<?xml version="1.0" encoding="utf-8" standalone="yes"?><rss version="2.0" xmlns:atom="http://www.w3.org/2005/Atom"><channel><title>Prostate Cancer on Michael’s Domain</title><link>https://jeltsch.org/en/tags/prostate-cancer/</link><description>Recent content in Prostate Cancer on Michael’s Domain</description><generator>Hugo</generator><language>en-us</language><copyright>Copyright © 2002 - 2026 Michael Jeltsch.</copyright><lastBuildDate>Fri, 24 Jul 2026 00:18:18 +0300</lastBuildDate><atom:link href="https://jeltsch.org/en/tags/prostate-cancer/index.xml" rel="self" type="application/rss+xml"/><item><title>KLK3: tumorigenic or not?</title><link>https://jeltsch.org/en/KLK3/</link><pubDate>Wed, 22 Dec 2021 00:00:00 +0000</pubDate><guid>https://jeltsch.org/en/KLK3/</guid><description>&lt;p&gt;We have just published our latest review about 
 &lt;a href="https://doi.org/10.3390/ijms222413545" target="_blank" rel="noopener noreferrer nofollow"&gt;the role of KLK3 as an activator of VEGF-C and VEGF-D in prostate cancer&amp;nbsp;






 
 
 
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. Prostate cancer is one of the most common cancers in males. It is not a question of whether you will get it but only when. Once you reach your 80s, the likelihood of you having prostate cancer is bigger than not having it. In a 
 &lt;a href="https://doi.org/10.1093/jnci/djt151" target="_blank" rel="noopener noreferrer nofollow"&gt;2013 autopsy study of Japanese males&amp;nbsp;






 
 
 
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, who died of other causes, 59% of those older than 80 had prostate cancer. It is likely that many of these cases were indolent and would never have caused any problems. Only a few of them might have become symptomatic had these men lived longer. So, there is a significant interest in distinguishing those cancers that are going to cause problems. Many prognostic markers have been proposed to do exactly that: to predict which cancers would become problematic.From the vascular biology point of view, angiogenesis and lymphangiogenesis are two hallmarks of cancers that have been previously proposed to have prognostic value. 
 &lt;a href="https://doi.org/10.7554/eLife.44478" target="_blank" rel="noopener noreferrer nofollow"&gt;When we stumbled upon the fact that prostate-specific antigen (PSA, also known as KLK3) is able to activate VEGF-C and VEGF-D&amp;nbsp;






 
 
 
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, we thought that this might have significance for prostate cancer. Meanwhile, further research has clarified some questions, and it really seems to be that both VEGF-C and VEGF-D are involved in cancer progression. it is not clear yet which proteases are responsible for the activation of VEGF-C and VEGF-D in real human cancers. KLK3- or Cathepsin D (CTSD)-activated VEGF-D might be a possible cause of the resistance of tumors to bevacizumab (Avastin) treatment. The consequences of VEGF-C activation, on the other hand, are more difficult to predict because activated VEGF-C does simultaneously both good and bad: On the one hand, it facilitates metastasis. On the other hand, it enables an enhanced immune response against the tumour. Interesting research lies ahead. Read more in our review: 
 &lt;a href="https://doi.org/10.3390/ijms222413545" target="_blank" rel="noopener noreferrer nofollow"&gt;https://doi.org/10.3390/ijms222413545&amp;nbsp;






 
 
 
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