Skip to content
Prof. Dr. Mustafa Özdoğan · Medical Oncologist

Turkish Professor Discovers a New Prostate Cancer Treatment

Turkish Professor Discovers a New Prostate Cancer Treatment
In this article

Prostate cancer is the most common cancer among men in Western countries. Approximately 1.3 million new cases occur worldwide each year. According to World Cancer Statistics , approximately 310.000 people die of prostate cancer annually. Effective treatments are therefore needed. In January 2019, Nature Communications published a study developing an effective approach against prostate cancer. It reflects 10 years of preclinical research in clinical practice.

The research was conducted under the leadership of a Turkish professor with his own laboratory in the Department of Biosciences at the University of Oslo, Norway, Fahri Saatçioğlu . In 2015, Professor Saatçioğlu discovered in prostate cancer cells 2 signaling pathways , one active and the other inactive. This study found that the active pathway, IRE1, is also important in activating oncogenes (a category of cancer-related genes). IRE1 was responsible for activating the cancer-related protein C-MYC. This pathway discovery relates to the endoplasmic reticulum, an organelle important in cellular responses to carcinogens. Our cells face “cellular stresses / carcinogens” in various ways. Cancer cells are under greater stress than normal cells because rapid proliferation requires sufficient oxygen and nutrients. They exploit normal stress responses. This study targeted that mechanism with MKC8866, developed by biotechnology company MannKind by screening 200.000 chemical compounds. MKC8866 is an anticancer agent in the hydroxyl-aryl-aldehyde group.

MKC8866 blocked the stress-response signaling pathway in targeted prostate cancer cells. It also successfully halted prostate cancer growth in cell culture and mouse models.

What Does This Study Mean for Us?

  • This discovery is an excellent example of basic science translating to clinical practice: an important prostate cancer signaling pathway was discovered, then a drug targeting it effectively destroyed cancer cells.
  • European clinical trials with these cellular-targeted anticancer agents are planned soon.
IRE1α XBP1 pathway triggers prostate cancer by activating c MYC signaling

Figure Explanation: The mechanism of MKC8866, which may become a prostate cancer drug, is shown. In prostate cancer cells, the androgen receptor drives IRE1-alpha expression (production). The IRE1 alpha enzyme then produces XBP1. XBP1 increases c-MYC activity, a powerful oncoprotein contributing to progression. MKC8866 inhibits XBP1 expression, substantially reducing c-MYC activity and consequently halting tumor growth. Prof.

Fahri Saatçioğlu began Ege University Faculty of Medicine in 1981 and completed half his university education in America. Frequently featured in our press for cancer discoveries, he is also known for research on Yoga and its health benefits.

Sources

Xia Sheng, Hatice Zeynep Nenseth, ... Fahri Saatcioglu ve ark.
IRE1α-XBP1s pathway promotes prostate cancer by activating c-MYC signaling.
Nature Communications, 24 January 2019.
DROZDOGAN AI

Explore this article together

Ask about the article and read answers alongside published sources from our site.

DROZDOGAN AI

Drozdogan Assistant

Turkish Professor Discovers a New Prostate Cancer Treatment

Ask about the article and read answers alongside published sources from our site.

Conversation and privacy information

Drozdogan Assistant answers this conversation. Authorized site administrators may review it for quality. Do not share personal information.

Replies use OpenAI infrastructure. Questions and replies are processed by that service; conversation records are stored on our site. Do not share identifying, contact or personal health information.

0 / 1000

For information only; no personal diagnosis or treatment advice.

Related articles

Explore other articles on this topic.

Stay informed

Receive new articles and scientific updates by email.

Google Analytics runs on public pages independently of this window and may use analytics cookies. Your choice here controls external services only.

Cookie policy