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

原癌基，胞发出和分裂的信号。

Now, interestingly, when scientists looked at the genome of elephants, for one particular tumor suppressor gene, they had 20 copies of it, and we have just one copy of it.

有趣的是，当科学家们查看大象的基组时，对于一个特定的抑癌基，它们有 20 个副本，而我们只有一个副本。

Over time, just like with squamous cell carcinoma, mutations might accumulate in either tumor suppressor genes or proto-oncogenes that control the division of these metaplastic cells, ultimately resulting in a malignant tumor.

此以往，和食管鳞癌一样，抑癌基和原癌基会积累一系列突变，那些制着化胞的胞周期的基突变最终会导致恶性肿。

Typically these are mutations in proto-oncogenes which results in a promotion of cell division, or mutations in tumor suppressor genes which results in a loss of inhibition of cell division.

通常，这些突变是原癌基突变，会促进胞分裂；或是抑癌基突变，导致胞分裂的正常抑制被解除。

And this is due to mutations in the TSC1 or TSC2 tumor suppressor genes, genes that usually suppress tumor growth, therefore a mutation leads to myocyte overgrowth.

由于TSC1和TSC2抑癌基的突变，这些基通常抑制肿，此此类基突变可导致肌胞过度。

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

致癌基加速胞增殖，而抑癌基使胞增殖变慢。

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

梭杆菌属是口腔中另一种会引发过度免疫应答、激活癌基的菌。

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

此，癌基或突变的抑癌基使胞不受制地增，导致肿发。

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

这时，有一些促进正常胞的基被称作原癌基。

So both an MYCN amplification or ALK gene fusion, where the oncogene is " turned on, " or a PHOX2B and chromosome 1 and 11 deletions, where tumor suppressor genes are " turned off, " can potentially cause uncontrolled cell growth.

此，MYCN基扩增或ALK基的融合，即致癌基被激活，或PHOX2B与1号、11号染色体缺失，即抑癌基的失活，都可能导致胞不受制。

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（如表皮子受体基、RAS基）被激活时，它们就变成了促进胞分裂的癌基。

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

你可以把原癌基看作是加速器或是油门，把抑癌基看作是刹车。

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

随着突变，原癌基变为癌基，这些癌基过度刺激胞。

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

鳞状胞癌产于经历了基突变的鳞状胞，基突变可能激活原癌基、或使抑癌基失活。

Mutations can occur in tumor suppressor genes, which normally code for proteins that stop the cell cycle or promote apoptosis - so they're the cell cycle's very own brake pedal.

基突变可能会发在抑癌基；抑癌基的功能是编码、阻断胞周期，或促进凋亡的蛋白质，所以它算是胞周期的“刹车片”。

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

为平衡胞，还有其它基，称作抑癌基，促进突变胞的凋亡或胞死亡。

But even though they are dividing, these polyps only become malignant - meaning they only invade nearby tissues if there are additional mutations in other tumor suppressor genes like the p53 gene or in proto-oncogenes like K-RAS.

但即便上皮胞在不断增殖，只有当另外的抑癌基（如p53基或K-RAS基）也同时突变时，这些息肉才会恶变，侵犯周围组织。

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.

基突变也可以发在原癌基；原癌基的功能是编码促进胞周期运转的蛋白质，所以它算是胞周期的“油门”。

And when tumor suppressor genes, like the genes that encode proteins p53, p16, and the retinoblastoma protein, also called pRb, are inactivated, it removes the inhibition to cell division.

当抑癌基（如编码蛋白质的p53基、p16基、成视网膜母胞蛋白或称pRb基）失活时，抑制胞分裂的机制就被去除了。

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

当原癌基被激活时，胞就会被指令快速增殖。