There seem to be two categories of genes involved in cancer: oncogenes, which code for proteins to regulate cell growth, and should not be stuck "on," much like the accelerator in a car; and tumor-suppressor genes, which work like the brakes on a car and must function! Let's begin with a look at the ras gene, which codes for a G protein and is an oncogene. Explain how a ras mutation leads to cancer

Two of the main types of genes involved in cancer are:

- Oncogenes, which include ras genes that code for proteins to regulate cell growth, and should not be stuck "on," much like the accelerator in a car; and

- Tumor-suppressor genes, which are normal genes that slow down cell division, like the brakes must function on a car. They repair DNA mistakes, programming cells death through a process called apoptosis. When tumor suppressor genes don't work properly, cells can grow out of control, which can lead to cancer.

Explanation:

Let's begin with a look at the oncogenes and a family within these genes called Ras. These genes are a bynary molecular GTP-binding protein, as protein G, that sends the growth signal to the nucleus; when a cell surface receptor is activated by the tyrosine kinases to grow, it transmits the signal to Ras. After the signal has been sent, GTP is hydrolyzed to GDP, and Ras becomes inactive once again. They are responsible for the signals transduction path in cells, as actin cytoskeletal integrity, cell proliferation, cell differentiation, cell adhesion, apoptosis, and cell migration that control the amount of cells growth that is allowed at any time, so mutations on Ras-regulated signal pathways controlling intracellular signaling networks can lead to cancer, switching Ras proteins function.

Members of the RAS gene family include KRAS, HRAS, and NRAS.

Note that there is an important difference between oncogenes that can cause cancer resulting from activation and tumor suppressor genes when they are inactivated.