My Mom, diagnosed with CC, who has not even started chemo yet, spends a great majority of the day asleep in bed.  She wakes up to eat, but usually get tired within an hour as her limit and goes back to sleep.

She has been like this for the past two months.  Does anybody else experience this symptom outside of chemo causing it?  I don't think it's calories related because she is definitely getting the required daily amount.


(0 replies, posted in Adverse Reactions & Side Effects)

My Mom, diagnosed with CC, has had anosmia / parosmia (cant smell / phantom putrid smells) for a good 6 months before bing diagnosed.

Our problem is that she can't eat lot of foods because the scent makes her vomit.  So she's on a strict Ensure diet just to get calories down, and very bland foods.  No meat at all is tolerated.  Even veggies are tough.

She hasn't even started chemo yet.

Does anybody else here have that symptom?


(5 replies, posted in Chemotherapy)

I have been able to make some progress on finding medical insurance!

For those who have been denied due to pre-existing medical conditions, there's hope:

The Pre-Existing Condition Insurance Plan makes health insurance available to people who have had a problem getting insurance due to a pre-existing condition.

The Pre-Existing Condition Insurance Plan:
Covers a broad range of health benefits, including primary and specialty care, hospital care, and prescription drugs.
Does not charge you a higher premium just because of your medical condition.
Does not base eligibility on income.


(5 replies, posted in New Developments)

Melatonin exerts by an autocrine loop antiproliferative effects in cholangiocarcinoma: its synthesis is reduced favoring cholangiocarcinoma growth.

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.

22-Oxa-1,25-Dihydroxyvitamin D3 Efficiently
Inhibits Tumor Growth in Inoculated Mice
and Primary Histoculutre of Cholangiocarcinoma … .25478/pdf

It is well known that 1a,25-Dihydroxyvitamin D3(1,25[OH]2D3) restrains cell proliferation and induces
differentiation and apoptosis in normal and tumor cells. The authors of this report recently demonstrated that
1,25(OH)2D3 effectively inhibits the proliferation of cholangiocarcinoma (CCA) cell lines. The antitumor activity and
the underlying mechanism of 22-oxa-D3, an analog of vitamin D, in mice and in tissue cultures from patients with
CCA were further explored in the current study. METHODS: Cell growth and cell cycle distribution were examined in
CCA cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Mice
were injected subcutaneously with 4  106 CCA cells at both flank sides and intraperitoneal injections with phosphate-
buffered saline or 22-oxa-D3(15 lg/kg/day) for 17 days thereafter. Tumors were removed the next day. The
expression levels of cyclin D1 and the cyclin-dependent kinase inhibitor p21 were determined by Western blot analysis
and immunohistochemistry. Growth inhibition of 22-oxa-D3 in fresh tissue samples from patients with CCA was analyzed
by using a histodrug response assay.

RESULTS: 22-Oxa-D3 effectively suppressed the growth of CCA cell lines
in a time-dependent and dose-dependent manner. 22-Oxa-D3 arrested CCA cells at G1 phase to S phase by the suppression
of cyclin D1 expression and the up-regulation of p21. Supplementation of 22-oxa-D3 to CCA-inoculated mice
significantly inhibited tumor growth without hypercalcemia or serious side effects. The treatment also induced cellular
apoptosis in tissue samples from patients with CCA.

CONCLUSIONS: 22-Oxa-D3 effectively suppressed tumor growth
in CCA-inoculated mice and induced cellular apoptosis in tissue samples from patients with CCA. The current data encourage
further investigation of 1,25(OH)2D3 or its analogues as therapeutic agents in the treatment of patients with
CCA. Cancer 2010;116:5535–43. VC 2010 American Cancer Society.


(5 replies, posted in Chemotherapy)

First of, thank you very much for reading this.  If you could help answer some of the questions below, we would sincerely appreciate it.

My Mom is an international patient with CC and has come to the United States to seek better medical care for her disease.  She has no medical insurance coverage in the United States, as such she must self-pay any and all medical costs.

Based on the doctor's recommendations for treatment, we have been provided an self-pay estimate of the treatment cost for Folfox-6.  Let's just say that we were quite shocked at the cost!  Now it could be just the area/hospital, so we are definitely looking into other possible options.


1)  For those of you who have had Folfox-6 treatment and self-payed, how much did it cost per cycle?

2)  For those who have insurance that covered Folfox-6 treatment, would you be able to share how much the hospital billed the insurance company, as well as how much the insurance company paid the hospital?

3)  For those with experience with non-US resident/citizen patients seeking medical treatment in the U.S. who have no medical insurance, do you have any advice on how we could possible get some financial assistance/insurance coverage for my Mom?

4)  My Mom actually has medical insurance coverage in her country of origin, just not here in the U.S.  Her insurance provider already said that if she upgraded her insurance to have U.S. coverage, she would not be able to use the benefit until 1 year later due to her "pre-existing medical condition."  Do you by any chance know of any recent laws that would make her despite the pre-existing medical condition?  I thought there was something - but I wasn't sure what to research.

Thank you again for reading.

Hi everybody-

I was doing some research and bumped into this study.  So I started looking for old threads of people here talking about this study or vitamin d3.  I saw a few posts about a few individuals who have been using/taking vitamin d3, although nothing widespread.  The study's title alone seems to indicate a curative potential, and even a synergistic effect with the noted chemotherapy drugs.  Although it was only in vitro and in vivo.  I did find one clinical study ( that intends to investigate  vitamin d3 in CC cases.

Anyway, my Mom has CC, and I am trying too figure out if supplementation of this vitamin could be helpful, what dosage is safe and would be potentially helpful.  My only concern is that Vitamin D3 is processed by the liver, which as we know is typically the compromised organ in CC patients.  She has not started chemo (folfox-6), but will be in the next week.

Anyway, I wanted to open discussion, opinions , and feedback to the general community on this vitamin.  All responses appreciated!  smile

Here's the study:

Vitamin D3 regulates cell viability in gastric cancer and cholangiocarcinoma.

AuthorsBaek S, et al. Show all Journal
Anat Cell Biol. 2011 Sep;44(3):204-9. Epub 2011 Sep 29.

Department of Anatomy, Pusan National University School of Medicine, Yangsan, Korea.

A low serum level of vitamin D has been associated with an increased incidence of gastrointestinal tract cancers. However, the effects of vitamin D3 have not been investigated in gastric cancer and cholangiocarcinoma. In the present study, we found that vitamin D3 treatment significantly suppressed the viability of gastric cancer and cholangiocarcinoma cells. Moreover, vitamin D3 had a synergistic effect with other anti-cancer drugs, such as paclitaxel, adriamycin, and vinblastine, for suppressing cell viability. To determine the underlying mechanism involved in the regulation of viability by vitamin D3, we examined the effects of vitamin D3 on expression of hedgehog signaling target genes, which has been associated with gastric cancer and cholangiocarcinoma. Vitamin D3 treatment decreased the level of mRNA expression of patched1, Gli1, cyclin D1, and Bcl2, suggesting the possibility that vitamin D3 may act through regulation of hedgehog signaling. From the above results, we conclude that vitamin D3 regulates cell viability in gastric cancer and cholangiocarcinoma.

Hello.  I am new here and this is actually my first post.  I was hoping I could get some opinions/questions answered from you kind folks.

My Mom was recently diagnosed with CC.  She was ineligible for surgery or other radiotherapy treatments.

Her first oncologist put her on Gemzar + Xeloda.  Before finishing the first treatment, they performed an MRI and learned that the tumors in her liver grew by about 30%.  At that point the Oncologist said that she didnt believe the Gemzar + Xeloda was going to work.

It was my belief that Gemzar + Ciscplatin is actually the standard treatment protocol for CC with the highest potential benefit.

So we went to a new Oncologist at one of the top-5 Cancer Center hospitals.  They agreed that they couldnt ignore the fact that Gemzar + Xeloda seemed to not work, and that in their opinion trying  Gemzar + Ciscplatin would just be asking "too much" of the second drug as Gemzar is the primary drug that does most of the legwork.  Is that true?

As such, they thought it was best to shift gears altogether and go with Folfox.  Does this recommendation make sense to those of you with experience on this?

The new Oncologist mentioned that they believed Folfox would likely become the treatment protocol in a few years (as opposed to Gemzar + Cisplatin today).   Does anybody know where can I get more information on the efficacy of Folfox, and any related studies pertaining to it?

Thank you very much in advanced for your reading my thread and I look forward to reading your answers.