Pub Date : 2024-04-25DOI: 10.1016/j.critrevonc.2024.104365
Ali Berro, Ahmad Assi, Mohamad Farhat, Lea Hatoum, Jean-Pierre Saad, Rami Mohanna, Anna Maria Antoun Bechara, Gilles Prince, Maria Catherine Rita Hachem, Ziad Zalaquett, Hampig-Raphael Kourie
Purpose
This systematic review summarizes evidence of VEGFR gene mutations and VEGF/VEGFR protein expression in glioblastoma multiforme (GBM) patients, alongside the efficacy and safety of anti-VEGFR tyrosine kinase inhibitors (TKIs) for GBM treatment.
Methods
A comprehensive literature review was conducted using PubMed up to August 2023. Boolean operators and MeSH term "glioma," along with specific VEGFR-related keywords, were utilized following thorough examination of existing literature.
Results
VEGFR correlates with glioma grade and GBM progression, presenting a viable therapeutic target. Regorafenib and axitinib show promise among studied TKIs. Other multi-targeted TKIs (MTKI) and combination therapies exhibit potential, albeit limited by blood-brain barrier penetration and toxicity. Combining treatments like radiotherapy and enhancing BBB penetration may benefit patients. Further research is warranted in patient quality of life and biomarker-guided selection.
Conclusion
While certain therapies hold promise for GBM, future research should prioritize personalized medicine and innovative strategies for improved treatment outcomes.
{"title":"Unlocking Hope: Anti-VEGFR inhibitors and their potential in glioblastoma treatment","authors":"Ali Berro, Ahmad Assi, Mohamad Farhat, Lea Hatoum, Jean-Pierre Saad, Rami Mohanna, Anna Maria Antoun Bechara, Gilles Prince, Maria Catherine Rita Hachem, Ziad Zalaquett, Hampig-Raphael Kourie","doi":"10.1016/j.critrevonc.2024.104365","DOIUrl":"10.1016/j.critrevonc.2024.104365","url":null,"abstract":"<div><h3>Purpose</h3><p>This systematic review summarizes evidence of VEGFR gene mutations and VEGF/VEGFR protein expression in glioblastoma multiforme (GBM) patients, alongside the efficacy and safety of anti-VEGFR tyrosine kinase inhibitors (TKIs) for GBM treatment.</p></div><div><h3>Methods</h3><p>A comprehensive literature review was conducted using PubMed up to August 2023. Boolean operators and MeSH term \"glioma,\" along with specific VEGFR-related keywords, were utilized following thorough examination of existing literature.</p></div><div><h3>Results</h3><p>VEGFR correlates with glioma grade and GBM progression, presenting a viable therapeutic target. Regorafenib and axitinib show promise among studied TKIs. Other multi-targeted TKIs (MTKI) and combination therapies exhibit potential, albeit limited by blood-brain barrier penetration and toxicity. Combining treatments like radiotherapy and enhancing BBB penetration may benefit patients. Further research is warranted in patient quality of life and biomarker-guided selection.</p></div><div><h3>Conclusion</h3><p>While certain therapies hold promise for GBM, future research should prioritize personalized medicine and innovative strategies for improved treatment outcomes.</p></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140757058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-23DOI: 10.1016/j.critrevonc.2024.104363
Yan Liu , Yanqing Xu , Wei Xu , Zhengzhong He , Cong Fu , Fen Du
Beyond tobacco smoking, radon takes its place as the second most significant contributor to lung cancer, excluding hereditary and other biologically related factors. Radon and its byproducts play a pivotal role in exposing humans to elevated levels of natural radiation. Approximately 10–20 % of lung cancer cases worldwide can be attributed to radon exposure, leading to between 3 % and 20 % of all lung cancer-related deaths. Nevertheless, a knowledge gap persists regarding the association between radon and lung cancer, impeding radon risk reduction initiatives globally. This review presents a comprehensive overview of the current state of research in epidemiology, cell biology, dosimetry, and risk modeling concerning radon exposure and its relevance to lung cancer. It also delves into methods for measuring radon concentrations, monitoring radon risk zones, and identifying priorities for future research.
{"title":"Radon and lung cancer: Current status and future prospects","authors":"Yan Liu , Yanqing Xu , Wei Xu , Zhengzhong He , Cong Fu , Fen Du","doi":"10.1016/j.critrevonc.2024.104363","DOIUrl":"10.1016/j.critrevonc.2024.104363","url":null,"abstract":"<div><p>Beyond tobacco smoking, radon takes its place as the second most significant contributor to lung cancer, excluding hereditary and other biologically related factors. Radon and its byproducts play a pivotal role in exposing humans to elevated levels of natural radiation. Approximately 10–20 % of lung cancer cases worldwide can be attributed to radon exposure, leading to between 3 % and 20 % of all lung cancer-related deaths. Nevertheless, a knowledge gap persists regarding the association between radon and lung cancer, impeding radon risk reduction initiatives globally. This review presents a comprehensive overview of the current state of research in epidemiology, cell biology, dosimetry, and risk modeling concerning radon exposure and its relevance to lung cancer. It also delves into methods for measuring radon concentrations, monitoring radon risk zones, and identifying priorities for future research.</p></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140764527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-18DOI: 10.1016/j.critrevonc.2024.104356
Shengfeng Fu , Qinyang Zhang , Changhe Zhang
Cholangiocarcinoma (CCA) is the second most common hepatobiliary malignancy after hepatocellular carcinoma. Due to the poor treatment effect and high mortality rate of CCA, it is of great significance to explore new therapeutic targets. Ferroptosis is a type of cell death caused by iron-dependent cell oxidative injury, which is closely related to the occurrence and development of numerous diseases. Novel ideas for the prevention and treatment of related diseases have been provided by ferroptosis, which has become a focus of research in recent years. This review introduces the underlying mechanisms related to ferroptosis, as well as a research update for ferroptosis in the occurrence and development of CCA. The clinical value of ferroptosis-related regulatory mechanisms in CCA will be elucidated.
胆管癌(CCA)是仅次于肝细胞癌的第二大肝胆恶性肿瘤。由于CCA治疗效果差、死亡率高,探索新的治疗靶点意义重大。铁中毒是一种由铁依赖性细胞氧化损伤引起的细胞死亡,与多种疾病的发生和发展密切相关。近年来,铁氧化还为相关疾病的预防和治疗提供了新思路,已成为研究的焦点。本综述介绍了与高铁血症相关的潜在机制,以及高铁血症在 CCA 发生和发展中的最新研究进展。此外,还将阐明 CCA 中与高铁血症相关的调控机制的临床价值。
{"title":"Research update for ferroptosis and cholangiocarcinoma","authors":"Shengfeng Fu , Qinyang Zhang , Changhe Zhang","doi":"10.1016/j.critrevonc.2024.104356","DOIUrl":"https://doi.org/10.1016/j.critrevonc.2024.104356","url":null,"abstract":"<div><p>Cholangiocarcinoma (CCA) is the second most common hepatobiliary malignancy after hepatocellular carcinoma. Due to the poor treatment effect and high mortality rate of CCA, it is of great significance to explore new therapeutic targets. Ferroptosis is a type of cell death caused by iron-dependent cell oxidative injury, which is closely related to the occurrence and development of numerous diseases. Novel ideas for the prevention and treatment of related diseases have been provided by ferroptosis, which has become a focus of research in recent years. This review introduces the underlying mechanisms related to ferroptosis, as well as a research update for ferroptosis in the occurrence and development of CCA. The clinical value of ferroptosis-related regulatory mechanisms in CCA will be elucidated.</p></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1040842824000994/pdfft?md5=506cc9564be4220ee4f85af02c746378&pid=1-s2.0-S1040842824000994-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140643974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-18DOI: 10.1016/j.critrevonc.2024.104350
Nicole Del Bianco , Anita Borsati , Linda Toniolo , Christian Ciurnielli , Lorenzo Belluomini , Jessica Insolda , Marco Sposito , Michele Milella , Federico Schena , Sara Pilotto , Alice Avancini
Purpose
Exercise before surgery, as part of prehabilitation, aiming to enhance patients' functional and physiological capacity, has become widespread, necessitating an in-depth understanding.
Methods
A systematic search was conducted on Pubmed, Cochrane, and Scopus to examine the effect of exercise as prehabilitation, alone or in combination with other interventions, in patients with cancer. Interventional studies applying a single-arm, randomized controlled, or nonrandomized design were included.
Results
A total of 96 studies were included, and categorized according to cancer types, i.e., gynecological, breast, urological, gastrointestinal and lung cancer. For each cancer site, the effect of exercise, on physical fitness parameters and postoperative outcomes, including length of hospital stay and postoperative complications, was reported.
Conclusion
Exercise as prehabilitation may have an important role in improving physical fitness, postoperative outcomes, and accelerating recovery, especially in certain types of malignancies.
{"title":"What is the role of physical exercise in the era of cancer prehabilitation? A systematic review","authors":"Nicole Del Bianco , Anita Borsati , Linda Toniolo , Christian Ciurnielli , Lorenzo Belluomini , Jessica Insolda , Marco Sposito , Michele Milella , Federico Schena , Sara Pilotto , Alice Avancini","doi":"10.1016/j.critrevonc.2024.104350","DOIUrl":"https://doi.org/10.1016/j.critrevonc.2024.104350","url":null,"abstract":"<div><h3>Purpose</h3><p>Exercise before surgery, as part of prehabilitation, aiming to enhance patients' functional and physiological capacity, has become widespread, necessitating an in-depth understanding.</p></div><div><h3>Methods</h3><p>A systematic search was conducted on Pubmed, Cochrane, and Scopus to examine the effect of exercise as prehabilitation, alone or in combination with other interventions, in patients with cancer. Interventional studies applying a single-arm, randomized controlled, or nonrandomized design were included.</p></div><div><h3>Results</h3><p>A total of 96 studies were included, and categorized according to cancer types, i.e., gynecological, breast, urological, gastrointestinal and lung cancer. For each cancer site, the effect of exercise, on physical fitness parameters and postoperative outcomes, including length of hospital stay and postoperative complications, was reported.</p></div><div><h3>Conclusion</h3><p>Exercise as prehabilitation may have an important role in improving physical fitness, postoperative outcomes, and accelerating recovery, especially in certain types of malignancies.</p></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1040842824000933/pdfft?md5=a059c18c28d0076fe7f48c57dda6bff8&pid=1-s2.0-S1040842824000933-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140643939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-16DOI: 10.1016/j.critrevonc.2024.104355
Miguel Martín , Atanasio Pandiella , Emilio Vargas-Castrillón , Elena Díaz-Rodríguez , Teresa Iglesias-Hernangómez , Concha Martínez Cano , Inés Fernández-Cuesta , Elena Winkow , Maria Francesca Perelló
Trastuzumab deruxtecan (T-DXd) is an antibody-drug conjugate (ADC) consisting of a humanised, anti-human epidermal growth factor receptor 2 (HER2) monoclonal antibody covalently linked to a topoisomerase I inhibitor cytotoxic payload (DXd). The high drug-to-antibody ratio (8:1) ensures a high DXd concentration is delivered to target tumour cells, following internalisation of T-DXd and subsequent cleavage of its tetrapeptide-based linker. DXd’s membrane-permeable nature enables it to cross cell membranes and potentially exert antitumour activity on surrounding tumour cells regardless of HER2 expression. T-DXd’s unique mechanism of action is reflected in its efficacy in clinical trials in patients with HER2-positive advanced breast cancer (in heavily pretreated populations and in those previously treated with a taxane and trastuzumab), as well as HER2-low metastatic breast cancer. Thus, ADCs such as T-DXd have the potential to change the treatment paradigm of targeting HER2 in metastatic breast cancer, including eventually within the adjuvant/neoadjuvant setting.
{"title":"Trastuzumab deruxtecan in breast cancer","authors":"Miguel Martín , Atanasio Pandiella , Emilio Vargas-Castrillón , Elena Díaz-Rodríguez , Teresa Iglesias-Hernangómez , Concha Martínez Cano , Inés Fernández-Cuesta , Elena Winkow , Maria Francesca Perelló","doi":"10.1016/j.critrevonc.2024.104355","DOIUrl":"https://doi.org/10.1016/j.critrevonc.2024.104355","url":null,"abstract":"<div><p>Trastuzumab deruxtecan (T-DXd) is an antibody-drug conjugate (ADC) consisting of a humanised, anti-human epidermal growth factor receptor 2 (HER2) monoclonal antibody covalently linked to a topoisomerase I inhibitor cytotoxic payload (DXd). The high drug-to-antibody ratio (8:1) ensures a high DXd concentration is delivered to target tumour cells, following internalisation of T-DXd and subsequent cleavage of its tetrapeptide-based linker. DXd’s membrane-permeable nature enables it to cross cell membranes and potentially exert antitumour activity on surrounding tumour cells regardless of HER2 expression. T-DXd’s unique mechanism of action is reflected in its efficacy in clinical trials in patients with HER2-positive advanced breast cancer (in heavily pretreated populations and in those previously treated with a taxane and trastuzumab), as well as HER2-low metastatic breast cancer. Thus, ADCs such as T-DXd have the potential to change the treatment paradigm of targeting HER2 in metastatic breast cancer, including eventually within the adjuvant/neoadjuvant setting.</p></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1040842824000982/pdfft?md5=5f18e1c66a63389354b151078ab3080a&pid=1-s2.0-S1040842824000982-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140643940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-16DOI: 10.1016/j.critrevonc.2024.104357
Xiaohong Kuang , Run Xu , Jian Li
Background
Whether PD-L1 testing is needed to identify patients receiving PD-1/PD-L1 inhibitors is an area of debate.
Methods
PubMed and Embase were searched for phase III randomized clinical trials. We assessed the heterogeneity of overall survival (OS) between patients with high and low PD-L1 expression using an interaction test.
Results
Seventy studies representing 44791 patients were included. Both the CPS and TPS can predict better survival from anti-PD-1/PD-L1 therapy in patients with high PD-L1 expression. However, only CPS 1 has the ability to select patients who are unlikely to respond to anti-PD-1/PD-L1 therapy, while an OS advantage can be obtained from PD-1/PD-L1 inhibitors both in patients with high and low PD-L1 expression defined by CPS 5, CPS 10 and TPS.
Conclusion
CPS 1 is recommended to select patients with the likelihood of benefiting from PD-1/PD-L1 inhibitors while excluding patients who may not respond.
{"title":"Association of PD-L1 expression with survival benefit from PD-1/PD-L1 inhibitors in advanced cancer: Systematic review and meta-analysis of phase III randomized clinical trials","authors":"Xiaohong Kuang , Run Xu , Jian Li","doi":"10.1016/j.critrevonc.2024.104357","DOIUrl":"https://doi.org/10.1016/j.critrevonc.2024.104357","url":null,"abstract":"<div><h3>Background</h3><p>Whether PD-L1 testing is needed to identify patients receiving PD-1/PD-L1 inhibitors is an area of debate.</p></div><div><h3>Methods</h3><p>PubMed and Embase were searched for phase III randomized clinical trials. We assessed the heterogeneity of overall survival (OS) between patients with high and low PD-L1 expression using an interaction test.</p></div><div><h3>Results</h3><p>Seventy studies representing 44791 patients were included. Both the CPS and TPS can predict better survival from anti-PD-1/PD-L1 therapy in patients with high PD-L1 expression. However, only CPS 1 has the ability to select patients who are unlikely to respond to anti-PD-1/PD-L1 therapy, while an OS advantage can be obtained from PD-1/PD-L1 inhibitors both in patients with high and low PD-L1 expression defined by CPS 5, CPS 10 and TPS.</p></div><div><h3>Conclusion</h3><p>CPS 1 is recommended to select patients with the likelihood of benefiting from PD-1/PD-L1 inhibitors while excluding patients who may not respond.</p></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140645206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-16DOI: 10.1016/j.critrevonc.2024.104352
Yu Fujiwara , Alexander B. Karol , Himanshu Joshi , Emma Reford , Sudeh Izadmehr , Deborah B. Doroshow , Matthew D. Galsky
C-reactive protein (CRP) may reflect a pro-inflammatory tumor microenvironment and could represent a biomarker to select patients with urothelial carcinoma more likely to benefit from therapies directed at modulating tumor-promoting inflammation. We performed a systematic review to evaluate survival outcomes based on pre-treatment CRP values in urothelial carcinoma. The hazard ratios (HRs) of survival such as overall survival (OS) and progression-free survival (PFS) between groups with high versus low CRP values were pooled by the random-effect model meta-analyses. Overall, 28 studies comprising 6789 patients were identified for meta-analyses. High CRP levels were associated with shorter OS (HR=1.96 [95% CI: 1.64–2.33], p < 0.01), particularly in advanced disease treated with immune checkpoint blockade (ICB, HR=1.78 [1.47–2.15], p < 0.01). Similar findings were observed in ICB-treated patients with PFS. These findings suggest that CRP could be an attractive biomarker to select patients with urothelial carcinoma for strategies seeking to modulate tumor-promoting inflammation.
{"title":"C-reactive protein (CRP) as a prognostic biomarker in patients with urothelial carcinoma: A systematic review and meta-analysis","authors":"Yu Fujiwara , Alexander B. Karol , Himanshu Joshi , Emma Reford , Sudeh Izadmehr , Deborah B. Doroshow , Matthew D. Galsky","doi":"10.1016/j.critrevonc.2024.104352","DOIUrl":"https://doi.org/10.1016/j.critrevonc.2024.104352","url":null,"abstract":"<div><p>C-reactive protein (CRP) may reflect a pro-inflammatory tumor microenvironment and could represent a biomarker to select patients with urothelial carcinoma more likely to benefit from therapies directed at modulating tumor-promoting inflammation. We performed a systematic review to evaluate survival outcomes based on pre-treatment CRP values in urothelial carcinoma. The hazard ratios (HRs) of survival such as overall survival (OS) and progression-free survival (PFS) between groups with high versus low CRP values were pooled by the random-effect model meta-analyses. Overall, 28 studies comprising 6789 patients were identified for meta-analyses. High CRP levels were associated with shorter OS (HR=1.96 [95% CI: 1.64–2.33], p < 0.01), particularly in advanced disease treated with immune checkpoint blockade (ICB, HR=1.78 [1.47–2.15], p < 0.01). Similar findings were observed in ICB-treated patients with PFS. These findings suggest that CRP could be an attractive biomarker to select patients with urothelial carcinoma for strategies seeking to modulate tumor-promoting inflammation.</p></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140555305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-16DOI: 10.1016/j.critrevonc.2024.104349
Qianghu Pang , Zhirou Tang , Lianxiang Luo
Ferroptosis, a novel form of cell death regulation, was identified in 2012. It is characterized by unique features that differentiate it from other types of cell death, including necrosis, apoptosis, autophagy, and pyroptosis. Ferroptosis is defined by an abundance of iron ions and lipid peroxidation, resulting in alterations in subcellular structures, an elevation in reactive oxygen species (ROS), a reduction in glutathione (GSH) levels, and an augmentation in Fe (II) cytokines. Ferroptosis, a regulated process, is controlled by an intricate network of signaling pathways, where multiple stimuli can either enhance or hinder the process. This review primarily examines the defensive mechanisms of ferroptosis and its interaction with the tumor microenvironment. The analysis focuses on the pathways that involve AMPK, p53, NF2, mTOR, System Xc-, Wnt, Hippo, Nrf2, and cGAS-STING. The text discusses the possibilities of employing a combination therapy that targets several pathways for the treatment of cancer. It emphasizes the necessity for additional study in this field.
{"title":"The crosstalk between oncogenic signaling and ferroptosis in cancer","authors":"Qianghu Pang , Zhirou Tang , Lianxiang Luo","doi":"10.1016/j.critrevonc.2024.104349","DOIUrl":"https://doi.org/10.1016/j.critrevonc.2024.104349","url":null,"abstract":"<div><p>Ferroptosis, a novel form of cell death regulation, was identified in 2012. It is characterized by unique features that differentiate it from other types of cell death, including necrosis, apoptosis, autophagy, and pyroptosis. Ferroptosis is defined by an abundance of iron ions and lipid peroxidation, resulting in alterations in subcellular structures, an elevation in reactive oxygen species (ROS), a reduction in glutathione (GSH) levels, and an augmentation in Fe (II) cytokines. Ferroptosis, a regulated process, is controlled by an intricate network of signaling pathways, where multiple stimuli can either enhance or hinder the process. This review primarily examines the defensive mechanisms of ferroptosis and its interaction with the tumor microenvironment. The analysis focuses on the pathways that involve AMPK, p53, NF2, mTOR, System Xc-, Wnt, Hippo, Nrf2, and cGAS-STING. The text discusses the possibilities of employing a combination therapy that targets several pathways for the treatment of cancer. It emphasizes the necessity for additional study in this field.</p></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140558485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-16DOI: 10.1016/j.critrevonc.2024.104361
Hanchen Cai , Ziqi Meng , Fujun Yu
Reactive oxidative species (ROS) is a crucial factor in the regulation of cellular biological activity and function, and aberrant levels of ROS can contribute to the development of a variety of diseases, particularly cancer. Numerous discoveries have affirmed that this process is strongly associated with "programmed cell death (PCD)," which refers to the suicide protection mechanism initiated by cells in response to external stimuli, such as apoptosis, autophagy, ferroptosis, etc. Research has demonstrated that ROS-induced PCD is crucial for the development of hepatocellular carcinoma (HCC). These activities serve a dual function in both facilitating and inhibiting cancer, suggesting the existence of a delicate balance within healthy cells that can be disrupted by the abnormal generation of reactive oxygen species (ROS), thereby influencing the eventual advancement or regression of a tumor. In this review, we summarize how ROS regulates PCD to influence the tumorigenesis and progression of HCC. Studying how ROS-induced PCD affects the progression of HCC at a molecular level can help develop better prevention and treatment methods and facilitate the design of more effective preventative and therapeutic strategies.
{"title":"The involvement of ROS-regulated programmed cell death in hepatocellular carcinoma","authors":"Hanchen Cai , Ziqi Meng , Fujun Yu","doi":"10.1016/j.critrevonc.2024.104361","DOIUrl":"https://doi.org/10.1016/j.critrevonc.2024.104361","url":null,"abstract":"<div><p>Reactive oxidative species (ROS) is a crucial factor in the regulation of cellular biological activity and function, and aberrant levels of ROS can contribute to the development of a variety of diseases, particularly cancer. Numerous discoveries have affirmed that this process is strongly associated with \"programmed cell death (PCD),\" which refers to the suicide protection mechanism initiated by cells in response to external stimuli, such as apoptosis, autophagy, ferroptosis, etc. Research has demonstrated that ROS-induced PCD is crucial for the development of hepatocellular carcinoma (HCC). These activities serve a dual function in both facilitating and inhibiting cancer, suggesting the existence of a delicate balance within healthy cells that can be disrupted by the abnormal generation of reactive oxygen species (ROS), thereby influencing the eventual advancement or regression of a tumor. In this review, we summarize how ROS regulates PCD to influence the tumorigenesis and progression of HCC. Studying how ROS-induced PCD affects the progression of HCC at a molecular level can help develop better prevention and treatment methods and facilitate the design of more effective preventative and therapeutic strategies.</p></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140604936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-13DOI: 10.1016/j.critrevonc.2024.104353
Yang Yang , Bing Zhao , Hongli Lan , Jinbing Sun , Guoli Wei
Bortezomib is the first-line standard and most effective chemotherapeutic for multiple myeloma; however, bortezomib-induced peripheral neuropathy (BIPN) severely affects the chemotherapy regimen and has long-term impact on patients under maintenance therapy. The pathogenesis of BIPN is poorly understood, and basic research and development of BIPN management drugs are in early stages. Besides chemotherapy dose reduction and regimen modification, no recommended prevention and treatment approaches are available for BIPN apart from the International Myeloma Working Group guidelines for peripheral neuropathy in myeloma. An in-depth exploration of the pathogenesis of BIPN, development of additional therapeutic approaches, and identification of risk factors are needed. Optimizing effective and standardized BIPN treatment plans and providing more decision-making evidence for clinical diagnosis and treatment of BIPN are necessary. This article reviews the recent advances in BIPN research; provides an overview of clinical features, underlying molecular mechanisms, and therapeutic approaches; and highlights areas for future studies.
{"title":"Bortezomib-induced peripheral neuropathy: Clinical features, molecular basis, and therapeutic approach","authors":"Yang Yang , Bing Zhao , Hongli Lan , Jinbing Sun , Guoli Wei","doi":"10.1016/j.critrevonc.2024.104353","DOIUrl":"https://doi.org/10.1016/j.critrevonc.2024.104353","url":null,"abstract":"<div><p>Bortezomib is the first-line standard and most effective chemotherapeutic for multiple myeloma; however, bortezomib-induced peripheral neuropathy (BIPN) severely affects the chemotherapy regimen and has long-term impact on patients under maintenance therapy. The pathogenesis of BIPN is poorly understood, and basic research and development of BIPN management drugs are in early stages. Besides chemotherapy dose reduction and regimen modification, no recommended prevention and treatment approaches are available for BIPN apart from the International Myeloma Working Group guidelines for peripheral neuropathy in myeloma. An in-depth exploration of the pathogenesis of BIPN, development of additional therapeutic approaches, and identification of risk factors are needed. Optimizing effective and standardized BIPN treatment plans and providing more decision-making evidence for clinical diagnosis and treatment of BIPN are necessary. This article reviews the recent advances in BIPN research; provides an overview of clinical features, underlying molecular mechanisms, and therapeutic approaches; and highlights areas for future studies.</p></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1040842824000969/pdfft?md5=feca42128439d868a83dc941207ca7b8&pid=1-s2.0-S1040842824000969-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140558436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}