ANTI-MEK ARE BETTER ANTI-VEGF

Based on what we know now, it is easy to see that in those diseases where Avastin has failed FDA approval, Anti-MEK will do better.  MEK is down stream and MEK is involved in much more, including VEGF expression.  MEK is part of the MEK/MAPK pathways, it is the door to Mesenchymal transformation (that is it the door to epithelial-mesenchymal transition), and therefore to angiogenesis, and to metastatic spread.
Anti-MEK also removes the negative inhibitory effect of the PTEN driven forces of the PI3K/MTOR pathways.

PTEN inhibits insulin-stimulated MEK/MAPK activation andcell growth by blocking IRS-1 phosphorylation and IRS-1/Grb-2/Sos complex formation in a breast cancer model

1. (Liang-Ping Weng1 at al.)   The involvement of the Sons of the Sevenless could signify a large implication on the RAS pathway.  And Anti-MEK were used as Medication to be used in lung cancer displaying amplification of the K-RAS 

Watch it now as Cabozantinib, Selumtinib, and Trametinib will rise in anything Avastin has touched.
Metastatic Colon Cancer is the Primary target!

Only the MTOR inhibitors add to these drugs

Inability of Doxorubicin to add to DTIC in Melanoma is due to amplification of these 2 pathways.

Anti-MEK and MTOR combination will do far better in Melanoma and Pancreatic cancers, mark my words.  We just need to brace ourselves to a new set of side effects.

TEMPLATE FOR HEPATOCELLULAR CARCINOMA FOLLOW-UP:

DOES THE PATIENT HAVE
- JAUNDICE OR ELEVATED LFT(S) FOR USE OF DOXORUBICIN
- POOR APPETITE
- ASCITES (?THROMBUS AT HEPATIC VEIN)
- ABDOMINAL PAIN
- NAUSEA ALREADY
- WEIGHT LOSS

HX OF DM-ROLE OF INSULIN
HX OF HEPATITIS B OR C
HX OF CIRRHOSIS (LOCAL INTERVENTION)
HX OF HEMOCHROMATOSIS

LAB
- ALPHA FETOPROTEIN LEVEL
- ? DES-GAMMA-CARBOXYPROTHROMBIN
- U/S FOR DETECTION
- CT FOR MEASUREMT OF LESIONS,
- MRI FOR EXISTENCE OF CAPSULE AND PERIPHERAL INVASION, EXACT NUMBER OF LESIONS,
- PET FOR METASTATIC LESIONS AND RESPONSE TO THERAPY

TYPE OF HISTOLOGY
- FIBROLAMELLAR
- PSEUDOGLANDULAR
- PLEIOMORPHIC (GIANT CELL)
- CLEAR CELL
- ANAPLASTIC

CANDIDATE FOR
- SANDOSTATIN
- TAMOXIFEN
- ORAL SYNTHETIC RETINOIDS
- GALLIUM

P53 STATUS, MICROSATELLITE INSTABILITY, MDR,
TO PREDICT RESPONSE TO DAORUBICIN, PLATINUM, 5-FU, INTERFERON, EPIRUBICIN, TAXOL,

SORAFENIB (FATIGUE,RASH,DIARRHEA,HYPERTENSION.HAND FOOT SYNDROME)
- EGFR,VEGF

CANDIDATE
- TRANSPLANT
- PERCUTANEOUS ETHANOL
- TACE (WATCH FOR TUMOR >8CM, PORTAL VEIN THROMBUS,LFT-BILURIBIN LEVEL, SHUNT)
- RADIOFREQUENCY ABLATION (TUMOR <5CM)
- STEREOTACTIC RT
- SIRT

WHAT ABOUT IMMUNEPHERESIS AND PEXA-VEC?????

MUTATIONS IN HEPATOMA?  (CONTINUE REVIEWING LITERATURE OF COURSE I DID NOT INVENT THIS)