Life – Terror. Ecstasy. Fight. Denial. Flight. Failure. PAIN. Forgiveness. Reconciliation. Hope. Love. Peace – Death.
Results day
My first results since getting back from a long, six weeks in Australia. CT scans – Abdomen, Pelvis, Chest, Thorax. Prostate Specific Antigen (PSA) test. I have been on immune system suppressant injections for several months since a sudden, catastrophic, immune system failure triggered by a flu jab led to a significant psoriasis/eczema attack that put me in hospital for 3 weeks.
Psoriasis injections are commonly used in people with moderate to severe psoriasis who do not respond to topical or oral treatments. Methotrexate, an immune suppressant drug, and biologic drugs such as Enbrel (etanercept), Humira (adalimumab), and Stelara (ustekinumab) are examples of injectable psoriasis medications.
Based upon my severe skin conditions & my metastatic prostate cancer prognosis it was agreed [myself, plus my cancer & dermatology consultants that, ‘for quality of life’, I should chance starting immune system inhibiting injections that should alleviate my worsening skin issues but could, severely [adversely] effect my cancer spread. Seven years ago I was refused such injections on the grounds it was too risky.
Some 6 months since starting Stelara (ustekinumab), this would be a tester to inform of any negative effects as in has my cancer spread accelerated significantly. I was expecting the worse, possibly a doubling of my PSA, or even worse…..much worse.
Telephone goes, 30 minutes earlier than expected, ‘Hello Mr Reynolds, it’s Dr Eswar, how are you?’ ‘I’m fucking wonderful, what do you think’! Actually, I’m fine sir, and yourself? We exchanged small talk, ‘your CT scans have shown no change, nothing to see and your PSA has dropped slightly, since July, from 2.7 to 2.5! WTF? Insane, not increase, a 7.5% decrease? Remarkable. I was that put back I forgot to ask, why? How can this be? I did ask about having another PET scan [much more accurate], to ‘make sure’, but as he rightly stated, that is hard [for him] to justify if there is nothing showing on a CT? He did advise me that there are PET scans available outside of the NHS. ‘Il see you in 4-5 months’. Then he was gone.
After telling Gail, Aubrey and Perri of my surprising, welcome, good news I got to thinking, what has changed, what is different? I remembered I had started a new diabetes drug, Dapagliflozin. I did some digging and sure enough there have been limited studies that found it to have a positive effect on prostate tumours. I also take Metformin for diabetes and this drug has also shown up several times in prostate cancer trials. I wonder if there have been any trials that combined both?
I will look into it further, especially the potential to vary dosage of either or? But whatever happens from now on, long may it continue!
Dapagliflozin [Forxiga], canagliflozin, empagliflozin are inhibitors of sodium-dependent glucose co-transporter 2 (SGLT2). They have been registered for the treatment of type 2 diabetes by the European Medicines Agency (EMA) and the Food and Drug Administration (FDA).
They competently, reversibly and highly selectively block SGLT2 located in the proximal nephron tubules, which are responsible for the resorption of approximately 90% of urinary glucose. As a consequence, glucose is excreted in the urine and its plasma concentration is normalized in an insulin-independent mechanism]. Scagoflio et al. in their work, based on immunohistochemical tests using specific antibodies, concluded that both SGLT1 and SGLT2 are expressed in human prostate adenocarcinoma. In tumor regions with normal histology, SGLT1 was expressed in prostate ducts, but SGLT2 was not detected.
In tumors obtained from patients, they detected SGLT2 expression in regions with high uptake of an SGLT-specific radioactive glucose analog, α-methyl-4-deoxy-4-[18F] fluoroglucopyranoside (Me4FDG), and its functional activity was blocked by specific SGLT inhibitors (phlorizin or dapagliflozin). Both phlorizin and dapagliflozin reduced malignant tissue uptake of Me4FDG.
Similar results were obtained during in vivo studies in PC-3 mouse xenograft models of prostate cancer in which Me4FDG uptake was blocked by dapagliflozin. They also provided preliminary evidence on the efficacy of SGLT2 inhibitors in reducing growth and/or increasing tumor necrosis in the pancreatic xenograft model.
It has been reported that SGLT1 may strongly interact with epidermal growth factor receptor (EGFR), which is overexpressed in more than 80% of the late stages of prostate cancer and is associated with poor prognosis. EGFR, by interacting with SGLT1, is involved in maintaining basal intracellular glucose levels in cancer cells. They showed that inhibition of SGLT1 by its inhibitor (florinsine) sensitized prostate cancer cells to treatment with an EGFR tyrosine kinase inhibitor (gefitinib and erlotinib).
Bonus, Dapagliflozin is used together with proper diet and exercise to treat type 2 diabetes. It works in the kidneys to prevent absorption of glucose (blood sugar). This helps lower the blood sugar level. It makes you lose weight, you literally piss out all of the sugar!
Thanks for Reading
Peace
Dying to Live 