Tumor suppressor genes, which signal a cell to stop dividing.

肿瘤抑制基因，向细胞发出停止分裂的信号。

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

因此，癌基因或突变的抑癌基因使细胞不受控制地增长，导致肿瘤发生。

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变慢。

Tumor suppressor genes work by acting as a kind of roadblock, keeping cell division from moving forward.

肿瘤抑制基因通过充当一种障碍来发挥作用，阻止细胞分裂继续发展。

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

你可以把原癌基因看作是加速器或是油门，把抑癌基因看作是刹车。

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

鳞状细胞癌产生于经历了基因突变的鳞状细胞，基因突变可能激活原癌基因、或使抑癌基因失活。

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

为平衡细胞生长，还有其它基因，称作抑癌基因，促进突变细胞的凋亡或细胞死亡。

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。

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。

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抑癌基因的突变，这些基因通常抑制肿瘤生长，因此此类基因突变可导致肌细胞过度生长。

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.

当抑癌基因（如编码蛋白质的p53基因、p16基因、成视网膜母细胞瘤蛋白或称pRb基因）失活时，抑制细胞分裂的机制就被去除了。

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，这些突变是原癌基因突变，会促进细胞分裂；或是抑癌基因突变，导致细胞分裂的正常抑制被解除。

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.

基因突变可能会发生在抑癌基因；抑癌基因的功能是编码、阻断细胞周期，或促进凋亡的蛋白质，所以它算是细胞周期的“刹车片”。

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.

长此以往，和食管鳞癌一样，抑癌基因和原癌基因会积累一系列突变，那些控制着化生细胞的细胞周期的基因突变最终会导致恶性肿瘤。

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.

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

Breast cancer has also been linked to specific mutations in tumor suppressor genes, such as Breast Cancer gene, or BRCA-1 and BRCA-2, and TP53, which normally slow down cell division or make cells die if they divide uncontrollably.

乳腺癌也与一些抑癌基因突变有关，如乳腺癌基因即BRCA-1、BRCA-2，以及TP53：它们可以降低细胞分裂速度或使分裂失控的细胞死亡。

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.

因此，MYCN基因扩增或ALK基因的融合，即致癌基因被激活，或PHOX2B与1号、11号染色体缺失，即抑癌基因的失活，都可能导致细胞生长不受控制。