International review of cell and molecular biology最新文献

{"title":"Cellular signaling in glioblastoma: A molecular and clinical perspective.","authors":"Debarati Ghosh, Brett Pryor, Nancy Jiang","doi":"10.1016/bs.ircmb.2024.01.007","DOIUrl":"10.1016/bs.ircmb.2024.01.007","url":null,"abstract":"<p><p>Glioblastoma multiforme (GBM) is the most aggressive brain tumor with an average life expectancy of less than 15 months. Such high patient mortality in GBM is pertaining to the presence of clinical and molecular heterogeneity attributed to various genetic and epigenetic alterations. Such alterations in critically important signaling pathways are attributed to aberrant gene signaling. Different subclasses of GBM show predominance of different genetic alterations and therefore, understanding the complex signaling pathways and their key molecular components in different subclasses of GBM is extremely important with respect to clinical management. In this book chapter, we summarize the common and important signaling pathways that play a significant role in different subclasses and discuss their therapeutic targeting approaches in terms of preclinical studies and clinical trials.</p>","PeriodicalId":14422,"journal":{"name":"International review of cell and molecular biology","volume":"386 ","pages":"1-47"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141087408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemokine receptors in COVID-19 infection.","authors":"Claudia Gutierrez-Chavez, Shalom Aperrigue-Lira, Brando Ortiz-Saavedra, Irmia Paz","doi":"10.1016/bs.ircmb.2024.05.002","DOIUrl":"https://doi.org/10.1016/bs.ircmb.2024.05.002","url":null,"abstract":"<p><p>Chemokine receptors play diverse roles in the immune response against pathogens by recruiting innate and adaptive immune cells to sites of infection. However, their involvement could also be detrimental, causing tissue damage and exacerbating respiratory diseases by triggering histological alterations such as fibrosis and remodeling. This chapter reviews the role of chemokine receptors in the immune defense against SARS-CoV-2 infection. In COVID-19, CXCR3 is expressed mainly in T cells, and its upregulation is related to an increase in SARS-CoV-2-specific antibodies but also to COVID-19 severity. CCR5 is a key player in T-cell recruitment, and its suppression leads to reduced inflammation and viremia levels. Conversely, CXCR6 is implicated in the aberrant migration of memory T cells within airways. On the other hand, increased CCR4+ cells in the blood and decreased CCR4+ cells in lung cells are associated with severe COVID-19. Additionally, CCR2 is associated with an increase in macrophage recruitment to lung tissues. Elevated levels of CXCR1 and CXCR2, which are predominantly expressed in neutrophils, are associated with the severity of the disease, and finally, the expression of CX3CR1 in cytotoxic T lymphocytes affects the retention of these cells in lung tissues, thereby impacting the severity of COVID-19. Despite the efforts of many clinical trials to find effective therapies for COVID-19 using chemokine receptor inhibitors, no conclusive results have been found due to the small number of patients, redundancy, and co-expression of chemokine receptors by immune cells, which explains the difficulty in finding a single therapeutic target or effective treatment.</p>","PeriodicalId":14422,"journal":{"name":"International review of cell and molecular biology","volume":"388 ","pages":"53-94"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142287341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preface.","authors":"Maroua Manai, Hamouda Boussen, Massimo Cristofanilli","doi":"10.1016/S1937-6448(24)00060-1","DOIUrl":"https://doi.org/10.1016/S1937-6448(24)00060-1","url":null,"abstract":"","PeriodicalId":14422,"journal":{"name":"International review of cell and molecular biology","volume":"384 ","pages":"xiii-xiv"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140852744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Drugging the undruggable: Advances in targeting KRAS signaling in solid tumors.","authors":"Prajna Tripathi, Rajni Kumari, Rajiv Pathak","doi":"10.1016/bs.ircmb.2023.11.004","DOIUrl":"10.1016/bs.ircmb.2023.11.004","url":null,"abstract":"<p><p>Cancer remains the leading cause of global mortality, prompting a paradigm shift in its treatment and outcomes with the advent of targeted therapies. Among the most prevalent mutations in RAS-driven cancers, Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations account for approximately 86% of cases worldwide, particularly in lung, pancreatic, and colon cancers, contributing to poor prognosis and reduced overall survival. Despite numerous efforts to understand the biology of KRAS mutants and their pivotal role in cancer development, the lack of well-defined drug-binding pockets has deemed KRAS an \"undruggable\" therapeutic target, presenting significant challenges for researchers and clinicians alike. Through significant biochemical and technological advances, the last decade has witnessed promising breakthroughs in targeted therapies for KRAS-mutated lung, colon, and pancreatic cancers, marking a critical turning point in the field. In this chapter, we provide an overview of the characteristics of KRAS mutations across various solid tumors, highlighting ongoing cutting-edge research on the immune microenvironment, the development of KRAS-driven mice models, and the recent progress in the exploration of specific KRAS mutant-targeted therapeutic approaches. By comprehensive understanding of the intricacies of KRAS signaling in solid tumors and the latest therapeutic developments, this chapter will shed light on the potential for novel therapeutic strategies to combat KRAS-driven tumors and improve patient outcomes.</p>","PeriodicalId":14422,"journal":{"name":"International review of cell and molecular biology","volume":"385 ","pages":"1-39"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140864136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic regulation of cancer.","authors":"Sheila Spada, Lorenzo Galluzzi","doi":"10.1016/S1937-6448(24)00113-8","DOIUrl":"https://doi.org/10.1016/S1937-6448(24)00113-8","url":null,"abstract":"","PeriodicalId":14422,"journal":{"name":"International review of cell and molecular biology","volume":"387 ","pages":"xiii-xvii"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142046657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preconditioning with immunogenic cell death-inducing treatments for subsequent immunotherapy.","authors":"Hui Pan, Peng Liu, Guido Kroemer, Oliver Kepp","doi":"10.1016/bs.ircmb.2023.06.001","DOIUrl":"10.1016/bs.ircmb.2023.06.001","url":null,"abstract":"<p><p>Since the dawn of anticancer immunotherapy, the clinical use of immune checkpoint inhibitors (ICI) has increased exponentially. Monoclonal antibodies targeting CTLA-4 and the PD-1/PD-L1 interaction were first introduced for the treatment of patients with unresectable melanoma. In melanoma, ICI lead to durable regression in a significant number of patients and have thus been clinically approved as a first-line treatment of advanced disease. Over the past years an increasing number of regulatory approvals have been granted for the use of ICI in patients affected by a large range of distinct carcinomas. In retrospect surprisingly, it has been discovered that particularly successful chemotherapeutic treatments are able to trigger anticancer immune responses because they induce immunogenic cell death (ICD), hence killing cancer cells in a way that they elicit an immune response against tumor-associated antigens. Logically, preclinical studies as well as clinical trials are currently exploring the possibility to combine ICD inducers with ICI to obtain optimal therapeutic effects. Here, we provide a broad overview of current strategies for the implementation of combinatorial approaches involving ICD induction followed by ICI in anticancer therapy.</p>","PeriodicalId":14422,"journal":{"name":"International review of cell and molecular biology","volume":"382 ","pages":"279-294"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139472122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of lipid and serine metabolism by the oncogene c-Myc.","authors":"Subhajit Chatterjee, Prarthana Prashanth, Vipin Rawat, Sounak Ghosh Roy","doi":"10.1016/bs.ircmb.2024.03.005","DOIUrl":"10.1016/bs.ircmb.2024.03.005","url":null,"abstract":"<p><p>Tumor formation is supported by metabolic reprogramming, characterized by increase nutrient uptake, glycolysis and glutaminolysis. The c-Myc proto-oncogene is a transcription factor, upregulated in most cancers and several reports showed the role of c-Myc in other metabolic pathways such as glucose, amino acid, and nucleotide metabolism. In this short report, we tried to summarize the existing takeaway points from studies conducted in different cancer types with respect to c-Myc and lipid and serine metabolism. Here, we report that c-Myc can activate both lipid and serine metabolism against the backdrop of tumor formation, and different therapies like aspirin and lomitapide target the links between c-Myc and metabolism to slow down tumor progression and invasion. We also report diverse upstream regulators that influence c-Myc in different cancers, and interestingly components of the lipid metabolism (like lipid phosphate phosphatase and leptin) and serine metabolism can also act upstream of c-Myc in certain occasions. Finally, we also summarize the existing knowledge on the involvement of epigenetic pathways and non-coding RNAs in regulating lipid and serine metabolism and c-Myc in tumor cells. Identification of non-coding factors and epigenetic mechanisms present a promising avenue of study that could empower researchers with novel anticancer treatment targeting c-Myc and lipid and serine metabolism pathways!</p>","PeriodicalId":14422,"journal":{"name":"International review of cell and molecular biology","volume":"389 ","pages":"236-256"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142465577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunological landscape of solid cancer: Interplay between tumor and autoimmunity.","authors":"Ajay K Singh, Phaneendra K Duddempudi, Divya Borasandra Kenchappa, Nityanand Srivastava, Nitin P Amdare","doi":"10.1016/bs.ircmb.2024.04.002","DOIUrl":"https://doi.org/10.1016/bs.ircmb.2024.04.002","url":null,"abstract":"<p><p>The immune system, a central player in maintaining homeostasis, emerges as a pivotal factor in the pathogenesis and progression of two seemingly disparate yet interconnected categories of diseases: autoimmunity and cancer. This chapter delves into the intricate and multifaceted role of the immune system, particularly T cells, in orchestrating responses that govern the delicate balance between immune surveillance and self-tolerance. T cells, pivotal immune system components, play a central role in both diseases. In autoimmunity, aberrant T cell activation drives damaging immune responses against normal tissues, while in cancer, T cells exhibit suppressed responses, allowing the growth of malignant tumors. Immune checkpoint receptors, example, initially explored in autoimmunity, now revolutionize cancer treatment via immune checkpoint blockade (ICB). Though effective in various tumors, ICB poses risks of immune-related adverse events (irAEs) akin to autoimmunity. This chapter underscores the importance of understanding tumor-associated antigens and their role in autoimmunity, immune checkpoint regulation, and their implications for both diseases. It also explores autoimmunity resulting from cancer immunotherapy and shared molecular pathways in solid tumors and autoimmune diseases, highlighting their interconnectedness at the molecular level. Additionally, it sheds light on common pathways and epigenetic features shared by autoimmunity and cancer, and the potential of repurposing drugs for therapeutic interventions. Delving deeper into these insights could unlock therapeutic strategies for both autoimmunity and cancer.</p>","PeriodicalId":14422,"journal":{"name":"International review of cell and molecular biology","volume":"389 ","pages":"163-235"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142465575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA damage response and neoantigens: A favorable target for triple-negative breast cancer immunotherapy and vaccine development.","authors":"Rajasekaran Subbarayan, Dhasarathdev Srinivasan, Ranjith Balakrishnan, Ajeet Kumar, Salman Sadullah Usmani, Nityanand Srivastava","doi":"10.1016/bs.ircmb.2024.05.001","DOIUrl":"https://doi.org/10.1016/bs.ircmb.2024.05.001","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) poses a significant clinical challenge due to its aggressive nature and limited therapeutic options. The interplay between DNA damage response (DDR) mechanisms and the emergence of neoantigens represents a promising avenue for developing targeted immunotherapeutic strategies and vaccines for TNBC. The DDR is a complex network of cellular mechanisms designed to maintain genomic integrity. In TNBC, where genetic instability is a hallmark, dysregulation of DDR components plays a pivotal role in tumorigenesis and progression. This review explores the intricate relationship between DDR and neoantigens, shedding light on the potential vulnerabilities of TNBC cells. Neoantigens, arising from somatic mutations in cancer cells, represent unique antigens that can be recognized by the immune system. TNBC's propensity for genomic instability leads to an increased mutational burden, consequently yielding a rich repertoire of neoantigens. The convergence of DDR and neoantigens in TNBC offers a distinctive opportunity for immunotherapeutic targeting. Immunotherapy has revolutionized cancer treatment by harnessing the immune system to selectively target cancer cells. The unique immunogenicity conferred by DDR-related neoantigens in TNBC positions them as ideal targets for immunotherapeutic interventions. This review also explores various immunotherapeutic modalities, including immune checkpoint inhibitors (ICIs), adoptive cell therapies, and cancer vaccines, that leverage the DDR and neoantigen interplay to enhance anti-tumor immune responses. Moreover, the potential for developing vaccines targeting DDR-related neoantigens opens new frontiers in preventive and therapeutic strategies for TNBC. The rational design of vaccines tailored to the individual mutational landscape of TNBC holds promise for precision medicine approaches. In conclusion, the convergence of DDR and neoantigens in TNBC presents a compelling rationale for the development of innovative immunotherapies and vaccines. Understanding and targeting these interconnected processes may pave the way for personalized and effective interventions, offering new hope for patients grappling with the challenges posed by TNBCs.</p>","PeriodicalId":14422,"journal":{"name":"International review of cell and molecular biology","volume":"389 ","pages":"104-152"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142465574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic and epigenetic features of neuroendocrine prostate cancer and their emerging applications.","authors":"Xintong Zhang, Edward Barnett, Jim Smith, Emma Wilkinson, Rathan M Subramaniam, Amir Zarrabi, Euan J Rodger, Aniruddha Chatterjee","doi":"10.1016/bs.ircmb.2023.06.002","DOIUrl":"10.1016/bs.ircmb.2023.06.002","url":null,"abstract":"<p><p>Prostate cancer is the second most prevalent cancer in men globally. De novo neuroendocrine prostate cancer (NEPC) is uncommon at initial diagnosis, however, (treatment-induced) t-NEPC emerges in up to 25% of prostate adenocarcinoma (PRAD) cases treated with androgen deprivation, carrying a drastically poor prognosis. The transition from PRAD to t-NEPC is underpinned by several key genetic mutations; TP53, RB1, and MYCN are the main genes implicated, bearing similarities to other neuroendocrine tumours. A broad range of epigenetic alterations, such as aberrations in DNA methylation, histone post-translational modifications, and non-coding RNAs, may drive lineage plasticity from PRAD to t-NEPC. The clinical diagnosis of NEPC is hampered by a lack of accessible biomarkers; recent advances in liquid biopsy techniques assessing circulating tumour cells and ctDNA in NEPC suggest that the advent of non-invasive means of monitoring progression to NEPC is on the horizon. Such techniques are vital for NEPC management; diagnosis of t-NEPC is crucial for implementing effective treatment, and precision medicine will be integral to providing the best outcomes for patients.</p>","PeriodicalId":14422,"journal":{"name":"International review of cell and molecular biology","volume":"383 ","pages":"41-66"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139740925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}