{"title":"口腔鳞状细胞癌中凋亡基因的启动子超甲基化","authors":"A. kumar Jha","doi":"10.19080/ctoij.2019.13.555872","DOIUrl":null,"url":null,"abstract":"Cancer stands among the foremost advanced human diseases with multiple levels of regulation. Despite the numerous progress that has been created in basic and clinical analysis, the incidence associated mortality rates related to malignant pathologies are still at high levels with an expected raised rate within the next fifteen years Irimie et al. [1]. The sixth most typical malignancy that has been found is Head and Neck cancer, wherever carcinoma represents the foremost frequent subtype inside this spectrum Irimie et al. [2], Hema et al. [3]. Also, Oral Squamous Cell Carcinoma (OSCC) accounts for roughly ninetieth of the oral subtype, being far and away the foremost common sort of malignancy inside the mouth Parkin et al. [4], Stewart et al. [5]. Apoptosis is that one pathway that could lead the elimination of oncogenic cells. Apoptosis can be explained as a process in which natural death of cells is initiated to maintain the cellular homeostasis. A variety of changes are done in the structure of cells by apoptotic proteins that eliminate the cell out of body. In this mechanism events occurs which result into formation of cascades that encounters the already anteceding cells leading them to demise, also known as “programmed cell death”, Elmore [6], Hervouet et al. [7]. The initiation and maturation of oral carcinoma caused by total of genetic changes combined with environmental risk factors (special mention to alcohol and tobacco use however various viral infectious agents and persistent inflammations) cause changes within the pursuit of cancer causing genes i.e., oncogenes and tumour suppressor genes Perez et al. [8], Irimie et al. [9].","PeriodicalId":9575,"journal":{"name":"Cancer Therapy & Oncology International Journal","volume":"11 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Promoter Hypermethylation of Apoptotic genes in Oral Squamous Cell Carcinoma\",\"authors\":\"A. kumar Jha\",\"doi\":\"10.19080/ctoij.2019.13.555872\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Cancer stands among the foremost advanced human diseases with multiple levels of regulation. Despite the numerous progress that has been created in basic and clinical analysis, the incidence associated mortality rates related to malignant pathologies are still at high levels with an expected raised rate within the next fifteen years Irimie et al. [1]. The sixth most typical malignancy that has been found is Head and Neck cancer, wherever carcinoma represents the foremost frequent subtype inside this spectrum Irimie et al. [2], Hema et al. [3]. Also, Oral Squamous Cell Carcinoma (OSCC) accounts for roughly ninetieth of the oral subtype, being far and away the foremost common sort of malignancy inside the mouth Parkin et al. [4], Stewart et al. [5]. Apoptosis is that one pathway that could lead the elimination of oncogenic cells. Apoptosis can be explained as a process in which natural death of cells is initiated to maintain the cellular homeostasis. A variety of changes are done in the structure of cells by apoptotic proteins that eliminate the cell out of body. In this mechanism events occurs which result into formation of cascades that encounters the already anteceding cells leading them to demise, also known as “programmed cell death”, Elmore [6], Hervouet et al. [7]. The initiation and maturation of oral carcinoma caused by total of genetic changes combined with environmental risk factors (special mention to alcohol and tobacco use however various viral infectious agents and persistent inflammations) cause changes within the pursuit of cancer causing genes i.e., oncogenes and tumour suppressor genes Perez et al. [8], Irimie et al. 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引用次数: 0
摘要
癌症是人类最先进的疾病之一,具有多层次的调控。尽管在基础和临床分析方面取得了许多进展,但与恶性病理有关的发病率和死亡率仍然很高,预计在今后15年内还会上升。已发现的第6个最典型的恶性肿瘤是头颈癌,其中癌是该光谱中最常见的亚型(Irimie et al. [3], Hema et al.[3])。此外,口腔鳞状细胞癌(Oral Squamous Cell Carcinoma, OSCC)约占口腔亚型的90%,是口腔内最常见的恶性肿瘤(Parkin et al. bbb, Stewart et al. bbb)。细胞凋亡是导致致癌细胞消失的一种途径。细胞凋亡可以解释为细胞自然死亡以维持细胞内稳态的过程。凋亡蛋白将细胞排除体外,从而使细胞结构发生多种变化。在这一机制中,发生的事件导致级联反应的形成,这些级联反应与已经在前面的细胞相遇,导致它们死亡,也被称为“程序性细胞死亡”。口腔癌的发生和成熟是由遗传变化和环境风险因素(特别提到酒精和烟草的使用,但各种病毒感染因子和持续炎症)引起的,在追求致癌基因,即致癌基因和肿瘤抑制基因(Perez et al. [8], Irimie et al.[8])的过程中发生变化。
Promoter Hypermethylation of Apoptotic genes in Oral Squamous Cell Carcinoma
Cancer stands among the foremost advanced human diseases with multiple levels of regulation. Despite the numerous progress that has been created in basic and clinical analysis, the incidence associated mortality rates related to malignant pathologies are still at high levels with an expected raised rate within the next fifteen years Irimie et al. [1]. The sixth most typical malignancy that has been found is Head and Neck cancer, wherever carcinoma represents the foremost frequent subtype inside this spectrum Irimie et al. [2], Hema et al. [3]. Also, Oral Squamous Cell Carcinoma (OSCC) accounts for roughly ninetieth of the oral subtype, being far and away the foremost common sort of malignancy inside the mouth Parkin et al. [4], Stewart et al. [5]. Apoptosis is that one pathway that could lead the elimination of oncogenic cells. Apoptosis can be explained as a process in which natural death of cells is initiated to maintain the cellular homeostasis. A variety of changes are done in the structure of cells by apoptotic proteins that eliminate the cell out of body. In this mechanism events occurs which result into formation of cascades that encounters the already anteceding cells leading them to demise, also known as “programmed cell death”, Elmore [6], Hervouet et al. [7]. The initiation and maturation of oral carcinoma caused by total of genetic changes combined with environmental risk factors (special mention to alcohol and tobacco use however various viral infectious agents and persistent inflammations) cause changes within the pursuit of cancer causing genes i.e., oncogenes and tumour suppressor genes Perez et al. [8], Irimie et al. [9].