Sweet-P: One Possible New Secret Ingredient Against Glioblastoma

According to a report from the University of Toledo, researchers developed a new molecule that could stop cancer in its tracks. The molecule, known as Sweet-P, works by targeting a protein expressed by several highly aggressive forms of cancer such as glioblastoma. Sweet-P appears to be able to stop these cancer cells from spreading to other parts of the body. Keep reading to learn more, or follow the original story here for further details.

What is Glioblastoma?

Glioblastoma is a rare type of cancer that forms in the brain from star-shaped astrocyte cells. The cancer typically begins in the cerebrum. Because glioblastomas are capable of creating their own blood supply, the cancer is able to grow rapidly and spread aggressively.

Symptoms of glioblastoma typically include difficulty in thinking or speaking, mood changes, persistent headaches, double vision, vomiting and seizures. Treatment may include surgical removal, radiation or chemotherapy, and electric-field therapy. Unfortunately, many glioblastomas regrow even after treatment.

Click here to learn more about glioblastoma.

Weighty Results

Sweet-P, surprisingly enough, was originally intended to be research on obesity. The research, led by Dr. Terry Hinds of UT Department of Physiology and Pharmacology, focused on a protein known as GR beta. During the research, Hinds experimented with GR beta and stem cells. The notion was that, if given enough GR beta, the stem cells would develop into large fat cells.

What happened instead was that the stem cells began to grow and replicate at surprising rates. GR beta seemed to accelerate the growth cycle of the cells. Because GR beta is known to have similar effects in some cancers, the team began to explore the protein further.

Sweet-P: A New Option

Hinds’ team began to examine a type of microRNA. The one they were studying, microRNA-144, is relatively mysterious. What is known, however, is that bladder cancer patients appear to present with higher levels of the microRNA.

Even more peculiar is that while most microRNAs turn genes off, microRNA-144 activates GR beta Sweet-P then came into existence as the first drug intended to target a specific microRNA reaction.

When tested on bladder cancer cells, Sweet-P successfully turned off the GR beta response. When the GR beta fails to function, the cancer cells stop spreading. They stay put.

Sweet-P offers hope, but is still has a long way to go before it could be approved as a treatment. There will need to be mice studies before it can even be brought to clinical trial in human patients. As a result of only targeting one specific gene interaction, Sweet-P, however, seems primed to be a potentially successful part of treatment while reducing dangerous side effects.


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