource that can be used to solve possible drug-related problems in the practice.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":0.9,"publicationDate":"2024-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139441915","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 : 2024-01-08DOI: 10.1515/oncologie-2023-0368
N. Murray
Abstract Matrix metalloproteinase-2 (MMP-2) is a gelatinase and is involved in multiple steps of the metastatic cascade. More than a decade ago an increased expression of MMP-2 in tumour cells or higher serum levels was reported to be a prognostic biomarker for a lower disease-free and overall survival rate. In recent years new evidence has indicated that MMP-2 has an important role in the tumour ecosystem. It is one of the many players in the onco-sphere, involved in interacting between tumour cells, host cells and the microenvironment. It plays a role in the dissemination of tumour cells, the epithelial–mesenchymal and mesenchymal–epithelial transitions, the formation of the pre-metastatic and metastatic niches, dormancy of tumour cells and modulating the immune system. The aim of this review is to highlight these multiple roles in the metastatic cascade and how many signalling pathways can up or down-regulate MMP-2 activity in the different stages of cancer progression and the effect of MMP-2 on the onco-sphere. Research in head and neck cancer is used as an example of these processes. The use of non-specific MMP inhibitors has been unsuccessful showing only limited benefits and associated with high toxicity as such that none have progressed past Phase III trials. Preclinical trials are undergoing using antibodies directed against specific matrix metalloproteinases, these targeted therapies may be potentially less toxic to the patients.
{"title":"The role of matrix metalloproteinase-2 in the metastatic cascade: a review","authors":"N. Murray","doi":"10.1515/oncologie-2023-0368","DOIUrl":"https://doi.org/10.1515/oncologie-2023-0368","url":null,"abstract":"Abstract Matrix metalloproteinase-2 (MMP-2) is a gelatinase and is involved in multiple steps of the metastatic cascade. More than a decade ago an increased expression of MMP-2 in tumour cells or higher serum levels was reported to be a prognostic biomarker for a lower disease-free and overall survival rate. In recent years new evidence has indicated that MMP-2 has an important role in the tumour ecosystem. It is one of the many players in the onco-sphere, involved in interacting between tumour cells, host cells and the microenvironment. It plays a role in the dissemination of tumour cells, the epithelial–mesenchymal and mesenchymal–epithelial transitions, the formation of the pre-metastatic and metastatic niches, dormancy of tumour cells and modulating the immune system. The aim of this review is to highlight these multiple roles in the metastatic cascade and how many signalling pathways can up or down-regulate MMP-2 activity in the different stages of cancer progression and the effect of MMP-2 on the onco-sphere. Research in head and neck cancer is used as an example of these processes. The use of non-specific MMP inhibitors has been unsuccessful showing only limited benefits and associated with high toxicity as such that none have progressed past Phase III trials. Preclinical trials are undergoing using antibodies directed against specific matrix metalloproteinases, these targeted therapies may be potentially less toxic to the patients.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":0.9,"publicationDate":"2024-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139380185","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 : 2024-01-05DOI: 10.1515/oncologie-2023-0472
Yu-Chia Chen, Hsin-Hung Chen, Po-Ming Chen
Abstract Objectives Liver hepatocellular carcinoma (LIHC) is the most common type of primary liver cancer and originates from hepatocytes, the main functional cells of the liver. It is a serious and aggressive cancer with a generally poor prognosis, especially when diagnosed at advanced stages. Reactive oxygen species (ROS) have been detected in LIHC and are involved in carcinogenesis and tumor progression. Here, a comprehensive analysis was performed to evaluate the effects of ROS-related genes on the prognosis of LIHC. Methods Using bioinformatical tools including Gene Expression Profiling Interactive Analysis (GEPIA2) and Q-omics, a comprehensive analysis was performed to evaluate the effects of ROS-related genes, including superoxide dismutases (SODs), glutathione peroxidases (GPXs), peroxiredoxins (PRDXs) and catalase (CAT) on the prognosis of LIHC using The Cancer Genome Atlas (TCGA) dataset and identified the most appropriate candidate genes. Then we further explored their effects on LIHC cell proliferation and drug selection for LIHC treatment. Results We found that CAT expression was significantly downregulated in late stage’s LIHC tissues compared to normal liver or early stage’s LIHC tissues, and high CAT expression was correlated with a favorable survival prognosis in LIHC. The expression of the CAT gene was associated with an inhibition of the “cell cycle” pathway. HepG2 and Hep3B cells’ growth was increased with a decrease in CAT expression by silencing its mRNA. As silencing of CAT in HepG2 and Hep3B cells, and its association with an increase in the expression of PLK1, CCNB1, CDC20, and PTTG1. A comparative 426 drug response in LIHC cells with different CAT expression, SU11274, a Met inhibitor, could serve as a therapeutic option when CAT levels are low in LIHC cells. Conclusions Our findings revealed that Met inhibitors could potentially control tumor progression and be used as a therapeutic option against LIHC with low CAT.
{"title":"Catalase expression is an independent prognostic marker in liver hepatocellular carcinoma","authors":"Yu-Chia Chen, Hsin-Hung Chen, Po-Ming Chen","doi":"10.1515/oncologie-2023-0472","DOIUrl":"https://doi.org/10.1515/oncologie-2023-0472","url":null,"abstract":"Abstract Objectives Liver hepatocellular carcinoma (LIHC) is the most common type of primary liver cancer and originates from hepatocytes, the main functional cells of the liver. It is a serious and aggressive cancer with a generally poor prognosis, especially when diagnosed at advanced stages. Reactive oxygen species (ROS) have been detected in LIHC and are involved in carcinogenesis and tumor progression. Here, a comprehensive analysis was performed to evaluate the effects of ROS-related genes on the prognosis of LIHC. Methods Using bioinformatical tools including Gene Expression Profiling Interactive Analysis (GEPIA2) and Q-omics, a comprehensive analysis was performed to evaluate the effects of ROS-related genes, including superoxide dismutases (SODs), glutathione peroxidases (GPXs), peroxiredoxins (PRDXs) and catalase (CAT) on the prognosis of LIHC using The Cancer Genome Atlas (TCGA) dataset and identified the most appropriate candidate genes. Then we further explored their effects on LIHC cell proliferation and drug selection for LIHC treatment. Results We found that CAT expression was significantly downregulated in late stage’s LIHC tissues compared to normal liver or early stage’s LIHC tissues, and high CAT expression was correlated with a favorable survival prognosis in LIHC. The expression of the CAT gene was associated with an inhibition of the “cell cycle” pathway. HepG2 and Hep3B cells’ growth was increased with a decrease in CAT expression by silencing its mRNA. As silencing of CAT in HepG2 and Hep3B cells, and its association with an increase in the expression of PLK1, CCNB1, CDC20, and PTTG1. A comparative 426 drug response in LIHC cells with different CAT expression, SU11274, a Met inhibitor, could serve as a therapeutic option when CAT levels are low in LIHC cells. Conclusions Our findings revealed that Met inhibitors could potentially control tumor progression and be used as a therapeutic option against LIHC with low CAT.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":0.9,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139383320","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 : 2024-01-03DOI: 10.1515/oncologie-2023-0384
Huan Liu, Shaohua He, L. Tan, Mingzhen Li, Cheng Chen, Ruiming Tan
Abstract Objectives Disulfidptosis is a novel form of cell death, whose modulation in tumor cells may present a promising therapeutic strategy for cancer treatment. However, the role of disulfidptosis-related long non-coding RNAs (lncRNAs) in non-small cell lung carcinoma (NSCLC) remains poorly elucidated. This study aims to investigate the prognostic significance of disulfidptosis-related lncRNAs (DRLs) and reveal their relationship to the immune microenvironment of NSCLC. Methods DRLs were identified through co-expression analysis of NSCLC transcriptomic data obtained from the Genomic Data Commons (GDC) data portal. The DRLs prognostic signature (DRLPS) was established using the least absolute shrinkage and selection operator (LASSO) and Cox regression analyses. Samples were separated into high-DS and low-DS groups based on the median disulfidptosis score (DS) of DRLPS. Integrated analyses were then implemented to unveil the association between DRLs and NSCLC microenvironment. These involved the evaluation of functional enrichments, immune cell infiltrations, genetic alterations, and drug sensitivity. Results A prognostic signature was developed based on six prognostic DRLs, which are AL606489.1, LINC00857, AP003555.1, AP000695.1, AC113346.1, and LINC01615. The Kaplan–Meier survival curves demonstrated the significant association between DRLPS and NSCLC prognosis. The functional enrichment assessment revealed the pivotal involvement of DRLs in immune regulation and metabolism in NSCLC. The low-DS and high-DS subgroups of NSCLC patients exhibited distinct differences in terms of immune infiltration and tumor mutation burden. The potential to predict immunotherapy benefit and drug sensitivity in NSCLC treatments was observed in DRLPS. Conclusions In this study, disulfidptosis-related lncRNAs were identified and their roles in NSCLC were revealed. A novel prognostic signature with the potential to predict drug response in NSCLC treatment was developed.
{"title":"Disulfidptosis-related long non-coding RNAs predict prognosis and indicate therapeutic response in non-small cell lung carcinoma","authors":"Huan Liu, Shaohua He, L. Tan, Mingzhen Li, Cheng Chen, Ruiming Tan","doi":"10.1515/oncologie-2023-0384","DOIUrl":"https://doi.org/10.1515/oncologie-2023-0384","url":null,"abstract":"Abstract Objectives Disulfidptosis is a novel form of cell death, whose modulation in tumor cells may present a promising therapeutic strategy for cancer treatment. However, the role of disulfidptosis-related long non-coding RNAs (lncRNAs) in non-small cell lung carcinoma (NSCLC) remains poorly elucidated. This study aims to investigate the prognostic significance of disulfidptosis-related lncRNAs (DRLs) and reveal their relationship to the immune microenvironment of NSCLC. Methods DRLs were identified through co-expression analysis of NSCLC transcriptomic data obtained from the Genomic Data Commons (GDC) data portal. The DRLs prognostic signature (DRLPS) was established using the least absolute shrinkage and selection operator (LASSO) and Cox regression analyses. Samples were separated into high-DS and low-DS groups based on the median disulfidptosis score (DS) of DRLPS. Integrated analyses were then implemented to unveil the association between DRLs and NSCLC microenvironment. These involved the evaluation of functional enrichments, immune cell infiltrations, genetic alterations, and drug sensitivity. Results A prognostic signature was developed based on six prognostic DRLs, which are AL606489.1, LINC00857, AP003555.1, AP000695.1, AC113346.1, and LINC01615. The Kaplan–Meier survival curves demonstrated the significant association between DRLPS and NSCLC prognosis. The functional enrichment assessment revealed the pivotal involvement of DRLs in immune regulation and metabolism in NSCLC. The low-DS and high-DS subgroups of NSCLC patients exhibited distinct differences in terms of immune infiltration and tumor mutation burden. The potential to predict immunotherapy benefit and drug sensitivity in NSCLC treatments was observed in DRLPS. Conclusions In this study, disulfidptosis-related lncRNAs were identified and their roles in NSCLC were revealed. A novel prognostic signature with the potential to predict drug response in NSCLC treatment was developed.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":0.9,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139121879","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}
Abstract Hepatocellular carcinoma (HCC) is a concerning liver cancer with rising incidence and mortality rates worldwide. The effectiveness of traditional therapies in managing advanced HCC is limited, necessitating the development of new therapeutic strategies. Immune checkpoint inhibitors (ICIs) have emerged as a promising strategy for HCC management. By preventing tumor cells from evading immune surveillance through immunological checkpoints, ICIs can restore the immune system’s ability to target and eliminate tumors. While ICIs show promise in enhancing the immune response against malignancies, challenges such as drug resistance and adverse reactions hinder their efficacy. To address these challenges, developing individualized ICI treatment strategies is critical. Combining targeted therapy and immunotherapy holds the potential for comprehensive therapeutic effects. Additionally, biomarker-based individualized ICI treatment strategies offer promise in predicting treatment response and guiding personalized patient care. Future research should explore emerging ICI treatment methods to optimize HCC immunotherapy. This review provides an overview of ICIs as a new treatment for HCC, demonstrating some success in promoting the tumor immune response. However, drug resistance and adverse reactions remain important considerations that must be addressed. As tailored treatment plans evolve, the prospect of immunotherapy for HCC is expected to grow, offering new opportunities for improved patient outcomes.
{"title":"Immunotherapy in hepatocellular carcinoma: an overview of immune checkpoint inhibitors, drug resistance, and adverse effects","authors":"Xuan-Yu Gu, Jin-Long Huo, Zhi-Yong Yu, Ji-Chang Jiang, Ya-Xuan Xu, Lijin Zhao","doi":"10.1515/oncologie-2023-0412","DOIUrl":"https://doi.org/10.1515/oncologie-2023-0412","url":null,"abstract":"Abstract Hepatocellular carcinoma (HCC) is a concerning liver cancer with rising incidence and mortality rates worldwide. The effectiveness of traditional therapies in managing advanced HCC is limited, necessitating the development of new therapeutic strategies. Immune checkpoint inhibitors (ICIs) have emerged as a promising strategy for HCC management. By preventing tumor cells from evading immune surveillance through immunological checkpoints, ICIs can restore the immune system’s ability to target and eliminate tumors. While ICIs show promise in enhancing the immune response against malignancies, challenges such as drug resistance and adverse reactions hinder their efficacy. To address these challenges, developing individualized ICI treatment strategies is critical. Combining targeted therapy and immunotherapy holds the potential for comprehensive therapeutic effects. Additionally, biomarker-based individualized ICI treatment strategies offer promise in predicting treatment response and guiding personalized patient care. Future research should explore emerging ICI treatment methods to optimize HCC immunotherapy. This review provides an overview of ICIs as a new treatment for HCC, demonstrating some success in promoting the tumor immune response. However, drug resistance and adverse reactions remain important considerations that must be addressed. As tailored treatment plans evolve, the prospect of immunotherapy for HCC is expected to grow, offering new opportunities for improved patient outcomes.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":0.9,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139119865","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 : 2024-01-03DOI: 10.1515/oncologie-2023-0459
Lingnan Meng, Ying Zheng, Hao Liu, Daiming Fan
Abstract Cancer is the second leading cause of death worldwide. Although multiple new cancer treatments have emerged in recent years, drug therapy, mainly comprising chemotherapy, targeted therapy, and immunotherapy, remains the most common approach. The multidrug resistance (MDR) of cancer cells to various treatments remains a challenge. Scientists have always focused on the acquired drug resistance mechanisms of tumor cells themselves. However, recent evidence shows that the tumor microenvironment (TME) plays a critical role in regulating tumor cell progression, metastasis, immune escape, and drug resistance. In the TME, interactions between cancer cells and non-malignant cells often modify the TME and facilitate drug resistance. Therefore, elucidating this complex interaction mechanism is essential for the development of effective treatments. This review focuses on the role of the TME in promoting chemoresistance in tumor cells through the following mechanisms: (i) inhibiting the immune clearance of tumor cells and facilitating immune escape responses; (ii) stimulating the release of soluble paracrine factors to enhance tumor survival and growth; (iii) promoting survival and altering drug delivery through metabolic reprogramming; (iv) obstructing drug absorption by inducing changes in stomatal cells and blood vessels surrounding the tumor; and (v) inducing the cancer stem cell phenotype. This review also addresses a clinical treatment strategy for targeting the TME, providing insights and a basis for reversing multidrug resistance.
{"title":"The tumor microenvironment: a key player in multidrug resistance in cancer","authors":"Lingnan Meng, Ying Zheng, Hao Liu, Daiming Fan","doi":"10.1515/oncologie-2023-0459","DOIUrl":"https://doi.org/10.1515/oncologie-2023-0459","url":null,"abstract":"Abstract Cancer is the second leading cause of death worldwide. Although multiple new cancer treatments have emerged in recent years, drug therapy, mainly comprising chemotherapy, targeted therapy, and immunotherapy, remains the most common approach. The multidrug resistance (MDR) of cancer cells to various treatments remains a challenge. Scientists have always focused on the acquired drug resistance mechanisms of tumor cells themselves. However, recent evidence shows that the tumor microenvironment (TME) plays a critical role in regulating tumor cell progression, metastasis, immune escape, and drug resistance. In the TME, interactions between cancer cells and non-malignant cells often modify the TME and facilitate drug resistance. Therefore, elucidating this complex interaction mechanism is essential for the development of effective treatments. This review focuses on the role of the TME in promoting chemoresistance in tumor cells through the following mechanisms: (i) inhibiting the immune clearance of tumor cells and facilitating immune escape responses; (ii) stimulating the release of soluble paracrine factors to enhance tumor survival and growth; (iii) promoting survival and altering drug delivery through metabolic reprogramming; (iv) obstructing drug absorption by inducing changes in stomatal cells and blood vessels surrounding the tumor; and (v) inducing the cancer stem cell phenotype. This review also addresses a clinical treatment strategy for targeting the TME, providing insights and a basis for reversing multidrug resistance.","PeriodicalId":54687,"journal":{"name":"Oncologie","volume":null,"pages":null},"PeriodicalIF":0.9,"publicationDate":"2024-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139120142","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：