NOMENCLATURE OF GENES TO LOOK FOR IN TRIPLE NEGATIVE BREAST CANCER

One may try to determine whether a breast cancer has bad prognosis in order to determine whether chemotherapy should be given (MammaPrint, Oncotypr DX), but more importantly, I believe, is to focus on genes of good prognosis which include driver genes against which we dispose of an answer in our Arsenal.
Currently we dispose of
1. Chemotherapy that attacks DNA and Microfilament/Microtubules,  (first and second law of nature)
2. Immune Modulators such as Interferon
3. Antibody to Membrane Receptor (EGFR/VEGF) Avastin
4.  Inhibitor to T-cell driven immunity (CTLA4)
5.  Inhibitors to sub-membrane or first line driver Mutations KRAS, HRAS, or the RAS family
6.  Inhibitors to 2nd line driver Mutations (anti MEK)
7. Inhibitor to Tertiary line driver Mutations and Mitochondrial level inhibition (MTOR, Metformin)
8. Anti-proteasome or inhibitor to cellular protein degradation (Velcade)
9. Inhibitors at Nuclear lever Include Histone Deacethylator and Acyl transferase inhibitor, check point controller inhibitors,  anti-Centrosome metabolism and inhibitors of various promoters and transcription factors.

Other opportunities not included in this classification go to specific genes of proliferation, Amplification, differentiation and metastasis that have been brought forth as indicator of either response to chemotherapy or simply as "Good prognosis" genes.  These will include the BRCA since a response to PARP inhibitors and Cisplatin based combinations should be anticipated.

Multikinase inhibitors such as Dasatinib (SRC+ BCR/ABL but also STAT5) and Arsenic Trioxide should be included   
LBK1: could predict early disease (inhibitor controlling initiation of metastasis)
DDR2: could predict anti MEK sensitivity
MEKK-1 sensitivity to Cisplatin
TFF1-could predict sensitivity to estrogen despite negative Estrogen
DYRK2, favorable in lung cancer
 
c-JUN amplification and over expression of 8q23-24 could predict  response to interferon/Interleukin
EGFR, VEGF, ALK,  and other Driver Mutations would match those discussed By DR Kris in lung cancer.

(to be continued!)

Building an Electronic Cancer Cell is a necessity

Natural death of cancer cells is the path to cure.
Experience of chemotherapy has shown that a blind and random attack of cancer cells is ineffective at assuring the death of cancer at a 100% curative rate. We believe that this is mostly due to the fact that chemotherapy most of the time does not inflict enough damage to the cell to lead to self destruction or Apoptosis. We believe that certain changes to the cell caused by chemotherapy could work counter the intended effect. This the basis of the trust in target therapy.
Now let us not approach Target therapy the same way we did for chemotherapy.  Target therapy has proven to work, no doubt about it. We need now to organize coordinated attacks on the cancer cells.  We know that Cancer cells' life processes seem to be organized in cascade, redundancy and escape mechanisms, but in a logical way. With one event following another.  This is why Target therapy works by cutting off or promoting upstream events in the cascade.The thing is that cells have downstream escape mechanisms, therefore that mechanism needs also to be struck down in a staged or coordinated attack.

We believe that the construction of an electronic model of a cell will help us identify gaps in the cascade of molecular events, and help identify critical new targets to go after, once these gaps are filled.
Some of the current targets
1. Adhesion Molecules
2. Cell membrane receptors
3. Signal transduction pathways
4. Transcription genes
5. Histones and promoter genes
6. Mitochondrial/ribosomes Metabolism disruption
7. Nuclear genetic material
8. Gene repair and mismatch repair mechanism
This list is not exhaustive, therefore the potential for investigation appears endless.