Breakthrough in tumor research: New protein slows brain tumor growth!

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Researchers discover the protein SFRP1, which slows the growth of glioblastomas in mice. New therapeutic approaches in sight.

Forschende entdecken das Protein SFRP1, das das Wachstum von Glioblastomen bei Mäusen verlangsamt. Neue Therapieansätze in Sicht.
Researchers discover the protein SFRP1, which slows the growth of glioblastomas in mice. New therapeutic approaches in sight.

Breakthrough in tumor research: New protein slows brain tumor growth!

Scientists at the German Cancer Research Center (DKFZ) in Heidelberg have achieved a significant breakthrough in the treatment of glioblastoma. Their research shows that the SFRP1 protein slows the growth of these aggressive brain tumors in mice. Glioblastomas are the most common and aggressive brain tumor that occurs in adults. They are known to often return after just a few months despite intensive therapies such as surgery, radiation and chemotherapy. The researchers' new method aims to prevent tumor recurrence by keeping cancer cells inactive over the long term.

The key to fighting these tumors lies in the structure of the glioblastoma cells, which have a pyramid-like structure. At the base there are resting cells, in the middle part there are active cells that divide, and at the tip there are differentiated tumor cells that have properties of nerve cells. While previous therapies have focused primarily on active cells, dormant cells are often ignored, which can lead to the formation of new tumors. This is where SFRP1 comes into play, which slows the transition from resting to active cells.

The role of SFRP1 in tumor suppression

Research has shown that loss of SFRP1 function through epigenetic inactivation, such as through DNA methylation or transcriptional silencing by microRNAs, is repeatedly associated with various types of cancer. This inactivation promotes uncontrolled cell proliferation and metastasis. More specifically, SFRP1 is classified as a tumor suppressor whose loss has been linked to colorectal cancer, prostate cancer, and renal cell carcinoma relapse, among others. Restoring SFRP1 expression could therefore offer new approaches in cancer therapy, as researchers from pmc.ncbi.nlm.nih.gov discovered.

In a clinical study with 55 patients, SFRP1 was identified as central to the inhibition of a signaling pathway that triggers the activation of stem cells. Animal experiments confirmed that targeting SFRP1 caused tumor cells to enter a sleep mode. This led to slowed tumor cell growth and prolonged survival of the mice.

Challenges in the fight against glioblastoma

Despite such progress, numerous challenges remain. One of the greatest difficulties in combating glioblastoma is the frequent mutations in growth factor receptors. Such receptors are mutated or amplified in approximately 67.3% of glioblastomas. Changes in the epidermal growth factor receptor (EGFR) are particularly common and are affected in 57.4% of cases. These mutations affect many cellular signaling pathways that are critical for tumor growth and prolonging cancer cell survival, as pmc.ncbi.nlm.nih.gov notes.

In addition to the challenge of gene mutations, the molecular heterogeneity of glioblastomas represents a significant obstacle. There is an urgent need for more specific inhibitors to increase the effectiveness of therapies while ensuring safety for patients. New approaches such as antibody-drug conjugates show promising results and could represent a valuable addition to existing treatment methods.

The ongoing research surrounding SFRP1 and its role in tumor biology is promising and could one day lead to more effective therapies for patients with glioblastoma. However, science continues to face the challenge of fully understanding the complex mechanisms that contribute to tumor development.

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