Natural Genetics just published the discovery of a mutation responsible for the progression of cancer.  This finding has the potential to help treat against numerous types of cancers since the mutation can be linked to various types of malignancies, rather than just in one type of cancer like many previous discoveries.

This mutation was discovered through the study of MicroRNAs (miRNAs).  Normally, the data stored in DNA is translated into RNA and the RNA is then translated into proteins, which then regulates gene expression.  In this study, the small pieces of RNA, miRNAs, were found to be blocking their translation into corresponding proteins.  Some of the miRNAs are hypothesized to suppress tumor formation and it was found that unusual levels of these molecules were present in all cancers studied.  This implies that this type of mutation could be responsible for cancer growth and progression in all types of cancers.  Following this hypothesis, continued research could possibly lead to a therapy that could reverse abnormal miRNA levels to treat multiple types of cancer.  The scientists working on this project believe that they could lead to an incredible discovery in cancer treatment.

Moving forward with the research, Sonia Melo is planning to analyze 12 different types of cancer in search of mutations in the pathway of miRNA formation.  In preliminary studies, she and her team found a protein called TARP2 that caused mutations in the pathway of miRNA formation, leading to low amounts of miRNA.  Upon the discovery of this protein and its pathway, the team later found that when functional TARBP2 was introduced to those cancerous cells, the miRNA returned to its normal levels.  In turn, those normal levels of miRNA that were reintroduced into the cancerous cells suggested to initiate tumor suppression functions.  This was found by comparing the levels of several known oncoproteins that promote tumorous functions when activated.

In vivo studies were performed by Melo and her team to verify their findings in SCID mice.  The team injected SCID some mice with new TARBP2 cells and other SCID mice with old TARBP2 from mutated cancer cells and compared the two groups.  The first group of mice with new TARBP2 cells either didn’t form tumors or formed a negligible amount of cancerous cells, while the second group of mice with old TARBP2 cells formed tumors relatively quickly.  This result confirmed the group’s theory that aberrant TARBP2 promotes tumor growth by reducing the amount of miRNA in cells.

A TARBP2 mutation in human cancer impairs microRNA processing and DICER1 function