Proto-oncogenes, which signal a cell to grow and divide.

原基因，向发出生长的信号。

Now, there are genes that promote normal cell growth called proto-oncogenes.

这时，有一些促进正常生长的基因被称作原基因。

With mutations, proto-oncogenes become oncogenes, and these overstimulate the cell growth.

随着突变，原基因变为基因，这些基因过度刺激生长。

Oncogenes help cells grow and proliferate, while tumor suppressor genes slow down cell growth and proliferation.

致基因加速生长增殖，而抑基因使生长增殖变慢。

Fusobacteria is another genus of bacteria in the mouth that produces excessive immune responses and activates oncogenes.

梭菌属是口腔中另一种会引发过度免疫应答、激活基因的菌。

You can think of proto-oncogenes as the accelerator or gas pedal and tumor suppressor genes as the brakes.

你可以把原基因看作是加速器或是油门，把抑基因看作是刹车。

So oncogenes or mutated tumor suppressor genes allow cells to keep growing uncontrollably resulting into tumors.

因此，基因或突变的抑基因使不受控制地增长，导致肿瘤发生。

Squamous cell cancers arise from squamous cells that undergo genetic mutations that either activate proto-oncogenes or inactivate tumor suppressor genes.

鳞状产生于经历了基因突变的鳞状，基因突变可能激活原基因、或使抑基因失活。

So if for example, your oncogenes switch back  on, they make oncogene proteins.

例如，如果您的基因重新启动，它们就会产生基因蛋白质。

The second crucial mutation can happen in your  oncogenes.

第二个关键突变可能发生在基因中。

When proto-oncogenes, like epidermal growth factor receptor and RAS, are activated, it turns them into oncogenes that promote cell division.

当原基因（如表皮生长因子受体基因、RAS基因）被激活时，它们就变成了促进的基因。

When oncogenes are turned on the cell is told to multiply rapidly.

当基因被打开时，就会迅速繁殖。

When your oncogenes get corrupted,   they basically turn on again.

当你的基因被破坏时，它们基本上会再次开启。

To balance out cell growth, there are other genes called tumor suppressor genes which promote apoptosis or cell death of mutated cells.

为平衡生长，还有其它基因，称作抑基因，促进突变的凋亡或死亡。

Abnormal cell division can occur either when active oncogenes are expressed or when tumor suppressor genes are lost.

当活性基因表达或肿瘤抑制基因丢失时，可发生异常。

This type of gene is called an anti-oncogene or tumor suppressor gene.

这种类型的基因被称为抗基因或肿瘤抑制基因。

Checking for the presence of mutations in a gene can confirm a diagnosis that is based on other clinical presentations.

在症的病例中，了解哪个基因发生了突变以及以什么样的方式发生突变，能够确定最佳治疗方案以及为开发新的治疗方法提供信息。

Or they can occur in proto-oncogenes, which normally code for proteins that promote the cell cycle - so they're the cell cycle's accelerator pedal.

基因突变也可以发生在原基因；原基因的功能是编码促进周期运转的蛋白质，所以它算是周期的“油门”。

Unlike other targetable oncogene drivers in NSCLC, KRAs G12C is most common in smokers Until recently, KRAS was an undruggable target.

与 NSCLC 中的其他靶向基因驱动因素不同，KRA G12C 在吸烟者中最常见。直到最近，KRAS 仍是一个不可药物治疗的靶点。

It usually involves several genetic mutations in endometrial cells, including of PTEN, a tumor suppressor gene; PIK3CA, an oncogene; and ARID1A, a gene regulating chromatin structure.

它通常涉及子宫内膜的几种基因突变，包括抑基因PTEN、原基因PIK3CA，及调控染色质结构的基因ARID1A。