hyaluronic acid

HA guy said:

HA
Hi Jimmy/Cleveland,

I have worked in the HA (Hyaluronic Acid) industry for the past 10 years in medical devices. Although we do not produce HA - I am aware of most of the studies in HA and have previously produced injectibles using HA and topical medical devices. That said - I have not seen any data that links HA "directly" to the cause and spread of cancer via the CD44 receptors. This included studies linking HA to causing irritation in low molecular weights. It seems that HA is more one of the few adaptive molecules the body uses in a variety of ways including lubrication, viscosupplementation and moisturisation. Because it's everywhere it's likely to be found in studies for both healthy individuals and those with cancer. It does play a part in healing and it seems that when applied to the body the natural production of HA increases. However the body is complex and the mechanisms and full understanding of the systems that are at work in the body are still under investigation. HA injections for Osteoarthritis is a large and mature market. It's likely patients with with PCa have had injections. Medical Device companies are required to monitor the products use in the market and attempt to trend customer feedback including any links with adverse events/reations. It's likely your doctor will be able to give you the brand/manufacturer of the particular HA Injectible he/she likes to use. You can take this information and contact the company directly for this informaiton. If it is available they will have it.
Hope this helps

HA Guy

HA Guy
Thanks for your informative reply on HA. The information that I read about HA not being recommended for Ca patients came from a Wikipedia search on the substance. Here is the part of the article that made me wonder:


Figure 1. The process of cancer metastasis in which HA-associated molecules play a role in the steps. Abbreviations: hyaluronic acid (HA), hyaluronic acid synthase (HAS), hyaluronic acid receptor (HAR), hyaluronidase (HAase/HYAL)As shown in Figure 1, the various types of molecules that interact with hyaluronan can contribute to many of the stages of cancer metastasis.

Hyaluronan synthases (HAS) play roles in all of the stages of cancer metastasis. By producing anti-adhesive HA, HAS can allow tumor cells to release from the primary tumor mass, and if HA associates with receptors such as CD44, the activation of Rho GTPases can promote epithelial-mesenchymal transition (EMT) of the cancer cells. During the processes of intravasation or extravasation, the interaction of HAS produced HA with receptors such as CD44 or RHAMM promote the cell changes that allow for the cancer cells to infiltrate the vascular or lymphatic systems. While traveling in these systems, HA produced by HAS protects the cancer cell from physical damage. Finally, in the formation of a metastatic lesion, HAS produces HA to allow the cancer cell to interact with native cells at the secondary site and to produce a tumor for itself.[43]

Hyaluronidases (HAase or HYAL) also play many roles in cancer metastasis. By helping to degrade the ECM surrounding the tumor, hyaluronidases help the cancer cell escape from the primary tumor mass and play a major role in intravasation by allowing degradation of the basement membrane of the lymph or blood vessel. Hyaluronidases again play these roles in establishment of a metastatic lesion by helping with extravasation and clearing the ECM of the secondary site.[44] Finally, hyaluronidases play a key role in the process of angiogenesis. HA fragments promote angiogenesis and hyaluronidases produce these fragments.[45] Interestingly, hypoxia also increases production of HA and activity of hyaluronidases.[46]

The hyaluronan receptors, CD44 and RHAMM, are most thoroughly studied in terms of their roles in cancer metastasis. Increased clinical CD44 expression has been positively correlated to metastasis in a number of tumor types.[47] In terms of mechanics, CD44 affects adhesion of cancer cells to each other and to endothelial cells, rearranges the cytoskeleton through the Rho GTPases, and increases the activity of ECM degrading enzymes.[48] Increased RHAMM expression has also been clinically correlated with cancer metastasis. In terms of mechanics, RHAMM promotes cancer cell motility through a number of pathways including focal adhesion kinase (FAK), Map kinase (MAPK), pp60(c-src), and the downstream targets of Rho kinase (ROK).[49] RHAMM can also cooperate with CD44 to promote angiogenesis toward the metastatic lesion.[50]