Heparin is a widely used injectable blood thinner. It is typically administrated as an injection IP (anyone can do it at home) or Intra Venous. It is used to treat and prevent deep vein thrombosis and pulmonary embolism (collectively known as venous thromboembolism).
According to Wikipedia, Heparin’s normal role in the body is unclear. Heparin is usually stored within the secretory granules of mast cells and released only into the vasculature at sites of tissue injury. It has been proposed that, rather than anticoagulation, the main purpose of heparin is defense at such sites against invading bacteria and other foreign materials. In addition, it is observed across a number of widely different species, including some invertebrates that do not have a similar blood coagulation system. (Ref.)
Heparin as a Cancer Treatment
Anti-Coagulant Slows Down Tumor Growth And Spread: A research group at University of Hull and Hull’s Castle Hill Hospital has revealed that Heparin can reduce the levels of a tissue factor (a protein that contributes to clotting) being secreted by tumors.
While tissue factor’s role in healthy people is to promote blood clotting in wounds and aid repair, tumors secrete tissue factor as an inflammatory response to their interaction with growth factors in the blood, which they hijack to help them grow and spread. High levels of tissue factor are known to cause thrombosis, which is one reason why cancer patients are particularly at risk of developing lethal deep vein blood clots.
Same researchers have previously shown that tumor cells which express high levels of tissue factor are more invasive, and other reports show that they metastasize rapidly and are resistant to therapy. As a result they concluded that finding new ways to suppress the expression of tissue factor are crucial.
Using Heparin to treat pancreatic, breast, melanoma, colorectal and ovarian cancer cells, they shown that this suppressed the cell’s interaction with growth factors, preventing tissue factor from being secreted, ” raising the possibility of a universal treatment strategy that could benefit all cancer patients.”
Same researchers conclude: “What we have here is experimental evidence that a drug that is already known to be safe in humans as an anti-coagulant may also suppress tumor growth directly and reduce resistance to treatment. I think this would also be a very useful way of lowering the risk of tumor regrowth in between chemotherapy and radiotherapy sessions.”
“… A potentially more significant issue, however, is whether taking heparin to treat blood clotting problems may have somehow slowed down the growth of Mrs. Benchley’s lung cancer. Based on cases like hers, doctors have begun to wonder if the human body’s blood clotting mechanism may somehow play a role in the growth of cancerous tumors. If that is so, then it would explain why a drug like heparin that fights blood clotting might actually stop or slow down tumor growth.”
“The possible reasons for this are not completely understood. To put them as simply as possible, cancerous tumors are usually surrounded by a substance called fibrin. Fibrin promotes the growth of the tumor and the growth of new blood vessels that supply the tumor with necessary nutrients. Heparin interferes with fibrin formation and perhaps directly inhibits the formation of new blood vessels. Both heparin and LMWH may also inhibit tumor growth in other ways.”
Researchers have discovered a novel mechanism regulating the development of breast cancer bone metastases and showed that heparin-like compounds can potentially be used to inhibit breast cancer metastasis to bone.
Exosomes are 30–100 nm-sized membranous vesicles, secreted from a variety of cell types into their surrounding extracellular space. Numerous studies have showed that tumor cell-derived exosomes play important roles in tumor growth and progression. The uptake of exosomes by oral squamous cell carcinoma (OSCC) cells and subsequent tumor progression was abrogated in the presence of heparin. Taken together, these data suggest that OSCC cell-derived exosomes might be a novel therapeutic target and the use of heparin to inhibit the uptake of OSCC-derived exosomes by OSCC cells may be useful for treatment.
Heparanase is an endo-β-D-glucuronidase that plays an important role in cancer progression, in particular during tumor angiogenesis and metastasis. Inhibiting this enzyme is considered as one of the most promising approaches in cancer therapy. Heparin is a complex glycoaminoglycan known as a strong inhibitor of heparanase.
Here, we provide evidence of a novel role of heparan sulfate proteoglycans (HSPGs) in the adaptive response of tumor cells to hypoxia and acidosis through increased internalization of lipoproteins, resulting in a lipid storing phenotype and enhanced tumor forming capacity. We show that stress mediated lipoprotein uptake is highly dependent on intact HSPG expression. The functional relevance of HSPG in the context of tumor cell stress was evidenced by HSPG-dependent lipoprotein cell signaling activation through the ERK/MAPK pathway, and by reversal of the LD-loaded phenotype by targeting of HSPGs. We conclude that HSPGs may have an important role in the adaptive response to major stress factors of the tumor microenvironment with functional consequences on tumor cell signaling, and metastatic potential.
Indeed it is known that the inhibition of lipid droplet (LD) formation may represent a serious anti cancer solution: https://www.cancertreatmentsresearch.com/?p=1447
Very good discussion on Heparin anti cancer effects: “Data from epidemiologic studies and clinical trials demonstrate a protective and therapeutic effect for heparin treatment on tumor growth and metastasis . In certain tumors, such as small-cell lung cancer, a portion of the survival benefit can clearly be ascribed to antithrombotic effects . However, the benefits of heparin treatment exceed the effects of anticoagulation, suggesting that other mechanisms are involved . Multiple mechanisms likely contribute to the therapeutic effects of heparin, including inhibition of selectin binding , inhibition of heparanase  and sulfatases , decreased platelet signaling to suppress tumor angiogenesis , and enhanced terminal differentiation of cancer cells .” For more, go to http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4065786/#S6title
- enzymatic depletion of mast cell heparin by injection of heparinase enzyme into tumor implants accelerated tumor growth and increased blood clotting within the tumors (Ref.)
- NDST-2 knockout mice are unable to synthesize mast cell heparin – tumor cells implanted into NDST-2 knockout mice grew faster than tumor cells implanted into wild-type mice that synthesized normal heparin (Ref.)
- “our observation that mast cells are abundantly present within the fibrous regions of tumors raises the intriguing possibility that a growth inhibitory mechanism similar to the one that we observed in our in vitro studies could also be naturally operative within tumors in vivo … we acknowledge, however, that this possibility seems to be at odds with the accumulating evidence that mast cells promote rather than inhibit tumor growth … In this regard, it should be emphasized that mast cell granules contain numerous biologically active compounds in addition to heparin, such as histamine, tryptase, and chymase. Some of these mast cell compounds and metabolites are likely to have significant effects on fibroblasts that remain to be defined. In addition, a number of other mediators from fibroblasts and mast cells could potentially influence tumor growth through a variety of mechanisms such as cyclooxygenase metabolites, heparanases, etc. The net effect on tumor growth, therefore, is likely to be the result of multiple complex interactions between the various components of mast cell granules and adjacent stromal cells such as vascular endothelium and fibroblasts.” (Ref.) The whole point of thsi is that heparin (produced by mast cells) has anti cancer effects while mast cells overall lead to tumor progression – therefore using Heparin as injection while if possible inhibiting mast cells may be best approach.
- NDST2 (N-Deacetylase/N-Sulfotransferase-2) Enzyme Regulates Heparan Sulfate Chain Length (Ref.)
- NDST-2 having a role in the formation of fully sulfated heparin – central role for NDST-2 in MC heparin synthesis – targeting of the NDST-2 gene was previously shown to result in strongly defective synthesis of heparin (Ref.)
- Mast Cell (MC) degranulation also caused an up-regulated expression of certain CS sulfotransferase genes, accompanied by a corresponding down-regulation of NDST-2. These results suggest that activated MCs predominantly synthesize CS over heparin and, indeed, the biosynthetic35S-sulfate labeling experiments supported an increased secretion of CS (Ref.)
Heparin is a great tool to help dissolve blood clots and thus enhance the penetration of treatments to the tumor site. Due to this property it may make sense to often use it just before starting the administration of other IV therapies. In addition to that, Heparin seems to have anti cancer action too and this strengthen the idea of using Heparin as a part of any anti cancer treatment.
Heparin can be found at any pharmacy and is very affordable. Here is an example: https://www.medizinfuchs.de/preisvergleich/heparin-natrium-25000-rati-5×5.0-ml-ratiopharm-gmbh-pzn-3029843.html
Dose, Administration, Safety:
Here info that we need to have references on what is safe in terms of administrated dose https://www.medicines.org.uk/emc/medicine/9796
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