INTEGRATING THE CAUSAL FACTORS OF GI MALIGNANCIES/QUESTIONS IN GI MALIGNANCIES

Indolency: one of the biggest unresolved question in cancer genetics is the clear determination of
what genes are determinant for indolency:  genes'role is defined by their position in a critical pathway and by the number of interactions they have.  It appears that a genes with multiple interactions (wild gene  i.e Grb2,Androgen gene,FYN) could definitely impact considerably cellular events and could indeed force things into the neoplastic way or direction.  There are gene that are critical as the are located upstream on an important gene.  Our own experience has stressed the importance of gene which induce malformation if lacking (i.e MITF)

MITF microphthalmia-associated transcription factor [ Homo sapiens (human) ]

Part of the "Indolent tumor gene" are those found in both preneoplastic and malignant diseases.  Although caution should be brought here since an early occuring Mutation could be just a normal irreversible process to full neoplasia.   Other than preneoplastic, there are Cancers that are truly indolent (with survival in years). The Neuroendocrine tumors are cited repeatedly (GIST also).  These are clearly identified as those cancers with a limited numbers of Driver Mutations or with gene abnormality responsive to some well known Target therapy or chemosensitivity!   Our experience is pointing to evidence that Regulator genes are generally bad actors!
TO BE CONTINUED==============================
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Hepatocarcinoma Vs Pancreatic Vs Neuroendocrnie cancers
Familial cancers different from random cancers (Genetically)
Known abormal CBF
what are the known targets
what are the known biomarkers

Ingestion of Irritant
Body mass: Insulin,lipolysis, Fat Acid, High TNF, metalloproteases,calories,salt,nitrates,iron in drinking water,type A
Genetic (racial factors)
location and culture (Anti-Oxidant, FE, Zinc, Magnesium,)

GERD influence Chronic irritation
meaning NF-KB C-JUN TGF, CYCLINS
Increased Gastric secretion? Glandular secretion MUC1
HLA
MEK-and Wnt, Notch- Metaplasia
Androgen, MTOR (Silencing, and TNF), smoking, ARYL Hydrocarbon

Medication may induce Atrophic and mitigateNeoplastic transformation