American institute for cancer research

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Cancer is, ultimately, a disease of genes. Typically, a series of several mutations is required before a cell becomes a cancer cell. We distinguish between oncogenes, which promote cancer when "switched on" by a mutation, and tumor suppressor genes, which prevent cancer unless "switched off" by a mutation. These mutations can have various causes: radiation or chemicals called carcinogens; some inherited predisposition is not uncommon; some viruses that can cause cancer have also been described. Usually, they carry in their genome some oncogene or tumor suppressor inactivating gene. In about 15% of all cancers, viruses seem to play a role; Bacteria, like Helicobacter pylori, also induce carcinogenesis by a process of chronic inflammation. Finally, damage by free radicals, which are a natural by-product of oxygen metabolism, can cause mutations in the DNA.

For most of the cancers, it cannot be told which event was the initial cause. However, with molecular biology, it is possible to characterize the mutations within a tumor, and to a certain extent predict its behavior. For example, about half of the tumors are deficient in the tumor suppressor gene p53, also known as "the guardian of the genome". This is associated with poor prospects for the patient, since those tumor cells are unlikely to go into apoptosis (programmed cell death) after they are damaged by therapy. There are more mutations that make a tumor more malignant. Telomerase mutations enable a tumor cell to divide indefinitely. Other mutations enable the tumor to grow new blood vessels to feed it, or to detach from the surrounding tissue, spreading to other parts of the body.

In cellular model systems, cells are exposed to carcinogenic influences (chemicals, radiation). In these systems, the first signs of a cell developing into a tumor cell are:

Immortality. The usual number of cell divisions for a mammalian cell is 50-60 (cell senescence), then it ceases to divide. Tumor cells keep dividing forever.
Altered morphology.
Building of cellular clusters (Foci).
Loss of contact inhibition.
Low or no need for growth factors.

Items 2-4 (above) can sometimes be traced to mutations in genes that result in a disruption of cell adhesion. Some cell adhesion proteins are oncogenes.

Romanian Cancer League
Eastern European organization with aims of education, prevention, treatment, support and advocacy.
Manage CINV
Offers patients and professionals information about chemotherapy-induced nausea and vomiting.
Suite 101
Articles and links about cancer treatments.
Mount Zion: Hyperthermia Treatment
Provides information about this treatment and research modality for use in cancer at the University of California at San Francisco.
Untangling The Web
Provides access to disability resources including those needed for cancer care support.

American institute for cancer research