After 12 years of vigorous research work following the creation of a transgenic mouse, the researchers at Jefferson’s Kimmel Cancer Center have come to the conclusive note that breast inflammation process is linked to the growth and promotion of cancer cells.

The December 15th issue of Cancer Research reports that the long suspected theory has finally been confirmed by these scientists who have now proven that inflammation process in the breast triggers cancerous cell activities which are directly linked with tumour development.

This also suggests that if the inflammation process can be halted then it would amount to the stoppage of breast cancer cells from spreading. Director of Kimmel Cancer Center Richard Pestell cites that inactivating the NFKB inflammatory path in the epithelial region of breast shall cease the progression of cancerous cells in living animals.

This finding is of great significance since it points to the need of just suppressing the breast inflammation for the desired result. Preventing the inflammation of the whole body, on the contrary, is likely to give rise to side effects.

Dr. Pestell has successfully demonstrated how NFKB pathway augments breast cancer. HER2 oncogene provides the first ‘insult’ which eventually activates NFKB. NFKB triggers inflammation and gives rise to tumour-growing factors.

But this theory was, hitherto, unverified as suppressing inflammation kills the mouse on which the test is conducted. Hence, this problem was addressed by creating a transgenic mouse in which the inflammatory system could be controlled. After 12 years of labour, the special mice have been developed in which selective inactivation of NFKB can be done.

Using this mice, they could demonstrate that inactivation of NFKB cells prevented the growth of tumours. It also reduced the number of cancerous stem cells in the breast. The transgenic mice can be used in future to conduct researches in relation to cardiac diseases, neuro-degeneration and other types of cancers.

Source: http://www.eurekalert.org/pub_releases/2010-12/tju-bii121410.php