Tumor development is initiated by an accumulation of genetic and epige的中文翻譯

Tumor development is initiated by a

Tumor development is initiated by an accumulation of genetic and epigenetic alterations, which promote tumor initiation, invasion and metastasis (1,2). During the development of human neoplasms, the hallmarks of cancer are acquired, including the sustainment of proliferative signaling, the evasion of growth suppressors, the resistance to cell death, the enabling of replicative immortality, the induction of angiogenesis, the activation of invasion and metastasis, genome instability and mutations, the tumor promotion of inflammation, the deregulation of cellular energetics and the avoidance of immune destruction. These hallmarks aid in our understanding of the diversity of neoplastic disease (3). With the continuous development of cancer research, our understanding of the molecular pathogenesis of cancer has been enhanced. Increasing efforts in cancer research have been focused on the study of oncogenes, tumor suppressors and signaling pathways. Since the development of a more in‑depth understanding of the molecular etiology of carcinogenesis, specific oncogenes have been identified and have led to the generation of ‘molecular‑targeted therapy’ (4). The development of a ‘pan‑cancer’ therapy may be possible by targeting an oncogene which is ubiquitously overexpressed in almost all types of cancer and has a regulatory role in the multistep processes of carcinogenesis (5).
A novel gene that has been identified is AEG‑1 [also known as Metadherin (MTDH) and Lysine‑rich CEACAM1 co‑isolated (LYRIC)], which has emerged as a potentially crucial mediator of malignant tumors, and a key converging point of a complex network of oncogenic signaling pathways (6,7). AEG‑1/MTDH presents as an ideal target for the development of the next generation of effective cancer therapeutics
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結果 (中文) 1: [復制]
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肿瘤的发展是由遗传和表观遗传的改变,促进肿瘤的发生、 侵袭和转移 (1,2) 积累发起的。在人类肿瘤的发展,收购癌症,包括增殖信号转导机制的维持、 生长抑制的逃税、 抗细胞死亡,使复制不朽,诱导的血管生成、 侵袭和转移、 基因组不稳定和突变激活、 炎症肿瘤促进、 细胞能量的放松管制和避免免疫破坏。这些特点帮助我们理解肿瘤性疾病 (3) 的多样性。癌症研究的不断发展,加强了我们对癌症的分子发病机制的理解。增加在癌症研究方面已集中的癌基因、 肿瘤抑制因子和信号通路的研究。以来更多的深入了解,癌变的分子病因的发展,特定基因已确定,导致 molecular‑targeted 疗法的一代 (4)。'Pan‑cancer' 疗法的发展可能通过靶向基因无处不在几乎所有类型的癌组织中高表达,癌变 (5) 多步过程中具有调节作用。已发现的新基因是 AEG‑1 [也被称为 Metadherin (MTDH) 和 Lysine‑rich CEACAM1 co‑isolated (抒情)],这已成为潜在关键的调解人的恶性肿瘤和致癌的信号通路 (6.7) 复杂网络关键的交汇点。AEG‑1/MTDH 提出了作为一个理想的目标,为下一代的有效的癌症疗法的发展
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