New study below.
Six months back I started a thread:
"Non-PCa Prescription Drugs: Thalidomide / Lenalidomide (Revlimid)"
healthunlocked.com/advanced...
18 months earlier, I had posted the Mainsail trial results where the addition of Lenalidomide to Docetaxel+Prednisone produced inferior results.
Odd, perhaps, that Thalidomide & Lenalidomide would show mixed results.
& now a cell study from India reports that:
"Thalidomide inhibited 'Cell cycle' and 'E2F network', possibly accounting for its synergistic effects with docetaxel. Conversely, lenalidomide promoted 'Cell cycle' and 'Cholesterol biosynthesis'."
"Hence, we propose that lenalidomide upregulates cholesterol synthesis followed by enhanced rate of cell cycle, thereby nurturing a hyperproliferative tumor microenvironment. In summary, this study offers a possible explanation for the differential outcomes in the treatment of mPCa with thalidomide and lenalidomide."
Those who have come across encouraging use of Thalidomide for PCa, should not assume that it would be better to use the kinder gentler modern version - Lenalidomide.
Incidentally, my wife is on Revlimid (Lenalidomide) & her insurance pays $14,000 / month (for 21 little pills). Thalidomide is presumably much more affordable.
-Patrick
ncbi.nlm.nih.gov/pubmed/301...
Future Oncol. 2018 Aug 24. doi: 10.2217/fon-2018-0090. [Epub ahead of print]
Mechanistic insights into the differential effects of thalidomide and lenalidomide in metastatic prostate cancer.
Sundaresan L1,2, Kumar P1, Chatterjee S1,2.
Author information
1
AU-KBC Research Center, Anna University, Chennai, India.
2
Department of Biotechnology, Anna University, Chennai, India.
Abstract
AIM:
To understand why thalidomide and lenalidomide exhibit different responses in metastatic prostate cancer (mPCa) treatment.
METHODS:
We analyzed the perturbation signatures of thalidomide, lenalidomide, flutamide treated mPCa cell line from Library of Integrated Network-based Cellular Signatures database and transcriptome of docetaxel-treated mPCa patients.
RESULTS:
Flutamide and docetaxel downregulated 'Steroid Biosynthesis', 'Cell cycle' and PCa specific transcription factor networks. Thalidomide inhibited 'Cell cycle' and 'E2F network', possibly accounting for its synergistic effects with docetaxel. Conversely, lenalidomide promoted 'Cell cycle' and 'Cholesterol biosynthesis'.
CONCLUSION:
Hence, we propose that lenalidomide upregulates cholesterol synthesis followed by enhanced rate of cell cycle, thereby nurturing a hyperproliferative tumor microenvironment. In summary, this study offers a possible explanation for the differential outcomes in the treatment of mPCa with thalidomide and lenalidomide.
KEYWORDS:
LINCS data; cell cycle; cholesterol biosynthesis; combinational therapy; docetaxel; flutamide; lenalidomide; metastatic prostate cancer; thalidomide; transcriptome
PMID: 30141351 DOI: 10.2217/fon-2018-0090