Follow-up at SAN ANTONIO

Researcher from Vanderbilt, namely Justin M Balko submitted a report where they examined tissue from 81 women who had undergone Neoadjuvant chemotherapy, in their study, they examined 450 genes as opposed to the 180 reported earlier.
90% of of all patient had at least 1 aberration in 5 signal pathways
1- PI3K/MTOR (therefore opening the door to Afinitor and related agents)
2. DNA repair  (May be PARP will have a role here)
3. Ras/MAP kinase   (Anti Myc /MEK inhibitor)
4. Cell cycle division (May be the Histone Deacetylase transferase inhibitor)
5. Growth Factor (Interferon and Interleukins)

Most common Mutations were in
-P53  (role  of Vitamin D can be discussed here)
- MCL-1(found in 56% of tissue) and Myc, found in 36% (Histone deacyltransferase inhibitors here  but also role of anti-actin/anti-Microtubule/anti-calmodulin )

The finding of prominent MCL-1, a Bcl-2 member goes directly to basic resistance to chemotherapy and actually could be reactive or an expression of primary refractoriness to chemotherapy.
JAK-2 was found in 11% (JAK2 inhitors could be tried)

Amplification in the MEK (cabozantinib)
PIM-1 would bring to bear Inteferon and Interleukins as therapeutic drugs (watch out PIM1 is an indicator that cyclins are an important drivers as they affect STAT3,5

The corollary question is whether to give the target therapy in maintenance setting or at time of progression.

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Medications and MCL-1 comment suggested here were not part of the report.  We are working hard at CRBCM!