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

随着突，原癌基因为癌基因，这些癌基因过度刺激细胞生长。

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

致癌基因加速细胞生长增殖，而抑癌基因使细胞生长增殖慢。

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

因此，癌基因或突的抑癌基因使细胞不受控制地增长，导致肿瘤发生。

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

梭杆属是口腔中另一种会引发过度免疫应答、激活癌基因的细。

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

当原癌基因（如表皮生长因受体基因、RAS基因）被激活时，它成了促进细胞分裂的癌基因。

One new treatment relies on a test to identify damaged genes called oncogenes that allow cancer cells to grow and spread.

一种新疗法是识别出名为致癌基因的破损基因，这种基因能使得癌细胞发展和蔓延。

The second crucial mutation can happen in your  oncogenes.

第二个关键突可能发生在你的原癌基因中。

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

当原癌基因被激活时，细胞会被指令快速增殖。

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

当你的原癌基因发生异时，它基本上会重新激活。

If several oncogenes are driven into action, the cell, unable to turn them off, becomes cancerous.

如果几个致癌基因被激活，细胞无法关闭它，会成癌细胞。

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

所以如果例如，你的原癌基因重新激活，它会产生原癌蛋白。

Anything from cosmic rays to radiation to diet may activate a dormant oncogene, but how remains unknown.

从宇宙射线到辐射再到饮食，任何因素都可能激活一个休眠的致癌基因，但具体机制仍然未知。

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

当活性癌基因表达或肿瘤抑制基因丢失时，可发生异常细胞分裂。

Oncologist Mark Kris from Memorial Sloan Kettering Cancer Center led a study that examined the role oncogenes play in the spread of cancer.

史隆凯特林癌症中心的肿瘤专家马克·克里斯负责了一项检验致癌基因在癌症蔓延中所起作用的研究。

The results showed that patients whose driver oncogenes were specifically targeted lived, on average, a year longer than those who received standard chemotherapy.

结果显示其致癌基因因得到针对性地治疗的患者存活了，平均来说他比那些接受标准疗的患者多活一年。

52 This suggests oncogene addiction, as seen occasionally and originally when first-generation EGFR-TKIs were withdrawn from patients with EGFR mutations.

52 这表明致癌基因成瘾，正如最初在从 EGFR 突患者体内撤回第一代 EGFR-TKI 时偶尔看到的那样。

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

与 NSCLC 中的其他靶向癌基因驱动因素不同，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。

But if it happens in certain genes that are important in cancer, like oncogenes or tumor suppressor genes, it can create deadly cancers like skin cancer.

但是如果它发生在某些对癌症很重要的基因中，比如致癌基因或肿瘤抑制基因，它会产生致命的癌症，比如皮肤癌。

These activate oncogenes, genes with the capacity to cause cancer, which drive abnormal cell proliferation or deactivate the body's natural tumour suppressor genes.

这些物质会激活致癌基因， 即那些具有引发癌症能力的基因，它推动异常细胞增殖， 或使人体天然的肿瘤抑制基因失活。

The result is that the cell receives a constant message to divide. This dominant " gain of function gene" is often called an oncogene.

结果是细胞接收一个恒定的息进行不断分裂。这种显性的" 获得功能基因" 通常被称为癌基因。