Molecular correlates the mutations

 Molecular correlates the mutations, gene copy
variety abnormalities, and patterns of protein expression
that drive carcinogenesis in epithelial lung tumors are largely
absent from mesothelioma. the underlying molecular lesions
to blame for uncontrolled tumor cell growth in mesothelioma
don't seem to be well understood. it's known that asbestos may
induce phosphorylation of egfr 388 stimulating tumor cell
growth and spread however egfr mutations commonly present
in an exceedinglydenocarcinoma haven't been found in mesothelioma. 389
genes that are overexpressed and could represent activation of
growth signal transduction embody hepatocyte growth factor
(hgf) 390 and notch, 391 however mutations and structural alterations
affecting these genes haven't been explored to date. in
reality, genomic alterations in mesothelioma are various 392
however consistent abnormalities affecting specific genes don't seem to be
defined.
it's been proposed that reactive oxygen and nitrogen
species created in response to asbestos fibers directly
induce dna injury in mesothelial cells, inflicting adduct
formation and ultimately mutation of vital tumor
suppressor genes inducing nf2, p15, and p16. in an exceedinglyddition,
sv-40 sequences are identified in mesothelioma.
393 sv-40 massive t antigen could be able to bind rb and p53
protein. binding of those proteins could result in tumor cell
proliferation and chromosomal instability. the role of sv-
forty in mesothelioma, in spite of this, has however to be confirmed and
clinical consequences of this potential association don't seem to be
established.