Osteosarcoma Biology

This information has been written for patients, their families and friends, and the general public to help them understand more about osteosarcoma: what it is and the different types. This information is produced in accordance with BCRT's information policy.

How do bone cells become cancerous (malignant)?

Doctors and scientists do not yet fully understand what causes a normal bone cell to become cancerous. It is known that cells contain important information in their genes, which instruct the cells to divide and grow in a highly regulated way. Damage to these genes can cause the cell to behave differently and grow abnormally, which can then lead to cancer

Doctors and scientists all over the World are involved in research to try to understand the difference between normal bone cells and osteosarcoma cells. This will enable them to find treatments, which can target the abnormal osteosarcoma cells rather than normal cells in the body.

BCRT raises money to fund research into improving the outcomes of people affected by primary bone cancer. This includes investigating why primary bone cancers start and trying to identify new targets for treatment.

Some people are known to have inherited damaged genes, which can cause them to have an increased risk of developing a cancer, including osteosarcoma. Some examples of this are in the section about risk factors for osteosarcoma.

The authors and reviewers of this information are committed to producing reliable, accurate and up to date content reflecting the best available research evidence, and best clinical practice. We aim to provide unbiased information free from any commercial conflicts of interest. This article is for information only and should not be used for the diagnosis or treatment of medical conditions. BCRT can answer questions about primary bone cancers, including treatments and research but we are unable to offer specific advice about individual patients. If you are worried about any symptoms please consult your doctor.

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Version 2 produced January 2013
Information will be reviewed in January 2015

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