New British study below [1].
"Pre-clinical models demonstrate that platelet activation is involved in the spread of malignancy."
(Metastasis is dependent on unwanted coagulation. This is why I use nattokinase to dissolve unwanted clots, and the D-dimer test to ensure that there are no active clots.)
It is well-known that low-dose aspirin can inhibit platelet aggregation - a necessary step for clot formation.
"Urinary 11-dehydro-thromboxane B2 (U-TXM), a biomarker of in vivo platelet activation ..."
Actually, thromboxane A2 triggers platelet activation. Thromboxane A2 is the precursor of thromboxane B2. Urinary thromboxane B2 can therefore be viewed as a surrogate for platelet activation.
Thromboxane ("thrombo" as in thrombosis) in cancer is a result of chronic nuclear factor-kappaB [NFkB] activation. One of the many proteins produced is COX-1, which acts on the omega-6 fatty acid arachidonic acid to generate thromboxane A2. Aspirin is a cox-1 inhibitor.
"716 patients (breast 260, colorectal 192, gastro-oesophageal 53, prostate 211) median age 61 years, 50% male were studied. Baseline median U-TXM were breast 782; colorectal 1060; gastro-oesophageal 1675 and prostate 826 pg/mg creatinine; higher than healthy individuals (~500 pg/mg creatinine)."
"Aspirin 100 mg daily decreased U-TXM similarly across all tumour types (median reductions: 77-82%)."
As expected, "Aspirin 300 mg daily provided no additional suppression of U-TXM compared with 100 mg."
"Thromboxane biosynthesis should be explored further as a biomarker of active malignancy and may identify patients likely to benefit from aspirin."
Aspirin, even at the low dose, is not without problems (would the FDA approve it today?). Following the aggregation of platelets, there begins the accumulation of fibrin to form the clot. I rely on nattokinase (to dissolve the fibrin) - and D-dimer testing - to deal with on-going clotting. Aspirin can be harsh on the stomach & kidneys. Aspirin users should periodically check D-dimer too.
***
From the old century, a Swedish study [2].
"Oestrogen has been proposed to influence platelet activity and formation of the vasoactive eicosanoids thromboxane and prostacyclin."
"Ten consecutive male patients with prostatic carcinoma participating in a randomized study comparing the effects of parenteral oestrogen therapy (n = 5) with orchidectomy (n = 5) were included. Oestrogen was given as polyestradiol phosphate 240 mg i.m. every month ..."
"We found a consistent decrease of in vivo formation of thromboxane by approximately 40% during parenteral oestrogen therapy ... and a doubling after surgical castration."
"In conclusion, oestrogen induced a marked decrease of in vivo formation of thromboxane and a marked increase in the ratio of prostacyclin to thromboxane formation in all patients. According to current knowledge this should be beneficial for the cardiovascular system."
The final study, from last year, looked at mortality in African-American men. [3]
"Thromboxane A2 (TXA2) is a platelet- and cyclooxygenase-derived eicosanoid that has been linked to metastasis."
"We measured urinary 11-dehydrothromboxane B2 (TXB2), a stable metabolite of TXA2"
"Urinary TXB2 was inversely associated with aspirin use."
"High TXB2 was positively associated with metastatic prostate cancer (OR = 2.60 ...)"
"Furthermore, high TXB2 was also associated with all-cause (adjusted hazard ratio = 1.59 ...) and prostate cancer-specific mortality (hazard ratio = 4.74 ...)"
-Patrick
[1] pubmed.ncbi.nlm.nih.gov/374...
