Nomenclature of 2 important genes in Ovarian cancer !

1.RASSF1A:  One of the thing cancer cell do is to Methylate some genes in order to block its path to death.
it appears this gene is a critical door to shut or disable.  It not only decrease the significance of RAS and MAPK in the pathogenesis of tumor that harbor this mutation.   It also remove blockage to proliferation by desensitizing the cell to the effect of P53, Cyclins.  Desensitize the cell to Death Receptor 6 and its Fas connection.  RASSF1a, demethylation is a valid target in ovarian cancer.

2.HNF1B:  " Hepatocyte Nuclear Factor 1α (HNF1α) is an atypical homeodomain-containing transcription factor that transactivates liver-specific genes including albumin, α-1-antitrypsin and α- and β-fibrinogen. Biallelic inactivating mutations of HNF1A have been frequently identified in hepatocellular adenomas (HCA), rare benign liver tumors usually developed in women under oral contraceptives, and in rare cases of hepatocellular carcinomas developed in non-cirrhotic liver. HNF1α-mutated HCA (H-HCA) are characterized by a marked steatosis and show activation of glycolysis, lipogenesis, translational machinery and mTOR pathway. We studied the consequences of HNF1α silencing in hepatic cell lines, HepG2 and Hep3B and we reproduced most of the deregulations identified in H-HCA."
 (Laura Pelletier et al)
This gene is the gene of differentiation for liver formation, it has the structure of a CBF (core binding Factor) therefore has a subunit binding the DNA, therefore silencing that portion, and another subunit having locations for enzymatic proteins or molecular structures that directly assume various functions intended by the cell (formation of Albumin, alpha Antitrypsine, and Beta Fibrinogen).
Interestingly enough, Steatosis is a prominent feature here.  This structure and gene may be of interest in LIPOSARCOMA?  
DOES ACTIVATION OF MTOR DEMONSTRATED HERE OPEN THE DOOR TO THE USE OF MTOR IN LIPOSARCOMA?

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)