My niece's son, aged 4 has just been diagnosed with Rhabdomyosarcoma of the
Bile duct and has had hiss gall bladder and bile duct removed. However,
there are still traces in the liver.

He's scheduled for chemo next week.

Can anybody help, please.

John

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This article speaks to the finding of higher than normal levels of
serum ferritin in those with this disease.
Serum ferritin is the marker of iron levels in the body.
Iron is KNOWN to 'feed' cancer .

Studies have shown the body has an upper LIMIT to the amount of
iron it can SAFELY hold .
Up until a year ago researchers had suspected this but had
always thought the transferrin had to be 100% full before the
iron became a 'problem'.
Problem being defined as not being held tightly away by the body.
They have found the iron becomes 'unsafe' or free when the transferrin
is only 35% full.

This is a compilation of articles which speak to this problem.
The NIH is funding studies as we speak to find suitable chelators..
iron binders ..which enter the body and remove this iron.

Subject: rhabdomyosarcoma

   Scand J Haematol 1977 Aug;19(2):153-8

Elevated serum ferritin in children with malignancies.

    Siimes MA, Wang WC, Dallman PR

   Serum ferritin (SF) is elevated in {*filter*}s with malignancies, chronic
   inflammatory disease, liver disease and iron overload. The purpose of
   this study was to determine whether the concentration of SF in
   children with a variety of malignancies correlated with the activity
   of their disease. Patients with acute lymphoblastic leukaemia (ALL) at
   initial diagnosis (n = 11) and relapse (n = 15) had a mean SF of 238
   and 338 ng/ml, respectively, compared to the normal mean of 31 ng/ml
   and range of 7 to 140 ng/ml in children. In 30 patients with ALL in
   remission the mean SF was 109 ng/ml, less than the values in patients
   with active disease and greater than the normal mean (P less than
   0.001). The concentration of SF was also increased in a group of 77
   patients with a variety of solid tumors. The 28 cases with active
   disease had a mean SF of 242 ng/ml, significantly higher (P less than
   0.001) that the value of 84 ng/ml in 49 patients with no evidence of
   residual tumor. The differences in SF concentration did reflect the
   activity of disease in the groups as a whole but it remains uncertain
   whether the assay will prove useful in following the response to
   treatment of patients with certain types of tumor.

   PMID: 197590, UI: 77258754
     _________________________________________________________________

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Subject: transferrin saturation/35%/iron

J Hepatol 2000 May;32(5):727-33

Determination of non-transferrin-bound iron in genetic hemochromatosis using a
new HPLC-based method.

    Loreal O, Gosriwatana I, Guyader D, Porter J, Brissot P, Hider RC

   INSERM U522, CHR Pontchaillou, Rennes, France.
   [Medline record in process]
   BACKGROUND/AIMS: Non-transferrin-bound iron may play a major
   pathogenic role in iron overload diseases due to its high hepatic
   uptake and potential damaging effect.
   The aim of this study was to
   evaluate the relevance of measuring serum non-transferrin-bound iron
   levels in genetic hemochromatosis using a new high performance liquid
   chromatography-based method.
   METHODS: This method includes a
   presaturation step of transferrin with cobalt(II) in order to avoid
   secondary deplacement of non-transferrin-bound iron toward transferrin
   during the assay.
   Six genetic hemochromatotic patients were followed
   serially during venesection treatment.

   RESULTS/CONCLUSIONS:
   The results indicate:
   (i) that this new method permits detection of
   non-transferrin-bound iron when transferrin is not fully saturated,
   (ii) that non-transferrin-bound iron levels persist almost until the
   completion of treatment,
   (iii) that non-transferrin-bound iron levels
   are well correlated with transferrin saturation for a given patient,
   and
   (iv) that despite some individual variations, a transferrin
   saturation value lower than 35% usually corresponds to the
   disappearance of non-transferrin-bound iron.

   PMID: 10845658, UI: 20302281

    _________________________________________________________________

Subject: cancer/kaposi

   J Invest Dermatol 2000 Nov;115(5):893-900

Iron chelators inhibit the growth and induce the apoptosis of Kaposi's sarcoma
cells and of their putative endothelial precursors.

    Simonart T, Degraef C, Andrei G, Mosselmans R, Hermans P, Van Vooren JP,
    Noel JC, Boelaert JR, Snoeck R, Heenen M

   Department of Dermatology, Erasme University Hospital, Brussels,

   Iron is suspected to be involved in the induction and/or progression
   of various human tumors. More particularly, iron may be involved in
   the pathogenesis of Kaposi's sarcoma, a tumor of probable vascular
   origin. This study was designed to investigate the effect of iron
   deprivation on Kaposi's sarcoma. The effects of iron chelators and
   iron deprivation associated with serum withdrawal were investigated on
   Kaposi's sarcoma-derived spindle cells, on a transformed Kaposi's
   sarcoma cell line (Kaposi's sarcoma Y-1) and on endothelial cells,
   which are the probable progenitors of Kaposi's sarcoma cells.
   Desferrioxamine and deferiprone, two chemically unrelated iron
   chelators, induced a time- and concentration-dependent inhibition of
   endothelial and Kaposi's sarcoma cell growth. The inhibition of cell
   growth was associated with a decrease in Ki-67 and in both stable and
   total proliferating cell nuclear antigen expression. Inhibition of the
   progression through the G1-phase of the cell cycle was further
   evidenced by decreased expression of cyclin D1 and of p34
   cyclin-dependent kinase 4. Terminal deoxynucleotidyl
   transferase-mediated desoxyuridinetriphosphate nick end labeling
   assay, flow cytometry with annexin-V-fluorescein and morphologic
   analysis indicated that iron chelation also induced a time- and
   concentration-dependent apoptosis. This apoptotic effect was prevented
   by the addition of exogenous iron. Induction of iron deprivation in
   the culture medium by serum withdrawal led to similar cell cycle
   effects, which, however, could only be partly reverted by the addition
   of exogenous iron. In conclusion, these results show that iron
   deprivation inhibits the growth and induces the apoptosis of Kaposi's
   sarcoma cells and of their putative endothelial precursors. This
   suggests that iron chelators may represent a potential therapeutic
   approach for the treatment of Kaposi's sarcoma.

   PMID: 11069629, UI: 20532598
     _________________________________________________________________

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Subject: chelator / cancer

   Carcinogenesis 2001 Oct;22(10):1607-14

p53-independent apoptosis mediated by tachpyridine, an anti-cancer iron
chelator.

    Abeysinghe RD, Greene BT, Haynes R, Willingham MC, Turner J, Planalp RP,
    Brechbiel MW, Torti FM, Torti SV

   Department of Biochemistry, Wake Forest University School of Medicine,
   Winston-Salem, NC, USA.

   [Medline record in process]

   Iron is involved in essential biochemical reactions ranging from
   respiration to DNA synthesis. Consequently, iron deprivation has been
   proposed as a strategy for inhibition of tumor cell growth. We
   recently described a novel iron chelator, tachypyridine
   [N,N',N"-tris(2-pyridylmethyl)-cis,cis-1,3,5-triaminocyclohexane], and
   demonstrated that it not only inhibited growth of cultured tumor
   cells, but was actively cytotoxic. Here we explore the mechanisms
   underlying tachpyridine cytotoxicity. Using several criteria,
   including time-lapse video microscopy, DNA staining and TUNEL assays,
   tachpyridine was shown to specifically induce apoptotic cell death.
   Further, unlike numerous cytotoxic chemotherapeutic {*filter*} which induce
   apoptosis by activating p53-dependent pathways, tachpyridine-mediated
   cell death did not require p53 activation. Although immunoblotting
   revealed rapid accumulation of p53 following treatment with
   tachpyridine, p21(WAF1) was not induced. Further, neither cytotoxicity
   nor apoptosis required p53. p53 null human lung cancer H1299 cells
   transfected with an ecdysone-inducible p53 exhibited equivalent
   sensitivity to tachpyridine in the presence and absence of p53,
   demonstrating the lack of requirement for p53 in an isogenic cell
   system. Further, time-lapse video microscopy and TUNEL assays
   demonstrated that both p53 null and p53 wild-type cells underwent
   apoptotic cell death in response to tachpyridine. In addition, in 55
   human cancer cell lines the mean GI(50) of tachpyridine in cells with
   mutant p53 was virtually identical to the GI(50) in cells with
   wild-type p53. These results demonstrate that tachpyridine initiates
   an apoptotic mode of cell death that does not require functional p53.
   Since over 50% of human tumors contain a functionally defective p53
   that reduces sensitivity to commonly used chemotherapeutic agents,
   such as etoposide and cisplatin, the ability of tachpyridine to induce
   apoptosis independently of p53 may offer an advantage in anti-tumor
   therapy.

   PMID: 11576999, UI: 21460375
     _________________________________________________________________

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...

read more »

I just checked out the nci Cancer Research Portfolio and only found two studies
that involved iron at all.

One had no description, the other contained this bit:

" The iron-CHD/cancer hypotheses have been supported by laboratory and animal
studies, but findings from small, less comprehensive epidemiologic studies are
inconsistent."

Is this the study to which you are referring?  If not, please post a link to
more information.

...lisa

John,
forget this jerk.

Rhabdo in kids is very responsive to chemotherapy, and I would think the
chances of cure are good.

This 'steph'.. fella? is an acupuncturist masquerading as
an oncologist ..
He has read up on chemotherapy and radiation and attempts to pass
himself off as a member in professional standing ..
Which by the way is against the law.. which is why his domain
and name do not exist on the web .. anonymity .. is the only
thing which save him from arrest ..

I posted many articles speaking to cancer .. all from Medline ..
the largest a most respected medical database in the world ..
used by the geniuses of the day in their research ..
Steph .. has yet to post an article .. plenty of 'heresay' ..
though ..

                             The Cancer Stopper

   Dateline: 04/02/98

   Researchers at the University of Maryland School of Medicine have
   found a potentially potent weapon in the fight against cancer. A sugar
   phosphate, called inositol hexaphosphate (IP6), was found to be
   effective against certain types of liver cancer in mice.

   IP6 is a sugar molecule with six phosphates attached. It occurs
   naturally in nature in such diverse things as wheat, rice bran,
   legumes and even in nearly all mammal cells. It helps to regulate
   cellular functions, particularly cell differentiation and
   proliferation.

   Scientists took human liver cells that were cancerous, treated them
   with various levels of IP6, and transplanted the treated cells into
   mice. IP6 was found to "check" the growth of the cancerous cells--not
   by destroying the cancer cells but by making the cancerous cells act
   like normal, healthy cells. Inositol hexaphosphate decreases the
   proliferation of the cancer cells, keeping them in "check."

   The higher the dose of IP6, the better the results. In the tests, mice
   that had transplanted cells with higher dosages of IP6 developed
   virtually no cancer. Those that had untreated cells developed the
   tumors we would expect from diseased cells.

   Some of the mice with tumors present were then tested as a follow-up.
   Injections of IP6 were given to the mice with tumors and, over the
   course of the treatment, the tumors decreased in size, sometimes
   almost five fold less than the size of the tumor at the start of the
   treatment.

   Interestingly enough, IP6 binds with several important minerals, like
   copper and zinc. Scientists suggested that taking the "pure" form of
   the substance rather than ingesting large quantities in the diet might
   prove more beneficial in fighting cancer.

   Scientists also hope that IP6 could be used in the treatment of other
   diseases and disorders, particularly in the fight against AIDS.

   Will IP6 prove to be a potent new weapon against cancer in the future,
   or is this another in the long line of substances that haven't lived
   up to their potential?

     __________________________________________________________________

Who loves ya.
Tom

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But only if it's untrue. Your posting is libellous, if I could be bothered,
by the way.

The only thing to save me from psychotic loonies like you, Tom.

I've told you before, Tom, just because someone gave you Medline to play
with, it doesn't make your opinions worth anything.

If you were intelligent, what would you say next.

That's all I needed to hear.  Steph comes across as an amateur who
will never admit being wrong.  What a {*filter*}wad.

--
Joel Crump

    snip the rest of the drivel emanating from a loonie!!!!!
    <plonk!> into the killfile.....

    That is something which we will =never= know!!!!!!!!!

I guess you have not been reading this or other cancer support newsgroups,
then.  Steph has been a staunch supporter of cancer patients and, as a member
of the medical community, has provided invaluable information.

Sometimes he may come across as rather abrubt.  Think about this...this is a
physician who is taking time our of his busy day to help people on the internet
for free.  That he does this at all is amazing.  A little brevity can be
understood in light of his contributions.

Before you begin supporting this person "watchman," I suggest you take a look
at his posts.  You happen to have gotten your judgements reversed when deciding
which of these two folks you label a f*wad.

...lisa

   Joel says:
<< Steph comes across as an amateur(plus other disparaging remarks) >>

Joel, you should be aware that publicly degrading a person's professional
status constitutes libel and is an actionable  civil and criminal offense.
Rolf

I somehow doubt this setting would qualify, but in any case, Steph
should feel free to do his worst.

--
Joel Crump

I wrote about my nephew who was diagnosed with cancer. I am amazed that this
subject has developed into an argument between different groups, which has
nothing to do with the predicament of my 4 year old nephew. Would anybody
who can offer me sound advice please email me. Thankyou.

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Hello John,

So sorry the little one has to go through this.

Besides the (other) arguing, some of us might have assumed that some people
e-mailed you privately.

Besides that, you didn't ask any specific question.  Nor provide many details
for anyone to comment on.
Like what the recommended chemo treatment is (where he's being treated) or
whether you are wanting opinions on what specialists in other centres might be
good for a 2nd opinion, etc etc.
Is this a re-occurrence (since none of the urls mention the gallbladder or the
liver).
Then one would ask, where's the primary?
May we assume that biopsy has confirmed the diagnosis?
And is the child in Stage IV? (ie Metastatic disease at diagnosis).

Anyways, here's some urls
http://www.acor.org/Cancerlist/sarcoma.html
http://oncolink.upenn.edu/disease/ped_sarcoma/
http://www.cancerindex.org/ccw/guide2t.htm
http://www.graylab.ac.uk/cancernet/200759.html
http://cancer.med.upenn.edu/pdq_html/1/engl/100759.html
http://www.nlm.nih.gov/medlineplus/ency/article/001429.htm
http://www.kids-cancer.org/rhabdomyosarcoma%20.htm (this last one mentions the
liver)

So hope the above helps in your search.
If you have specific questions, please post them.
Best,
J (not a doctor).

[]