Researchers at the Imperial College London have now identified a novel protein –LMTK3, which is involved in the process of drug resistance in breast cancer. This protein can purportedly act as a target for new treatments.
Breast cancer is the most common cancer in the UK and affects around 46,000 women annually. Although anti-oestrogen drugs like tamoxifen act as an appropriate treatment for breast cancer, most patients might develop resistance to these medications.
A mouse model of breast cancer was used for blocking production of the protein. The team of researchers adopted genetic techniques to shrink tumours and are now searching for drugs that could accomplish a related effect.
The protein called LMTK3 was apparently blocked within human cancer cells, which were resistant to tamoxifen. When genetic techniques were used for blocking the production of LMTK3, a momentous decrease in the size of breast tumours was observed.
Senior researcher, Professor Justin Stebbing, from the Department of Surgery and Cancer at Imperial College London, said the anti-oestrogen drugs have been a roaring success at letting women with breast cancer to live longer, but resistance to these drugs was found to be a common problem. Their results suggest that the action of LMTK3 on the oestrogen receptor has an important role in the development of drug resistance.
The team is now searching for drugs that can block the effect of LMTK3 that could hopefully prevent patients from becoming resistant to hormone therapy. The whole process is expected to take at least five to ten years to create new treatments that are risk-free to be used in humans.
The researchers also measured levels of LMTK3 in tissue samples taken from women with breast cancer. Those with increased levels of LMTK3 in their tumours were in all likelihood found to live less longer and were also less likely to react to hormone therapy. Some mutations in the gene coding for LMTK3 were obviously associated with the endurance of a patient.
Experiments conducted by the team have disclosed that resistance to hormone therapy happens when the oestrogen receptor is adapted by enzymes called kinases. LMTK3 is considered to be a approving treatment target for kinases, which affect the way cancer cells respond to oestrogen. DNA sequences in the gene coding for LMTK3 among human beings was compared to that of chimps, as because chimps are not sensitized to oestrogen receptor positive breast cancer. Significant differences that have evolved in these sequences between the two species were registered.
Dr Georgios Giamas, who designed and led the research, from the Department of Surgery and Cancer at Imperial College London, believes that humans and chimpanzees have evolved these differences in the LMTK3 gene, since genes are related between the two species. He states that the evolutionary alterations in this gene may have given humans a degree of advantage, but also made us more sensitive to breast cancer.
The study was published in the May 2011 issue of the Nature Medicine journal. The research was funded by the US National Institutes of Health, Cancer Research UK and the Department of Health.
