Nomenclature of some Genes in Ovarian Cancer:
BRAC1
BRAC2
CDO1
HER-2
CPG ISLAND
TMS1
ER alpha
PRB
MEK
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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. Desensititize the cell to Death Receptor 6 and its Fas connection. RASSF1a, demethylation is a valid target in ovarian cancer
RARbeta
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STRATIFIN.
LAM et al.
" stratifin,
also known as 14-3-3 sigma protein, stimulates matrix metalloproteinase
(MMP)-1 expression in dermal fibroblasts. Treatment of dermal fibroblasts with stratifin
resulted in rapid and transient upregulation of c-jun and c-fos mRNA
levels.
Stratifin was demonstrated to increase MMP-1 protein levels. Microarray analysis of stratifin-treated fibroblasts shows an
increase in Elk4/Sap1 mRNA expression and this finding was confirmed by
northern blot analysis. Our results indicate that stratifin markedly
increase Elk4/Sap1 mRNA expression in a time-dependent fashion. In
conclusion, stratifin stimulates fibroblast MMP-1 levels through the
activation of c-fos and MAPK pathway."
Our interpretation is that stratifin is part of an intergrin, its release in the Cytoplasm indeed stimulate MAPK C-JUN and c-fos. This means it is interpretated by the cell as a chemical stressor. The NF-kB is not far away. One of the most important hidden information here is the note by the authors that there is an increase of ELK4/Sap1.
ELK4 has been shown to
interact with
Serum response factor[4][5] and
BRCA1.
[6]
Serum response factor has been shown to
interact with
NFYA,
[10] Src,
[11] CREB-binding protein,
[12] GTF2I,
[13][14] ATF6,
[15] Nuclear receptor co-repressor 2,
[16] CEBPB,
[17][18] GATA4,
[19][20] Myogenin,
[21][22] GTF2F1,
[23][24] TEAD1,
[25] ELK4,
[15][26] Promyelocytic leukemia protein[12] and
ASCC3.
[27]
(wikipedia)
ELK4 therefore control BRCA1 and serum response factor which control NFYA. This uncover what the cancer cell has to do to start the neoplastic process. It has to derail genetic repair by abrogating the action of BRAC1, but it also has to take controles of CBF complexes and NFYA and ZHXY. Remember CBF complexes control the direction of the metabolism, In essence, when it comes to function in the cell, the role of Core Binding Factors (CBF) is indistinguishable from that of TRANSCRIPTION FACTORS. They all impose the direction that the cell metabolism should take.
Remember also that because the Stratifin engages the MAPK mostly through the certain well selected CDK, it will tend to stop cell division. In Breast cancer, Stratifin is one of the earliest methylated gene slated for silencing.
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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 a 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 direct assume various functions intended by the cell (formation of Albumin,alpha Antitrypsine, and Beta Fibrinogen) Interestingly enough, Steatosi 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 USE OF MTOR IN LIPOSARCOMA?
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p16INK4A
p14
CYCLIN D2
SLIT2
CDH13
PTEN
CLAUDIN 3,4
HE4
MUCIN1 OR MUC1
MESOTHELIN
ApoE, J
PIK3CA
P53 AND CHEK2
MLH1
MSH2,6
PMS2
CA-125
STK11
LKB1
PTCH
ATM
This is just the beginning, lets go to work! love those recurring genes as they cross over with presence in other cancers to strengthen their importance, Please remember those that lead to hypothrophy of muscles and extremities are probably more important for therapeutic intervention. And those with a "q" location on chromosome arm are most likely of poor prognosis or dramatic phenotype expression! Always do remember that Multidrug resistance (MDR-1) is in play HERE!
