大多數(shù)人都已經(jīng)知道人類遺傳信息儲(chǔ)存在DNA中，并通過(guò)我們的基因來(lái)表現(xiàn)出來(lái),。但是,，很少有人知道“表觀遺傳學(xué)”，我們的細(xì)胞進(jìn)化出了各種不同的方式，在不改變DNA的情況下來(lái)傳遞可遺傳變化,。
在其他一些情況下,，表觀遺傳對(duì)細(xì)胞與細(xì)胞之間的差異的形成至關(guān)重要，并且也是干細(xì)胞秘密的核心,。
基因組印記（Genomic imprinting）是一種類型的表觀遺傳變化,，能導(dǎo)致特定基因的一個(gè)拷貝被關(guān)閉。表觀遺傳主要通過(guò)基因的甲基化模式的來(lái)起作用,，而不是DNA序列,。這些甲基化模式在從一代傳遞到下一代時(shí)能夠被重置。
研究人員在20多年前就已經(jīng)發(fā)現(xiàn)癌細(xì)胞中的甲基化模式發(fā)生異常,。但是腫瘤細(xì)胞出現(xiàn)異常的方面很多,，但一直很難確定癌癥和表觀遺傳改變之間的精確的直接因果關(guān)系。
現(xiàn)在,，約翰霍普金斯醫(yī)學(xué)院的Andrew Feinberg對(duì)基因組印記有了新的了解,，并且證實(shí)它能夠作為一種癌癥傾向因子。Feinberg分析了一種常見(jiàn)的表觀遺傳變化,。這種變化能夠通常人群中5％－10％的人中發(fā)現(xiàn),，包括一種累胰島素生長(zhǎng)因子基因IGF2上印記的丟失。
IGF2的印記丟失與結(jié)腸癌有關(guān),。在喪失了IGF2印記的小鼠模型中,，F(xiàn)einberg發(fā)現(xiàn)小鼠中腫瘤的發(fā)生頻率增加，這種小鼠的癌癥相關(guān)基因Apc發(fā)生了突變,。在突變Apc小鼠中,，IGF2印記的丟失似乎尤其會(huì)影響成體干細(xì)胞的行為。這或許在結(jié)腸癌風(fēng)險(xiǎn)的增加中起到一定的作用,。
確定人類表觀遺傳標(biāo)記物在未來(lái)將可能成為預(yù)防癌癥的重要策略,。研究人員指出，有關(guān)通過(guò)分析健康人結(jié)腸細(xì)胞中的表觀遺傳變化來(lái)確定結(jié)腸癌風(fēng)險(xiǎn),。
英文原文：
Inheritance outside DNA
Most people have heard that human inheritance is spelled out in our DNA and activated through our genes. Yet few know anything about epigenetics, a variety of methods that our cells have evolved to transmit heritable changes without changing DNA.
Among other things, epigenetics is crucial to differentiation, the process which makes one cell from another, and thus is at the heart of the mystery of stem cells.
Genomic imprinting is a type of epigenetic change that causes one copy of a particular gene to be turned off, depending on its parental origin. It works largely by altering the methylation patterns"the addition or subtraction of methyl groups"around a gene, but not the DNA sequence itself. These methylation patterns are reprogrammed when passed from generation to generation, carrying instructions related to the parent from whom that copy was inherited but without altering the DNA.
Abnormal methylation patterns in cancerous cells were discovered more than 20 years ago. Yet tumor cells have so many things wrong with them, including methylation abnormalities, that a precise cause-and-effect relationship between cancer and epigenetic alterations has been difficult to pin down, says Andrew Feinberg of the John Hopkins School of Medicine, who has been a pioneer in unraveling the epigenetics of cancer.
Now Feinberg has taken a new look at genomic imprinting, as a cancer-predisposing factor. Feinberg analyzed a common epigenetic alteration—found in 5–10 percent of the general population—that involves the loss of imprinting on an insulin-like growth factor gene called IGF2. Loss of imprinting of IGF2 has been associated statistically with individuals who have personal and familial histories of colorectal cancer. Turning to mice that modeled the loss of IGF2 imprinting, Feinberg found an increase in frequency of tumors in mice who also had mutations in a cancer-associated gene called Apc. In the mutant Apc mice, the loss of IGF2 imprinting seems to particularly affect the behavior of the adult stem cells that continually regenerate the colon in mice. This probably plays a role in the increased risk of colon cancer, says Feinberg.
Spotting epigenetic markers like lost IGF2 in humans could be used in future cancer-prevention strategies. Says Feinberg, “It could be possible to screen for colon cancer risk by looking at the epigenetic changes in colon cells of healthy people.”
