Melatonin and Cholangiocarcinoma
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Hi Tiffany,
Yes, it’s the same melatonin. If it helps you sleep, I say it’s good! As a mom of two young kids, you need good sleep.
As far as medical mambo-jambo goes, this article is one of the worst I’ve seen. It seems to say that CC cells generate less melatonin than normal cells. They think — and it’s just a theory — that lack of melatonin contributes to CC growth. When they added melatonin to CC cells implanted in mice, melatonin decreased tumor growth. Keep in mind, what works in mice might not work in humans. Don’t increase your melatonin dose like crazy just because of this one cryptic article.
BTW, Sloan-Kettering has a nicely written page about melatonin. It’s all in plain English.
http://www.mskcc.org/cancer-care/herb/melatoninS-K page contains this warning:
Quote:Because melatonin can alter levels of estrogen, patients with hormone sensitive cancer should consult their physicians before considering melatonin supplementation.Tiffany, talk to Dr.Javle about this warning. I seem to recall that ICC might be hormone sensitive.
P.S. Happy birthday to Madison!!
Tiff, don’t feel bad, I honestly don’t understand much of these ‘medical posts’ and am wondering if this is a Professional posting them? I really feel inadequate as I don’t even know what half the words mean. I am confused and not on chemo so I am wondering if this is confusing those who are suffering from CC and perhaps not understanding these posts.
Is this talking about the melatonin I take to help me sleep? I’m confused by this. LOL Is melatonin good or bad?
Melatonin exerts by an autocrine loop antiproliferative effects in cholangiocarcinoma: its synthesis is reduced favoring cholangiocarcinoma growth.
http://www.ncbi.nlm.nih.gov/pubmed/21778461
Abstract
Cholangiocarcinoma (CCA) is a devastating biliary cancer. Melatonin is synthesized in the pineal gland and peripheral organs from serotonin by two enzymes, serotonin N-acetyltransferase (AANAT) and acetylserotonin O-methyltransferase (ASMT). Cholangiocytes secrete neuroendocrine factors, including serotonin-regulating CCA growth by autocrine mechanisms. Melatonin exerts its effects by interaction with melatonin receptor type 1A/1B (MT1/MT2) receptors. We propose that 1) in CCA, there is decreased expression of AANAT and ASMT and secretion of melatonin, changes that stimulate CCA growth; and 2) in vitro overexpression of AANAT decreases CCA growth. We evaluated the 1) expression of AANAT, ASMT, melatonin, and MT1/MT2 in human nonmalignant and CCA lines and control and CCA biopsy samples; 2) melatonin levels in nonmalignant and CCA lines, and bile and serum from controls and patients with intrahepatic CCA; 3) effect of melatonin on the growth and expression of AANAT/ASMT and MT1/MT2 in CCA lines implanted into nude mice; and 4) effect of AANAT overexpression on the proliferation, apoptosis, and expression of MT1/MT2 in Mz-ChA-1 cells. The expression of AANAT, ASMT, and melatonin decreased, whereas MT1/MT2 expression increased in CCA lines and biopsy samples. Melatonin secretion decreased in the supernatant of CCA lines and bile of CCA patients. Melatonin decreased xenograft CCA tumor growth in nude mice by increased AANAT/ASMT and melatonin, along with reduced MT1/MT2 expression. Overexpression of AANAT in Mz-ChA-1 cells inhibited proliferation and MT1/MT2 expression and increased apoptosis. There is dysregulation of the AANAT/ASMT/melatonin → melatonin receptor axis in CCA, which inhibited melatonin secretion and subsequently enhanced CCA growth.
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