New clues to mechanism of thyroid cancer

Thyroid cancer occurs when abnormal cells grow in the thyroid gland, an organ that makes hormones to regulate heart rate, blood pressure, body temperature and weight. The cancer is relatively uncommon compared to other cancers. Most patients do very well because the cancer is usually found early and treatment works well. Women are much more likely to have thyroid cancer than men. Thyroid cancer can affect people of all ages, but it is most common in people after the age of 30. The aggressiveness of thyroid cancer increases significantly in older patients.

A research appearing in Proceedings of the National Academy of Sciences now reveals a new genetic mechanism of thyroid cancer and a biomarker that can help predict response to treatment. The research, conducted by scientists from the University of Pittsburgh, Zhejiang University, and Affymetrix, would have profound complications in the intervention of many types of cancer.

Although the precise mechanism of thyroid cancer is not clear, the presence of genetic changes contributes to disease progression. Genetic mutations allow cells to grow and divide rapidly, and the cells eventually become cancerous and form a tumor. In severe cases, the cancer cells metastasize to other parts of the body. Approximately 90% of all thyroid cancer cases are driven by known genetic alterations, whereas driver mutations in the remaining tumors are unknown.

The aim of the new study is to find new genetic alterations related to the cancer. Yuri E. Nikiforov, who led the study, and co-workers focused on papillary thyroid carcinomas, the most common type of the thyroid gland that comprises up to 80% of all thyroid cancer cases. Using whole-transcriptome and whole-genome analyses, they examined a series of papillary thyroid carcinomas that had no known mutations. They identified a genetic alteration involving fusion of the THADA gene to a region near the IGF2BP3 gene. This alteration led to increased expression of IGF2BP3 protein. It is known that IGF2BP3 is involved in the IGF1R protein signaling pathway, which can drive tumor formation and growth.

Prior studies have suggested that THADA mutations contribute to thyroid cancer. But how they work remains a mystery. Nikiforov noted that their findings provided a mechanism of thyroid cancer.

The researchers also discovered that increased IGF2BP3 was found in other cancers, such as lung, pancreatic, colon and ovarian cancer, and inhibiting IGF1R pathway reduced the growth of IGF2BP3-driven cells and tumors. Collectively, the data indicate that IGF2BP3 could be a biomarker to predict which patients would respond to IGF1R inhibitors.
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