ANOTHER CONFIRMATION THAT TRIPLE NEGATIVE BREAST CANCER IS ANOTHER BEAST ALL TOGETHER. AS WE HAVE SHOWN, HERE THE RECEPTORS ARE COMPLETELY DESENSITIZED, YOU HAVE TO GO TO MEDICATION DEALING WITH THE FIRST AND SECOND LAWS TO ATTACK THE CELL. YOU HAVE TO GO "NUCLEAR" BY BREAKING DNA AND INTERFERING WITH MACROTUBULES.
WHAT IS UNCLEAR YET IS HOW THE DISEASE FINALLY ESCAPE. CISPLATIN RESISTANCE MAY BE THROUGH INCREASING REPAIR OF DNA.
"These data demonstrated that overexpression of c-erbB-2/neu can lead to intrinsic Taxol resistance independent from mdr-1 mechanisms.
"AURORA-A amplification overrides the mitotic spindle assembly checkpoint, inducing resistance to Taxol"
"Defective microtubule-kinetochore attachment and spindle formation
Authors: Yan Li,"
Resistance to Taxol in lung cancer cells associated with increased microtubule dynamicsA. Gonçalves*
Prediction of paclitaxel sensitivity by CDK1 and CDK2 activity in human breast cancer cellsSatoshi Nakayama1
"We found that changes in CDK1 specific activity after paclitaxel treatment predicted the paclitaxel sensitivity of breast cancer cells and xenograft tumors. Baseline CDK2 specific activity was higher in tumors that were sensitive to paclitaxel than in tumors that were resistant to paclitaxel."