The human body is composed of trillions of cells, each responsible for regulating their respective life cycles. Mutations within genes—or the non-coding sequences that regulate them—accountable for growth, division, and programmed cell death can cause normal cells to ignore their regulatory rules and begin dividing rapidly and uncontrollably.

Cancer can start nearly anywhere. These renegade cells propagate in number and can form tumors, invade surrounding areas, and spread through blood and lymphatic systems to colonize organs and tissues far from their origin.

No two cancers are genetically identical, but all cancers arise from changes or mutations in DNA that impact proper cell function. Cancer or an increased risk of developing cancer may be due to random errors during cell division, DNA damage from environmental or dietary factors, or inherited gene mutations (approximately 5%-10%). Pinpointing the precise mutation in DNA that results in cancer is not always possible which may complicate targeted treatment therapies.

Types of genes that may contribute to cancer or increased cancer risk include genes involved in cell growth (proto-oncogenes), genes that regulate cell division (tumor suppressors), and those that repair damaged DNA. Both proto-oncogenes and tumor suppressor genes are well categorized subtypes that govern normal cell growth, division, and apoptosis (programmed cell death), yet when they are mutated, they can lead to uncensored cell division. The best studied tumor suppressor and DNA repair gene, p53, when mutated can cause cells to become cancerous.

Cancer is categorized by which type of cell or system it originates in. According to the National Cancer Institute, carcinomas, the most common types of cancer, begin in cells lining the inside and outside surfaces of organs and include breast, colon, stomach, lung, bladder, and kidney cancer. Sarcomas form in bone and tissues like muscle, fat, and tendons. Leukemia originates in bone marrow and results in the proliferation of abnormal white blood cells. There are many other classes including lymphoma, myeloma, melanoma, and cancers of the brain and spine.

Early detection is likely the best indicator of a positive prognosis or cure. However, with hundreds of different cancers, their classification based on which body system is impacted may make certain types more aggressive or difficult to detect or treat.

Different types of cancer frequently require different treatment regimens, with a combination-based approach being most common. Sometimes a specific treatment type may be effective on multiple cancers due to shared genetic commonalities, while specialized treatments are necessary to target uncommon cancers.

Treatment and prevention can be correlated for the small percentage of heritable cancers. For example, treatment for women carrying a BRCA gene (implicated in breast and ovarian cancer) may include frequent screening or prophylactic surgery.

The World Health Organization estimates that nearly half of all cancers can be prevented. Cigarette smoking, proven beyond doubt by a wealth of data, is the leading cause of lung cancer. Additional methods to remediate the likelihood of developing cancer include maintaining a healthy diet and weight, liberal application of sunscreen to prevent skin cancer, exercising regularly, and limiting or avoiding consuming alcohol and other substances.

While a cancer-free world may be decades in the future, research has led to a better understanding of the disease and more effective treatments for many individuals. Several scientists at the Stowers Institute are engaged in increasing our understanding of how our genome, genes, and proteins are regulated for normal cellular function to help explain how these regulatory mechanisms are disrupted in cancer. Learn more about the research related to cancer in each of our labs by watching the videos on this page.