醫(yī)學界至今仍不斷研究根治癌癥方法,，年僅27歲的香港小子梁子宇，透過老鼠胚胎干細胞和基因研究,，首次發(fā)現(xiàn)將癌癥連根拔起的曙光,。他發(fā)現(xiàn)，透過控制一種名為ESET的蛋白,，便可將致癌干細胞殲滅而不影響正常細胞,，是啟發(fā)根治癌癥的新突破。報告已于4月8日出版的國際權(quán)威科學期刊《自然》(Nature)上發(fā)表,。
據(jù)香港明報報道,，本身也從事基因研究的香港大學校長徐立之對此研究也感可喜，并指香港極需此類優(yōu)秀人才回流,。
梁子宇的父親是香港執(zhí)業(yè)西醫(yī),，但他并無繼承父業(yè)讀醫(yī)，而是自創(chuàng)新天地,。他13歲隨家人移居加拿大,，在當?shù)赝瓿芍袑W課程后，先后考入英國倫敦大學學院 (UCL)和倫敦帝國學院(IC)學士及碩士畢業(yè),，一直鉆研香港較冷門的基因研究,，專注“表觀基因?qū)W”。3年前他返回加拿大在英屬哥倫比亞大學(UBC)攻讀博士課程至今,。
他透過長途電話接受訪問時說,，“香港的確是少人研究此學科，但正因為少,，就應該去做,。”梁子宇擁有一顆赤子心，希望透過所學知識,，研究出治療疾病的新突破,，造福病人。
“現(xiàn)時治療癌癥的傳統(tǒng)方法,，是將腫瘤切除,，然后做化療、電療等,，但化療和電療除會將癌細胞殺死,，就連一些正常的細胞也被殺死；我們的發(fā)現(xiàn)可針對致癌的干細胞,，做到清除癌細胞但不影響正常細胞,。”他與日本京都大學一名也是30出頭的研究員松井稔幸研究以往較少人關(guān)注的蛋白“ESET”,，找到根治癌癥的曙光,。
年紀輕輕便在國際科學舞臺露光芒，被問及是否已有香港的大學向他招手，梁子宇說,，確有香港的大學教授找他,，但他指自己仍未博士畢業(yè),，回流加盟是言之尚早,。
梁子宇“放洋”多年，但家在香港,，每年放假也會回港,，對這片土地很有歸屬感。他立下決心,，學成后一定回來作貢獻,，但不會是短期內(nèi)的事。“我想在國外從事研究一段時間,，希望有一番成績后,，才返香港領(lǐng)導研究隊伍從事研究。”
港大校長徐立之表示,，香港年輕人能在科研上有成就并獲國際認同,，值得恭喜，港大當然有興趣汲納世界各地不同年齡和學科的優(yōu)秀人才,，而香港本身也有很多優(yōu)秀的科學家,。（生物谷Bioon.com)
相關(guān)專題：癌癥干細胞
生物谷推薦原文出處：
Nature doi:10.1038/nature08858;
Proviral silencing in embryonic stem cells requires the histone methyltransferase ESET
Toshiyuki Matsui1,2,5, Danny Leung3,5, Hiroki Miyashita1,2, Irina A. Maksakova3, Hitoshi Miyachi1, Hiroshi Kimura4, Makoto Tachibana1,2, Matthew C. Lorincz3 & Yoichi Shinkai1,2
1Experimental Research Center for Infectious Diseases, Institute for Virus Research, and,
2Graduate School of Biostudies, Kyoto University, 53 Shogoin, Kawara-cho, Sakyo-ku, Kyoto 606-8507, Japan
3Department of Medical Genetics, Life Sciences Institute, The University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada
4Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan
5These authors contributed equally to this work.
Endogenous retroviruses (ERVs), retrovirus-like elements with long terminal repeats, are widely dispersed in the euchromatic compartment in mammalian cells, comprising ~10% of the mouse genome1. These parasitic elements are responsible for >10% of spontaneous mutations2. Whereas DNA methylation has an important role in proviral silencing in somatic and germ-lineage cells3, 4, 5, an additional DNA-methylation-independent pathway also functions in embryonal carcinoma and embryonic stem (ES) cells to inhibit transcription of the exogenous gammaretrovirus murine leukaemia virus (MLV)6, 7, 8. Notably, a recent genome-wide study revealed that ERVs are also marked by histone H3 lysine 9 trimethylation (H3K9me3) and H4K20me3 in ES cells but not in mouse embryonic fibroblasts9. However, the role that these marks have in proviral silencing remains unexplored. Here we show that the H3K9 methyltransferase ESET (also called SETDB1 or KMT1E) and the Krüppel-associated box (KRAB)-associated protein 1 (KAP1, also called TRIM28)10, 11 are required for H3K9me3 and silencing of endogenous and introduced retroviruses specifically in mouse ES cells. Furthermore, whereas ESET enzymatic activity is crucial for HP1 binding and efficient proviral silencing, the H4K20 methyltransferases Suv420h1 and Suv420h2 are dispensable for silencing. Notably, in DNA methyltransferase triple knockout (Dnmt1-/-Dnmt3a-/-Dnmt3b-/-) mouse ES cells, ESET and KAP1 binding and ESET-mediated H3K9me3 are maintained and ERVs are minimally derepressed. We propose that a DNA-methylation-independent pathway involving KAP1 and ESET/ESET-mediated H3K9me3 is required for proviral silencing during the period early in embryogenesis when DNA methylation is dynamically reprogrammed.
