{"title":"C-myc 致癌基因多样性对实体肿瘤和淋巴恶性肿瘤的临床影响","authors":"Sotirios Papouliakos, Aristeidis Chrysovergis, Vasileios Papanikolaou, Despoina Spyropoulou, Georgios Papanastasiou, Asimakis D Asimakopoulos, Sofianiki Mastronikoli, Panagiotis Stathopoulos, Dimitrios Roukas, Maria Adamopoulou, Evangelos Tsiambas, Dimitrios Peschos, Pavlos Pantos, Vasileios Ragos, Nicholas Mastronikolis, Efthymios Kyrodimos","doi":"10.26574/maedica.2024.19.2.355","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Onset and progression of malignant tumors is a multistep process including a variety of gross chromosomal and specific genes' deregulation. Among oncogenes that are frequently altered in solid and also in hematological malignancies, the C-myc (gene locus: 8q24.21) plays a pivotal role. C-myc is a proto-oncogene encoding for a nuclear phosphoprotein implicated in cell cycle progression, apoptosis and cellular differentiation and transformation.</p><p><strong>Objective: </strong>The purpose of the current molecular review was to explore the differences of C-myc oncogenic activity in solid and lymphoid malignancies that modify its clinical impact on them.</p><p><strong>Material and method: </strong>A systematic review of the literature in the international database PubMed was carried out. The year 2010 was set as a prominent time limit for the publication date of articles in the majority of them, whereas specific references of great importance and historical value in the field of C-myc gene discovery and analysis were also included. The following keywords were used: C-myc, oncogene, signaling pathway, malignancies, carcinoma, lymphoma. A pool of 43 important articles were selected for the present study at the basis of combining molecular knowledge with new targeted therapeutic strategies.</p><p><strong>Results: </strong>C-myc oncogene demonstrates two different mechanisms of deregulation: amplification, mutation and translocation patterns. These particular aspects of gene alteration are unique for solid and non-solid (hematological) malignancies, respectively.</p><p><strong>Conclusions: </strong>C-myc is characterized by diversity regarding its deregulation mechanisms in malignancies derived from different tissues. C-myc translocation is sporadically combined with amplification (\"complicon\" formation) or mutations creating exotic genetic signatures. This \"bi-phasic\" C-myc deregulation model in the corresponding malignant tumor categories clinically affects the corresponding patients, also modifying the targeted therapeutic strategies on them.</p>","PeriodicalId":74094,"journal":{"name":"Maedica","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11345059/pdf/","citationCount":"0","resultStr":"{\"title\":\"Clinical Impact of C-myc Oncogenic Diversity on Solid and Lymphoid Malignancies.\",\"authors\":\"Sotirios Papouliakos, Aristeidis Chrysovergis, Vasileios Papanikolaou, Despoina Spyropoulou, Georgios Papanastasiou, Asimakis D Asimakopoulos, Sofianiki Mastronikoli, Panagiotis Stathopoulos, Dimitrios Roukas, Maria Adamopoulou, Evangelos Tsiambas, Dimitrios Peschos, Pavlos Pantos, Vasileios Ragos, Nicholas Mastronikolis, Efthymios Kyrodimos\",\"doi\":\"10.26574/maedica.2024.19.2.355\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Onset and progression of malignant tumors is a multistep process including a variety of gross chromosomal and specific genes' deregulation. Among oncogenes that are frequently altered in solid and also in hematological malignancies, the C-myc (gene locus: 8q24.21) plays a pivotal role. C-myc is a proto-oncogene encoding for a nuclear phosphoprotein implicated in cell cycle progression, apoptosis and cellular differentiation and transformation.</p><p><strong>Objective: </strong>The purpose of the current molecular review was to explore the differences of C-myc oncogenic activity in solid and lymphoid malignancies that modify its clinical impact on them.</p><p><strong>Material and method: </strong>A systematic review of the literature in the international database PubMed was carried out. The year 2010 was set as a prominent time limit for the publication date of articles in the majority of them, whereas specific references of great importance and historical value in the field of C-myc gene discovery and analysis were also included. The following keywords were used: C-myc, oncogene, signaling pathway, malignancies, carcinoma, lymphoma. A pool of 43 important articles were selected for the present study at the basis of combining molecular knowledge with new targeted therapeutic strategies.</p><p><strong>Results: </strong>C-myc oncogene demonstrates two different mechanisms of deregulation: amplification, mutation and translocation patterns. These particular aspects of gene alteration are unique for solid and non-solid (hematological) malignancies, respectively.</p><p><strong>Conclusions: </strong>C-myc is characterized by diversity regarding its deregulation mechanisms in malignancies derived from different tissues. C-myc translocation is sporadically combined with amplification (\\\"complicon\\\" formation) or mutations creating exotic genetic signatures. This \\\"bi-phasic\\\" C-myc deregulation model in the corresponding malignant tumor categories clinically affects the corresponding patients, also modifying the targeted therapeutic strategies on them.</p>\",\"PeriodicalId\":74094,\"journal\":{\"name\":\"Maedica\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11345059/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Maedica\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.26574/maedica.2024.19.2.355\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Maedica","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.26574/maedica.2024.19.2.355","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Clinical Impact of C-myc Oncogenic Diversity on Solid and Lymphoid Malignancies.
Introduction: Onset and progression of malignant tumors is a multistep process including a variety of gross chromosomal and specific genes' deregulation. Among oncogenes that are frequently altered in solid and also in hematological malignancies, the C-myc (gene locus: 8q24.21) plays a pivotal role. C-myc is a proto-oncogene encoding for a nuclear phosphoprotein implicated in cell cycle progression, apoptosis and cellular differentiation and transformation.
Objective: The purpose of the current molecular review was to explore the differences of C-myc oncogenic activity in solid and lymphoid malignancies that modify its clinical impact on them.
Material and method: A systematic review of the literature in the international database PubMed was carried out. The year 2010 was set as a prominent time limit for the publication date of articles in the majority of them, whereas specific references of great importance and historical value in the field of C-myc gene discovery and analysis were also included. The following keywords were used: C-myc, oncogene, signaling pathway, malignancies, carcinoma, lymphoma. A pool of 43 important articles were selected for the present study at the basis of combining molecular knowledge with new targeted therapeutic strategies.
Results: C-myc oncogene demonstrates two different mechanisms of deregulation: amplification, mutation and translocation patterns. These particular aspects of gene alteration are unique for solid and non-solid (hematological) malignancies, respectively.
Conclusions: C-myc is characterized by diversity regarding its deregulation mechanisms in malignancies derived from different tissues. C-myc translocation is sporadically combined with amplification ("complicon" formation) or mutations creating exotic genetic signatures. This "bi-phasic" C-myc deregulation model in the corresponding malignant tumor categories clinically affects the corresponding patients, also modifying the targeted therapeutic strategies on them.