transitional cell cancer
pack back
husband has had 3 different chemos and the cancer is back. They want to do
radiation, can anyone help.
Steph
"pack back" <pcb...@intelos.net> wrote in message
news:3h9%7.4183$wd4.7...@atlpnn01.usenetserver.com...
Radiation is a potentially curative treatment for TCC of the bladder.
Prognosis depends on stage. If the chemo you are talking about was
intravesical chemo, then the tumour is fairly superficial. In that case
radiotherapy stands a good chance of controlling or curing it. More advanced
tumours usually require radiation plus chemo therapy, or even cystectomy.
watchman
These two articles speak to the fact they have known for awhile .. iron is
involved in this disease.
Ferritin and transferrin are iron and gallium nitrate affects the iron.
Am J Hematol 1992 Dec;41(4):232-40
Treatment with gallium nitrate: evidence for interference with iron metabolism
in vivo.
Seligman PA, Moran PL, Schleicher RB, Crawford ED
Department of Medicine, University of Colorado Health Sciences Center,
Denver 80262.
Gallium, when bound to transferrin, has been previously shown to cause
tumor cell cytotoxicity by preventing cellular uptake of transferrin
bound iron in vitro. Patients treated with constant infusion gallium
nitrate for carcinoma show a rise in serum iron within 6 hr of the
start of treatment. Serum iron returns to baseline by 24 hr
post-infusion. Atomic analysis of iron and gallium content of Sephadex
G-150 fractions of treatment sera indicate that about an equimolar
amount of gallium and iron are associated with transferrin. These
gallium and iron concentrations result in inhibition of transferrin
mediated iron uptake in vitro, and in vivo allow for > 90% saturation
of transferrin with metal. All seven patients who completed two
courses of gallium therapy exhibited hypochromic microcytic anemia
(mean fall in hemoglobin 3.5 grams %). Evidence for red cell iron
depletion was confirmed by an increase (mean 3.3-fold) in zinc
protoporphyrin levels. Since transferrin receptor increases on gallium
treated iron requiring cells in vitro, we assessed cell surface
transferrin receptor on peripheral blood lymphocytes by measuring
fluorescent transferrin receptor antibody binding. A population of
highly transferrin receptor positive cells peaks at 48 hr into the
infusion. DNA analysis as well as double staining indicate the
majority of transferrin receptor positive cells are unstimulated B
lymphocytes. These studies provide the first documentation that
constant infusion gallium treatment results in significant
interference with iron metabolism and evidence for tissue iron
depletion in vivo. These changes may correlate with therapeutic
effects of gallium such as tumor response.
PMID: 1337663, UI: 93167236
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Clin Sci (Lond) 1995 Jun;88(6):701-6
Clinical significance of urinary ferritin excretion in patients with
transitional cell carcinoma.
Chow NH, Chang CJ, Cheng PE, Tzai TS, Huang CM, Lin JS
Department of Pathology, National Cheng Kung University, Tainan,
Taiwan, Republic of China.
1. The serum ferritin level provides a valuable index of the body iron
store. An increase in serum ferritin has often been observed in
patients with neoplastic disease and correlates well with the stage of
cancer. A few studies have suggested the potential of urinary ferritin
as a marker for transitional cell carcinoma. The rationale of the
measurement, however, has not been investigated in detail. 2. Urinary
ferritin levels were evaluated in patients with diverse urological
diseases to investigate their potential clinical implications. 3.
Analysis of logarithmic transformed values (ng/mg creatinine) showed
that patients with both neoplastic and non-neoplastic urological
diseases had significantly higher ferritin levels than normal control
subjects (P = 0.02). There was no apparent difference between
subgroups of patients with urological disease (P > 0.5). For patients
with urothelial carcinoma, univariate analysis revealed a strong
positive relationship between urinary ferritin levels and the density
of lymphoid cells in tumour stroma (P = 0.0001), while no important
association was observed with tumour grade (P = 0.32), stage (P =
0.29) or urinary cytology detection (P = 0.33). Patients with
muscle-invasive tumour had significantly higher ferritin levels than
those with papillary, superficial cancer (P < 0.05). For patients with
non-neoplastic urological disease (n = 19), urinary ferritin levels
tend to correlate with the severity of tissue inflammation (P = 0.03).
4. The results suggest that urinary ferritin may reflect the degree of
local inflammatory reaction in the urinary tract.
PMID: 7634755, UI: 95361451
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There is a problem more and more researchers are becoming aware
of ..
This is the heme iron from the meat we eat ..
They have shown the body controls the iron we have in it by
absorption and once a set limit is met .. the body begins to
downregulate the PERCENTAGE of iron we absorb.
It has been shown the heme iron though .. found in meat / blood
is NOT controlled and bypasses the bodies processes which would
normally not allow too much iron to be absorbed.
Below you will find a compilation of articles which speak to the
problem of iron and what researchers / scientists are beginning
to find seem to have some good .. results.
Chelators are as we speak being funded by the NIH in order to
remove iron from disease ..
Oxidation / free radicals / rust have been closely linked to
cancer.
Each article speaks to the role of iron in disease .. and the leading
edge treatments being developed and approved as we speak .. with the
underlying root .. iron .
This first article specifically shows the iron .. the elevated iron in
this study group .. stems from the eating of meat .. or heme iron.
Eur J Haematol 2001 Feb;66(2):115-25
Iron status markers in 224 indigenous Greenlanders: influence of age, residence
and traditional foods.
Milman N, Byg KE, Mulvad G, Pedersen HS, Bjerregaard P
Department of Medicine, Naestved Hospital, Naestved, Denmark.
m...@cn.stam.dk
OBJECTIVE: To evaluate iron status in indigenous Greenlanders and its
relationship to gender, age and intake of traditional Greenlandic
foods. Methods: Serum ferritin, serum transferrin saturation and
haemoglobin were evaluated in a population survey in 1993-1994
comprising 224 Greenlandic individuals (109 men) aged 19-82 yr. The
participants were residents in the capital Nuuk (n=73) with a
predominantly Western style of living, the town Ilulissat (n=60) with
a mixture of Western and Greenlandic style of living, and the small
town Uummannaq (n=91) with a predominantly Greenlandic style of
living. Consumption of traditional foods was assessed by
questionnaire. RESULTS: Intake of traditional foods was more prevalent
among elderly than among young individuals and more frequent in
Uummannaq than in Ilulissat and Nuuk. Ferritin levels were higher in
men than in women (p<0.0001). Median ferritin levels were lowest in
Nuuk (men, 92 microg/L; women, 40 microg/L), higher in Ilulissat (men,
104 microg/L; women, 69 microg/L) and in Uummannaq (men, 118 microg/L;
women, 46 microg/L) (p<0.001). The prevalence of iron load (ferritin
>200 microg/L) was lowest in Nuuk (men: 13.8%, women: 2.3%)
intermediate in Ilulissat (men, 11.1%; women, 9.1%) and highest in
Uummannaq (men, 32.1%; women, 21.1%). The prevalence of iron depletion
(ferritin <16 microg/L) was high in Nuuk (men, 0%; women, 20.5%), and
lower in Ilulissat (men, 3.7%; women, 6.1%) and in Uummannaq (men, 0%;
women, 10.5%). The prevalence of iron deficiency anaemia (ferritin <13
microg/L and Hb <5th percentile for iron-replete men and women) was
0.92% in men and 0.87% in women. Correlations between age and ferritin
were lowest in Nuuk (men, r(s)=0.26, p=0.2; women, r(s)=0.50, p=0.001)
intermediary in Ilulissat (men, r(s)=0.37, p=0.06; women, r(s)=0.73,
p<0.0001) and highest in Uummannaq (men, r(s)=0.59, p<0.0001; women,
rs=0.74, p<0.0001). Intake of traditional foods was correlated with
ferritin in men (r(s)=0.29, p=0.01) and women (r(s)=0.40, p<0.0001).
CONCLUSION: The observed differences in estimated body iron stores in
Greenlanders from the three residential areas can be explained by
differences in the dietary intake of haem iron.
PMID: 11168519, UI: 21099797
_________________________________________________________________
Subject: cancer/moderate iron
Int J Cancer 1994 Feb 1;56(3):364-9
Moderate elevation of body iron level and increased risk of cancer occurrence
and death.
Stevens RG, Graubard BI, Micozzi MS, Neriishi K, Blumberg BS
Pacific Northwest Laboratory, Life Sciences Center, Richland, WA
99352.
The purpose of the study was to address the hypothesis that elevated
body iron increases the risk of cancer occurrence and death, and to
determine the dose response. Subjects were 3,287 men and 5,269 women
participating in the first National Health and Nutrition Examination
Survey who had a transferrin saturation determination at enrollment
(1971-1975), who remained alive and cancer-free for at least 4 years,
and who were followed to 1988 for cancer outcome. Among 379 men who
developed cancer over the study period, the mean transferrin
saturation at enrollment was 32.1% whereas among 2,908 who remained
cancer-free it was 30.7%; the difference for mortality was 32.3% among
233 deaths vs. 30.8% among 3,054 men not dying of cancer. The mean
differences among women were not significant. The mean differences in
TIBC and serum iron among men were consistent with the findings for
transferrin saturation, and all 3 differences were stable over time
when examined by years since blood test. Men and women were divided
into 5 groups on the basis of baseline transferrin saturation: 0 to
30%, 30-40%, 40-50%, 50-60%, and 60% and higher. Nineteen percent of
men had a baseline transferrin saturation above 40% (the last 3
groups), whereas only 10 percent of women had transferrin saturation
above 40%. For men and women combined, risk of cancer occurrence in
each group relative to the first was 1.0, 0.95, 1.16, 1.38 and 1.81;
for mortality the relative risks were 1.0, 0.96, 1.22, 1.29 and 1.73.
There is evidence, in this cohort, of elevated cancer risk in those
with moderately elevated iron level. This pattern was seen in women as
well as in men.
PMID: 8314323, UI: 94148541
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Cancer Lett 1988 Aug 30;41(3):251-6
Dietary iron enhances the tumor rate in dimethylhydrazine-induced colon
carcinogenesis in mice.
Siegers CP, Bumann D, Baretton G, Younes M
Institute of Toxicology, Medical University of Lubeck, F.R.G.
Treatment of male mice with 20 mg/kg dimethylhydrazine (DMH) s.c. for
10 weeks caused a mean tumour rate of 3.5 after 20 weeks. Dietary iron
(3.5% Fefumarate for 10 weeks) enhanced the mean tumour rate to 13.9.
All tumours detected were localized exclusively in the distal colon
and rectum. The iron load caused a 6.5-fold increase in the mucosal
Fe-concentration in the proximal as well as distal colon.
DMH-demethylase activity was not influenced by iron and did not differ
between proximal and distal segments. Cytosolic alcohol dehydrogenase
(ADH) activity was also not altered by iron, but was 3.3-fold higher
in the distal colon and rectum as compared to proximal segments; this
might explain the DMH-induced tumorigenesis in the distal colon only.
It is suggested that iron ions might evoke cocarcinogenic activity by
a stimulation of cell proliferation.
PMID: 3409203, UI: 88310811
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This article speaks to the finding of an upper LIMIT to the amount of iron
the body can SAFELY contain.
Safely being defined as the 'spillage/leaking' of iron once a certain
limit has been met.
Up until now researchers had believed the iron did not become toxic until
the transferrin was 100% full.
This article specifically shows the iron begins to leak and forms the
NTBI - non transferrin bound iron when it is ONLY.. 35% saturated and NOT
the 100% they had thought until now.
This leaked iron is also known as NPBI - non protein bound iron or 'free'
iron. This iron forms what is known as the labile iron pool or LIP.
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
_________________________________________________________________
These articles speak to the use and developement of chelators / iron
binders in cancer .. various cancers.
Subject: lung cancer
CANCERLIT®
AUTHOR: Sakai H, Wang H, Murai Y, Soukejima S, Kagamimori S
TITLE: [Study of remanent magnetization of the human body: lung and
liver tissues]
SOURCE: Nippon Eiseigaku Zasshi; 56(2):523-7 2001 UI: 21410934
ABSTRACT: In this study, we used lung and liver tissue specimens
distracted from tissue to investigate remanant magnetization, and
found that specimens with a volume of 6 mm3 had an intensity of
10(-10) Am2, which was significantly stronger than the noise level of
the superconducting magnetometer. This finding indicates that both
lung and liver tissues contain magnetic materials. We speculated that
biological magnetite is the magnetic material in these tissues. In
addition, we found that lung tissue specimens with strong
magnetization had correspondingly strong magnetized findings in the
liver tissue specimens. In a comparison of magnetization in lung
cancer tissue specimens and normal lung tissue, no significant
relationship was noted, but two of the lung cancer tissue specimens
showed strong magnetization. The number of lung cancer specimens
studies was insufficient to investigate the relation between the
magnetization (accumulation of magnetic materials) and lung cancer,
and further studies are necessary. The magnetic properties of two lung
cancer tissue specimens showing strong magnetization were further
investigated, and an alternating field demagnetization experiment
showed that their magnetization was composed of a unit stable vector,
which indicates that the lung tissue may have been magnetized after
the accumulation of magnetic materials. The Wohlfarth ratio (Moskowitz
et al., 1989) of them was less than 0.5, which suggests that magnetic
materials are distributed in clusters in lung tissue.
MESH TERMS: Aged
Aged, 80 and over
English Abstract
Human
Iron/*Analysis
Liver/*Metabolism
Lung/*Metabolism
Lung Neoplasms/Metabolism
Magnetics
Oxides/*Analysis
Support, Non-U.S. Gov't
LANGUAGE: JPN
PUBLICATION TYPE: JOURNAL ARTICLE
TITLE ABBREVIATION: Nippon Eiseigaku Zasshi
YEAR: 2001
ADDRESS: Department of Earth Sciences, Faculty of Science, Toyama
University, Gofuku 3190, Toyama 930-8555, Japan.
ENTRY MONTH: 200110
CAS NO.: 0 (Oxides)
1317-61-9 (ferrosoferric oxide)
7439-89-6 (Iron)
_________________________________________________________________
National Cancer Institute
CANCERLIT®
AUTHOR: Li J, Zheng LM, King I, Doyle TW, Chen SH
TITLE: Syntheses and antitumor activities of potent inhibitors of
ribonucleotide reductase:
3-amino-4-methylpyridine-2-carboxaldehyde-thiosemicarba-zone (3-AMP),
3-amino-pyridine-2-carboxaldehyde-thiosemicarbazone (3-AP) and its
water-soluble prodrugs.
SOURCE: Curr Med Chem; 8(2):121-33 2001 UI: 21111217
ABSTRACT: The reductive conversion of ribonucleotides to
deoxyribonucleotides by ribonucleotide reductase (RR) is a crucial and
rate-controlling step in the pathway leading to the biosynthesis of
DNA, since deoxyribonucleotides are present in extremely low levels in
mammalian cells. Mammalian ribonucleotide reductase (RR) is composed
of two dissimilar proteins, often referred to as R(1), which contains
polythiols and R(2), which contains non-heme iron and a free tyrosyl
radical. Both the R(1) and R(2) subunits contribute to the active site
of the enzyme. Currently, there are two broad classes of RR
inhibitors. The first class includes nucleoside analogs which bind to
the R1 subunit of the enzyme, several of which are in development.
Among those, Gemcitabine and MDL 101,731 have demonstrated impressive
efficacy against various solid tumors. Gemcitabine has now been
approved for the treatment of pancreatic cancer and non-small cell
lung cancer. The most promising second class of inhibitors of RR
includes HCTs [alpha--(N)-heterocyclic carboxaldehyde
thiosemicarbazones, e.g., 3-AP and 3-AMP], which exert enzyme
inhibitory effect through high affinity binding with non-heme iron.
Based on the clinical success achieved by Gemcitabine, it seems
reasonable that a strong inhibitor of RR, which is essential for
cellular replication, would be a useful addition to the existing
therapeutic agents against cancer. In this chapter, we wish to report
several highly efficient syntheses for both 3-AP and 3-AMP based upon
palladium mediated Stille/Suzuki/Heck coupling reactions. Based upon
the in vivo efficacy profile observed with these two agents, 3-AP was
chosen over 3-AMP as the candidate for further optimization with the
intention to improve its biological and pharmaceutical properties. In
this vein, we have completed the synthesis of two water soluble
phosphate containing prodrugs and one disulfide-linked prodrug of
3-AP. As expected, bioconversion study using either alkaline
phosphatase or glutathione showed that these prodrugs were indeed
converted to the parent 3-AP. When evaluated against the murine M-109
lung carcinoma as well as the B16-F10 murine melanoma xenograft
models, the newly prepared phosphate prodrugs displayed improved
efficacy and safety profiles than that found with the parent. More
significantly, the ortho-phosphate prodrug 21 demonstrated impressive
antitumor effect using once-a-day dosing regimen. In summary, the
results disclosed herein demonstrated that some of 3-AP prodrugs
prepared indeed demonstrated improved pharmaceutical, biological and
toxicity profiles over the parent 3-AP. Efforts directed towards
further optimization of 3-AP prodrugs as novel anticancer agents is
clearly warranted.
MESH TERMS: Animal
Antineoplastic Agents/*Chemical Synthesis/*Pharmacology
Enzyme Inhibitors/*Chemical Synthesis/*Pharmacology
Human
Prodrugs/*Chemical Synthesis/Chemistry/*Pharmacology
Pyridines/*Chemical Synthesis/Chemistry/*Pharmacology
Ribonucleotide Reductases/*Antagonists and Inhib
Support, U.S. Gov't, P.H.S.
Thiosemicarbazones/*Chemical Synthesis/Chemistry/*Pharmacology
LANGUAGE: ENG
PUBLICATION TYPE: JOURNAL ARTICLE
REVIEW
REVIEW, TUTORIAL
TITLE ABBREVIATION: Curr Med Chem
YEAR: 2001
ADDRESS: Vion Pharmaceuticals, Inc, Four Science Park, New Haven, CT
06511, USA.
ENTRY MONTH: 200104
CAS NO.: 0 (Antineoplastic Agents)
0 (Enzyme Inhibitors)
0 (Prodrugs)
0 (Pyridines)
0 (Thiosemicarbazones)
143621-35-6 (3-aminopyridine-2-carboxaldehyde thiosemicarbazone)
143621-37-8 (3-amino-4-methylpyridine-2-carboxaldehyde
thiosemicarbazone)
EC 1.17.4 (Ribonucleotide Reductases)
_________________________________________________________________
home help dictionary search
National Cancer Institute
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 drugs 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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Clin Cancer Res 2001 Nov;7(11):3574-9
Inhibition of Malignant Cell Growth by 311, a Novel Iron Chelator of the
Pyridoxal Isonicotinoyl Hydrazone Class: Effect on the R2 subunit of
Ribonucleotide Reductase.
Green DA, Antholine WE, Wong SJ, Richardson DR, Chitambar CR
Division of Hematology/Oncology [D. A. G., S. J. W., C. R. C.] and the
Biophysics Research Institute [W. E. A.], Medical College of
Wisconsin, Milwaukee, Wisconsin 53226, and the Heart Research
Institute, Sydney, New South Wales, Australia 2050 [D. R. R.].
[Medline record in process]
The key roles of iron and iron proteins in cell proliferation make
them potential targets for cancer therapy. However, clinical trials
directed toward perturbation of tumor iron homeostasis by iron
chelation have been limited to the use of deferoxamine (DFO). There is
thus a need to develop agents with greater efficacy. In the present
study, we investigated the mechanism of cytotoxicity of 311
(2-hydroxy-1-naphthylaldehyde benzoyl hydrazone), a novel iron
chelator of the pyridoxal isonicotinoyl class. We found that 311
inhibited the growth of CCRF-CEM cells in a time- and
concentration-dependent fashion with an IC(50) that was approximately
20-fold lower than that of DFO. 311 also inhibited the growth of
breast, bladder, and head and neck cancer cell lines. Using electron
spin resonance (ESR) spectroscopy analysis, we found that a 12-h
exposure of CCRF-CEM cells to 311 inhibited the tyrosyl radical ESR
signal of the R2 subunit of ribonucleotide reductase. However,
overproduction of the R2 subunit in hydroxyurea-resistant CCRF-CEM
cells was associated with a decrease in sensitivity of cells to 311
but not to DFO. Our studies show that 311 is a more potent cytotoxic
agent than DFO, with activity against both hematopoietic and
nonhematopoietic cell lines regardless of their p53 status.
Furthermore, the ESR studies suggest that inhibition of the R2 subunit
of ribonucleotide reductase is at least one mechanism by which 311
blocks cell proliferation.
PMID: 11705879, UI: 21562478
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There is a NATURAL chelator found in any health food store and is
compared to the 'prescribed' chelators .. (Medline)
It is called phytic acid or Ip6.
It is found in most of our plant food but chiefly in our grains but our
modern refining of our grain into flour effectively removes it.
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?
__________________________________________________________________
__________________________________________________________________
Subject: Ip6/phytic acid
_________________________________________________________________
Antitumor Activity of Physic Acid (Inositol Hexaphosphate) in Murine
Transplanted and Metastatic Fibrosarcoma, a Pilot Study
Authors: Vucenik I, Tomazic VJ, Fabian D, Shamsuddin AM
Source: Cancer Letters. 1992; 65:9-13.
_________________________________________________________________
Comparison of Pure Inositol Hexaphosphate and High-Bran Diet in the
Prevention of DMBA-Induced Rat Mammary Carcinogenesis
Authors: Vucenik I, Yang G, Shamsuddin AM
Source: Nutrition and Cancer. 1997; 28(1):7-13.
_________________________________________________________________
Dose-dependent Inhibition of Large Intestinal Cancer by Inositol
Hexaphosphate in F344 Rats
Authors: Ullah A, Shamsuddin AM
Source: Carcinogenesis. 1990; 2(12):2219-2222.
_________________________________________________________________
Effects of Inositol Hexaphosphate on Growth and Differentiation in
K-562 Erythroleukemia Cell Line
Authors: Shamsuddin AM, Baten A, Lalwani ND
Source: Cancer Letters. 1992; 64:195-202.
_________________________________________________________________
Growth Inhibition and Differentiation of HT-29 Cells in vitro by
Inositol Hexaphosphate (Phytic Acid)
Authors: Sakamoto K, Venkatraman G, Shamsuddin AM
Source: Carcinogenesis. 1993; l4(9):l815-1819.
_________________________________________________________________
IP6-Induced Growth Inhibition and Differentiation of HT-29 Human Colon
Cancer Cells: Involvement of Intracellular Inositol Phosphates
Authors: Yang G, Shamsuddin AM
Source: Anticancer Research. 1995; 15:2479-2488.
_________________________________________________________________
IP6: A Novel Anti-Cancer Agent
Authors: Shamsuddin AM, Vucenik I, Cole KE
Source: Life Sciences. 1997; 61(4):343-354.
_________________________________________________________________
Inhibition of Rat Mammary Carcinogenesis by Inositol Hexaphosphate
(Phytic Acid). A Pilot Study.
Authors: Vucenik I, Sakamoto K, Bansal M, Shamsuddin AM
Source: Cancer Letters.1993; 75:95-102.
_________________________________________________________________
Inositol Hexaphosphate Inhibits Cell Transformation and Activator
Protein 1 Activation by Targeting Phosphatidylinositol-3'
Kinase
Authors: Huang C, Ma W, Hecht SS, Dong Z
Source: Cancer Research. 1997; 57:2873-2878.
_________________________________________________________________
Inositol Hexaphosphate Inhibits Growth and Induces Differentiation of
PC-3 Human Prostate Cancer Cells
Authors: Shamsuddin AM, Yang G
Source: Carcinogenesis. 1995; 16(8):1975-1979.
_________________________________________________________________
Inositol Hexaphosphate Inhibits Large Intestinal Cancer in F344 Rats 5
Months After Induction by Azoxymethane
Authors: Shamsuddin AM, Wah A
Source: Carcinogenesis. 1989; l0(3):625-626.
_________________________________________________________________
Inositol Hexaphosphate and Inositol Inhibit DMBA-induced Rat Mammary
Cancer
Authors: Vucenik I, Yang G, Shamsuddin AM
Source: Carcinogenesis. 1995; l6(5):l055-1058.
_________________________________________________________________
Inositol Phosphates Have Novel Anticancer Function
Authors: Shamsuddin AM
Source: J. Nutr. 1995; 125:725S-732S.
_________________________________________________________________
Inositol and Inositol Hexaphosphate Suppress Cell Proliferation and
Tumor Formation in CD-1 Mice
Authors: Shamsuddin AM, Ullah A, Chakravarthy AK
Source: Carcinogenesis. 1989; 10(8):1461-1463.
_________________________________________________________________
Inositol-phosphate-induced Enhancement of Natural Killer Cell Activity
Correlates with Tumor Suppression
Authors: Baten A, Ullah A, Tomazic VJ, Shamsuddin AM
Source: Carcinogenesis. 1989; 10(9):1595-1598.
_________________________________________________________________
Novel Anti-Cancer Functions of IP6: Growth Inhibition and
Differentiation of Human Mammary Cancer Cell Lines in Vitro
Authors: Shamsuddin AM, Yang GY, Vucenik I
Source: Anticancer Research. 1996; 16:3287-3292.
_________________________________________________________________
Novel Anticancer Function of Inositol Hexaphosphate: Inhibition of
Human Rhabdomyosarcoma in Vitro and in Vivo
Authors: Vucenik I, Kalebic T, Tantivejkul K, Shamsuddin AM
Source: Anticancer Research. 1998; 18:1377-1384.
_________________________________________________________________
Suppression of Large Intestinal Cancer in F344 Rats by Inositol
Hexaphosphate
Authors: Shamsuddin AM, Elsayed AM, Ullah A
Source: Carcinogenesis. 1988; 9(4):577-580.
_________________________________________________________________
Up-regulation of the Tumor Suppressor Gene p53 and WAF1 gene
expression by IP6 in HT-29 Human Colon Carcinoma Cell Line
Authors: Saied IT, Shamsuddin AM
Source: Anticancer Res. 1998; 18(3A):1479-1484.
_________________________________________________________________
[3H]Inositol Hexaphosphate (Phytic Acid) Is Rapidly Absorbed and
Metabolized by Murine and Human Malignant Cells In Vitro
Authors: Vucenik I, Shamsuddin AM
Source: J. Nutr. 1994; 124:861-868.
_________________________________________________________________
[3H]Phytic Acid (Inositol Hexaphosphate) Is Absorbed and Distributed
to Various Tissues in Rats
Authors: Sakamoto K, Vucenik I, Shamsuddin AM
Source: J. Nutr. 1993; 123:713-720.
_________________________________________________________________
Subject: cancer/low iron diet
Anticancer Res 1999 Jan-Feb;19(1A):445-50
Inhibitory effect of deferoxamine mesylate and low iron diet on the 13762NF rat
mammary adenocarcinoma.
Wang F, Elliott RL, Head JF
Mastology Research Institute, Elliott Mastology Center, Baton Rouge,
LA 70806, USA.
The iron chelator deferoxamine mesylate has been shown to inhibit the
growth of a variety of human malignant cell lines and the rat 13762NF
mammary adenocarcinoma cell line. In vivo studies in mice have also
demonstrated that an iron deficiency induced by either feeding a low
iron diet or injecting the iron chelator deferoxamine mesylate
decreases tumor growth. In this study Fisher rats were transplanted
with the 13762NF mammary adenocarcinoma and divided into four groups:
normal diet, normal diet plus deferoxamine mesylate treatment, low
iron diet and low iron diet plus deferoxamine mesylate treatment. The
measurements of tumor size and body weight were recorded weekly. We
found that treatment with either deferoxamine mesylate or a low iron
diet decreased rat tumor growth, but the greatest inhibitory effect on
tumor growth occurred when the rats were treated with deferoxamine
mesylate injections plus fed a low iron diet. These treatments did not
significantly inhibit the weight gain of the rats. At the end of the
experiments measurement of serum iron proved that these treatments
caused iron deficiency, but there was no significant treatment related
alteration in blood hematocrit. We therefore concluded that
deferoxamine mesylate may be a useful chemotherapeutic agent in the
treatment of breast cancer, when used in combination with standard
chemotherapeutic regiments or with other agents that interfere with
iron metabolism, and further that the restricting of iron intake
should be considered when planning chemotherapy for all cancer
patients.
PMID: 10226580, UI: 99243167
_________________________________________________________________
_________________________________________________________________
From The June 2000 Issue of Nutrition Science News
Feature
Too Much of a Good Thing
by Bill Sardi
fortified bread Recent studies reveal that blood donors exhibit lower
rates of many diseases and experience better than average health.
Additionally, the centuries-old practice of bloodletting is being
revived as a treatment for disorders such as heart disease, cancer and
Alzheimer's.1 Why would blood reduction improve health parameters? In
part, because blood removal helps to control circulating iron levels.
Iron is an essential component of hemoglobin in red blood cells, is
associated with strength, and is required for oxygen transport, DNA
synthesis and other processes. But it also has a destructive nature.
In its free form, unbound from hemoglobin or other binding proteins,
it accelerates oxidation or "rusting" of body tissues. Since
iron-induced oxidation worsens the course of virtually every disease,
iron control could be a universal approach to disease prevention and
therapy.2
Whereas poor iron intake, or impaired absorption, may lead to anemia,
too much iron--iron overload--is even more problematic.3 After full
growth is achieved, at about age 18 or so, excess iron accumulates in
the blood of all humans at the rate of 1 mg per day.2 About 80 percent
of the body's iron stores are in the blood. Women are less at risk for
iron buildup than men because of the blood they lose monthly during
menstruation. As a result, women have somewhere around half the
circulating iron levels as men. Their rates for heart disease, cancer
and diabetes are also about half those of males. Because men have no
direct outlet for iron, by age 40 their iron levels are similar to
those of a postmenopausal 70-year-old woman. This amount of iron can
lead to premature aging and diseases such as arthritis, cancer,
cataracts, diabetes, osteoporosis, and retinal, liver and brain
disorders.4 Postmenopausal women, or women who have undergone early
hysterectomy in their 20s, 30s and early 40s, may experience similar
problems.5
Recognizing the Problem
Iron overload hasn't gone completely unnoticed. There are a number of
books on the topic, but most are written for health professionals,
leaving the public largely unaware of the problem. Also, some
confusion exists regarding the role of iron in health and disease.
First, there is a mistaken idea that the majority of the people
affected by iron overload diseases have the genetic form, called
hemochromatosis, which affects only about 1 million of the estimated
275 million Americans. In fact, the potential threat of iron overload
is universal. It comes with advancing age and regardless of genetic
factors. Second, the emphasis on preventing anemia in children and
menstruating women has detracted attention from progressive iron
buildup in adult men and postmenopausal women.6
Upon closer inspection, many health-promoting practices inadvertently
control iron. For example, taking an aspirin a day to prevent heart
attacks and strokes causes blood loss via the digestive tract on the
order of about a tablespoon per day. This results in iron loss.7
Raymond Hohl, M.D., an assistant professor of internal medicine and
pharmacology at the University of Iowa in Iowa City, says even chronic
use of a baby aspirin may help to control iron and in some cases can
induce iron-deficiency anemia.8 Aspirin also appears to increase the
production of ferritin, an iron-binding protein that prevents iron
from inducing oxidation.9 By exercising, a person loses about 1 mg of
iron through sweat.10 Fasting and vegetarian diets, both of which
promote longevity in animals and humans, limit iron consumption
because red meat contains the highly absorbable heme iron. Whether or
not related to iron consumption, restricting red meat consumption has
been shown in various studies to reduce the risk of colon cancer.11
Normal Iron Regulation
In healthy individuals there is little if any unbound iron circulating
in the blood. In all disease states, however, unbound iron (also
called free iron) is released at sites of inflammation and can spark
uncontrolled oxidation.12 Fortunately, there are numerous automatic
mechanisms in the body that help to control iron, many by
chelation--compounds that bind to a toxic substance (such as iron) and
render it nontoxic or nonactive. Albumin, a simple protein found in
blood, acts as a chelator by loosely binding to iron.13 Ferritin,
produced in the liver, is another iron-binding protein.14 Transferrin
is a protein that chelates iron and totes it back to the liver, where
it is metabolized and excreted.15 The liver produces lactoferrin,
another iron chelator, when challenged by infectious agents.16 This is
important because pathogenic organisms such as viruses, bacteria and
fungi require iron for growth. Furthermore, as iron stores increase,
the gastric absorption of iron decreases. So the body employs numerous
mechanisms to control iron that are activated when threatened by
disease. However, these defensive mechanisms can be overwhelmed.
Blood tests for iron levels (i.e., hemoglobin and ferritin levels are
checked for transferrin saturation percentages) are often useful, but
the results of these tests are confounded in states of prolonged
inflammation or disease.17 A skilled hematologist is often the best
professional from whom to obtain personal information concerning blood
iron levels.
Differentiating between anemia and iron overload can be difficult
because both conditions cause fatigue. One study at the Department of
Medicine, University of Western Ontario in Canada, found that iron
overload can produce a wide range of symptoms, such as joint pain
(particularly hip), unexplained gastric pain, frequent infections,
skin bronzing, elevated liver enzymes, cessation of menstruation, hair
loss and heart flutters (fibrillation). Yet, of 410 iron-overload
patients, 27 percent experienced no symptoms whatsoever.18 Common
symptoms of iron-deficiency anemia are lowered resistance to
infections, fainting, breath holding, mental fatigue, sleepiness, cold
hands and feet, and cravings for ice, meat or tomatoes, all which are
more likely to occur among women.19
Dietary Iron Control
Various dietary practices can help control iron levels. In a
relatively short period of time, dietary changes can result in anemia,
iron overload or an ideal state of iron control. Anemia can be induced
in about 120 days, while symptoms of iron overload can come on in just
60 days.
Humans absorb only a fraction of the iron they consume, but there are
many controlling factors.20 Iron absorption rates from food vary
widely, from less than 1 percent to nearly 100 percent.21 Cooks who
use iron or stainless steel pots increase the amount of iron they
consume.22 Generally, iron in plant foods is not as well absorbed as
iron from meat: Only 5 percent of iron in plant foods is available,
vs. 30 to 50 percent of iron from meat.23 Olive oil and spices such as
anise, caraway, cumin, licorice and mint promote iron absorption,24
while antacids, eggs and soy reduce availability.25 Since dairy
products contain lactoferrin, milk also inhibits the absorption of
iron.26 Moderate alcohol consumption is unlikely to pose a problem
with iron absorption, but excessive amounts of alcohol is associated
with iron overload, particularly in adult males.27
Vitamin C also increases iron absorption.28 However, there is no
evidence that vitamin C leads to iron overload. Thus vitamin C should
not be avoided by meat-eaters for this reason, since studies show
high-dose vitamin C supplements are associated with a decreased risk
for heart disease, cancer, cataracts and other disorders.29 A
vegetarian diet does not generally cause iron-deficiency anemia
because there is more vitamin C in plant-food diets, which enhances
absorption.30
A 1982 human study was conducted to assess the effect of various
drinks on iron absorption. A subject ate a standard meal of a
hamburger, string beans, mashed potatoes and water. When green tea was
drunk instead of water, iron absorption was reduced by 62 percent.
Coffee reduced iron absorption by 35 percent, whereas orange juice (as
a source of vitamin C) increased absorption by 85 percent. Contrary to
other studies, milk and beer had no significant effect.31
Bioflavonoids (found in berries, coffee, green tea, pine bark,
quercetin and the rind of citrus fruits, particularly blueberry,
cranberry, elderberry and grape seed) and phytic acid (a component of
whole grains and seeds such as sesame) bind to iron and other minerals
in the gastric tract and help to limit iron availability. If
bioflavonoids and phytic acid haven't bound to minerals in the
digestive tract they will get into the bloodstream, where they can
bind to free iron, acting as blood-cleansing iron chelators.
Therefore, maximum iron chelation in the blood circulation is achieved
when these iron binders are consumed apart from meals.
Phytic acid--also called inositol hexaphosphate, or IP6--is comprised
of six phosphorus molecules and one molecule of inositol. It has been
mistakenly described for decades as an "anti-nutrient" because it
impairs mineral absorption. However, in the 1980s food biochemist
Ernst Graf, Ph.D., began to tout phytic acid for its beneficial
antioxidant properties achieved through mineral chelation.32
Phytic acid in foods or bran should be distinguished from supplemental
phytic acid, which is derived from rice bran extract. In foods, phytic
acid binds to iron and other minerals in the digestive tract and may
interfere with mineral absorption. As a purified extract of rice bran,
taken between meals so it will not bind to minerals in the digestive
tract, phytic acid is readily absorbed into the bloodstream, where it
acts as a potent mineral chelator.33 Phytic acid binds to any free
iron or other minerals (even heavy metals such as mercury, lead and
cadmium) in the blood, which are then eliminated through the kidneys.
Phytic acid removes only excess or unbound minerals, not mineral ions
already attached to proteins.
Phytic acid is such a potent--but safe--iron and mineral chelator that
it may someday replace intravenous chelation therapy such as the
mineral-chelator EDTA or iron-binding drugs such as desferrioxamine
(Desferal). Because of its ability to bind to iron and block
iron-driven hydroxyl radical generation (water-based) as well as
suppress lipid peroxidation (fat-based), phytic acid has been used
successfully as an antioxidant food preservative.34
Phytic acid supplements should not be taken during pregnancy since the
developing fetus requires minerals for proper development. Because
aspirin causes a small loss of blood and consequently helps to control
iron levels, the simultaneous use of phytic acid with a daily aspirin
tablet is not advised. A three-month course of phytic acid should
achieve adequate iron chelation, and prolonged daily supplementation
may lead to iron-deficiency anemia. Anemic individuals who take phytic
acid as a food supplement are likely to feel weak shortly after
consumption, whereas iron-overloaded individuals are likely to feel
increased energy.
For those at risk for iron overload, it may be wise to avoid iron in
multivitamins and shun fortified foods that provide more than 25
percent of the recommended daily intake for iron. No doctor should
prescribe iron tablets for patients who complain of fatigue without
blood tests and a thorough health history. Iron-rich foods such as red
meat and molasses may prevent anemia and build strength during the
growing years but in adulthood may lead to iron overload among men and
postmenopausal women. Those individuals who learn how to achieve iron
balance will maintain the most desirable state of health throughout
life.
Sidebars:
Why Fortify Foods?
Bill Sardi is a health journalist and consumer advocate in Diamond
Bar, Calif. He recently published
The Iron Time Bomb (Bill Sardi, 1999).
References
1.Bonkovsky HL, et al. Iron in liver diseases other than
hemochromatosis. Semin Liver Dis 1996;16:65-82.
2. Gutteridge JMC, Halliwell B. Antioxidants in nutrition, health and
disease. New York: Oxford University Press; 1994. p 24-39.
3. McCord JM. Iron, free radicals, and oxidative injury. Sem in Hem
1998;35:5-12.
4. Crawford RD. Proposed role for a combination of citric acid and
ascorbic acid in the production of dietary iron overload: a
fundamental cause of disease. Biochem Mol Med 1995;54:1-11.
5. Emery TF. Iron and your health. Boca Raton (FL): CRC Press; 1991. p
1-13.
6.Arthur CK, Isbister JP. Iron deficiency. Drugs 1987;33:171-82.
7. Rider JA, et al. Double-blind comparison of effects of aspirin and
namoxyrate on pH of gastric secretions, fecal blood loss, serum iron
and iron-binding capacity in normal volunteers. Curr Ther Res
1965;7:633-8.
8. Bankhead C. In assessing anemia, doctors must decipher role of iron
deficiency. Med Tribune Clin Focus 1997 Mar; 20:24.
9. Oberle S, et al. Aspirin increases ferritin synthesis in
endothelial cells: a novel antioxidant pathway. Circ Res
1998;82:1016-20.
10. Vellar OD. Studies on sweat losses of nutrients. Scand J Clin Lab
Invest 1968;21:157-67.
11. Kampman E, et al. Meat consumption, genetic susceptibility, and
colon cancer risk. Cancer Epid Biomarker Prev 1999;8:15-24.
12. Griffiths, E. Iron and infection. New York: John Wiley &
Sons;1987. p 1-25.
13. Goldwasser P, Feldman J. Association of serum albumin and
mortality risk. J Clin Epid 1997;50:693-703.
14. Aust SD. Ferritin as a source of iron and protection from
iron-induced toxicities. Toxicol Lett 1995;82:941-4.
15. Aisen P, Brown EB. The iron-binding function of transferrin in
iron metabolism. Sem Hematol 1977;14:31-46.
16. Baker EN, et al. Three-dimensional structure of lactoferrin. Adv
Exp Med Biol 1998;443:1-14.
17. Hulten L, et al. Iron absorption from the whole diet in men: how
effective is the regulation of iron absorption? Am J Clin Nut
1997;66:347-56.
18. Adams PC, et al. The relationship between iron overload, clinical
symptoms and age in 410 persons with genetic hemochromatosis.
Hepatology 1997;25:162-6.
19. Marinella MA. Tomatophagia and iron-deficiency anemia. N Eng J Med
1999;341:60-1.
20. Monsen ER. The ironies of iron. Am J Clin Nutr 1999;69:831-2.
21. Hurrell RF. Preventing iron deficiency through food fortification.
Nut Rev 1997;55:210-22.
22. Park J, Brittin HC. Increased iron content of food due to
stainless steel cookware. J Am Diet Assoc 1997;97:659-61.
23. U.S. Agricultural Research Service, USDA Bulletin. 1998 Dec 23.
24. El-Shobaki FA, et al. The effect of some beverage extracts on
intestinal iron absorption. Z Ernahrungswiss 1990;29:264-9.
25. Morris ER. An overview of current information on bioavailability
of dietary iron to humans. Fed Proc 1983;42:1716-20.
26. Davidsson L, et al. Influence of ascorbic acid on iron absorption
from an iron-fortified chocolate-flavored milk drink in Jamaican
children. Am J Clin Nut 1998:67:873-7.
27. Fletcher LM. Alcohol and iron: one glass of red or more? J Gastro
Hepatol 1996;11:1039-41.
28. Derman DP, et al. Importance of ascorbic acid in the absorption of
iron from infant foods. Scand J Haematol 1980;25: 193-201.
29. Gerster H. High-dose vitamin C: a risk for persons with high iron
stores? Int J Vitam Nutr Res 1999;69:67-82.
30. Craig WJ. Iron status of vegetarians. Am J Clin Nut 1994 May; 59(5
Suppl):12335-7.
31. Hallberg L, Rossander L. Effect of different drinks on the
absorption of non-heme iron from composite meals. Hum Nutr Appl Nutr
1982;36:116-23.
32. Graf E, et al. Phytic acid--a natural antioxidant. J Biol Chem
1987;262:11647-50.
33. [No authors listed] Phytic acid: new doors open for a chelator.
Lancet 1987 Sept 19:2;2(8560):664-6.
34. Lee BJ, Hendricks DG. Phytic acid protective effect against beef
round muscle lipid peroxidation. J Food Sci 1995;60:241-4.
_________________________________________________________________
If radiation is being used .. this article speaks to the use of chelators
and radiation ..
CANCERLIT®
AUTHOR: Cook J
TITLE: Radiation sensitization of mammalian cells by metal chelators.
SOURCE: Radiat Res; 155(2):304-10 2001 UI: 21107885
ABSTRACT: The cell cycle effects, alteration in radiation response,
and inherent cytotoxicity of the metal chelators mimosine,
desferrioxamine (DFO),
N,N'-bis(o-hydroxybenzyl)-ethylenediamine-N,N'-diacetic acid (HBED),
and deferiprone (L1) were studied in exponentially growing Chinese
hamster V79 cells. Incubation of cells with 200-1000 microM mimosine
for 12 h reduced clonogenic survival to 50-60%, while incubation for
24 h reduced survival further to 0.5%. Mimosine treatment resulted in
cell cycle blocks at the G(1)/S-phase border and in S phase. Pulse
labeling with 5-bromodeoxyuridine indicated that the S-phase cells
ceased to actively replicate DNA after only 2 h of mimosine treatment
and were unable to replicate DNA for extended periods. Treatment of
V79 cells with 600 microM mimosine for 12 h resulted in
radiosensitization, yielding a sensitizer enhancement ratio (SER) of
2.7 +/- 0.3 at the 10% survival level. To study the kinetics of the
sensitization, V79 cells were incubated with mimosine for various
times up to 12 h and irradiated with a single 10-Gy dose of X rays. It
was found that the radiosensitization increased continually up to 8 h
(from a 3- to a 100-fold difference in survival) and then reached a
plateau after 8 h. Mimosine also equally radiosensitized human lung
cancer cells having either a normal or mutated TP53 gene, suggesting a
TP53-independent mechanism. To test whether iron binding by mimosine
was responsible for the observed radiosensitization, additional
experiments were performed using the iron chelators DFO, HBED and L1.
V79 cells treated with 500 microM of these agents for 8 h followed by
various doses of X rays gave SERs similar to that for mimosine
(2.0-2.7). These studies indicate that metal chelators are potent
radiosensitizers in V79 and human cells. Importantly, when the DFO was
preloaded together with Fe(3+) [Fe(III)-DFO], the radiosensitizing
effect was lost. These preliminary findings warrant further studies
for the possible application of metal chelators as radiation
sensitizers in radiation oncology.
MESH TERMS: Animal
Cell Cycle/Drug Effects
Chelating Agents/*Pharmacology
Colony-Forming Units Assay
Comparative Study
Cricetulus
DNA Replication/Drug Effects
Deferoxamine/*Pharmacology
Edetic Acid/Analogs and Derivatives/*Pharmacology
Fibroblasts/*Drug Effects/Radiation Effects
Genes, p53
Hamsters
Human
Iron Chelating Agents/Pharmacology
Lung/Cytology/Radiation Effects
Lung Neoplasms/Genetics/Pathology
Mimosine/*Pharmacology/Toxicity
Pyridones/*Pharmacology
Radiation-Sensitizing Agents/*Pharmacology
S Phase/Drug Effects
Tumor Cells, Cultured/Drug Effects/Radiation Effects
LANGUAGE: ENG
PUBLICATION TYPE: JOURNAL ARTICLE
TITLE ABBREVIATION: Radiat Res
YEAR: 2001
ADDRESS: Cellular Biochemistry and Human Genetics, Schools of Medicine
and Dentistry, Hebrew University, Jerusalem 91120, Israel.
ENTRY MONTH: 200104
CAS NO.: 0 (Chelating Agents)
0 (Iron Chelating Agents)
0 (Pyridones)
0 (Radiation-Sensitizing Agents)
30652-11-0 (1,2-dimethyl-3-hydroxypyrid-4-one)
35998-29-9 (N,N'-bis(2-hydroxybenzyl)ethylenediamine-N,N'-diacetic
acid)
500-44-7 (Mimosine)
60-00-4 (Edetic Acid)
70-51-9 (Deferoxamine)
_________________________________________________________________
home help dictionary search
National Cancer Institute
Who loves ya.
Tom
--
Jesus was a Vegetarian! http://www.nucleus.com/watchman
Moses was a Mystic! http://www.nucleus.com/watchman/light.html
Steph
"watchman" <watc...@nucleus.com> wrote in message
news:3c3d...@news.nucleus.com...
> pack back <pcb...@intelos.net> wrote:
> > Has anyone out there gone through radaition for transitional cell
cancer? My
> > husband has had 3 different chemos and the cancer is back. They want to
do
> > radiation, can anyone help.
>
> These two articles speak to
Tom,
when you post garbage (as you always do) please post short
garbage............
Cat in the Hat
Steph <st...@vancouvers.island> wrote in message
news:_ck%7.1891$N9....@news.bc.tac.net...
"Pack Back", meet Tom the Watchman. His cure for every ill known to mankind
is to tell you you have too much iron in your body. He is a complete lunatic
and spams most newsgroups I'm on and quite a few I'm not. He is the worst
sort of troll and gets horrifically irate if you question his genius. Iron
deficiency (which he advocates as a cure) is not a cure for everything,
contrary to what he tells everyone.
Wonder what he'd do if someone had problems with anemia??!!
Robert, who highly recommends you killfile him
watchman
> Tom,
> when you post garbage (as you always do) please post short
> garbage............
Look pal .. I am getting real tired of a salesman on a cancer list
badmouthing articles directly out of Cancerlit and Medline ..
If you were on any other list you would be considered an MLMer .. a double
one at that ..
Oncology / drug pusher .. and acupuncture / quackery ..
So read my lips and S. T. F. U ..
I believe all of you will be rather dismayed when you read
the following article I am going to post that states:
68 to 72% of revenues for Oncologists come from Chemotherapy sales.
These 2 articles together shed a very poor light on the Professionals
who are supposed to have our best interests at heart. No one knows
better than an Oncologist that Chemo. is at its best ineffective but
without it they lose 70% of their income. The only way they justify
recommending Chemo. is that the FDA has approved each of these
poisons."
How Oncologists get Paid
http://www.aishealth.com/PhysMgmt/Business%20Tools/Oncologists.htm
Oncologists Use Production Pay, But Some Prefer Equal Shares
Reprinted from PHYSICIAN COMPENSATION REPORT, the nation's
leading source of news and data on the actual pay plans used by
medical group practices. For more information on PHYSICIAN
COMPENSATION REPORT
Production and equal share pay systems are both found
frequently in single specialty hematology/oncology groups - as in
many other specialties such as gastroenterology and ophthalmology.
Those groups that use production often use fairly unusual
production gauges such as the number of consults with new or
established patients, and the number of office visits.
The economics of oncology are marked by the highest operating
costs of any specialty, according to MGMA's recently published Cost
Survey: 2000 Report Based on 1999 Data and Cost Survey for
Hematology/Oncology Practices: 2000 Report Based on 1999 Data. Most
revenues in single specialty oncology groups, usually about 68% to
72%, are for sales of chemotherapy drugs, says Thomas Barr, executive
director of Texas Cancer Care in Arlington, Texas. In nearly all
other specialties, most revenues are for physician services, Barr
notes. Median operating costs as a percentage of revenue rose more
than 6% from 1998 to 1999, from 65% to 71%, the MGMA
Hematology/Oncology survey indicates.
In some cases, cost hikes for drugs and staff have actually led
to a downturn in physician income. Such has been the case in a
Southeastern oncology group for each of the last three years, says
its administrator. Like several oncology practices, it has attracted
long-term employees with excellent pay and benefits. But for most
oncology groups, incomes are rising.
Production Pay Spurs Hard Work
At Columbus (Ohio) Oncology Associates, the pay pool of
revenues minus expenses is divided by each physician's relative score
on three measures: established patient office visits (with a weight
of 42%); physician work RVUs for professional services (42% weight);
and attendance at monthly compliance meetings (16% weight).
All eight physicians, including new hires, are paid this way.
While new hires have a guaranteed salary,
they can usually exceed it under the production formula within
six months, administrator Ruth Lander, FACMPE, says. As a result, the
group attracts the "cream of the crop," says Lander, and everyone
works hard.
This pay system, in place for several years, "works well" for
the group. The equal share method is often accompanied by declining
production, she warns.
Internal Medicine Associates in Yakima, Wash., which has 18
physicians of whom five are oncologists, pays by a "salary-based
production bonus payment" system, says Judy Hagarty, FACMPE. Until
recently, she was the administrator of the five-physician oncology
practice. Hagarty is now a practice consultant, specializing in
oncology.
Under the system, salary is paid at a maximum of 80% of the
physician's long-term collections, reduced by a percentage to reflect
the operating costs for bringing in the revenues. The rest of the
money available for physician pay is divided mainly by the ratio of
the physicians' consultations with new patients. This is akin to an
RVU system, Hagarty explains, although it uses evaluation and
management codes for consults. Like several other oncology
administrators, she says that the RVUs credited for office visits,
even for the most intensive visit (99215), are wholly inadequate for
a visit with a new cancer patient.
The time and complex judgments needed to set up a treatment
plan usually far exceed what can be reimbursed under the 99215 code.
Another reason for using the number of consults is that it
"evens out the score" between types of cancer, Hagarty adds. Some
cancers require more chemotherapy or more expensive chemotherapy than
other cancers. But the work in setting up the treatment plan is about
the same, so pay should not be pegged to the kind of therapy
prescribed. It should also not be pegged to the type of cancer a
physician subspecializes in, she explains.
A third reason to use consults is that pay cannot be allocated
according to chemotherapy revenue under a cautious interpretation of
the Stark rules. The statute, passed in 1994, does not mention chemo
drugs, but the proposed rule, which came out early in 1998, does. The
final rule has yet to come out.
The group's targets for overall income are the MGMA medians for oncology.
Equal Shares Come With a Difference
At New Hampshire Oncology in Hooksett, N.H., the six partners
are on equal shares, drawing a base salary and quarterly bonuses that
are precisely equal, says administrator Elaine Towle, CMPE. The one
new physician is on salary, and prices in the recruiting market are
rising.
Despite sharp increases in physical production, Towle's
partners' incomes have been fairly stagnant for the last several
years. She terms Medicare reimbursements "pretty desirable these
days," because managed care prices have in many cases fallen below
Medicare levels.
At five-partner, seven-physician Texas Cancer Care in
Arlington, Texas, the partners are nearly on equal shares. Salaries
are established for all physicians in light of marketplace levels and
what the practice can afford given the investments it is making, and
then the partners split their bonus money equally. With bonuses,
partners are earning about the MGMA 80th percentile for oncologists.
Employed physicians are at roughly the oncologist median. That
means bringing in new physicians at $185,000 to $200,000 with a
two-year partnership track. The goal for paying clinical and
administrative staff is about the 75th percentile as revealed in the
MGMA Hematology/Oncology Survey.
However, this past year and for the next two, the partners are
plowing their bonus money into a major capital investment in
information systems to make possible the archiving and retrieval of
data on the complete course of treatment of all patients. This will
enable the practice to keep up to date with innovation and to sell
information on the actual use and effects of chemotherapy drugs to
pharmaceutical companies and others who may be interested, says
executive director Thomas Barr. Such data is extremely useful for
post-FDA-approval clinical testing, and for research into drugs, such
as SmithKline Beecham's ProCrit, that try to take the edge off
chemotherapy's often severe side effects. The data will include "how
patients feel.[and] why they make those therapeutic decisions with
their physicians."
Forgoing raises except cost of living allowances for the next
three years was a "big deal" among the partners, Barr said. However,
they are committed to "leaving a practice legacy behind, a business
structure for the physicians coming in." Over the next three years,
the group wants to hire four physicians because the founders are in
their mid-50s and want to slow down. The investment the group is
making is proving to be a strong recruiting pitch to high quality
fellowship grads.
Oncology is very demanding emotionally, Barr notes. "Success
for an oncologist is keeping people alive and functional."
Chemotherapy is, of course, hard on people, and many patients are old
and have other conditions.
The fall in profit margins from sales of chemotherapy agents,
which Barr expects will continue, is the business inspiration for the
information systems investments. The group had to figure out other
sources of revenue to replace chemotherapy profits, he explains.
A Southeastern oncology practice with five physicians, all
partners, pays each one a salary of $260,000. There are quarterly
bonuses that range widely with how the practice is doing financially.
The bonuses are divided by a method that is part equal shares
and part production, the administrator explains. Those who produce
from 95% to 115% of the group's average - as it usually is for three
of the physicians - receive the same amount, about one-fifth of the
bonus pool. One consistently high producer receives about 10% more in
bonus money. One newer physician whose production is lower receives a
smaller bonus.
This two-year-old pay system has "made everybody feel good" by
showing where other physicians are and where each would like to go,
the administrator says.
--
=======================
watchman
> Oh =hell=. I thought Tom was locked up somewhere, hopefully for good.
> "Pack Back", meet Tom the Watchman. His cure for every ill known to mankind
> is to tell you you have too much iron in your body. He is a complete lunatic
> and spams most newsgroups I'm on and quite a few I'm not. He is the worst
> sort of troll and gets horrifically irate if you question his genius. Iron
> deficiency (which he advocates as a cure) is not a cure for everything,
> contrary to what he tells everyone.
Meet cat .. the man who has every disease .. and his wife does too .
It's too bad they let guys like him breed .. but THAT too .. is a matter
of contention .. seeing that the ages , sex and number of children he has
seems to change .. at the 'drop of the hat ' ..
Oh yeah .. another 'anonymous' poster .. much like 'Steph' the
'oncologist' who lives in the sixties who believes sitting close to a
color television has the 'possibility' of curing your cancer .. due to
its' radiation ..
Steph
> Steph <st...@vancouvers.island> wrote:
>
> > Tom,
> > when you post garbage (as you always do) please post short
> > garbage............
>
> Look pal .. I am getting real tired of a salesman on a cancer list
> badmouthing articles directly out of Cancerlit and Medline ..
>
I'm really glad you're getting tired. Stop posting the garbage and you'll be
less tired quite quickly.
> If you were on any other list you would be considered an MLMer .. a double
> one at that ..
I'm not on any of your "other lists", thank God.
> Oncology / drug pusher .. and acupuncture / quackery ..
>
> So read my lips and S. T. F. U ..
>
Spit it out Tom
> I believe all of you will be rather dismayed when you read
> the following article I am going to post that states:
> 68 to 72% of revenues for Oncologists come from Chemotherapy sales.
> These 2 articles together shed a very poor light on the Professionals
> who are supposed to have our best interests at heart. No one knows
> better than an Oncologist that Chemo. is at its best ineffective but
> without it they lose 70% of their income. The only way they justify
> recommending Chemo. is that the FDA has approved each of these
> poisons."
>
> How Oncologists get Paid
But Tom, I don't get ANY income from chemotherapy sales.
If you were intelligent, what would you say next?
Sorry, unfair question.
Steph
> Cat in the Hat <n...@chance.mate> wrote:
> > Oh =hell=. I thought Tom was locked up somewhere, hopefully for
good.
> > "Pack Back", meet Tom the Watchman. His cure for every ill known to
mankind
> > is to tell you you have too much iron in your body. He is a complete
lunatic
> > and spams most newsgroups I'm on and quite a few I'm not. He is the
worst
> > sort of troll and gets horrifically irate if you question his genius.
Iron
> > deficiency (which he advocates as a cure) is not a cure for everything,
> > contrary to what he tells everyone.
>
> Meet cat .. the man who has every disease .. and his wife does too .
> It's too bad they let guys like him breed .. but THAT too .. is a matter
> of contention .. seeing that the ages , sex and number of children he has
> seems to change .. at the 'drop of the hat ' ..
>
> Oh yeah .. another 'anonymous' poster .. much like 'Steph' the
> 'oncologist' who lives in the sixties who believes sitting close to a
> color television has the 'possibility' of curing your cancer .. due to
> its' radiation ..
>
Tom,
your desperation is showing............
Lbucc
It's ironic that you complain about being tired. We're all pretty darned tired
of you replying to everything inisisting that iron is the root of all evil.
...lisa
watchman
> ab...@nucleus.net
Take a hike ..
I reply to people who ask about their cancer..
If you believe the story is going to change .. don't hold your breath ..
Let me give you some advice .. 'block sender' .. 'killfile'..
Steph
> Lbucc <lb...@cs.com> wrote:
> > ab...@nucleus.net
>
> > It's ironic that you complain about being tired. We're all pretty
darned tired
> > of you replying to everything inisisting that iron is the root of all
evil.
>
> Take a hike ..
Classy as always, Tom.
> I reply to people who ask about their cancer..
Unfortunately your "replies" never have anything to do with the question.
> If you believe the story is going to change .. don't hold your breath ..
>
None of us believe the story is going to change, because you're a one-tune
fiddle.
> Let me give you some advice .. 'block sender' .. 'killfile'..
>
Let me give you some advice. Take more antipsychotics. You'll regain some
insight.
watchman
> Let me give you some advice. Take more antipsychotics. You'll regain some
> insight.
So since you and 'cat' seem to be 'cut from the same bolt of cloth' .. I
will take this to mean you are speaking from .. personal experience..
Lbucc
You apparently do not understand the meaning of support. This is a cancer
support newsgroup. What you do is come and post responses to messages that do
not have anything to do with the original post. No one would be picking on you
if you posted messages that were related to the original post.
But you don't.
Why don't you find some newsgroup where your input would be appreciated? Or,
do you simply need to have people dislike you for some perverse reason? Why
don't you do like the Barrett's guy does if you need to spread your "word?"
Create a post and put the same thing in the newsgroup once a week or, better
yet, once a month.
You are not helping anyone, only pissing people off and wasting resources.
...lisa
Steph
>
> > Let me give you some advice. Take more antipsychotics. You'll regain
some
> > insight.
>
> So since you and 'cat' seem to be 'cut from the same bolt of cloth' .. I
> will take this to mean you are speaking from .. personal experience..
>
Personal experience of sanity? Sure.
Try it sometime.
Steph
"Lbucc" <lb...@cs.com> wrote in message
news:20020111143059...@mb-cq.news.cs.com...
> Tom,
>
> You apparently do not understand the meaning of support. This is a cancer
> support newsgroup. What you do is come and post responses to messages
that do
> not have anything to do with the original post. No one would be picking
on you
> if you posted messages that were related to the original post.
>
> But you don't.
>
> Why don't you find some newsgroup where your input would be appreciated?
Lisa, ever tried opening a can of beans with a banana? Mission impossible.
watchman
> Tom,
> You apparently do not understand the meaning of support. This is a cancer
> support newsgroup. What you do is come and post responses to messages that do
> not have anything to do with the original post. No one would be picking on you
> if you posted messages that were related to the original post.
Other people don't seem to understand what 'support' means then either ..
eh .. lbucc ..
They come here and ask about 'specific' measures to take .. and I answer
them ..
As to 'not relating' to original post.. just because YOU or 'steph' .. SAY
.. they don't relate .. doesn't mean they don't.
If you get half the education I have .. THEN and maybe then can you even
comment on ANY of my posts ..
> But you don't.
Yeh .. like transitional cell cancer DOESN'T relate to bladder cancer ..?
Like I said .. stay with what you know best ..
'Mental support' .. and stay away from anything relating to 'medical' ..
support ..
> Why don't you find some newsgroup where your input would be appreciated? Or,
> do you simply need to have people dislike you for some perverse reason? Why
> don't you do like the Barrett's guy does if you need to spread your "word?"
> Create a post and put the same thing in the newsgroup once a week or, better
> yet, once a month.
I tell you what .. I don't really care whether YOU 'like me' or not ..
Get a life .. find somewhere where people like you congregate .. like ..
alt.Ihadcancerwhichmakesmeanexpert ..
> You are not helping anyone, only pissing people off and wasting resources.
Wasting resources ..?
Another little 'tactic' used by your 'ilk' ..
Take a hike ..
Steph
> comment on ANY of my posts ..
>
ROTFLMAO!
watchman
Again .. based on personal experience?
Jeez .. and you'd think that would be an 'obvious' .. stupid thing to try
.. but .. it seems your stupidity extends far beyond medicince ..
Steph
>
> > "Lbucc" <lb...@cs.com> wrote in message
> > news:20020111143059...@mb-cq.news.cs.com...
> >> Tom,
> >>
> >> You apparently do not understand the meaning of support. This is a
cancer
> >> support newsgroup. What you do is come and post responses to messages
> > that do
> >> not have anything to do with the original post. No one would be
picking
> > on you
> >> if you posted messages that were related to the original post.
> >>
> >> But you don't.
> >>
> >> Why don't you find some newsgroup where your input would be
appreciated?
>
> > Lisa, ever tried opening a can of beans with a banana? Mission
impossible.
>
> Again .. based on personal experience?
>
> Jeez .. and you'd think that would be an 'obvious' .. stupid thing to try
> .. but .. it seems your stupidity extends far beyond medicince ..
>
That's the point Tom.
With your extensive education, I would have thought you'd realise that
opening a can of beans with a banana is as likely as you finding a newsgroup
where your input would be appreciated.
I wouldn't have to explain that to 99.9% of the population, but I do
understand that you are special.
Cat in the Hat
Steph <st...@vancouvers.island> wrote in message
> That's the point Tom.
> With your extensive education, I would have thought you'd realise that
> opening a can of beans with a banana is as likely as you finding a
newsgroup
> where your input would be appreciated.
>
> I wouldn't have to explain that to 99.9% of the population, but I do
> understand that you are special.
Yeah, he's got Special Education; I used to teach a room full of those
kids when I was a teacher..... finally got where one of them could say his
name; well actually, he said his mother's maiden name, never could teach him
to say his own.....
Tom is easily the most hated Usenet troll I've ever seen and I've seen
quite a few.......
Tom is a nuisance on the following ngs:
alt.animals.ethics.vegetarian.snm
alt.animals.rights.promotion.snm
alt.bible.prophecy.snm
alt.fan.heinlein.snm
alt.gathering.rainbow.snm
alt.lawyers.snm
alt.legend.king-arthur.snm
alt.med.cfs.snm
alt.med.fibromyalgia.snm
alt.privacy.snm
alt.rec.crafts.metalworking.snm
alt.religion.christian.roman-catholic.snm
alt.support.asthma.snm
alt.support.cancer.snm
alt.support.crohns-colitis.snm
alt.support.endometriosis.snm
alt.support.epilepsy.snm
alt.support.impotence.snm
alt.support.kidney-failure.snm
alt.support.mult-sclerosis.snm
alt.support.schizoaffective.snm
alt.support.schizophrenia.snm
alt.support.thyroid.snm
misc.fitness.misc.snm
misc.fitness.weights.snm
misc.health.aids.snm
misc.health.alternative.snm
misc.health.arthritis.snm
misc.health.diabetes.snm
misc.kids.breastfeeding.snm
misc.health.infertility.snm
misc.kids.health.snm
misc.kids.pregnancy.snm
misc.rural.snm
misc.survivalism.snm
rec.crafts.metalworking.snm
rec.drugs.cannabis.snm
rec.food.cooking.snm
rec.food.veg.snm
rec.gardens.edible.snm
rec.music.classical.recordings.snm
rec.music.gdead.snm
rec.outdoors.fishing.bass.snm
rec.pets.birds.snm
rec.pets.dogs.behavior.snm
sci.anthropology.snm
sci.chem.analytical.snm
sci.chem.snm
sci.geo.geology.snm
sci.life-extension.snm
sci.med.cardiology.snm
sci.med.dentistry.snm
sci.med.diseases.cancer.snm
sci.med.diseases.hepatitis.snm
sci.med.diseases.lyme.snm
sci.med.laboratory.snm
sci.med.nursing.snm
sci.med.nutrition.snm
sci.med.pathology.snm
sci.med.pharmacy.snm
sci.med.prostate.prostatitis.snm
sci.med.radiology.interventional.snm
sci.med.radiology.snm
sci.med.snm
soc.culture.african.american.snm
sci.physics.electromag.snm
soc.culture.cuba.snm
soc.culture.british.snm
soc.culture.greek.snm
soc.culture.indian.snm
soc.culture.jewish.moderated.snm
soc.culture.nigeria.snm
soc.culture.quebec.snm
soc.culture.south-africa.snm
soc.history.what-if.snm
soc.religion.quaker.snm
talk.atheism.snm
talk.politics.animals.snm
tnn.religion.catholic.snm
talk.politics.medicine.snm
uk.philosophy.humanism.snm
watchman
> quite a few.......
> Tom is a nuisance on the following ngs:
And you sir are a loser ..
How does that feel?
Who loves ya.
Tom
Steph
> Cat in the Hat <n...@chance.mate> wrote:
> > Tom is easily the most hated Usenet troll I've ever seen and I've
seen
> > quite a few.......
> > Tom is a nuisance on the following ngs:
>
> And you sir are a loser ..
> How does that feel?
>
Gosh, Tom, that was cutting!
You must have been reading Oscar Wilde again?
Edweirdo
Steph wrote:
lol.....
So, here I am, gettin' my daily feed of learnin' all that I can with cancer,
and lo and behold, flames wars here too! lol A newsgroup that's dedicated to
one of the most serious issues known to man, and people flame each other, how
loverly! lol
I've learned one thing being online, let alone real life. Some people think
they can open a can with a bannana, some people think it's impossible. I say,
oh well, to each their own. Nobody forces nobody to change their opinions or
ways in life, here or elsewhere. I dunno Watchmen. I'm *just* getting to know
Steph. But both have their own ideas and beliefs and conclusions towards
stuff. Who cares. Duh! It's up to us, as individuals, to sift thru the crap
and the truths. Watchmen thinks he's right. Steph thinks he's right. EDDIE
thinks he's right. Who's gonna ever say somethin' *knowingly* wrong?
Am I making sense here? Doubt it, just woke up, java hasn't kicked in yet.
Rock on Watchman.
Rock on Steph.
Rock on Ed.
Hell, EVERYBODY rock on..........
Cat in the Hat
> Cat in the Hat <n...@chance.mate> wrote:
> > Tom is easily the most hated Usenet troll I've ever seen and I've
seen
> > quite a few.......
> > Tom is a nuisance on the following ngs:
>
> And you sir are a loser ..
> How does that feel?
homosexual?
Michele
wrote:
> Tom, you thrive on hatred. Are you by any chance a Jehovahs Witness or a
>homosexual?
You think that Jehovahs' Witnesses and gays thrive on hatred?
Michele, puzzled
Edweirdo
Michele wrote:
Against the hatred of the 'wordly people', Jw's do, I used to be one, 20 years
ago, the rest of my family are still in it. In fact, part of their hatred can be
geared towards those that have been disfellowshipped, ( kicked out from the
cult), which includes family members, such as I. But it's crazy ya know, my
parents just left my home after staying a week to visit my boys. So, I guess it
depends how one takes their ( JW laws) religion.
Eddie
Cat in the Hat
Michele <book...@bigfoot.com> wrote in message
news:3c40e95a....@news.telus.net...
JW's are taught to get right in your face, harass you, and never leave
you alone. I had one call me a murderer because I own a gun. That really
made me mad, and if you get mad and tell them to go away, they consider that
to be suffering for the Lord and putting little stars in their crown......
The really amusing part about their entire organization is that the very
same verse of scripture they take their name from disproves their whole
system of theology! LOL!
Gays that =I= have known =mostly= seem bent on pushing it in my face,
including my brother, and I hate that. I have a friend who is the soul of
discretion, you would never guess he was gay except for the fact that his
boyfriend is like the first type mentioned above. Worse than my brother....
sheesh..... He thrives on grossing people out. His goal is to be universally
annoying and despised.
The question still remains: Tom do you thrive on hatred? Because that is
surely all I've seen you getting anywhere.....
Oh yeah, check out my spiffy new tag line!
Robert <><
--
Click here for a laughable mess!
http://www.nucleus.com/watchman
The World's Worst Usenet Troll,
the one, the only, Tom Hennessy!
Cat in the Hat
Edweirdo <Edwe...@shaw.ca>
> Against the hatred of the 'wordly people', Jw's do, I used to be one, 20
years
> ago, the rest of my family are still in it. In fact, part of their hatred
can be
> geared towards those that have been disfellowshipped, ( kicked out from
the
> cult), which includes family members, such as I. But it's crazy ya know,
my
> parents just left my home after staying a week to visit my boys. So, I
guess it
> depends how one takes their ( JW laws) religion.
ones in Heaven because of their great amount of "Fruitage" meaning preaching
their gospel door-to-door. I replied that was only true if their gospel
wasn't the pack of lies I'd just proven it to be.
If you have any interest in a private conversation on this, say the
word, or not. No probs, I'm easy! :-)
Robert
PS- Glad your parents love you! The WTB&TS hasn't got 'em yet.....
Edweirdo
Cat in the Hat wrote:
>
> The last one that came to my house told me the JW's would be the only
> ones in Heaven because of their great amount of "Fruitage" meaning preaching
> their gospel door-to-door. I replied that was only true if their gospel
> wasn't the pack of lies I'd just proven it to be.
Actually Robert, according to them, only a 144,000 would go to heaven.
>
> If you have any interest in a private conversation on this, say the
> word, or not. No probs, I'm easy! :-)
I'd really like that Robert. If and when you do email me, lemme know what yer
interest is with it k?
>
> Robert
> PS- Glad your parents love you! The WTB&TS hasn't got 'em yet.....
Well, seems like yer pretty familiar with those catch words huh?
But I'm afraid they *do* got 'em. Except my dad has gotten sick over these last
few months as well as getting into his mid 70's. I think he's reflecting now.
And I believe he's turning a bit towards what real love is as well.
Michele
wrote:
<snip>
> Gays that =I= have known =mostly= seem bent on pushing it in my face,
>including my brother, and I hate that.
Seems to me that you have the problem with hatred, then.
> I have a friend who is the soul of
>discretion, you would never guess he was gay except for the fact that his
>boyfriend is like the first type mentioned above. Worse than my brother....
>sheesh..... He thrives on grossing people out. His goal is to be universally
>annoying and despised.
Maybe his goal is to not have to hide who he is.
Michele
ber...@charter.net
All you are doing is encouraging him. If you ignore him maybe he'll go
away.
Post a warning to his imaginations, and leave it alone.
Berky the Warrior
Folie à Deux
Steph
<ber...@charter.net> wrote in message
news:u42ct6h...@corp.supernews.com...
Berky,
I'm trying to annoy him.
I know it's childish and unlikley to work, but it pleases me.
piet Jansen
Are you by any chance a homosexual?
I have never hated anybody, not even Tom.
--
Darn! an evil hen.
Michele <book...@bigfoot.com> schreef in berichtnieuws
3c40e95a....@news.telus.net...
Cat in the Hat
Steph <st...@vancouver.island>
> Berky,
> I'm trying to annoy him.
>
> I know it's childish and unlikley to work, but it pleases me.
that the best way to really tick him off is to recommend people look at his
website, which as you know, is the stupidest concoction of idiocy ever known
to man. Then when everyone really knows what he's all about, he may finally
get the message. Of course, I personally believe it is impossible to talk an
insane person back into sanity.... soooo, probably not.
Cat in the Hat
Edweirdo <Edwe...@shaw.ca> wrote
> I'd really like that Robert. If and when you do email me, lemme know what
yer
> interest is with it k?
period, or if you went elsewhere to a Christian church. I'm a Bible student,
though not a "Dawn" Bible student, if you know what I mean ;-) and I'm
always interested in what someone who leaves a major cult thinks afterwards.
I spent a brief period of time in the Mormons, til it became obvious they
were clueless...
> Well, seems like yer pretty familiar with those catch words huh?
I have studied virtually every major and a lot of minor cultic orgs. It
fascinates me how something as plain as the Bible can be mangled into so
many different things...
I can destroy the core of JW theology in less than 5 minutes, using 2
verses of Scripture.
> But I'm afraid they *do* got 'em. Except my dad has gotten sick over these
last
> few months as well as getting into his mid 70's. I think he's reflecting
now.
> And I believe he's turning a bit towards what real love is as well.
Blood is thicker than water; he will have a good chance of coming around
now that your son is ill. Romans 8:28
I'll continue to pray for your family, you guys need it. We =all= do! I
wouldn't be here if I didn't need help.
Robert <><
PS- I love your nickname! LOL!
Edweirdo
Hey man, I doubt this topic interests anyone here so I'll reply to this and send
it to your personal email address k?
Eddie
Cat in the Hat wrote: