Pub Date : 2024-09-17DOI: 10.1007/s12032-024-02441-2
Marie-Eve Letellier, Marize Ibrahim, Anna Towers, Geneviève Chaput
Cancer-related lymphedema (CRL) lacks internationally accepted definition and diagnostic criteria. The accurate incidence of CRL is therefore a challenge and the condition is likely underreported. Patients treated for cancer can develop CRL as a result of surgery, chemotherapy, and/or radiotherapy, which can lead to considerable psychosocial and physical morbidity, and decreased quality of life. Determining CRL incidence is crucial to inform care access and resource allocation, to best support patients affected by this lifelong condition. This review aimed to provide the latest CRL incidence estimates. Using four core databases (MEDLINE, Embase, Web of Science Core Collection, Cochrane Library), a literature search was performed to capture publications dated between 2015 and 2023. A total of 48 articles (33 prospective studies, 15 systematic reviews) met inclusion criteria, providing a sample size of 234,079 cancer patients. Findings revealed CRL incidence across cancer types varied, reported 2–74% in breast, 8–45% in gynecological and urological, 71–90% in head and neck and 2–29% in melanoma cancers. CRL incidence varied between 3 and 21% in preventative lymphedema surgery patients. Projected increases in cancer incidence and improved survival rates are expected to further escalate CRL incidence. Healthcare systems and professionals alike must therefore prepare to meet the growing needs of CRL patients.
{"title":"Incidence of lymphedema related to various cancers","authors":"Marie-Eve Letellier, Marize Ibrahim, Anna Towers, Geneviève Chaput","doi":"10.1007/s12032-024-02441-2","DOIUrl":"https://doi.org/10.1007/s12032-024-02441-2","url":null,"abstract":"<p>Cancer-related lymphedema (CRL) lacks internationally accepted definition and diagnostic criteria. The accurate incidence of CRL is therefore a challenge and the condition is likely underreported. Patients treated for cancer can develop CRL as a result of surgery, chemotherapy, and/or radiotherapy, which can lead to considerable psychosocial and physical morbidity, and decreased quality of life. Determining CRL incidence is crucial to inform care access and resource allocation, to best support patients affected by this lifelong condition. This review aimed to provide the latest CRL incidence estimates. Using four core databases (MEDLINE, Embase, Web of Science Core Collection, Cochrane Library), a literature search was performed to capture publications dated between 2015 and 2023. A total of 48 articles (33 prospective studies, 15 systematic reviews) met inclusion criteria, providing a sample size of 234,079 cancer patients. Findings revealed CRL incidence across cancer types varied, reported 2–74% in breast, 8–45% in gynecological and urological, 71–90% in head and neck and 2–29% in melanoma cancers. CRL incidence varied between 3 and 21% in preventative lymphedema surgery patients. Projected increases in cancer incidence and improved survival rates are expected to further escalate CRL incidence. Healthcare systems and professionals alike must therefore prepare to meet the growing needs of CRL patients.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142254131","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 : 2024-09-11DOI: 10.1007/s12032-024-02494-3
Suleiman Ibrahim Shelash Mohammad, Asokan Vasudevan, Felix Oghenemaro Enwa, Jaya Bansal, Mamata Chahar, Mamdouh Eldesoqui, Muhammad Ikram Ullah, Zhanna R. Gardanova, Hanen Mahmod Hulail, Ahmed Hussein Zwamel
The likelihood of survival for cancer patients has greatly improved due to chemotherapy medicines. However, these antitumor agents might also have unfavorable effects on the cardiovascular system, which could result in sudden or gradual cardiac failure. The production of free radicals that result in oxidative stress appears to be the key mechanism by which chemotherapy-induced cardiotoxicity (CIC) happens. Reports suggest that the Sirtuin-1 (Sirt1)/Nuclear factor E2-associated factor 2 (Nrf2) signaling pathway has been considered an alternative path for counteracting cardiotoxicity by suppressing oxidative stress, inflammation, and apoptosis. This review concludes recent knowledge about CIC with a special focus on the anti-oxidative regulation properties of the Sirt1/Nrf2 pathway.
{"title":"The Sirt1/Nrf2 pathway is a key factor for drug therapy in chemotherapy-induced cardiotoxicity: a Mini-Review","authors":"Suleiman Ibrahim Shelash Mohammad, Asokan Vasudevan, Felix Oghenemaro Enwa, Jaya Bansal, Mamata Chahar, Mamdouh Eldesoqui, Muhammad Ikram Ullah, Zhanna R. Gardanova, Hanen Mahmod Hulail, Ahmed Hussein Zwamel","doi":"10.1007/s12032-024-02494-3","DOIUrl":"https://doi.org/10.1007/s12032-024-02494-3","url":null,"abstract":"<p>The likelihood of survival for cancer patients has greatly improved due to chemotherapy medicines. However, these antitumor agents might also have unfavorable effects on the cardiovascular system, which could result in sudden or gradual cardiac failure. The production of free radicals that result in oxidative stress appears to be the key mechanism by which chemotherapy-induced cardiotoxicity (CIC) happens. Reports suggest that the Sirtuin-1 (Sirt1)/Nuclear factor E2-associated factor 2 (Nrf2) signaling pathway has been considered an alternative path for counteracting cardiotoxicity by suppressing oxidative stress, inflammation, and apoptosis. This review concludes recent knowledge about CIC with a special focus on the anti-oxidative regulation properties of the Sirt1/Nrf2 pathway.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142183342","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 : 2024-09-06DOI: 10.1007/s12032-024-02484-5
Mustafa Khalid Abduljabbar, Mohammed Merza, Abdulqader Aziz, Soumya V Menon, Mandeep Kaur, Zafar Aminov, Safia Obaidur Rab, Ahmed Hjazi, Yasser Fakri Mustafa, Benien C Gabel
This study investigates the intricate mechanisms underlying the correlation between elevated consumption of harmful fats and the onset of kidney malignancies. The rise in global obesity rates has been accompanied by an increased prevalence of renal cancers, prompting an exploration into the molecular pathways and biological processes linking these phenomena. Through an extensive review of current literature and clinical studies, we identify potential key factors contributing to the carcinogenic influence of harmful fats on renal tissues. Our analysis highlights the role of adipose tissue-derived factors, inflammatory mediators, and lipid metabolism dysregulation in fostering a microenvironment conducive to renal tumorigenesis. Furthermore, we delve into the impact of harmful fats on signaling pathways associated with cell proliferation, apoptosis evasion, and angiogenesis within the renal parenchyma. This review underscores the importance of elucidating the molecular intricacies linking lipid metabolism and kidney malignancies, offering a foundation for future research and the development of targeted preventive and therapeutic interventions. The findings discussed herein contribute to our understanding of the complex relationship between lipid mediators and renal cancer, providing a basis for public health strategies aimed at mitigating the impact of harmful fats on kidney health.
{"title":"Lipid metabolism reprogramming in renal cell carcinomas.","authors":"Mustafa Khalid Abduljabbar, Mohammed Merza, Abdulqader Aziz, Soumya V Menon, Mandeep Kaur, Zafar Aminov, Safia Obaidur Rab, Ahmed Hjazi, Yasser Fakri Mustafa, Benien C Gabel","doi":"10.1007/s12032-024-02484-5","DOIUrl":"https://doi.org/10.1007/s12032-024-02484-5","url":null,"abstract":"<p><p>This study investigates the intricate mechanisms underlying the correlation between elevated consumption of harmful fats and the onset of kidney malignancies. The rise in global obesity rates has been accompanied by an increased prevalence of renal cancers, prompting an exploration into the molecular pathways and biological processes linking these phenomena. Through an extensive review of current literature and clinical studies, we identify potential key factors contributing to the carcinogenic influence of harmful fats on renal tissues. Our analysis highlights the role of adipose tissue-derived factors, inflammatory mediators, and lipid metabolism dysregulation in fostering a microenvironment conducive to renal tumorigenesis. Furthermore, we delve into the impact of harmful fats on signaling pathways associated with cell proliferation, apoptosis evasion, and angiogenesis within the renal parenchyma. This review underscores the importance of elucidating the molecular intricacies linking lipid metabolism and kidney malignancies, offering a foundation for future research and the development of targeted preventive and therapeutic interventions. The findings discussed herein contribute to our understanding of the complex relationship between lipid mediators and renal cancer, providing a basis for public health strategies aimed at mitigating the impact of harmful fats on kidney health.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140506","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 : 2024-09-05DOI: 10.1007/s12032-024-02486-3
Fouad Attieh, Marc Boutros, Hampig Raphaël Kourie, Mervat Mahrous
In recent years, kidney cancer has shown an increased worldwide incidence of more than 400 000 novel cases annually. Although more than half of patients are diagnosed at a localised stage, this disease presents a high-risk of relapse after surgery. Thus, there is a need for adjuvant therapy post-resection to reduce cancer recurrence and prolong disease-free and overall survival. Thorough investigation of adjuvant drugs for renal cell carcinoma (RCC) has shown little promise in the last fifty years, with no recorded overall survival benefits. This was the case until pembrolizumab, an immune checkpoint inhibitor, was introduced into the adjuvant RCC space through the KEYNOTE-564 trial. The adjuvant administration of this novel anti-PD-1 drug demonstrated a significant overall survival benefit which has led to an update in the current treatment guidelines of RCC. This substantial change in the standard of care also caused an investigation of possible treatment combinations and an adoption of innovative predictive biomarkers. In this review, we will present the evolution of past adjuvant ICI trials for the treatment of RCC, the implications of pembrolizumab's overall survival benefits and a discussion of future directions concerning new RCC drug trials and liquid biopsy-based biomarkers.
{"title":"Turning the tide: pembrolizumab's triumph in adjuvant RCC therapy.","authors":"Fouad Attieh, Marc Boutros, Hampig Raphaël Kourie, Mervat Mahrous","doi":"10.1007/s12032-024-02486-3","DOIUrl":"https://doi.org/10.1007/s12032-024-02486-3","url":null,"abstract":"<p><p>In recent years, kidney cancer has shown an increased worldwide incidence of more than 400 000 novel cases annually. Although more than half of patients are diagnosed at a localised stage, this disease presents a high-risk of relapse after surgery. Thus, there is a need for adjuvant therapy post-resection to reduce cancer recurrence and prolong disease-free and overall survival. Thorough investigation of adjuvant drugs for renal cell carcinoma (RCC) has shown little promise in the last fifty years, with no recorded overall survival benefits. This was the case until pembrolizumab, an immune checkpoint inhibitor, was introduced into the adjuvant RCC space through the KEYNOTE-564 trial. The adjuvant administration of this novel anti-PD-1 drug demonstrated a significant overall survival benefit which has led to an update in the current treatment guidelines of RCC. This substantial change in the standard of care also caused an investigation of possible treatment combinations and an adoption of innovative predictive biomarkers. In this review, we will present the evolution of past adjuvant ICI trials for the treatment of RCC, the implications of pembrolizumab's overall survival benefits and a discussion of future directions concerning new RCC drug trials and liquid biopsy-based biomarkers.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142140507","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 : 2024-09-05DOI: 10.1007/s12032-024-02481-8
Zachary E Hunzeker, Lei Zhao, Austin M Kim, Jacob M Parker, Ziwen Zhu, Huaping Xiao, Qian Bai, Mark R Wakefield, Yujiang Fang
Interleukin-22, discovered in the year of 2000, is a pleiotropic Th17 cytokine from the IL-10 family of cytokines. IL-22 signals through the type 2 cytokine receptor complex IL-22R and predominantly activates STAT3. This pathway leads to the transcription of several different types of genes, giving IL-22 context-specific functions ranging from inducing antimicrobial peptide expression to target cell proliferation. In recent years, it has been shown that IL-22 is involved in the pathogenesis of neoplasia in some cancers through its pro-proliferative and anti-apoptotic effects. This review highlights studies with recent discoveries and conclusions drawn on IL-22 and its involvement and function in various cancers. Such a study may be helpful to better understand the role of IL-22 in cancer so that new treatment could be developed targeting IL-22.
{"title":"The role of IL-22 in cancer.","authors":"Zachary E Hunzeker, Lei Zhao, Austin M Kim, Jacob M Parker, Ziwen Zhu, Huaping Xiao, Qian Bai, Mark R Wakefield, Yujiang Fang","doi":"10.1007/s12032-024-02481-8","DOIUrl":"https://doi.org/10.1007/s12032-024-02481-8","url":null,"abstract":"<p><p>Interleukin-22, discovered in the year of 2000, is a pleiotropic Th17 cytokine from the IL-10 family of cytokines. IL-22 signals through the type 2 cytokine receptor complex IL-22R and predominantly activates STAT3. This pathway leads to the transcription of several different types of genes, giving IL-22 context-specific functions ranging from inducing antimicrobial peptide expression to target cell proliferation. In recent years, it has been shown that IL-22 is involved in the pathogenesis of neoplasia in some cancers through its pro-proliferative and anti-apoptotic effects. This review highlights studies with recent discoveries and conclusions drawn on IL-22 and its involvement and function in various cancers. Such a study may be helpful to better understand the role of IL-22 in cancer so that new treatment could be developed targeting IL-22.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142133103","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 : 2024-09-05DOI: 10.1007/s12032-024-02472-9
Mary Vargo, Melissa Aldrich, Paula Donahue, Emily Iker, Louise Koelmeyer, Rachelle Crescenzi, Andrea Cheville
Lymphedema evaluation entails multifaceted considerations for which options continue to evolve and emerge. This paper provides a critical review of the current status of diagnostic and quantitative measures for lymphedema, from traditional and novel bedside assessment tools for volumetric and fluid assessment, to advanced imaging modalities. Modalities are contrasted with regard to empirical support and feasibility of clinical implementation. The manuscript proposes a grid framework for comparing the ability of each modality to quantify specific lymphedema characteristics, including distribution, dysmorphism, tissue composition and fluid content, lymphatic anatomy and function, metaplasia, clinical symptoms, and quality of life and function. This review additionally applies a similar framework approach to consider how well assessment tools support important clinical needs, including: (1) screening, (2) diagnosis and differential diagnosis, (3) individualization of treatment, and (4) monitoring treatment response. The framework highlights which clinical needs are served by an abundance of assessment tools and identifies others that have problematically few. The framework clarifies which tools have greater or lesser empirical support. The framework is designed to assist stakeholders in selecting appropriate diagnostic and surveillance modalities, gauging levels of confidence when applying tools to specific clinical needs, elucidating overarching patterns of diagnostic and quantitative strengths and weaknesses, and informing future investigation.
{"title":"Current diagnostic and quantitative techniques in the field of lymphedema management: a critical review.","authors":"Mary Vargo, Melissa Aldrich, Paula Donahue, Emily Iker, Louise Koelmeyer, Rachelle Crescenzi, Andrea Cheville","doi":"10.1007/s12032-024-02472-9","DOIUrl":"10.1007/s12032-024-02472-9","url":null,"abstract":"<p><p>Lymphedema evaluation entails multifaceted considerations for which options continue to evolve and emerge. This paper provides a critical review of the current status of diagnostic and quantitative measures for lymphedema, from traditional and novel bedside assessment tools for volumetric and fluid assessment, to advanced imaging modalities. Modalities are contrasted with regard to empirical support and feasibility of clinical implementation. The manuscript proposes a grid framework for comparing the ability of each modality to quantify specific lymphedema characteristics, including distribution, dysmorphism, tissue composition and fluid content, lymphatic anatomy and function, metaplasia, clinical symptoms, and quality of life and function. This review additionally applies a similar framework approach to consider how well assessment tools support important clinical needs, including: (1) screening, (2) diagnosis and differential diagnosis, (3) individualization of treatment, and (4) monitoring treatment response. The framework highlights which clinical needs are served by an abundance of assessment tools and identifies others that have problematically few. The framework clarifies which tools have greater or lesser empirical support. The framework is designed to assist stakeholders in selecting appropriate diagnostic and surveillance modalities, gauging levels of confidence when applying tools to specific clinical needs, elucidating overarching patterns of diagnostic and quantitative strengths and weaknesses, and informing future investigation.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11377676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142133102","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 : 2024-09-04DOI: 10.1007/s12032-024-02478-3
Akbar Oghalaie, Mahmoud Eshagh Hosseini, Mohammad Hosseininejad-Chafi, Zohre Eftekhari, Mahdi Behdani, Fatemeh Kazemi-Lomedasht
Immunotoxins (ITs) are specialized therapeutic agents designed for targeted treatment, particularly in cancer therapy. They consist of a monoclonal antibody or antibody fragment linked to a potent cytotoxic agent, such as bacterial- or plant-derived toxins like diphtheria toxin, ricin, or pseudomonas exotoxin. The monoclonal antibody component specifically binds to antigens expressed on the surface of target cells, facilitating the internalization of the IT. Once inside the cell, the cytotoxic agent is released, disrupting essential cellular processes and leading to cell death. This targeted approach minimizes damage to healthy tissues while effectively eliminating diseased cells. The production of ITs involves two primary methods: recombinant fusion and chemical conjugation. In recombinant fusion, genetic engineering is used to create a fusion protein that combines the antibody and toxin, ensuring precise control over their ratio and functionality. In chemical conjugation, pre-existing antibodies are chemically linked to toxins, allowing for greater flexibility in combining different antibodies and cytotoxic agents. Each method has its advantages and challenges, influencing the specificity, production complexity, and therapeutic potential of the resulting ITs. As research advances, ITs continue to show promise not only in oncology but also in treating other diseases, including inflammatory conditions and atherosclerosis. The precise targeting and potent effects of ITs make them a valuable tool in the development of new therapeutic strategies.
免疫毒素(ITs)是专为靶向治疗(尤其是癌症治疗)而设计的特殊治疗剂。它们由单克隆抗体或抗体片段与强效细胞毒剂(如白喉毒素、蓖麻毒素或假单胞菌外毒素等细菌或植物毒素)连接组成。单克隆抗体成分与靶细胞表面表达的抗原特异性结合,促进 IT 的内化。一旦进入细胞,细胞毒剂就会释放出来,破坏细胞的基本过程,导致细胞死亡。这种有针对性的方法在有效消灭病变细胞的同时,最大限度地减少了对健康组织的损害。生产 ITs 涉及两种主要方法:重组融合和化学合成。在重组融合法中,利用基因工程制造出一种融合蛋白,将抗体和毒素结合在一起,确保精确控制它们的比例和功能。在化学合成中,预先存在的抗体与毒素通过化学反应结合在一起,这样就能更灵活地将不同的抗体和细胞毒剂结合在一起。每种方法都有其优势和挑战,影响着所制成的 ITs 的特异性、生产复杂性和治疗潜力。随着研究的不断深入,ITs 不仅在肿瘤学领域,而且在治疗其他疾病(包括炎症和动脉粥样硬化)方面也大有可为。ITs 的精确靶向性和强效作用使其成为开发新治疗策略的重要工具。
{"title":"Advances in immunotoxin engineering: precision therapeutic strategies in modern oncology.","authors":"Akbar Oghalaie, Mahmoud Eshagh Hosseini, Mohammad Hosseininejad-Chafi, Zohre Eftekhari, Mahdi Behdani, Fatemeh Kazemi-Lomedasht","doi":"10.1007/s12032-024-02478-3","DOIUrl":"https://doi.org/10.1007/s12032-024-02478-3","url":null,"abstract":"<p><p>Immunotoxins (ITs) are specialized therapeutic agents designed for targeted treatment, particularly in cancer therapy. They consist of a monoclonal antibody or antibody fragment linked to a potent cytotoxic agent, such as bacterial- or plant-derived toxins like diphtheria toxin, ricin, or pseudomonas exotoxin. The monoclonal antibody component specifically binds to antigens expressed on the surface of target cells, facilitating the internalization of the IT. Once inside the cell, the cytotoxic agent is released, disrupting essential cellular processes and leading to cell death. This targeted approach minimizes damage to healthy tissues while effectively eliminating diseased cells. The production of ITs involves two primary methods: recombinant fusion and chemical conjugation. In recombinant fusion, genetic engineering is used to create a fusion protein that combines the antibody and toxin, ensuring precise control over their ratio and functionality. In chemical conjugation, pre-existing antibodies are chemically linked to toxins, allowing for greater flexibility in combining different antibodies and cytotoxic agents. Each method has its advantages and challenges, influencing the specificity, production complexity, and therapeutic potential of the resulting ITs. As research advances, ITs continue to show promise not only in oncology but also in treating other diseases, including inflammatory conditions and atherosclerosis. The precise targeting and potent effects of ITs make them a valuable tool in the development of new therapeutic strategies.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142126152","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}
Despite the high incidence of breast cancer in women worldwide, there are still great challenges in the treatment process. Mitochondria are highly dynamic organelles, and their dynamics involve cellular energy conversion, signal conduction and other processes. In recent years, an increasing number of studies have affirmed the dynamics of mitochondria as the basis for cancer progression and metastasis; that is, an imbalance between mitochondrial fission and fusion may lead to the progression and metastasis of breast cancer. Here, we review the latest insights into mitochondrial dynamics in the progression of breast cancer and emphasize the clinical value of mitochondrial dynamics in diagnosis and prognosis, as well as important advances in clinical research.
{"title":"How mitochondrial dynamics imbalance affects the progression of breast cancer:a mini review.","authors":"Jingwen Kuang, Hao Liu, Linlin Feng, Yuan Xue, Huiyi Tang, Pengcheng Xu","doi":"10.1007/s12032-024-02479-2","DOIUrl":"10.1007/s12032-024-02479-2","url":null,"abstract":"<p><p>Despite the high incidence of breast cancer in women worldwide, there are still great challenges in the treatment process. Mitochondria are highly dynamic organelles, and their dynamics involve cellular energy conversion, signal conduction and other processes. In recent years, an increasing number of studies have affirmed the dynamics of mitochondria as the basis for cancer progression and metastasis; that is, an imbalance between mitochondrial fission and fusion may lead to the progression and metastasis of breast cancer. Here, we review the latest insights into mitochondrial dynamics in the progression of breast cancer and emphasize the clinical value of mitochondrial dynamics in diagnosis and prognosis, as well as important advances in clinical research.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11366726/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109227","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 : 2024-08-30DOI: 10.1007/s12032-024-02487-2
Murali Santhoshkumar
{"title":"Letter to the editor: comment on \"Probiotic-derived silver nanoparticles target mTOR/MMP-9/BCL-2/dependent AMPK activation for hepatic cancer treatment\".","authors":"Murali Santhoshkumar","doi":"10.1007/s12032-024-02487-2","DOIUrl":"10.1007/s12032-024-02487-2","url":null,"abstract":"","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109151","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 : 2024-08-29DOI: 10.1007/s12032-024-02456-9
Yi Hu, Chen Wang, Huishi Liang, Jie Li, Qiong Yang
Triple-negative breast cancer (TNBC) tumors are biologically aggressive breast cancer. On the molecular level, TNBC is a highly heterogeneous disease; more biotechnologies are gradually being used to advance the understanding of TNBC subtypes and help establish more targeted therapies. Multiple TNBC target-related agents are already approved by the Food and Drug Administration for clinical use, including PI3K/AKT/mTOR inhibitors, PRAP inhibitors, and antibody-drug conjugates. Some innovative approaches, like peptide strategies, also promise to treat TNBC. Currently, the interplay between TNBC tumors and their tumor microenvironment provides a promising prospect for improving the efficacy of immunotherapy. In this review, we summarize the prevalent TNBC subtype methodologies, discuss the evolving therapeutic strategies, and propose new therapeutic possibilities based on existing foundational theories, with the attempt to serve as a reference to further advance tailoring treatment of TNBC.
{"title":"The treatment landscape of triple-negative breast cancer.","authors":"Yi Hu, Chen Wang, Huishi Liang, Jie Li, Qiong Yang","doi":"10.1007/s12032-024-02456-9","DOIUrl":"https://doi.org/10.1007/s12032-024-02456-9","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) tumors are biologically aggressive breast cancer. On the molecular level, TNBC is a highly heterogeneous disease; more biotechnologies are gradually being used to advance the understanding of TNBC subtypes and help establish more targeted therapies. Multiple TNBC target-related agents are already approved by the Food and Drug Administration for clinical use, including PI3K/AKT/mTOR inhibitors, PRAP inhibitors, and antibody-drug conjugates. Some innovative approaches, like peptide strategies, also promise to treat TNBC. Currently, the interplay between TNBC tumors and their tumor microenvironment provides a promising prospect for improving the efficacy of immunotherapy. In this review, we summarize the prevalent TNBC subtype methodologies, discuss the evolving therapeutic strategies, and propose new therapeutic possibilities based on existing foundational theories, with the attempt to serve as a reference to further advance tailoring treatment of TNBC.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142109152","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}