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J Invest Dermatol 2000 Nov;115(5):893-900
Iron chelators inhibit the growth and induce the apoptosis of Kaposi's sarcoma
cells and of their putative endothelial precursors.
Simonart T, Degraef C, Andrei G, Mosselmans R, Hermans P, Van Vooren JP,
Noel JC, Boelaert JR, Snoeck R, Heenen M
Department of Dermatology, Erasme University Hospital, Brussels,
Belgium. simonart@erasme.ulb.ac.be
Iron is suspected to be involved in the induction and/or progression
of various human tumors. More particularly, iron may be involved in
the pathogenesis of Kaposi's sarcoma, a tumor of probable vascular
origin. This study was designed to investigate the effect of iron
deprivation on Kaposi's sarcoma. The effects of iron chelators and
iron deprivation associated with serum withdrawal were investigated on
Kaposi's sarcoma-derived spindle cells, on a transformed Kaposi's
sarcoma cell line (Kaposi's sarcoma Y-1) and on endothelial cells,
which are the probable progenitors of Kaposi's sarcoma cells.
Desferrioxamine and deferiprone, two chemically unrelated iron
chelators, induced a time- and concentration-dependent inhibition of
endothelial and Kaposi's sarcoma cell growth. The inhibition of cell
growth was associated with a decrease in Ki-67 and in both stable and
total proliferating cell nuclear antigen expression. Inhibition of the
progression through the G1-phase of the cell cycle was further
evidenced by decreased expression of cyclin D1 and of p34
cyclin-dependent kinase 4. Terminal deoxynucleotidyl
transferase-mediated desoxyuridinetriphosphate nick end labeling
assay, flow cytometry with annexin-V-fluorescein and morphologic
analysis indicated that iron chelation also induced a time- and
concentration-dependent apoptosis. This apoptotic effect was prevented
by the addition of exogenous iron. Induction of iron deprivation in
the culture medium by serum withdrawal led to similar cell cycle
effects, which, however, could only be partly reverted by the addition
of exogenous iron. In conclusion, these results show that iron
deprivation inhibits the growth and induces the apoptosis of Kaposi's
sarcoma cells and of their putative endothelial precursors. This
suggests that iron chelators may represent a potential therapeutic
approach for the treatment of Kaposi's sarcoma.
PMID: 11069629, UI: 20532598
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Subject: free radicals/breast cancer
Clin Biochem 1999 Mar;32(2):131-6
Association between oxidative stress and changes of trace elements in patients
with breast cancer.
Huang YL, Sheu JY, Lin TH
Graduate Institute of Medicine and School of Technology for Medical
Sciences, Kaohsiung Medical College, Taiwan, ROC.
OBJECTIVES: To investigate the association between oxidative stress
and certain trace elements in the blood of breast cancer patients.
DESIGN AND METHODS: Malondialdehyde (MDA) was measured in serum of
patients with breast cancer (n = 35) and controls (n = 35) by high
performance liquid chromatography. Trace elements were determined by
atomic absorption spectrophotometry. RESULTS: In the present study,
significantly increased lipid peroxidation, measured as MDA, was
demonstrated in the serum of breast cancer patients (p < 0.01). The
concentrations of zinc and iron remained unaltered. However, the mean
serum copper level in patients with breast cancer was significantly
higher than the control group (p < 0.01). In addition, the mean serum
selenium level in patients with stage III was significantly lower than
the control group (p < 0.05). Moreover, a positive correlation was
also observed between copper and MDA levels in the patient group but
not in the control group. CONCLUSION: In the present study, the
presence of an association between oxidative stress and trace elements
was observed in patients with breast cancer. We suggest that increased
oxidative stress in patients with breast cancer may result from
changes in the levels of certain trace elements.
Publication Types:
* Clinical trial
* Controlled clinical trial
PMID: 10211630, UI: 99226612
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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
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Subject: chelator/cancer/iron
Gen Pharmacol 1999 Jan;32(1):155-8
Dexrazoxane (ICRF-187).
Weiss G, Loyevsky M, Gordeuk VR
Department of Internal Medicine, University Hospital, Innsbruck,
Austria. guenter.weiss@uibk.ac.at
1. Dexrazoxane (ICRF-187) is the only clinically approved drug for use
in cancer patients to prevent anthracycline mediated cardiotoxicity.
2. The mode of action appears to be mainly due to the potential of the
drug to remove iron from iron/anthracycline complexes and thus reduce
free radical formation by these complexes. 3. Dexrazoxane also
influences cell biology by its ability to inhibit topoisomerase II and
its effects on the regulation of cellular iron homeostasis. 4.
Although the cardioprotective effect of dexrazoxane in cancer patients
undergoing chemotherapy with anthracyclines is well documented, the
potential of this drug to modulate topoisomerase II activity and
cellular iron metabolism may hold the key for future applications of
dexrazoxane in cancer therapy, immunology, or infectious diseases.
Publication Types:
* Review
* Review, tutorial
PMID: 9888268, UI: 99103343
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Subject: breast cancer/alcohol/free radicals
Free Radic Biol Med 1999 Feb;26(3-4):348-54
Alcohol-induced breast cancer: a proposed mechanism.
Wright RM, McManaman JL, Repine JE
Webb-Waring Antioxidant Research Institute and University of Colorado
Health Sciences Center, Denver 80262, USA. richard.m.wright@uchsc.edu
Alcohol consumption increases the risk for breast cancer in women by
still undefined means. Alcohol metabolism is known to produce reactive
oxygen species (ROS), and breast cancer is associated with high levels
of hydroxyl radical (*OH) modified DNA, point mutations, single strand
nicks, and chromosome rearrangement. Furthermore, ROS modification of
DNA can produce the mutations and DNA damage found in breast cancer.
Alcohol dehydrogenase (ADH) and xanthine oxidoreductase (XOR) are
expressed and regulated in breast tissues and aldehyde oxidase (AOX)
may be present as well. Mammary gland XOR is an efficient source of
ROS. Recently, hepatic XOR and AOX were found to generate ROS in two
ways from alcohol metabolism: by acetaldehyde consumption and by the
intrinsic NADH oxidase activity of both XOR and AOX. The data obtained
suggests that: (1) expression of ADH and XOR or AOX in breast tissue
provides the enzymes that generate ROS; (2) metabolism of alcohol
produces acetaldehyde and NADH that can both be substrates for XOR or
AOX and thereby result in ROS formation; and (3) ROS generated by XOR
or AOX can induce the carcinogenic mutations and DNA damage found in
breast cancer. Accumulation of iron coupled with diminished
antioxidant defenses in breast tissue with advancing age provide
additional support for this hypothesis because both result in elevated
ROS damage that may exacerbate the risk for ROS-induced breast cancer.
Publication Types:
* Review
* Review, tutorial
PMID: 9895226, UI: 99110517
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Subject: HEME IRON AND COLON CANCER
Cancer Res 1999 Nov 15;59(22):5704-9
Red meat and colon cancer: the cytotoxic and hyperproliferative effects of
dietary heme.
Sesink AL, Termont DS, Kleibeuker JH, Van der Meer R
Wageningen Centre for Food Sciences, Netherlands Institute for Dairy
Research Food Research, Ede. Sesink@nizo.nl
[Medline record in process]
The intake of a Western diet with a high amount of red meat is
associated with a high risk for colon cancer. We hypothesize that
heme, the iron carrier of red meat, is involved in diet-induced
colonic epithelial damage, resulting in increased epithelial
proliferation. Rats were fed purified control diets, or purified diets
supplemented with 1.3 micromol/g of hemin (ferriheme), protoporphyrin
IX, ferric citrate, or bilirubin (n = 8/group) for 14 days. Feces were
collected for biochemical analyses. Fecal cytotoxicity was determined
from the degree of lysis of erythrocytes by fecal water. Colonic
epithelial proliferation was measured in vivo using [3H]thymidine
incorporation into colonic mucosa. The colonic epithelial
proliferation in heme-fed rats was significantly increased compared to
control rats [55.2 +/- 5.8 versus 32.6 +/- 6.3 dpm/microg DNA (mean
+/- SE); P < 0.05]. The fecal water of the heme group was highly
cytotoxic compared to the controls (90 +/- 2% versus 2 +/- 1%; P <
0.001), although the concentrations of cytotoxic bile acids and fatty
acids were significantly lower. Organic iron was significantly
increased compared to the controls (257 +/- 26 versus 80 +/- 21,
microM; P < 0.001). Spectrophotometric analyses suggest that this
organic iron is heme-associated. Thiobarbituric acid-reactive
substances were greatly increased in the fecal water of heme-fed rats
compared to the controls (177 +/- 12 versus 59 +/- 7 microM; P <
0.05). Heme itself could not account for the increased cytotoxicity
because the addition of heme to the fecal water of the control group,
which was equimolar to the organic iron content of the fecal water of
the heme group, did not influence the cytotoxicity. Hence, an
additional heme-induced cytotoxic factor is involved, which may be
modulated by the generation of luminal-reactive oxygen species.
Protoporphyrin IX, ferric citrate, and bilirubin did not increase
proliferation and cytotoxicity. In conclusion, dietary heme leads to
the formation of an unknown, highly cytotoxic factor in the colonic
lumen. This suggests that, in heme-fed rats, colonic mucosa is damaged
by the intestinal contents. This results in a compensatory
hyperproliferation of the epithelium, which supposedly increases the
risk for colon cancer.
PMID: 10582688, UI: 20047513
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Subject: fibroid/ferritin
Chung Hua Fu Chan Ko Tsa Chih 1991 Jan;26(1):21-3, 61
[Evaluation of serum ferritin in female genital neoplasms].
[Article in Chinese]
Dong MY
Obstetric and Gynecologic Hospital, Zhejiang Medical University,
Hangzhou.
Serum ferritin concentrations of 50 normal women and 90 patients with
neoplasms of female genital tract were determined by radioimmunoassay.
The mean value of serum ferritin in 23 cases of ovarian carcinoma was
402.04 micrograms/L, significantly higher than that of normal subjects
and patients with benign genital neoplasms. Serum ferritin levels in
patients with endometrial carcinoma, endometrial stromal sarcoma, and
benign genital neoplasms were significantly higher than that of the
normal subjects. There was a positive correlation between the serum
ferritin level and the clinical stage of ovarian carcinoma. The serum
ferritin determination is useful in the diagnosis, differential
diagnosis and prognosis of ovarian cancers.
PMID: 1848498, UI: 91168663
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Subject: fibroid/ferritin
Chung Hua Fu Chan Ko Tsa Chih 1991 Jan;26(1):21-3, 61
[Evaluation of serum ferritin in female genital neoplasms].
[Article in Chinese]
Dong MY
Obstetric and Gynecologic Hospital, Zhejiang Medical University,
Hangzhou.
Serum ferritin concentrations of 50 normal women and 90 patients with
neoplasms of female genital tract were determined by radioimmunoassay.
The mean value of serum ferritin in 23 cases of ovarian carcinoma was
402.04 micrograms/L, significantly higher than that of normal subjects
and patients with benign genital neoplasms. Serum ferritin levels in
patients with endometrial carcinoma, endometrial stromal sarcoma, and
benign genital neoplasms were significantly higher than that of the
normal subjects. There was a positive correlation between the serum
ferritin level and the clinical stage of ovarian carcinoma. The serum
ferritin determination is useful in the diagnosis, differential
diagnosis and prognosis of ovarian cancers.
PMID: 1848498, UI: 91168663
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Subject: iron/magnetic/cancer
Med Hypotheses 2000 Feb;54(2):177-9
Selective treatment of neoplastic cells using ferritin-mediated electromagnetic
hyperthermia.
Babincova M, Leszczynska D, Sourivong P, Babinec P
Department of Biophysics and Chemical Physics, Comenius University,
Bratislava, Slovakia. babincova@fmph.uniba.sk
A new method of cancer treatment is proposed, based on the unique
magnetic properties of ferritin iron core which, in alternating
magnetic field of frequency approximately 100 kHz, is easily heated to
temperatures sufficiently high to destroy neoplastic cells containing
an excess of this protein, without damaging the normal cells.
Copyright 2000 Harcourt Publishers Ltd.
PMID: 10790746, UI: 20253813
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Subject: cancer/iron/diet/rectum/Uruguay
Eur J Cancer Prev 1999 Dec;8(6):501-8
Dietary iron and cancer of the rectum: a case-control study in Uruguay.
Deneo-Pellegrini H, De Stefani E, Boffetta P, Ronco A, Mendilaharsu M
Registro Nacional de Cancer, Montevideo, Uruguay.
In order to examine the relationship between dietary iron intake and
risk of rectal cancer, a case-control study was carried out in
Montevideo, Uruguay. In the time period 1994-1998, 216 newly diagnosed
and microscopically verified cases of adenocarcinoma and 433 controls
hospitalized for diseases not related with long-term changes in diet
were enrolled in the study. Controls were frequency matched to cases
on age, sex, residence and urban/rural status. Both series of patients
were interviewed face-to-face in the four major hospitals in
Montevideo by two trained social workers. Dietary iron was associated
with significant increases in risk in men, women, and in both sexes
together [odds ratio (OR) 3.2, 95% confidence interval (CI) 1.9-5.3
for the highest tertile of consumption versus the lowest one]. Since
meat and its major macronutrients were potential confounders, iron
intake was adjusted for these variables without major changes in the
results. Furthermore, dietary iron and total fat combined its effects
according to a multiplicative model (OR 3.3, 95% CI 1.8-5.8). Finally,
an interaction between dietary iron and vitamin C was found. According
to the results, iron displayed a significant increase in risk at low
levels of vitamin C intake (OR 4.9, 95% CI 2.3-10.5). These results,
together with the existing epidemiological and experimental evidence,
suggest that dietary iron could play an important role in rectal
carcinogenesis.
PMID: 10643939, UI: 20106755
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Subject: vitamin E/tocopherol/cancer
Molecular Medicine
VITAMIN E SUCCINATE INDUCES APOPTOSIS IN HUMAN PROSTATE CANCER CELLS: ROLE
FOR FAS IN VITAMIN E SUCCINATE-TRIGGERED APOPTOSIS
Compare the effects of VES on human prostate carcinoma cells and normal
prostate cells in vitro.
Nutrition and Cancer 36(1):90-100, 2000
http://www.medscape.com/26577.rhtml
Read it Here
Subject: vitamin E/cancer
Carcinogenesis 2000 Aug;21(8):1531-1536
Effects of vitamin E and selenium supplementation on esophageal
adenocarcinogenesis in a surgical model with rats.
Chen X, Mikhail SS, Ding YW, Yang Gy, Bondoc F, Yang CS
Laboratory for Cancer Research, College of Pharmacy, Rutgers
University, 164 Frelinghuysen Road, Piscataway, NJ 08854, USA.
[Record supplied by publisher]
Two well-known antioxidative nutrients, vitamin E and selenium, were
used in this study to investigate possible inhibitory action against
the formation of esophageal adenocarcinoma (EAC) in rats. In this
model, carcinogenesis is believed to be driven by oxidative stress.
Male Sprague-Dawley rats (8 weeks old) were divided into four groups
and received esophagoduodenal anastomosis (EDA) surgery plus iron
supplementation (12 mg/kg/week). Vitamin E and selenium were
supplemented in the diet in the forms of alpha-tocopheryl acetate (750
IU/kg) and sodium selenate (1.7 mg Se/kg), which were 10 times the
regular amounts in the basic AIN93M diet. At 40 weeks after surgery,
all the EDA groups had lower body weights than the non-operated
control group. Iron nutrition (hemoglobin, total serum iron and
transferrin saturation) was normal as a result of iron supplementation
after EDA. Vitamin E supplementation maintained the normal plasma
level of alpha-tocopherol in EDA rats, but not those of
gamma-tocopherol and retinol. Selenium supplementation increased the
serum and liver selenium contents of the EDA rats. Histopathological
analysis showed that selenium supplementation increased the incidence
of EAC and the tumor volume. The selenium level in the tumor is higher
than that in the duodenum of the same animal.Vitamin E
supplementation, however, inhibited carcinogenesis, especially in the
selenium-supplemented group. We believe that vitamin E exerts its
effect through its antioxidative properties, and a high dose of
inorganic selenium may promote carcinogenesis by enhancing oxidative
stress.
PMID: 10910955
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Subject: bacteria/iron
Clin Microbiol Rev 1996 Oct;9(4):435-447
Mycobacterium haemophilum: microbiology and expanding clinical and geographic
spectra of disease in humans.
Saubolle MA, Kiehn TE, White MH, Rudinsky MF, Armstrong D
Department of Pathology, Good Samaritan Regional Medical Center,
Phoenix, Arizona 85006, USA.
Reports of the association of Mycobacterium haemophilum with disease
in humans have greatly increased. At least 64 cases have now been
reported, with symptoms ranging from focal lesions to widespread,
systemic disease. The organism is now known to cause primarily
cutaneous and subcutaneous infection, septic arthritis, osteomyelitis,
and pneumonitis in patients who are immunologically compromised and
lymphadenitis in apparently immunocompetent children. Underlying
conditions in the compromised patients have included AIDS; renal, bone
marrow, and cardiac transplantation; lymphoma; rheumatoid arthritis;
marrow hypoplasia; and Crohn's disease. Reports have originated from
diverse geographic areas worldwide. The epidemiology of M. haemophilum
remains poorly defined; there appears to be a genetic diversity
between strains isolated from different regions. The organism is
probably present in the environment, but recovery by sampling has not
been successful. M. haemophilum has several unique traits, including
predilection for lower temperatures (30 to 32 degrees C) and
requirement for iron supplementation (ferric ammonium citrate or
hemin). These may in the past have compromised recovery in the
laboratory. Therapy has not been well elucidated, and the outcome
appears to be influenced by the patient's underlying
immunosuppression. The organisms are most susceptible to
ciprofloxacin, clarithromycin, rifabutin, and rifampin. Timely
diagnosis and therapy require communication between clinician and the
laboratory.
Publication Types:
* Review
* Review, academic
PMID: 8894345, UI: 97049617
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Subject: estrogen and iron
Carcinogenesis 1998 Jul;19(7):1285-90
Enhancement of estrogen-induced renal tumorigenesis in hamsters by dietary
iron.
Wyllie S, Liehr JG
Department of Pharmacology and Toxicology, University of Texas Medical
Branch, Galveston 77555-1031, USA.
Iron participates in the generation of hydroxyl radicals by the
iron-catalyzed Fenton reaction. Its role in estrogen-induced
carcinogenesis has been examined in this study by investigating the
effects of iron content of hamster diets on tumor induction by
estradiol. The renal tumor incidence and number of tumor nodules in
hamsters treated with estradiol plus a diet enriched with iron (384
p.p.m. Fe as ferric citrate) for 5 months were 2- and 4-fold higher,
respectively, than those observed in animals on an iron-poor diet plus
estradiol (3.9 p.p.m. Fe, as ferric citrate). Tumor incidence and
number of tumor nodules in estradiol-treated hamsters on the
iron-deficient diet were not different from those of animals on a
normal rodent chow. No tumors were detected in hamsters treated only
with the low or high iron diets. Total serum iron was significantly
increased in animals treated with the high iron diet plus estradiol
compared with the low iron diet plus estradiol group and the high and
low iron controls. Estrogen treatment increased non-heme iron in liver
of both high and low iron treatment groups and in kidney of the
hamsters on the low iron diet. It is concluded that dietary iron
enrichment enhances the incidence and severity of estrogen-induced
tumor induction.
PMID: 9683190, UI: 98346720
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Subject: stomach cancer/iron supplements
J Reprod Med 1999 Nov;44(11):986-8
Gastric adenocarcinoma presenting with persistent, mild gastrointestinal
symptoms in pregnancy. A case report.
Chan YM, Ngai SW, Lao TT
Department of Obstetrics and Gynecology, University of Hong Kong,
Queen Mary Hospital, China.
BACKGROUND: Mild gastrointestinal symptoms are common during pregnancy
but can also be the only symptoms in stomach cancer until the late
stage. Clinicians' reluctance to pursue diagnostic studies appears to
be a major contributing factor to delayed diagnosis and poor outcome.
We report a case of maternal death to alert clinicians to this rare
possibility. CASE: A 36-year-old woman had persistent, mild epigastric
discomfort, nausea, vomiting and frequent episodes of dark stools
since the second trimester of pregnancy. These were attributed to
peptic ulcer and an iron supplement given, without investigation.
Gastroscopy was performed only at 32 weeks of gestation, when the
patient had heavy hematemesis. Biopsy confirmed the diagnosis of
poorly differentiated adenocarcinoma of the stomach. Cesarean section
was performed after steroid therapy. Advanced stomach cancer with
stomach perforation was found. Curative surgery was not possible. The
patient died four weeks after delivery. CONCLUSION: Stomach cancer is
a rare complication of pregnancy. Delay in diagnosis is commonly due
to clinicians' reluctance to request diagnostic studies and the
nonspecific symptoms of the disease. Early recognition and diagnosis
are the only possibilities for a better outcome. Clinicians must be
alert to this possibility and include this in the differential
diagnosis of minor gastrointestinal discomfort during pregnancy.
PMID: 10589414, UI: 20056854
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Subject: iron/testicular cancer
Med Hypotheses 1998 Aug;51(2):129-32
The case for iron repletion as a promoter in testicular cancer.
Crawford RD
Department of Chemistry and Biochemistry, Loyola Marymount University,
Los Angeles, CA 90045-8225, USA.
[Medline record in process]
The incidence of testicular cancer has increased considerably in this
century. Current hypotheses (most specifically, those concerning
environmental estrogens) show inconsistencies with this increase,
either in terms of time course or individual exposure to proposed
promoters. This new hypothesis, which attributes the increased
incidence in testicular cancer to our current more iron-replete
dietary status, is devoid of these inconsistencies. Evidence to
support this hypothesis includes the following: (a) the iron-related
mechanism of drugs used in the treatment of testicular cancer, (b)
dietary associations with disease frequency, (c) the similarity of
time course between historic increases in testicular cancer incidence
and dietary iron availability, and (d) potential genetic associations
with hemochromatosis. The link between incidence of the cancer and
cyptorchidism is also addressed. The article concludes with potential
experimental approaches to test the hypothesis.
PMID: 9881819, UI: 99096146
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Subject: zinc/thyroid
J Endocrinol 2001 May;169(2):417-24
Induction of apoptosis and necrosis by zinc in human thyroid cancer cell lines.
Iitaka M, Kakinuma S, Fujimaki S, Oosuga I, Fujita T, Yamanaka K, Wada S,
Katayama S
Department of Internal Medicine 4, Saitama Medical School, 38
Morohongo, Moroyama, Iruma-gun, Saitama 350-0495, Japan.
Zinc at concentrations of 150, microM or higher induced necrosis as
well as apoptosis in thyroid cancer cell lines. Necrosis was induced
by zinc in a dose-dependent manner, whereas apoptosis did not increase
at higher concentrations of zinc. The expression of the antiapoptotic
protein phosphorylated Bad was markedly increased, whereas the
expression of the proapoptotic proteins Bax and Bad decreased
following Zn(2+) exposure. Zn(2+) induced rapid degradation of
IkappaB, and an increase in the binding of nuclear transcription
factor-kappaB (NF-kappaB). These observations indicate that
antiapoptotic pathways were activated in thyroid cancer cells
following exposure to Zn(2+). This may be a self-defence mechanism
against apoptosis and may underlie the general resistance of thyroid
cancer cells to apoptotic stimuli. Zinc may be a potential cytotoxic
agent for the treatment of thyroid cancer.
PMID: 11312158, UI: 21211517
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