In a healthy cell, tumor suppressor genes act as the gatekeepers that control cell growth and proliferation and promote cell apoptosis.

Hence, when a tumor suppressor gene is inactivated, cells may start growing out of control leading to cancer.

Fortunately, in most cases, the inactivation of a single allele of a tumor suppressor gene does not lead to tumor progression. Both of the alleles must lose their function for the cells to become cancerous.

Such loss of function mutations in tumor suppressor genes can be caused by genetic alterations such as point mutations, chromosomal deletion, or errors in chromosome segregation.

However, a few epigenetic changes can also permanently inactivate the tumor suppressor genes. For example, if a gene undergoes modifications in its promoter region or gets packaged into the heterochromatin region of a chromosome, it can make irreversible and heritable changes to the gene expression pattern.

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.

When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell cycle. It's only when both the copies of the gene are inactivated or lost that the cells lose control and become cancerous.

Some common tumor suppressor genes that have implications in human cancer include TP53, Rb, INK4, PTEN, APC, BRCA1/BRCA2, and MADR2. Loss of function mutations in these tumor suppressor genes has implications in many types of cancers, including ovarian, lung, colorectal, head and neck, pancreatic, uterine, breast, and bladder cancer.

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