Oncogenes and Carcinogenesis最新文献

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Introductory Chapter: Interactions between Environmental Chemicals and KRAS Oncogene in Different Cancers - Special Focus on Colorectal, Pancreatic, and Lung Cancers 导论章:环境化学物质与KRAS癌基因在不同癌症中的相互作用-特别关注结直肠癌,胰腺癌和肺癌
Oncogenes and Carcinogenesis Pub Date : 2018-12-07 DOI: 10.5772/INTECHOPEN.82459
P. Erkekoğlu
{"title":"Introductory Chapter: Interactions between Environmental Chemicals and KRAS Oncogene in Different Cancers - Special Focus on Colorectal, Pancreatic, and Lung Cancers","authors":"P. Erkekoğlu","doi":"10.5772/INTECHOPEN.82459","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.82459","url":null,"abstract":"","PeriodicalId":332728,"journal":{"name":"Oncogenes and Carcinogenesis","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130340848","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
MicroRNAs (miRNAs) in Colorectal Cancer 结直肠癌中的MicroRNAs (miRNAs)
Oncogenes and Carcinogenesis Pub Date : 2018-11-07 DOI: 10.5772/INTECHOPEN.80828
Burçin Baran, Nazli Mert Ozupek, G. C. Kocal, Y. Baskın
{"title":"MicroRNAs (miRNAs) in Colorectal Cancer","authors":"Burçin Baran, Nazli Mert Ozupek, G. C. Kocal, Y. Baskın","doi":"10.5772/INTECHOPEN.80828","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.80828","url":null,"abstract":"Colorectal cancer (CRC) is the third most common cancer in the world and third leading cause of cancer-related deaths in men and women as well. While early screening procedures and removal of small polyps improve the survival rates among the patients, there is still need for new diagnostic and therapeutic approaches for developing more effective treatments. MicroRNAs (miRNAs) are short noncoding RNA fragments, which involve in posttranscriptional regulation of gene expression, and they are shown to involve in tumorigenesis either targeting oncogenes or tumor suppressor genes. Based on the current studies, miRNAs are now suggested as potential biomarkers for CRC diagnosis, prognosis, and therapeutic responses. In this chapter, the latest findings on the role of miRNA in CRC in many aspects are reviewed: diagnosis (role of circular miRNAs in blood and miRNAs from tissue biopsies and their potential role in pathophysiology and diagnosis of CRC), prognosis (miRNAs related with metastasis, recurrence, and survival rates in CRC), and therapeutic responses (role of miRNAs both in chemotherapies and/or in targeted therapies in CRC). In conclusion, miRNAs are promising molecules for diagnosis, prognosis, and therapeutic responses of CRC. the microprocessor complex) nucleotide (nt) pre-miRNAs. Pre-miRNA, which is by the nuclear export factor exportin-5, is transferred to the cytoplasm. In the cytoplasm, the cytoplasmic RNase Dicer cleaves the pre-miRNA hairpin to its mature length. Dicer in complex with the transactivation response (TAR) RNA-binding protein (also known as TRBP and TARBP2) and argonaute (AGO) 1–4 mediate the processing of pre-miRNA and the assembly of the RISC (RNA-induced silencing complex). With the formation of this complex structure, one strand of the miRNA duplex is removed and single-stranded miRNA is generated. Interaction complex and target induces posttranscriptional silencing destabilization of and suppression between miR-27b, miR-148a, and miR-326 expression levels and progression-free","PeriodicalId":332728,"journal":{"name":"Oncogenes and Carcinogenesis","volume":"19 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124610769","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
A Molecular Link between the Circadian Clock, DNA Damage Responses, and Oncogene Activation 生物钟、DNA损伤反应和癌基因激活之间的分子联系
Oncogenes and Carcinogenesis Pub Date : 2018-11-05 DOI: 10.5772/INTECHOPEN.81063
Yoshimi Okamoto-Uchida, J. Izawa, J. Hirayama
{"title":"A Molecular Link between the Circadian Clock, DNA Damage Responses, and Oncogene Activation","authors":"Yoshimi Okamoto-Uchida, J. Izawa, J. Hirayama","doi":"10.5772/INTECHOPEN.81063","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.81063","url":null,"abstract":"Circadian clocks enhance the efficiency and survival of living things by organizing their behavior and body functions. There has been a long history of research seeking a link between circadian clock and tumorigenesis. Studies of animal models and human tumor samples have revealed that the dysregulation of circadian clocks is an important endogenous factor causing mammalian cancer development. The core circadian clock regulators have been implicated in the control of both the cell cycle and DNA damage responses (DDR). Conversely, several intracellular signaling cascades that play important roles in regulation of the cell cycle and the DDR also contribute to circadian clock regulation. This review describes selected regulatory aspects of circadian clocks, providing evidence of a molecular link of the circadian clocks with cellular DDR. ROS stimulate intracellular MAPK/ERK signaling pathway, which transduces photic signal to zCry1a expression. The light-induced zCRY1a interacts directly with the zCLOCK:zBMAL complex and modifies its transcriptional capacity. Notably, the zCLOCK:zBMAL complex regulates the transcription of a variety of genes involved in cellular stress responses and DDR. UV component of sunlight induces DNA damage. Light-induced ROS and activation of MAPK/ERK pathway also induce expression of a DNA repair enzyme, zPHR. The induced zPHR repairs UV-damaged DNA in a light-dependent manner.","PeriodicalId":332728,"journal":{"name":"Oncogenes and Carcinogenesis","volume":"94 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132291511","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
Oncogenetics of Lung Cancer Induced by Environmental Carcinogens 环境致癌物诱发肺癌的肿瘤遗传学研究
Oncogenes and Carcinogenesis Pub Date : 2018-11-05 DOI: 10.5772/INTECHOPEN.81064
Victor D. Martinez, Adam P Sage, E. Marshall, Miwa Suzuki, A. A. Goodarzi, G. Dellaire, W. Lam
{"title":"Oncogenetics of Lung Cancer Induced by Environmental Carcinogens","authors":"Victor D. Martinez, Adam P Sage, E. Marshall, Miwa Suzuki, A. A. Goodarzi, G. Dellaire, W. Lam","doi":"10.5772/INTECHOPEN.81064","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.81064","url":null,"abstract":"The molecular landscape of non-tobacco-induced primary lung tumors displays specific oncogenetic features. The etiology of these tumors has been largely associated with exposure to well-established environmental lung carcinogens such as radon, arsenic, and asbestos. Environmental carcinogens can induce specific genetic and epigenetic alterations in lung tissue, leading to aberrant function of lung cancer oncogenes and tumor suppressor genes. These molecular events result in the disruption of key cellular mechanisms, such as protection against oxidative stress and DNA damage-repair, which promotes tumor development and progression. This chapter provides a comprehensive discussion of the specific carcinogenic mechanisms associated with exposure to radon, arsenic, and asbestos. It also summarizes the main protein-coding and non-coding genes affected by exposure to these environmental agents, and the underlying molecular mechanisms promoting their deregulation in lung cancer. Finally, the chapter examines the anticipated challenges in personalized intervention strategies in non-tobacco-induced lung cancer.","PeriodicalId":332728,"journal":{"name":"Oncogenes and Carcinogenesis","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126638117","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
The AIB1/NCOA3/SRC-3 Oncogene AIB1/NCOA3/SRC-3癌基因
Oncogenes and Carcinogenesis Pub Date : 2018-11-05 DOI: 10.5772/INTECHOPEN.80925
Max H Kushner, A. Riegel, G. Sharif
{"title":"The AIB1/NCOA3/SRC-3 Oncogene","authors":"Max H Kushner, A. Riegel, G. Sharif","doi":"10.5772/INTECHOPEN.80925","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.80925","url":null,"abstract":"A member of the NCOA/SRC/p160 co-activator family, AIB1 is amplified and overexpressed in multiple cancer types, notably breast, ovarian, and pancreatic cancer. Common to all members of the NCOA/SRC/p160 family are bHLH-PAS, receptor interaction, and CBP/p300 interacting activation domains. The protein acts as a scaffold to support the transcriptional activity of many DNA binding transcription factors, such as the ER, AP-1, E2F, NF κ B, and TEADs. In doing so, the multi-domain protein facilitates chromatin remodeling and oncogenic gene transcription. Further, the AIB1Δ4 isoform promotes tumorigenesis and metastasis through interaction with chromatin in the nucleus or at the periphery of the cell. Pathologically, AIB1 promotes the transformation of normal tissue to cancerous lesions in multiple diseases, and loss delays progression. AIB1 has also been implicated in cancer recurrence and pharmacological resistance. We will discuss the structure and isoforms of AIB1, the physiological consequences of its interaction with transcription factors and hormone receptors, and clinical significance of the protein.","PeriodicalId":332728,"journal":{"name":"Oncogenes and Carcinogenesis","volume":"29 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130946832","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: 3
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