Hi everyone, I’m about to start chemo round 4 out of 6 and I’m changing from FEC- T to Docetaxel for my triple negative BC.
Has anyone else been on this treatment course? Looking for reassurance and experiences as the 2 minute chat with a substitute oncologist in prep for starting tomorrow has left me really scared.
Thank you all 💕
Phosphocholine derivative of docetaxel‐conjugated lithocholic acid can form stable sub‐100 nm nanomicelles (DTX‐PC NMs). DTX‐PC NMs exhibit superior tolerance and pharmacokinetics over FDA‐approved formulation. DTX‐PC NMs can retard tumor progression in murine models and induce upregulation of tumor suppressor genes. Superior pharmacokinetic profiling in non‐human primates makes them an ideal platform for clinical applications.
Abstract
In this study, we describe the engineering of sub‐100 nm nanomicelles (DTX‐PC NMs) derived from phosphocholine derivative of docetaxel (DTX)‐conjugated lithocholic acid (DTX‐PC) and poly(ethylene glycol)‐tethered lithocholic acid. Administration of DTX‐PC NMs decelerate tumor progression and increase the mice survivability compared to Taxotere (DTX‐TS), the FDA‐approved formulation of DTX. Unlike DTX‐TS, DTX‐PC NMs do not cause any systemic toxicity and slow the decay rate of plasma DTX concentration in rodents and non‐rodent species including non‐human primates. We further demonstrate that DTX‐PC NMs target demethylation of CpG islands of Sparcl1 (a tumor suppressor gene) by suppressing DNA methyltransferase activity and increase the expression of Sparcl1 that leads to tumor regression. Therefore, this unique system has the potential to improve the quality of life in cancer patients and can be translated as a next‐generation chemotherapeutic.
https://ift.tt/2JgzseM
No side effects other than heartburn for my aged 75 year old mother after the first cycle of the chemo regimen mentioned above. Prior to that, she was on Keytruda immunotherapy for 9 months until the cancer began to progress again. This second line chemo, second cycle, was on Wednesday, and she went to the ER Friday morning complaining of shortness of breath, which I read is a severe side effect of either the Neulasta or decadron (steroid given to reduce inflammation potentially caused by the Taxotere) resulting in ARDS (Acute Respiratory Distress Syndrome). The cyramza immune agent can possibly cause a blood clot, so when admitted, she was found to have edema in the lungs as well as the RVMT. Seems any of these drugs given could have caused this. She has prior heart damage from massive radiation 22 years ago for her breast cancer.
This clot, though... they put her on Eliquis while in the hospital, and gave her an Rx to stay on for the duration of her cancer. However, just like with Keytruda, before we made the decision to go with it, the pros and cons were 50/50 - life-saving pros, and really bad high grade side effects - seems the same go with this Eliquis. Pros - no more clots, Cons - internal fatal bleeding. She had no issues with the Keytruda, but the Eliquis, I can't gauge if it's the right call or not. She'll be done with this chemo regimen in a few months, if not before that, but I don't know when these fatalities with Eliquis happened after beginning the drug. Would she be safe to take it for just a couple of months or could the bleeding begin quite quick?
Phosphocholine derivative of docetaxel‐conjugated lithocholic acid can form stable sub‐100 nm nanomicelles (DTX‐PC NMs). DTX‐PC NMs exhibit superior tolerance and pharmacokinetics over FDA‐approved formulation. DTX‐PC NMs can retard tumor progression in murine models and induce upregulation of tumor suppressor genes. Superior pharmacokinetic profiling in non‐human primates makes them an ideal platform for clinical applications.
Abstract
In this study, we describe the engineering of sub‐100 nm nanomicelles (DTX‐PC NMs) derived from phosphocholine derivative of docetaxel (DTX)‐conjugated lithocholic acid (DTX‐PC) and poly(ethylene glycol)‐tethered lithocholic acid. Administration of DTX‐PC NMs decelerate tumor progression and increase the mice survivability compared to Taxotere (DTX‐TS), the FDA‐approved formulation of DTX. Unlike DTX‐TS, DTX‐PC NMs do not cause any systemic toxicity and slow the decay rate of plasma DTX concentration in rodents and non‐rodent species including non‐human primates. We further demonstrate that DTX‐PC NMs target demethylation of CpG islands of Sparcl1 (a tumor suppressor gene) by suppressing DNA methyltransferase activity and increase the expression of Sparcl1 that leads to tumor regression. Therefore, this unique system has the potential to improve the quality of life in cancer patients and can be translated as a next‐generation chemotherapeutic.
https://ift.tt/2JgzseM
