Ding-Wu Shen

TL;DR: Decreased accumulation is one of the most common features resulting in cisplatin resistance, and seems to be a consequence of numerous epigenetic and genetic changes leading to the loss of cell-surface binding sites and/or transporters for cisPlatin, and decreased fluid phase endocytosis.

TL;DR: Evidence is presented that multidrug-resistant sublines of human KB carcinoma cells, selected for resistance to either colchicine, vinblastine, or Adriamycin (doxorubicin), display amplification of two different DNA sequences homologous to the hamster mdr gene, suggesting that the mdr1 gene is involved inMultidrug resistance in human cells.

TL;DR: It is suggested that only a limited number of protein changes occur in multidrug-resistant cell lines, which are associated with a loss of translatable mRNA for these proteins.

TL;DR: A model that helps reconcile the disparate literature by describing multiple pathways for Pt-containing drugs into and out of the cell is suggested.

TL;DR: The results suggest that [Gd@C82(OH)22]n nanoparticles overcome tumor resistance to cisplatin by increasing its intracellular accumulation through the mechanism of restoring defective endocytosis of the CP-r cancer cells.