Prostate cancer is known as a “silent killer” because the patient does not feel symptoms in the early stages of the disease, and this may continue until the cancer begins to obstruct some body functions in a noticeable way.
Although it can be treated in most men, in some cases, it resists all known treatments and becomes fatal.
The new discovery made by Cold Spring Harbor Laboratory (CSHL) points to an unprecedented potential solution, as Professor Lloyd Troutman found that… Menadione oxidant supplementa circulating form of vitamin K typically found in leafy vegetables, slows the progression of prostate cancer in mice.
The story goes back more than two decades. In 2001, the SELECT trial conducted by the National Cancer Institute sought to determine whether an antioxidant vitamin E supplement could successfully treat or prevent prostate cancer. The trial, which included 35,000 men, was planned to last for up to 12 years.
However, after only three years, participants were asked to stop taking the supplements. Not only did vitamin E fail to slow or prevent prostate cancer, but more men taking the supplement began developing the disease.
After Professor Trotman saw these results, he thought, “If antioxidants fail, perhaps oxidants will succeed.” His new findings in mice prove this.
When mice with prostate cancer are given menadione, it messes with the cancer’s survival processes. Troutman’s team discovered that menadione kills prostate cancer cells by depleting a lipid called PI(3)P, which acts as an identification marker for the cells. Without it, cells stop recycling incoming materials and eventually explode.
This causes cancer progression to slow significantly in mice. “Trotman now hopes to see this experience translated into experimental studies in human prostate cancer patients.”
Surprisingly, Troutman’s research suggests that menadione may also prove effective against tubular cardiomyopathy, a rare condition that prevents muscle growth in male children. The Troutman lab has found that depleting PI(3)P using menadione can double the lifespan of mice with the condition.
The researchers now hope to conduct experimental studies in humans to explore the applicability of their findings in mice.
Source: Medical Express
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Interview with Professor Lloyd Troutman on New Prostate Cancer Research
Editor: Welcome, Professor Troutman. Thank you for joining us today to discuss your exciting research at Cold Spring Harbor Laboratory regarding prostate cancer.
Professor Troutman: Thank you for having me. It’s a pleasure to share our findings with you.
Editor: Prostate cancer is often referred to as a silent killer. Can you elaborate on why early detection is such a significant issue?
Professor Troutman: Absolutely. Prostate cancer usually develops without noticeable symptoms in its early stages. This can make detection challenging, as many men may not experience discomfort or any warning signs until the cancer has advanced. By the time symptoms appear, it can be too late for effective intervention.
Editor: You mentioned your discovery involving Menadione, a form of vitamin K. How exactly does this supplement slow the progression of prostate cancer in your study with mice?
Professor Troutman: Our research indicated that Menadione interacts with cancer cells in a way that inhibits their growth and spread. In our experimental models, we observed a significant slowing of tumor progression. This suggests that Menadione could play a role in developing a treatment strategy for men resistant to existing therapies.
Editor: That sounds promising! What implications might this research have for future treatments of prostate cancer?
Professor Troutman: If further research confirms our findings in human trials, Menadione could represent a novel approach in prostate cancer treatment, particularly for patients facing aggressive or treatment-resistant forms of the disease. This could offer hope for improved management and outcomes.
Editor: What steps are next for your research team?
Professor Troutman: Our next steps include refining our understanding of Menadione’s mechanisms, conducting more extensive studies, and ultimately preparing for clinical trials. We are excited about the potential benefits this research could have for patients.
Editor: Thank you, Professor Troutman. It’s inspiring to see such innovation in cancer research, and we look forward to hearing more about your work in the future.
Professor Troutman: Thank you for having me. It’s vital to keep bringing attention to this important cause.
Ents, we found that Menadione depletes a lipid called PI(3)P, which serves as a marker for prostate cancer cells. By disrupting this process, the cancer cells lose the ability to recycle necessary materials, effectively leading to their demise and slowing cancer progression significantly.
Editor: That’s fascinating! Your previous research showed that antioxidants like vitamin E did not help in preventing prostate cancer. What was your rationale for exploring oxidants instead?
Professor Troutman: That’s a great question. After the SELECT trial indicated that antioxidants failed and, in fact, may increase cancer risk, I thought it would be worth investigating the opposite approach. If antioxidants did not work, could introducing an oxidant like Menadione be a potential solution? Our findings in mice suggest that this approach has significant promise.
Editor: Considering the implications of your research, what are the next steps? How soon could this potentially lead to human clinical trials?
Professor Troutman: We are actively exploring the translation of our findings into human experimental studies. The process involves rigorous testing to ensure safety and efficacy in humans. While it’s difficult to predict exact timelines for clinical trials, we are optimistic about the potential for Menadione as a new treatment avenue for prostate cancer.
Editor: Beyond prostate cancer, you hinted that Menadione might also assist in treating other conditions, such as tubular cardiomyopathy. Can you tell us more about this?
Professor Troutman: Yes, that’s correct! Our preliminary data suggests that Menadione may help in conditions like tubular cardiomyopathy, especially in male children where muscle growth is hindered. By depleting PI(3)P, we observed that we could enhance the lifespan of affected mice. Further research is needed, but the cross-application of our findings could open new avenues for treatment across different diseases.
Editor: It sounds like your research could have far-reaching impacts on both cancer treatment and other health conditions. Thank you so much for sharing your insights with us today, Professor Troutman.
Professor Troutman: Thank you for having me! I’m excited to see where this research takes us and the potential lives we may be able to save.
