Sunifiram and Brain Cancer

Full study: http://ge.tt/5bR5qkj/v/0?c

>Chemical carcinogens
such as nitrosamines, present in tobacco smoke, are
known to modulate PKC isoenzyme ratio. Specifi-
cally, nitrosamines have been shown to induce
increased expression and activation of PKC
a
and
b
while PKC
d
is downregulated
[70–72]
. Introduction
of oncogenic Ras to keratinocytes has been shown to
upregulate PKC
a
and downregulate PKC
d
activation,
and inhibition PKC
a
expression in Ras transformed
cells leads to more differentiated phenotype
[73–76]
.
Furthermore, oncogenic Ras has been shown to
induce PKC
a
overexpression in colon cancer cells
[77]
. c-myc oncogene induces increased PKC
b
expression and PKC
b
is thought to partially mediate
c-myc induced malignant phenotype
[78,79]
. p53
mediated signaling has also been linked to regulation
of PKC
a
expression since wild-type p53 suppresses
PKC
a
expression through transcriptional block
[80]
.
Based on these notions, one could speculate that Ras,
c-myc and p53 mutations occurring very frequently in
human cancers could at least partially explain the
increased PKC
a
/
b
activity or expression of some
cancer types.

So it seems that carcinogens don't just activate PKCa, but modify the expression of the subreceptors. Making the jump from that to sunifiram potentially causing cancer due to PKC activation is a little bit much. Activation of PKC alpha receptors is crucial in many processes, including hydrolyzing phosphatidylcholine. If mere activation of that subreceptor caused cancer, then we are all screwed. Not that the mechanisms should be overlooked. But don't jump to conclusions just yet.