Is there help in this group for esophageal cancer? It's not
rare but information is somewhat scarce. Tom
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esophageal cancer
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Quoted message said:
Subject: esophageal cancer
From: "Tom" [email hidden]
Date: 7/3/2004 12:00 PM Mountain Daylight Time
Message-id: <[email hidden]>Is there help in this group for esophageal cancer? It's not
rare but information is somewhat scarce. Tomherbivore.7h.comcancerpost.htmlOpen ↗
They are now speaking to TARGETING of the iron in leukemia ,
neuroblastoma , bladder and hepatocellular carcinoma ..Esophageal cancer can't be too far behind ..
J Neurooncol. 2004 May;67(3):367-77. Related Articles, Links
Desferoxamine (DFO)--mediated iron chelation: rationale for
a novel approach to therapy for brain cancer.Dayani PN, Bishop MC, Black K, Zeltzer PM.
Northwestern University Medical School, Chicago, IL, USA.
Iron homeostasis is crucial to normal cell metabolism, and
its deficiency or excess is associated with numerous disease
states. The association of increased iron load with cancer
may be due to several factors including free radical
production, reduction of the body's protective mechanism to
combat oxidative stress, inhibition of immune systems,
inhibition of essential nutrient functions, facilitation of
cancer growth, suppression of antitumor actions of
macrophages, and lowering of the ratio of T4-T8 positive
lymphocytes. Antiproliferative effects of desferoxamine
(DFO) both in vitro and in vivo are mediated by an
intracellular pool of iron that is necessary for DNA
synthesis rather than prevention of iron uptake from
transferrin. Several clinical studies have shown it to have
antitumor activity in the treatment of neuroblastoma,
leukemia, bladder carcinoma, and hepatocellular carcinoma.
Human neural tumor cells are susceptible to the effects of
DFO. Continued study of DFO is necessary to further
elucidate its antineoplastic profile and its use as an
adjunct to current chemotherapy regimens. Given the lack of
satisfactory treatment of central nervous system neoplasms,
DFO could serve as an important tool in the management of
such cancers.PMID: 15164994 [PubMed - in process]
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------Who loves ya. Tom
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Tom said:
Is there help in this group for esophageal cancer? It's
not rare but information is somewhat scarce. TomHi Tom, there's lots of info out there. What would you
like to know?We often refer people to Cathy's EC Cafe. There's a link
there to the ACOR ec-group.But if there's specific questions, some of the doctors here
might comment. Best, J -
Tom said:
Is there help in this group for esophageal cancer? It's
not rare but information is somewhat scarce. TomI forgot this in my earlier reply eccafe.orgeccafe.orgOpen ↗
Cathy's EC CafeJ
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Quoted message said:
Subject: esophageal cancer
From: "Tom" [email hidden]
Date: 7/3/2004 12:00 PM Mountain Daylight Time
Message-id: <[email hidden]>Is there help in this group for esophageal cancer? It's not
rare but information is somewhat scarce. TomThis study speaks DIRECTLY to the involvement of iron ..
<<snip>> When the operated animals were supplemented
with iron, EAC occurred at a high rate (73%) after 30
weeks, <<snip>>Carcinogenesis 1997 Nov;18(11):2265-70
Development of esophageal metaplasia and adenocarcinoma in a
rat surgical model without the use of a carcinogen.Goldstein SR, Yang GY, Curtis SK, Reuhl KR, Liu BC, Mirvish
SS, Newmark HL, Yang CS Laboratory for Cancer Research,
College of Pharmacy, Rutgers University, Piscataway, NJ
08855, USA.In order to establish an animal model for studying the
cause and prevention of esophageal adenocarcinoma (EAC) and
its frequent precursor, Barrett's esophagus (BE), factors
affecting the pathogenic processes were investigated in an
esophagoduodenal anastomosis model with rats. Experiments
by us and others have shown that surgical treatment
produced reflux esophagitis with cell hyperproliferation,
but not EAC. Additional treatment with a carcinogen has
been shown to be necessary for the development of EAC,
squamous cell carcinomas (SCC) or EAC/SCC mixtures. We
found that the surgically treated animals developed anemia
due possibly to reduced iron absorption. When the operated
animals were supplemented with iron, EAC occurred at a high
rate (73%) after 30 weeks, and treatment with N'-
nitrosonornicotine did not enhance the rate of
tumorigenesis. Treatment with carcinogen, however, induced
SCC in the group of rats killed after 22 weeks. The results
suggest that iron overload, which is known to cause
oxidative damage, is an enhancing factor for
adenocarcinogenesis. The pathogenesis of EAC in the iron-
supplemented, non-carcinogen treated group resembles human
esophageal adenocarcinogenesis in many features. All the BE
was the specialized type with goblet cells (containing
sialomucin or sulfomucin) and columnar cells (containing
acid or neutral mucin) as well as an incompletely developed
brush border. Almost all of the BE was located at the
bottom of the esophagus and was continuous with the
duodenal mucosa; dysplasia became more frequent at later
time points. All of the cancers were well-differentiated
mucinous EAC, and most of the EAC had an adjacent area of
BE with dysplasia. The results are consistent with the
proposed human sequence for pathogenic events of BE
progression to 'BE with dysplasia' and then to EAC.
Esophagoduodenal anastomosis and iron treatment in rats
produces a high rate of BE and EAC which are
morphologically similar to human BE and EAC; this may be a
useful animal model to study the development and prevention
of EAC in humans.PMID: 9395230, UI: 98055608
-----------------------------------------------
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I'm familiar with Kathy's Cafe, and I'm a subscriber to the
EC group. I have a medical question. My Med Onc and I are
working together on this. If a small recurrance of squamous
CC pops up after extended 5FU/Cisplatin + Radiation has
given me 4 months of NED (according to CT and PET) does
that mean the cancer is now resistant to the previous
therapy. Should we try more of the same or try the
Carbo/Taxol option? -
Tom said:
I'm familiar with Kathy's Cafe, and I'm a subscriber to
the EC group. I have a medical question. My Med Onc and I
are working together on this. If a small recurrance of
squamous CC pops up after extended 5FU/Cisplatin +
Radiation has given me 4 months of NED (according to CT
and PET) does that mean the cancer is now resistant to the
previous therapy. Should we try more of the same or try
the Carbo/Taxol option?I'm wondering why they can't do radiation on the "small
recurrance"? J
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