Coagulation and Cancer




Coagulopathy is an important aspect of cancer:


1) Treat inflammation:    Wobenzym   6 pills    5 times a day AWAY from food   (see


2) Enhance immunity  New Eden   1 tablespoon twice a day  


3) Enhance blood flow (with all its beneficial nutrients)  with  Heparin 5000 units twice a day  (sublingual or IM).

See articles below   We should test whether your blood is hypercoagulated with the ISAC test:  Bob, check out and search test: ISAC


4) Vitamin C    1 gram every hour while awake – up to bowel tolerance (if the stools get loose, cut back)


5) restart RAW enzymatically buffed foods   (shift metabolism to alkaline)


6)     aerobic exercise to oxygenate the blood



Anti-angiogenic mechanisms and efficacy of the low molecular weight heparin, tinzaparin: anti-cancer efficacy.

Mousa SA, Mohamed S.

Oncol Rep. 2004 Oct;12(4):683-8.

Pharmaceutical Research Institute, Albany College of Pharmacy, Albany, NY 12208, USA.

Inhibitors of angiogenesis are potential anti-cancer agents in that they deprive tumors of the blood necessary for growth and metastasis. The anti-angiogenic efficacy of tinzaparin, a known anticoagulant low molecular weight heparin (LMWH), was examined in vitro in endothelial cell tube formation assay and in vivo in the chick chorioallantoic membrane model. The observed anti-angiogenic effects of tinzaparin were shown to be dose-related and dependent on the relatively higher molecular weight tinzaparin fragments. These experiments demonstrated that tinzaparin is a potent inhibitor of angiogenesis (ED90-100 range, 0.05-0.1 mg) regardless of the angiogenic factor and suggest that its effect is mediated via cellular release of tissue factor pathway inhibitor (TFPI). This was evident by the reversal of either tinzaparin or r-TFPI anti-angiogenesis efficacy by a specific monoclonal TFPI antibody. The ED90-100 for the inhibition of angiogenesis for r-TFPI ranged from 0.01 to 0.03 mg in the chorioallantoic membrane model regardless of the proangiogenic factor. In addition, either tinzaparin or r-TFPI inhibited the growth of colon carcinoma tumors, human fibrosarcoma tumors, and human lung carcinoma in the chorioallantoic membrane tumor implant model. Thus, the LMWH tinzaparin, in addition to its anticoagulant effects, may offer important benefits in treatment of cancer and other disorders supported by pathologic angiogenesis.

PMID: 15375485 [PubMed – in process]

2: Ugeskr Laeger. 2004 Aug 9;166(33):2781-4.

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[Hypercoagulation and cancer. New treatment possibilities]

[Article in Danish]

Lykke J, Nielsen HJ.

H:S Hvidovre Hospital, Gastroenheden, Kirurgisk sektion.

Publication Types:

·         Review

·         Review, Tutorial

PMID: 15344855 [PubMed – indexed for MEDLINE]

3: J Support Oncol. 2003 Nov-Dec;1(4):235-8, 240-2; discussion 239-40, 243-5.

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Management of thrombosis in the cancer patient.

Andrea N, Ansell J.

Department of Medicine, Boston University Medical Center, Boston, Massachusetts 02118, USA.

The treatment of venous thromboembolism in the cancer patient presents many challenges. The safety and efficacy of anticoagulation in these patients are still evolving. The clinical scenario is often unique to each patient and dictates careful consideration of the method of anticoagulation. Various issues that need to be considered are the length of anticoagulation, the method of administration, and the potential pitfalls of initiating one therapy over another. This review attempts to provide an approach to these issues in the treatment of the cancer patient with venous thromboembolism. The role of warfarin, heparin, and low-molecular-weight heparin is discussed. Additionally, adjunctive measures, such as vena cava filter insertion and thrombotic complications associated with central venous catheters, are discussed. The review is meant to provide clinicians with practical guidelines through a review of the pertinent literature.

PMID: 15334865 [PubMed – in process]

4: Cancer Res. 2004 Aug 15;64(16):5720-7.

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Heparin-binding EGF-like growth factor is a promising target for ovarian cancer therapy.

Miyamoto S, Hirata M, Yamazaki A, Kageyama T, Hasuwa H, Mizushima H, Tanaka Y, Yagi H, Sonoda K, Kai M, Kanoh H, Nakano H, Mekada E.

Department of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Ovarian cancer is the most frequent cause of cancer death among all gynecologic cancers. We demonstrate here that lysophosphatidic acid (LPA)-induced ectodomain shedding of heparin-binding EGF-like growth factor (HB-EGF) is a critical to tumor formation in ovarian cancer. We found that among the epidermal growth factor receptor (EGFR) family of growth factors, HB-EGF gene expression in cancerous tissues and HB-EGF protein levels in patients’ ascites fluid were significantly elevated. The human ovarian cancer cell lines SKOV3 and RMG-1 form tumors in nude mice. Tumor formation of these cells was enhanced by exogenous expression of pro-HB-EGF and completely blocked by pro-HB-EGF gene RNA interference or by CRM197, a specific HB-EGF inhibitor. Transfection with mutant forms of HB-EGF indicated that the release of soluble HB-EGF is essential for tumor formation. LPA, which is constitutively produced by ovarian cancer cells, induced HB-EGF ectodomain shedding in SKOV3 and RMG-1 cells, resulting in the transactivation of EGFR and the downstream kinase extracellular signal-regulated kinase/mitogen-activated protein kinase. LPA-induced transactivation was abrogated by HB-EGF gene RNA interference or by CRM197. Introduction of lipid phosphate phosphohydrolase, which hydrolyzes LPA, decreased the constitutive shedding of HB-EGF, EGFR transactivation, and the tumorigenic potential of SKOV3 and RMG-1 cells. These results indicate that HB-EGF is the primary member of the EGFR family of growth factors expressed in ovarian cancer and that LPA-induced ectodomain shedding of this growth factor is a critical step in tumor formation, making HB-EGF a novel therapeutic target for ovarian cancer.

PMID: 15313912 [PubMed – indexed for MEDLINE]

5: J Thromb Haemost. 2004 Aug;2(8):1311-5.

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Fixed-dose low-molecular-weight heparin for secondary prevention of venous thromboembolism in patients with disseminated cancer: a prospective cohort study.

Monreal M, Zacharski L, Jimenez JA, Roncales J, Vilaseca B.

Servicio de Medicina Interna, Hospital Universitari Germans Trias i Pujol, Badalona, Spain.

INTRODUCTION: Secondary prevention of venous thromboembolism (VTE) with vitamin K antagonists is often problematic in patients with cancer. We prospectively evaluated the effectiveness and safety of long-term subcutaneous dalteparin in a series of consecutive patients with symptomatic VTE and metastatic cancer. PATIENTS AND METHODS : The study included 203 patients, aged 36-96 years. The initial treatment consisted of a 7-day course of subcutaneous dalteparin according to body weight. Then, patients received a fixed dose of 10 000 IU dalteparin once daily for at least 3 months. In patients developing transient thrombocytopenia the dose was reduced to 5000 IU daily while the platelet count remained <50,000; and to 2500 IU daily while it remained <10 000. Patients undergoing any surgical intervention during the study were put on 5000 IU daily during the first 4 days, switching thereafter to 10,000 IU. Patients undergoing any other invasive procedure (i.e. biopsies, punctures) received a 5000 IU dose the same day, instead of 10 000 IU. RESULTS: Eleven patients (5.4%) developed major bleeding complications (6 fatal) during the 3-month study period, and 18 patients (8.9%) developed VTE recurrences (2 patients died). There were no higher complication rates in patients with either liver or brain metastases, nor during thrombocytopenia, surgery or invasive procedures. CONCLUSIONS: Fixed dose 10,000 IU subcutaneous dalteparin once daily for 3 months was not associated with more complications in patients with liver or brain metastases. The dose adjustment for patients with thrombocytopenia, surgery or invasive procedures was safe too.

PMID: 15304036 [PubMed – in process]

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