Critical Reviews in Oncogenesis最新文献_第10页

Diagnostic and Prognostic Implications of Cardiac Markers for Hepatocellular Carcinoma. 肝细胞癌心脏标志物的诊断和预后意义。

Critical Reviews in Oncogenesis Pub Date : 2021-01-01 DOI: 10.1615/CritRevOncog.2020036305

Mohan Krishna Ghanta, Afzal Khan Akbar Khan, L V K S Bhaskar

引用次数: 0

Circadian Rhythm and Melatonin in Liver Carcinogenesis: Updates on Current Findings. 肝癌发生过程中的昼夜节律和褪黑激素：最新研究成果。

Critical Reviews in Oncogenesis Pub Date : 2021-01-01 DOI: 10.1615/CritRevOncog.2021039881

Yuyan Han, Lixian Chen, Leonardo Baiocchi, Ludovica Ceci, Shannon Glaser, Heather Francis, Gianfranco Alpini, Lindsey Kennedy

{"title":"Circadian Rhythm and Melatonin in Liver Carcinogenesis: Updates on Current Findings.","authors":"Yuyan Han, Lixian Chen, Leonardo Baiocchi, Ludovica Ceci, Shannon Glaser, Heather Francis, Gianfranco Alpini, Lindsey Kennedy","doi":"10.1615/CritRevOncog.2021039881","DOIUrl":"10.1615/CritRevOncog.2021039881","url":null,"abstract":"Liver cancer, including hepatocellular carcinoma and cholangiocarcinoma, can be devastating if not treated early. The risk factors of liver cancer include alcoholic liver disease, non-alcoholic fatty liver disease, disruption of melatonin levels, and dysregulated circadian rhythm. The circadian rhythm is a 24-hour biological clock that regulates the physiological activities at both central and peripheral levels. Its molecular mechanism exists in every cell in mammals. Disruption of the circadian rhythm has found in liver cancers as an independent risk factor. This review summarized the most recent findings about the molecular mechanisms of circadian rhythm, the crosstalk between core clock genes and melatonin, as well as the role of circadian rhythm and melatonin played in chronic liver diseases and liver cancer. Finally, we discussed the potential clinical application of circadian rhythm and melatonin for the treatment of liver cancer and discussed future perspectives of how understanding the circadian rhythm in liver cancer progression could provide new clinical applications for liver cancer treatment and diagnosis.","PeriodicalId":35617,"journal":{"name":"Critical Reviews in Oncogenesis","volume":"26 3","pages":"69-85"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9755746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Potential Oncostatic Effects of Melatonin against Prostate Cancer. 褪黑素对前列腺癌的潜在抑癌作用。

Critical Reviews in Oncogenesis Pub Date : 2021-01-01 DOI: 10.1615/critrevoncog.2021041260

S. Samanta

{"title":"The Potential Oncostatic Effects of Melatonin against Prostate Cancer.","authors":"S. Samanta","doi":"10.1615/critrevoncog.2021041260","DOIUrl":"https://doi.org/10.1615/critrevoncog.2021041260","url":null,"abstract":"Melatonin is an endogenous indolamine, synthesized and secreted from the pineal gland. The environmental light-dark cycle is the primary regulator of melatonin synthesis. Darkness during the subjective night induces noradrenaline secretion, which stimulates pinealocytes for melatonin production. Melatonin exhibits anticancer effects and different physiological functions through the membrane-bound G-protein-coupled MT1 and MT2 receptors. Impaired circadian activity, indoor or outdoor light pollution, shift work, night work, and jet lag suppress normal melatonin synthesis. Decreased melatonin concentration causes impaired anticancer effects that adversely affect the progression of different cancers, including prostate. Melatonin differentially regulates the cell cycle, cell survival, and metabolism in malignant cells in contrast to normal prostate epithelial cells. Melatonin promotes the nuclear exclusion of androgen receptors without suppressing the expression of this receptor. This indirect effect blocks the androgenic response in prostate cancer cells. It acts as a cytostatic and cytotoxic agent, prevents cell proliferation, and activates an apoptotic response. Melatonin also inhibits HIF-1α activity and the expression of vascular endothelial growth factors to suppress angiogenesis. This indolamine restricts alteration of metabolic activity, invasion, and metastasis. Melatonin has therapeutic importance. It decreases the side effects of anticancer treatment and mitigates adverse effects after prostatectomy and radiotherapy. Melatonin blocks the recurrence of prostate cancer as well as hormone-refractory effects during androgen deprivation therapy. The present review discusses the multifaceted effects of melatonin against prostate cancer.","PeriodicalId":35617,"journal":{"name":"Critical Reviews in Oncogenesis","volume":"26 3 1","pages":"53-67"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67428494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Cross Talk between the Circadian Clock Proteins and TP53 in Cancer and Therapeutic Significance. 肿瘤中生物钟蛋白与TP53的串扰及其治疗意义。

Critical Reviews in Oncogenesis Pub Date : 2021-01-01 DOI: 10.1615/critrevoncog.2022042860

Brandon Valafar, A. Zaravinos, B. Bonavida

{"title":"Cross Talk between the Circadian Clock Proteins and TP53 in Cancer and Therapeutic Significance.","authors":"Brandon Valafar, A. Zaravinos, B. Bonavida","doi":"10.1615/critrevoncog.2022042860","DOIUrl":"https://doi.org/10.1615/critrevoncog.2022042860","url":null,"abstract":"The circadian rhythms regulate physiological and cellular processes that maintain normal homeostasis, keeping our cells synchronized to the dark-light cycle. The disruption of circadian clock genes has been associated with various diseases, including cancer. The clock genes impact several cancer-related signaling trajectories, including the tumor suppressor's p53 pathway involvement in the regulation of the cell cycle and apoptosis. In most human cancers, p53 loses its normal functions and tumor-suppressive activity through function-inactivating mutations. Herein, we review the roles of each of the clock genes (PER1-3, CRY1/2, BMAL1, CLOCK, REV-ERBα/β, RORα, and SIRT1) in their association and regulation of p53. We analyzed by bioinformatics the expression of several clock genes (CLOCK, CRY1-2, PER1-3), p53, and apoptotic and metabolic genes across all tumors in the TCGA platform, and found deregulated patterns in many cases. Our findings support the development of new therapies targeted against some clock genes to restore p53 activities and the inhibition of tumor development. Such therapies will complement a large number of currently tested treatments targeting the restoration of wild-type p53 to prevent tumor growth and lead cancer cells to apoptosis.","PeriodicalId":35617,"journal":{"name":"Critical Reviews in Oncogenesis","volume":"26 4 1","pages":"19-36"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67428631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Commentary: Photodynamic Therapy-Induced Oxidative Stress and the Circadian Rhythm. 评论:光动力疗法诱导的氧化应激和昼夜节律。

Critical Reviews in Oncogenesis Pub Date : 2021-01-01 DOI: 10.1615/critrevoncog.2022043185

V. Rapozzi, B. Bonavida

引用次数: 0

The Rhythmicity of Life: A Review of the Circadian Clocks. 生命的节律性:生理时钟研究综述。

Critical Reviews in Oncogenesis Pub Date : 2021-01-01 DOI: 10.1615/critrevoncog.2022042786

Eda Acikgoz, S. Karahuseyinoglu, Ş. Ayla, G. Oktem

{"title":"The Rhythmicity of Life: A Review of the Circadian Clocks.","authors":"Eda Acikgoz, S. Karahuseyinoglu, Ş. Ayla, G. Oktem","doi":"10.1615/critrevoncog.2022042786","DOIUrl":"https://doi.org/10.1615/critrevoncog.2022042786","url":null,"abstract":"Physiology of the mammalian body has been adapted to diurnal cycles of around 24 h, an evolutionary situation that affects a wide spectrum of biological events including sleep-to-wake transitions, feeding/fasting, body temperature, and hormonal regulations. The patterns of the diurnal cycle occur due to rhythmic oscillations that arise from the suprachiasmatic nucleus of hypothalamus, which also can be defined as the pacemaker of the system. The clock can be defined as a molecular machinery driven by the core clock genes that encode clock proteins in a rhythmic oscillatory fashion maintained by the light/dark cycles of the environment. Although the well-established knowledge refers to the function of the circadian rhythm as maintenance of the normal physiology, growing evidence shows that disruptions in the system usually caused by genetic and/or epigenetic misregulations may have a direct effect to lead major pathological conditions, such as carcinogenesis. This review outlines the main molecular aspects of circadian physiology, and reveals the reasons for and results of the circadian disruptions at different levels. In spite of the fact that more proof is needed for a direct correlation between circadian disruptions and oncogenesis and other pathological events, data obtained from current research supports the role of circadian rhythms in malfunctioning of the normal cellular metabolism.","PeriodicalId":35617,"journal":{"name":"Critical Reviews in Oncogenesis","volume":"26 4 1","pages":"37-53"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67428617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Understanding the Alterations in Lipid Metabolism in NAFLD Progression: Current Trends and Future Directions. 了解NAFLD进展中脂质代谢的变化:当前趋势和未来方向。

Critical Reviews in Oncogenesis Pub Date : 2021-01-01 DOI: 10.1615/CritRevOncog.2020035839

Sathish Kumar Mungamuri, Sukesh Narayan Sinha, Yamini Javvadi

{"title":"Understanding the Alterations in Lipid Metabolism in NAFLD Progression: Current Trends and Future Directions.","authors":"Sathish Kumar Mungamuri, Sukesh Narayan Sinha, Yamini Javvadi","doi":"10.1615/CritRevOncog.2020035839","DOIUrl":"https://doi.org/10.1615/CritRevOncog.2020035839","url":null,"abstract":"Nonalcoholic fatty liver disease (NAFLD) is a pathological condition, wherein fat deposition exceeds the allowable limits of the healthy person. If the condition persists for a long time, the patient will eventually develop NASH (nonalcoholic steatohepatitis), which will probably lead to HCC (hepatocellular carcinoma). The incidence of NAFLD is rising at an alarming rate, and still there are no drugs approved by the U.S. Food and Drug Administration for this devastating health condition. To combat and treat NAFLD successfully, it is essential to understand how routine lipid metabolism in the liver is altered under these conditions. In this review, we discuss specifically during the NAFLD progression how the signaling pathways leading to excess fat accumulation in the liver are changed. We also address variations in the mechanisms underlying hepatic lipid uptake and changes in fatty acid oxidation mechanisms. We will also highlight the role of transcription factors and other lipolytic enzymes that stringently regulate the hepatic de novo lipolysis (DNL) and emphasize how they are altered during NAFLD progression. Finally, we will also touch upon how the lipid disposal from the liver goes wrong during the NAFLD progression. A comprehensive understanding of the changes in lipid metabolism is essential for developing successful therapies for NAFLD.","PeriodicalId":35617,"journal":{"name":"Critical Reviews in Oncogenesis","volume":"26 1","pages":"35-49"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25413703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Long Noncoding RNAs: Potential Mediators of Liver Cancer Metastasis. 长链非编码rna:肝癌转移的潜在介质。

Critical Reviews in Oncogenesis Pub Date : 2021-01-01 DOI: 10.1615/CritRevOncog.2020035666

Rama Rao Malla

引用次数: 2

Growth Factor-Induced Angiogenesis in Hepatocellular Carcinoma. 生长因子诱导的肝细胞癌血管生成。

Critical Reviews in Oncogenesis Pub Date : 2021-01-01 DOI: 10.1615/CritRevOncog.2020035703

Santoshi Muppala

引用次数: 2

Hepatocellular Carcinoma: A Difficult Cancer to Treat. 肝细胞癌:一种难以治疗的癌症。

Critical Reviews in Oncogenesis Pub Date : 2021-01-01 DOI: 10.1615/CritRevOncog.2020036234

Antonella Cusimano, Maurizio Soresi, Giuseppe Montalto, Giuseppa Augello, Maria Rita Emma, Antonina Azzolina, Melchiorre Cervello, Lydia Giannitrapani

{"title":"Hepatocellular Carcinoma: A Difficult Cancer to Treat.","authors":"Antonella Cusimano, Maurizio Soresi, Giuseppe Montalto, Giuseppa Augello, Maria Rita Emma, Antonina Azzolina, Melchiorre Cervello, Lydia Giannitrapani","doi":"10.1615/CritRevOncog.2020036234","DOIUrl":"https://doi.org/10.1615/CritRevOncog.2020036234","url":null,"abstract":"Hepatocellular carcinoma (HCC) is a very peculiar cancer because it presents several molecular alterations linked to the activation of survival and antiapoptotic signal pathways that are protein in form and not easily targetable by even the newest targeted therapies. In addition, it is almost always a consequence of liver cirrhosis, a serious disease condition in which several drugs are often not tolerated. This is why the study of HCC was such a challenge for Professor Natale D'Alessandro, to whom this work is dedicated, during the latter years of his career. The aim of this review is to summarize studies on different molecules involved in the development, progression, and chemoresistance of HCC, topics on which we have focused our research over the last decade. In particular, we have analyzed the role of inflammatory mediators, such as the cyclooxygenase (COX) enzymes, nuclear factor κB (NF-κB), interleukin 6 (IL-6), as well as other important factors, such as Yin Yang 1 (YY1), in HCC. Moreover, we have reviewed some more recent literature on research aimed at identifying druggable targets in HCC as well as candidate agents for its prevention and treatment.","PeriodicalId":35617,"journal":{"name":"Critical Reviews in Oncogenesis","volume":"26 2","pages":"11-25"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39274775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2