Mixed-lineage leukemia or MLL is one of the most aggressive forms of blood cancer. A study shows that MLL makes up to 5 percent of leukemia cases and that this disease may have started developing during infancy.
Particularly treatment-resistant and pervasive, MLL owes its success to a protein which becomes a by-product when the MLL gene acquires mutations, altering normal cellular functions and leading to the formation of cancer cells.
Researchers from CSHL or Cold Spring Harbor Laboratory in New York have found out that this protein known as ZPF64 is found in many human tissue types and tends to be reliant on another. Based on their research, CHSL has found out a definitive association between ZPF64 and the malignant protein which is the MLL fusion protein.
ZPF64: What it Is and Why It is Important
Just like other ZPFs, Zinc-Finger Protein 64 or ZPF64 acts as a regulator of DNA expressions. It is responsible for the regulation of the human RNA polymerase II and is present in a number of cell types for this same purpose. The key functions of the ZPF64 protein include the following:
- Manage human RNA polymerase II
- Aid in the expression of the hepatic, muscle-associated, and brain tissue-related genes
- Regulate inherent immune system functions
Generally, ZPF64 tends to be important to support the health and normal functions of many tissues in the body. It also appears, however, that this protein allows for the expression of the malignant MLL fusion protein. It turns out in the study that the MLL tumor appears to depend on ZPF64 in up-regulating this expression. Thus, withdrawing ZPF64 supply prohibits the formations of MLL fusion protein.
A New Avenue for Aggressive Leukemia Treatment
A team of researchers from the CHSL lab headed by Dr Bin Lu is now arguing that controlling ZPF64 production is the key to the eventual failure of the MLL tumor and offers a promising channel for the treatment of the aggressive blood cancer.
However, while the future for these findings looks promising, thorough research is still needed before any conclusions can be made. As research is still underway, very few is known about the risks involved in ZPF64 inactivation. What is largely known though, is that the protein serves a number of functions in regulating many genes and tissues in the body.
In an earlier study, ZPF64 has been determined to play an important role in regulating the effects of the ILDR2 activation which is a gene linked to the risk of diabetes. Altering ZPF64 will most likely increase the risk of fatty liver disease. Eliminating ZPF64 altogether may also disrupt macrophage functions which are vital for the body’s immune system.
Furthermore, in another study, the level of ZPF64 protein in the genes altered through adding methyl groups to the DNA molecule has been associated with an increased risk to a certain sub-type of colorectal cancer. All of these mean that targeting ZPF64 in cases of MLL still requires more validation and a thorough approach. On the other hand, this new study can be an important avenue that could lead the way towards finding a new therapy to treat MLL.