大多数人都已经知道人类遗传信息储存在DNA中，并通过我们的基因来表现出来。但是，很少有人知道“表观遗传学”，我们的细胞进化出了各种不同的方式，在不改变DNA的情况下来传递可遗传变化。
在其他一些情况下，表观遗传对细胞与细胞之间的差异的形成至关重要，并且也是干细胞秘密的核心。
基因组印记（Genomic imprinting）是一种类型的表观遗传变化，能导致特定基因的一个拷贝被关闭。表观遗传主要通过基因的甲基化模式的来起作用，而不是DNA序列。这些甲基化模式在从一代传递到下一代时能够被重置。
研究人员在20多年前就已经发现癌细胞中的甲基化模式发生异常。但是肿瘤细胞出现异常的方面很多，但一直很难确定癌症和表观遗传改变之间的精确的直接因果关系。
现在，约翰霍普金斯医学院的Andrew Feinberg对基因组印记有了新的了解，并且证实它能够作为一种癌症倾向因子。Feinberg分析了一种常见的表观遗传变化。这种变化能够通常人群中5％－10％的人中发现，包括一种累胰岛素生长因子基因IGF2上印记的丢失。
IGF2的印记丢失与结肠癌有关。在丧失了IGF2印记的小鼠模型中，Feinberg发现小鼠中肿瘤的发生频率增加，这种小鼠的癌症相关基因Apc发生了突变。在突变Apc小鼠中，IGF2印记的丢失似乎尤其会影响成体干细胞的行为。这或许在结肠癌风险的增加中起到一定的作用。
确定人类表观遗传标记物在未来将可能成为预防癌症的重要策略。研究人员指出，有关通过分析健康人结肠细胞中的表观遗传变化来确定结肠癌风险。
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.”
