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Chronic myelogenous leukemia (CML) is known to be a cancer of the white blood cells. Apparently, investigators from the Duke University Medical Center have found a mechanism that can reveal the way patients move into the worst phase of chronic myelogenous leukemia (CML). It is believed that the protein Mushashi, known to restrict cells from maturing, creating a large population of immature cells is one of the distinct feature of CML.

The experts claim the same pathway to be associated with other aggressive leukemias, breast cancer and solid tumors like glioblastoma which is an extreme type of brain cancer. In the course of the research, the researchers examined 120 human specimens from patients in various phases of CML progression. The outcome was that a significant elevation in the levels of Musashi was reported with advancement in the ailment.

The CML progression is ascertained to be indicated by a block in cell maturation known as differentiation and an addition in immature cells. Therefore, the scientists investigated whether an abnormal reversal of the signals controlling cell differentiation led to the progression of the disease. The molecule Numb that is believed to regulate control differentiation during normal development was inspected by the scientists.

Tannishtha Reya, Ph.D., an associate professor of pharmacology, senior author and cancer biology at Duke enlightened, “We found high levels of Musashi in all of the human advanced phase CML samples we studied. The fact that this pattern was seen in all of the human cells, regardless of patients’ gender or ethnicity, and in people on three continents, marked it as potentially a major signal that needed to be studied in as much depth as possible.”

In order to compare the chronic which is the less harmful with the blast-crisis that is the most harmful and severe phases of CML, the investigators observed mice. The investigation enabled the researchers to inspect the way Numb was being curbed in advanced disease and, if this repression aids in the sustenance of blast-crisis phase. The RNA-binding protein Musashi was thoroughly scrutinized as it is assumed to hold back Numb in other systems.

Musashi may be admitted to contribute to the growth of immature cells in cancers also, because it heightens in stem cells and is required for their growth. The investigators elucidate that Musashi expression was 10 times higher in the more immature blast crisis CML phase. By blocking Musashi, cancer growth may be blocked, so future therapies can target Musashi. The latest research has suggested activating Numb, or blocking Musashi to prevent blast-crisis CML.

Reya said “It is not always clear if a pathway that appears to be important in mouse models will be relevant in human disease. In this case, however, the data and patterns are so strong in human patient samples that pursuing these findings becomes critical.”

To overcome cancer cell growth either the programmed cell death in cancer cells is activated, or the growth is blocked directly. In instances wherein cancer is composed of immature cells, these cells are supposedly impelled to mature and differentiate. Depletion of immature cells may adversely hamper the continued growth of the cancer.

Since an early marker of advanced CML is claimed to be elevated levels of Musashi, the patient prognosis can be understood in detail by examining the levels of the protein. It was concluded that heightened levels of Musashi in glioblastoma and lower levels of Numb in high-grade breast cancer seemingly indicate the Musashi-Numb pathway to be encompassed in solid cancers.

The research is published in Nature online on July 18.