Sadly for all researchers in the field, the way cancer works is highly varied and dependent on the specific type. Because of that, each different type of cancer has to be investigated separately and all of the mechanisms involved deciphered one by one, meaning any proper treatment or cure for a single type of cancer will take far more work than if cancer was just a single disease.
However, sometimes there are genes and molecules that cross the gaps between different cancers, giving researchers the opportunity to advance understanding of cancer formation with a giant leap. On that note, this new study to be published in October in the International Journal of Cancer discusses using transgenic mice to figure out what role Kif14 has on the development of a rare form of cancer known as retinoblastoma, but which has added involvement in a number of other cancers.
Kif14 is a type of kinesin, which are motor proteins responsible for transporting other substances around the cell. This kinesin is specifically involved during mitosis, when the cell is in the processing of dividing into two, and helps collect and transport needed proteins during the last phases of cytokinesis, the actual splitting of the cell.
Previous studies have shown that over-expression of Kif14 is involved somehow with the development of retinoblastoma and a number of other carcinoma-type cancers. Due to this, the researchers noted that the gene involved in expressing Kif14 is likely an oncogene, a gene that has the potential to cause tumor formation under certain circumstances.
This study is based around tracing the effects of Kif14 within a transgenic mice model made to also express the simian virus 40 large T-antigen retinoblastoma (TAg-RB) gene, which as can be guessed is an oncogene that also aggravates retinoblastoma development. This is just to ensure that a large amount of the experimental group develop retinoblastoma so that the influence of Kif14 can be more easily focused on. The control group for the experiment was also a set of transgenic rats made to express TAg-RB, so the extra effects coming from Kif14 in tandem could be compared.
It was found by the researchers that over-expression of Kif14 did indeed speed initial forming of tumors and also significantly reduced the amount of time required for the tumor to double in cell number from nearly 3 weeks to just over a week and a half. This information gives more insight for scientists on how oncogenes like Kif14 affect the onset of cancer and open up future opportunities and therapies that can target such genes in order to delay or even eradicate that onset.