Biswal Biranchi Narayan, Das Surya Narayan, Das Bijoy Kumar, Rath Rachna
Department of Oral Pathology and Microbiology, S.C.B. Dental College and Hospital, Cuttack, Odisha, India.
J Oral Maxillofac Pathol. 2017 May-Aug;21(2):244-251. doi: 10.4103/jomfp.JOMFP_60_17.
Transformation of a normal cell into a cancerous phenotype is essentially backed by genetic mutations that trigger several oncogenic signaling pathways. These signaling pathways rewire the cellular metabolism to meet the bioenergetic and biomass requirement of proliferating cell, which is different from a quiescent cell. Although the change of metabolism in a cancer cell was observed and studied in the mid-20 century, it was not adequate to explain oncogenesis. Now, equipped with a revolution of oncogenes, we have a genetic basis to explain the transformation. Through several studies, it is clear now that such metabolic alterations not only promote cancer progression but also contribute to the chemoresistance of cancer. Targeting specific enzymes and combinations of enzymes can improve the efficacy of cancer therapy and help to overcome the therapeutic resistance.
正常细胞向癌性表型的转变本质上是由引发多种致癌信号通路的基因突变所支持的。这些信号通路重新连接细胞代谢，以满足增殖细胞的生物能量和生物量需求，这与静止细胞不同。尽管癌细胞代谢的变化在20世纪中叶就已被观察和研究，但这不足以解释肿瘤发生。现在，随着癌基因研究的革新，我们有了一个解释这种转变的遗传基础。通过多项研究，现在很清楚，这种代谢改变不仅促进癌症进展，还导致癌症的化疗耐药性。靶向特定酶和酶的组合可以提高癌症治疗的疗效，并有助于克服治疗耐药性。
