Showing posts with label xeloda. Show all posts
Showing posts with label xeloda. Show all posts

Sunday, March 10, 2013

METASTATIC COLON CANCER

*It is interesting to note that in current clinical practice  3/4 of Oncologist still give Avastin instead of Cetuximab as their first choice in KRAS wild type metastatic colon cancer, and they chose it in combination with FOLFOX.   Why to do the test at onset.  And 12 cycles won rather than "until disease progression" in Metastatic setting.
* If you worry about Mismatch repair, it did not come up!

*Avastin-Xeloda superior to Xeloda alone with
- progression free survival (PFS) 9.1 months Vs 6.1months
- Overall survival (OS) 20.7 months Vs 16.8 months

* In Maintenance setting, Combining Avastin to Erlotinib was superior to Avastin alone  (OPTIMOX3) in terms of progression free survival.

*In the VELOUR study
Aflibercept +FOLFIRI was superior to Folfiri alone in terms of PFS and OS.

*new kid on the block Regorafenib (brings back use of EUCERIN cream for patients palms)




Wednesday, December 19, 2012

COMBINATION OF XELODA, AND ANTICALMODULIN AND AN ANTI-P35 ANTIBODY FOR TRIPLE NEGATIVE BREAST CANCER.,

OR TAXOTERE-XELODA-VELCADE-ANTI-P35

If the fighting cancer strategy is to disrupt the cell where it hurts the most, the above combinations make the most sense.  These combinations achieve the following:

1.  Disruption of Microfilaments/Microtubules which in turn disrupt Anaphases in dividing cancer cells.  This also disrupts membrane attachment of  Cytochromes in Mitochondria by disrupting the Cytoskeleton, and leads to Caspase release.
2. Xeloda leads to an increase of intracellular 5-FU and to DNA breakage which triggers activation of P53 induced stoppage of cell division.
3. The Anti-Calmodulin will add and increase an intracellular release of Calcium leading to stimulation of Endonucleases which will further damage the DNA.
4. The Anti-P35 decreases resistance to Caspases since P35 is an inhibitor of  Caspases.
5. To lead to growth advantage, most cancers get a mutation of the MDM2 which leads to increased ubiquitination proteins/cyclins  favorable to apoptosis, making Velcade a powerful drug as it disrupts the proteasomes!

With these combinations, we are trying to harvest the strongest destructive forces in a cell!