The
Effect Of EMF on Rat Mammary Carcinoma
Douglas M. Evans, M.D., et al.
The
following study was a cell culture study aimed at investigating
possible enhancing effect of EMF on cancer growth, as was the
prevailing sentiment at the time, and not designed to
demonstrate a therapeutic advantage. It was conducted in the
early 1990's at a private laboratory , hence the names of
the associate researchers and the
laboratory will be withheld. Attempts were made to publish the
study at the time, but no one was inclined to do so. Permission
to publish the following study on my website was graciously
given by the primary researcher.
Overview:
I was going to
write an overview for the layman (including myself), but
excerpts from a letter by Dr. Evans will be more accurate:
"My
initial interest was directed to the possible etiologic effects
of emf fields. As I'm sure you know there was considerable furor
over some epidemiologic studies linking cancer in children who
lived near hightension wires, brain
cancer in cell phone users, some instances in breast cancer etc.
Some of this still lingers on as far as cell phone usage is
concerned.
Our approach
started with applying electrical, magnetic and combined electrical
and magnetic fields to cells using capacitors created by gluing
plates on both
surfaces of standard petri dishes, by constructing a large coil
which would
accommodate several petri dishes at a time and using a stepped
down power source
which was monitored by a sophisticated potentiometer.
We had a physicist who was in charge of field production. So, we
were using electrical and magnetic fields and both combined as
sources of the energy exposures and living cells in cell culture
all conducted in a big incubator.
Rather than
establishing an etiologic pathway between emf and cancer we
found that the application of these fields in strengths
comparable to what could be considered reasonably to be within
range of environmental exposure to suppress the growth of cancer
cells as well as their ability to invade as measured in standard
invasion chambers.
We also
measured the effect on one of the known enzymatic requirements
for cancer cell invasion, i.e. the urokinase activator/receptor
axis. This was done on several cell lines including human breast
cancer cells. The bulk of the work was done using rat mammary
cancer cells. The bottom line of all this was to demonstrate a
suppressant effect by the application of emf to cancer
cells."
Project
Summary:
The
Effect of Electromagnetic Fields on Rat Mammary Carcinoma
Douglas M.
Evans, M.D., et al.
The processes
of cancer cell invasion involve the many faces of the
fibrinolytic system. What was initially thought to be a
mechanism to control the effects of intravascular thrombus
formation has been shown to be far more complex. The
fibrinolytic cascade is nearly as complex as the coagulation
cascade. A major role in the capability of cells to migrate
through tissue has been recognized to belong to this biologic
system. The aspects of this system that are important from the
aspect of tumor invasive and metastatic potential are the
collagenolytic activities indicated.
Incorporated into this system are several levels of checks and
balances in the form of inhibitors and stimulators. Not
surprisingly, this same system facilitates the migration of
inflammatory cells and fibroblasts, making it a vital part of
the host defense mechanism. Ironically, this vital biologic
asset becomes a significant liability when coded into tumor
cells. This is not unlike the transformation of rational adults
into congressmen, thereby converting protection into invasion.
The key to the invasive potential imparted by this system is
that the activated plasmin produced by the
cascade is bound to the cell surface at the receptor site uPAR.
Even more unusual is the finding that most tumor systems studied
to date show cellular capability of producing the uPA which then
binds to its own surface
receptors and initiates the cascade. It is also worthy of note
that the resultant bound plasmin is some how protected from the
normal inactivation mechanism of alpha 2 antiplasmin. In some
tumor systems there can be as many as several hundred such sites
per cell, allowing for matrix dissolution in all directions. In
contrast, inflammatory cells have
their receptors grouped in only one locale, providing a
unidirectional migratory pattern, in addition to the direct
collagenolytic effect of surface bound plasmin, this
uPA/uPAR/plasmin complex causes activation of other tissue
components, particularly the metalloproteases, which intensify
the matrix degradation required for invasion andmetastasis. In
essence then, as illustrated in this slide, we have an
aberration of a normal mechanism which
allows a lethal process to perpetuate itself. That same system
which promotes healing, wound repair, infection control, ova
fertilization and implantation and the spontaneous resolution of
intravascular thrombosis can be parasitized by the malignant
cell and utilized for the invasion and spread of the malignant
process. The purpose of the exercise I am here to describe is to
investigate the effect of electromagnetic fields on the
capability of the cancer cell to pervert the fibrinolytic
system.
The Fisher rat
MATB tumor cell line was chosen for this study because it is of
mammary origin, and has been shown previously in the laboratory
to produce uPA. The degree of tumor production can be readily
reproduced from a given size of the inoculum. In order to
establish that uPA was indeed essential to the care and feeding
of these cells, a preliminary study was done to establish that
the inhibition of uPA would impair the growth of this tumor. PAI
2, the uPA inhibitor, was graciously donated by (name withheld)
and was utilized as the inhibitory agent of uPA. The tumor model
used was the creation of lung metastases by injecting the tumor
cells into the external iuqular vein of the Fisher rat and
counting the number of metastases produced in standardized lung
sections. The inhibitor was given
separately via the osmotic pump in the first half of the
experiment, and by mixing the inhibitor with the tumor cells in
the pump in the second stage.
The results
confirm that this tumor system is susceptible to uPA suppression
and that the model is productive in creating metastases in
predictable numbers.
An in vitro
assay of uPA output of the cells in tissue culture was carried
out under varying levels of exposure to electrical, magnetic and
electromagnetic fields. uPA was assayed from the culture media.
The levels obtained from
field exposure produced by 300uA of current and a 106 gauss
magnetic field are shown here. Exposure times were 1 hour q 12
hrs x 48. These exposures were not selected with the view of
mimicking physiologic situations, but rather to establish the
presence or absence of a gross effect.
The methods of exposure are shown in these slides. Anticipating
that increased amounts of uPA production would produce bigger
and better tumors the pilot study was set up as follows. Forty
Fisher rats were divided into four groups of ten each. The`
control group received 10 MATB cells injected into the gluteus
muscle by direct vision. Ten rats received cells exposed to the
electrical fields as described, ten received cells exposed to
the magnetic fields and the final ten received cells exposed
simultaneously to both electrical and magnetic fields. The study
was terminated at ten days post tumor inoculation. The tumors
were harvested, measured, weighed and preserved for electron
microscopy. To my surprise the tumors produced by the exposed
cells were uniformly and significantly smaller than
the controls. (slides) When viewed under the electron microscope
the cell membranes were grossly different, but this needs be
interpreted with some caution.The
cell membrane of cultured cells, represented by the controls,
tend to show more echinosis than those taken from a confluent
mass. The appearance of microtubules did not seem to show
morphologic change.
Being forced to
reconcile the evidence that the treated cells consistently
produced smaller tumors in the face of what was deemed to be an
increased production of uPA it was recalled that the action in
terms of tissue invasion was via surface bound uPA/plasmin
complexes. The assay was repeated using both media and cellular
homogenate and using plasmin as the assay target rather than
free uPA. These results suggest that significantly less surface
bound plasmin is produced by the treated cells than that
produced by the control cells. Those levels of plasmin correlate
roughly with the tumor sizes generated by the corresponding
treated cell groups. Referring back to the electron microscopic
findings, the appearance of the cell membranes of the treated
cells could suggest that the receptor sites for uPA may be
either reduced in number or otherwise defunctionalized by the
field exposures, thereby resulting in measurably less
bound plasmin and consequently reduced penetrating power.
The apparent
increase in free uPA demonstrated by the media assay would
then be accounted
for by having notably fewer binding sites for the uPA produced
by the tumor cells with a larger fraction available in the free
state while a proportionally smaller fraction is converted to
the surface bound plasmin required for tissue matrix
dissolution. This latter hypothesis is currently in the process
of verification by monoclonal antibody labeling of the receptor
sites for uPA.
This line of
inquiry is obviously barely in its initial stages. At this point
we have only a suspicion of an iceberg. if indeed there is an
iceberg here, it is entirely submerged and a great amount of
exploration will be required to
determine its dimensions.





Abstract:
EMF
exposure and MATB Effects of Exposure of MATB Rat Mammary Cancer
Cells to Electric, Magnetic and Electromagnetic Fields:
Increased Cell Growth and
Proliferation, Decreased Tumor Growth and Cell Invasiveness
Douglas M.
Evans, M.D. , et al.
EMF
Effect on Induced Ca
The implication
of environmental exposure of electromagnetic fields on the
incidence of certain malignancies is of continued interest. This
study shows inhibitory effects of exposure of rat mammary cancer
cells to electrical, magnetic and combined electromagnetic
fields on tumor growth and cell invasive capacity, while cell
proliferation was enhanced. Tumor growth was measured in Fisher
344 rats by direct intramuscular inoculation of EMF
exposed/unexposed MATB rat mammary cancer cells. Invasive
capacity was measured by incubating exposed/unexposed cells in
Matrigel invasion chambers. Cell proliferation was measured by
thymidine uptake combined with numerical counts of
exposed/unexposed cells. Cell exposure in each aspect of this
study was identical in field strength and exposure time to
unexposed controls. While each field caused significant
suppression of tumor growth and invasive capacity, as well as
cell proliferation enhancement, the responses to the combined
fields were somewhat greater. The determinations demonstrated
strong dose related inhibitory response. Key words: Cancer
Inhibition; Tumor Inhibition Environmental
and occupational electromagnetic field (EMF) exposure have been
implicated as a causese of certain malignancies. Leukemia and
the lymphomas have been the primary neoplasms in question
[1,2,3,4,5,6,7] although there are also reports of an increase
in the incidence of breast cancer in employees exposed to
electrical fields in the workplace [8,9,10,11], and questions of
a link between brain cancer and occupational exposure to EMF
[12]. The basis for these reports in each instance has been
retrospective epidemiological data. Accurate retrospective
measurement of the intensity of field exposures in these studies
is not possible. While an approximation of field strength can be
made in some instances, i.e. proximity to power lines, the use
of household appliances, electric blankets etc., the
extent of exposure to these field sources is uncertain. There
have been recent
studies on the impact of EMF exposure on gene expression in
exposed human leukemic, HL60 and Daudi cells [13,14,15], the
results of which are in conflict. To date there have been no
reports of prospective approaches to permit comparisons of
quantified exposures over defined periods of time to biologic
effects. Moreover, while there have been numerous reports of the
possible linkage between EMF exposure and the etiology of
specific malignancies, there have been no studies aimed at the
impact of such exposures on the invasive and growth
characteristics of cancer cells. To this end, this study was
designed to investigate the effect of measured EMF exposures on
cancer cells with respect to the capacity to invade, to
proliferate and to the growth of tumors induced by exposed vs.
unexposed cells. Since
the actual biologic effects of field exposures are ill defined,
the field components were assessed separately. Electrical fields
(E) were created through the conversion of petri dishes to
capacitors in order to deliver pure voltage to the cultures
without the effect of electrolysis on the culture media. The
application of a
defined voltage to the capacitors using a current-limited
transformer at a static strength of 235.4 milliVolts (mV)
produced an electric potential of 300 milliAmps (mA)/meter2. A
variable voltage filtered power supply with the addition of an
inline transformer was used to provide either direct current or
alternating current. A 11.5cm diameter coil (10 turns/cm) with
an internal nonconducting platform onto which the culture dishes
were placed provided magnetic field exposures (M) to the cells.
60Hz alternating current at 1.47 Amps created a 10 Gauss field
within the coil. Combined exposures (EM) were provided by
connecting the DC power supply to the capacitors, during
exposure to a 10G field within the interior of the coil. All
exposures were accomplished within the confines of an incubator
at 37 degrees
centigrade and 5% C02. MATB 13762 rat mammary cancer cells
(ATCC, Rockville, Md.) were maintained in culture with McCoy's
5A(90%) Bovine Serum (FBS) (10%) and penicillin-streptomycin 1%.
MATB cells centrifuged and counted for viability with Trypan
blue stain on a hemacytometer. Millicells (30mm,3um; Millipore
Corp., Bedford MA) were used inside the petri dishes to provide
an elevated surface for growth
so the cells would not contact the capacitor surface. The pore
size of the Millicells obstructed passage of the MATB cells but
permitted diffusion of the media. For cellular field exposures
106 MATB cells were distributed into the Millicells and the
outer petri dish was filled with 30 ml of media. In each phase
of the experiment control (unexposed) cells were prepared in an
identical paired fashion but
conducted in an incubator separate from that in which the fields
were generated.
Determination
of the effect of field exposure on tumor growth utilized cells
exposed to each field (E, M, and EM) for one hour periods twice
daily for 48 hours. Ten Fisher 344 rats per exposure type were
subsequently inoculated by intramuscular injection with l0u
viable exposed cells. An identical inoculum of 10u unexposed
cells was carried out on 10 Fisher 344 rats for controlled
comparison. The central gluteal musculature was selected as the
inoculation site under direct vision by virtue of a 3mm skin
incision. The same inoculation schedule was followed for two
groups of
forty rats each. At 10 days post inoculation the tumors were
harvested, measured and weighed. Data was analysed by t-test
with comparison of each exposure group to unexposed controls.
The effect of
field exposure on the capability of MATB cells to invade was
determined using the synthetic basement membrane Matrigel
(Collaborative Biomedical Products, Bradford, MA), and standard
invasion chambers. Matrigel
(100mg/cm2) was layered into Millicells (12 mm, 12 um) in 24-
well plates. The size of the invasion chamber inoculation
remained at l0u exposed viable cells. Field exposures were again
imposed within the confines of an incubator at 37 degrees C. and
5% CO2 incubators. Exposure lengths were expanded to 24, 48 and
72 hours with one and two hour exposure times. A separate set of
12 individual chambers was used for each combination of field
exposures. The cells were separately retrieved from each layer
and counted by Trypan blue stain. The percentage of invasion was
calculated by numbers of cells in the outer well of the invasion
chamber divided by the total numbers of cells retrieved.
Statistical analysis was by t-test for individual comparison of
the exposure group to the unexposed controls. ANOVA was added
for comparison of invasion values with respect to length and
duration of exposure.
The effect of
field exposures on cellular growth and proliferation was
measured by both H-thymidine incorporation and by cell counts
following incubation during field exposures. MATB cells were
prepared, placed in Millicells and intermittently exposed to E,
M, and EM fields as with the tumor growth and invasion
experiments. The exposure length for this section of the study
was Z hours twice daily over a duration of 72 hours. The media
was removed from the outer portion of the petri dish and
replaced with serum-free media to quiesce the cells for 48
hours, prior to exposure. The cells were removed from the
exposure and control chambers and counted with Trypan blue stain
in ahemocytometer. MATB cells were resuspended in media
containing 10% fetal bovine serum and 0.25 Ci/ml of H-thymidine
(NEN Dupont, Boston MA). 10 viable cells per well were
aliquotted into 6 wells per exposure group and incubated for 48
hours. The suspended cells from each well were transferred to
microcentrufuge tubes, centrifuged and media aspirated. The
wells and pellets were washed with media to remove non-specific
binding. MATB pellets and
attached cells were lysed with 0.5ml of 0.25 NaOH and incubated
for 30 minutes at room temperature. The lysates were diluted
with 5ml of Ecolite scintillation cocktail and counted on a
Packard PLD beta counter. Growth and proliferation analysis was
compared by t-test for each exposure group.
The results of
the tumor growth aspect at the study are depicted graphically in
Figure 1. Comparison
of tumor weights showed significant reduction of tumor mass (all
comparisons p<0.02) in lesions produced by exposed cells over
those by controls. Tumors produced by unexposed MATB cells
weighed 0.9766 -+10.16 grams, those receiving electrical
exposure weighed 0.5334+/-0.10 gms., those receiving magnetic
exposure weighed 0.43424+/- 0.07 gms. and those receiving
combined exposure weighed 0.3597 -+0.06gms. EMF significantly
decreased the growth and local
invasio0n of the MATB cells. The
invasive capacity of MATB cells showed variable results with the
exposure durations of 24 and 48 hours, but more consistent
effects were observed with 72 hour exposure periods (Figs 2
& 3). Compared to unexposed cells, those exposed to
electrical fields showed invasiveness of 60% of controls
(p=<O.OO2), those exposed to magnetic fields showed 64%
invasiveness of controls (p=<0.05) and cells exposed to
electromagnetic fields revealed 38$ invasiveness of controls
(p=<0.001). Further analysis indicated a dose response from
the effect on exposed cells that correlated to the effect on
cell invasiveness. Exposure of the cells for 2 hours showed no
more
pronounced effect than that for 1 hour, but a direct effect was
observed with respect to the duration of exposure. Consistent
with the decreased tumor growth of EMF exposed cells noted a
significant decrease was noted in the invasion of Matrigel by
when field exposure was extended to 72 hours. The more
pronounced effect was produced by the combined fields.


EMF effects on
MATB cellular proliferation by incorporation of 3H-thymidine and
growth by cell counts were compared to the indices of unexposed
cells (100%). Exposure to electrical fields increased cell
proliferation to 150% of control, exposure to magnetic fields
increased proliferation to 160% of control and combined field
exposure produced increases of 228%. All field exposures
increased the cellular proliferation (P<0.001) of the MATB
cells. Furthermore, cell counts for the E, M and EM exposed
cells showed increased cell growth (Table
1) to 105% of control, 116% of control and 137% of control for
respective p values of 0.32, 0.053 and 0.005. The results
confirm that the MATB cells remain
viable through EMF exposure. In contrast, the increased growth
and proliferative capacities of the exposed cells did not
correlate with their resultant tumor size and invasive activity.
The potential for
biologic effects of exposure to electromagnetic fields was
raised initially in the mid 1960s by Asanova and Rakov [16]
reporting from the Soviet
Union. A complex of symptoms including malaise, headache,
insomnia, fatigue, loss of libido and cardiovascular disorders
was indentified among railroad switchyard workers. Subsequent
studies of workers with similar levels of exposure in western
countries were nonconfirmatory [17,108,19). The report of
Wertheimer and Leeper
[1] in 1979 first raised the question of possible linkage
between field exposures and cancer. A two- to three-fold
increase in cancer was reported among children living in
proximity to electrical lines of high-current configuration.
Leukemia. lymphoma and central nervous system tumors were the
prominent lesions found in this study. Subsequently at least 50
epidemiologic studies have been reported, focusing on either
occupational or residential exposures. The results and
appropriate abstracts of these studies have been presented in
extensive literature reviews by Creasey and Goldberg [20] and
Ahlbom [21] These may be summarized as showing a plausible but
weak and unproven relationship between specific neoplasms and
electromagnetic exposures. Some of the data suggest a possible
role of EMF exposures serving a promotional rather than
causative role with respect to the incidence of certain cancers.
In support of
the concept of a promotional role for EMF exposures, Leung et al
[22] reported an increased number of rat mammary tumors produced
in animals exposed to both dimethylbenzanthracene (DMBA) and
60Hz electrical fields. Bemiashvili [23] likewise showed
promotional effects of both static and variable magnetic fields
imposed on rats previously injected with nitrosomethyl urea
(NMU). The results reported by Rannug [24, 25] in two separate
studies of promotional effects of magnetic fields on the
production of liver tumors were inconclusive. Loscher [26]
studied the promotional influence of magnetic fields in DMBA
treated female rats. Varying ranges of magnetic field exposures
were used with equivocal results. Conversely, inhibition of
expected growth of spontaneous tumors In animals exposed
to pulsed magnetic fields has been reported by Bellossi [27],
Rius [28] and Iur'ev [29]. It should be noted that the levels of
energy of the induced fields in these studies were at
considerable variance. Of
the several studies focused on the influence of EMF exposures on
tumor growth, only the study reported here investigated both the
effects of EMF exposure on tumor cells
of the same type and at the same levels of exposure. Rius [28]
reported inhibition of growth of a mouse mammary tumor cell
line, demonstrated. Conversely, Phillips and associates [30]
reported the increased growth of two separate cell lines of
human colon cancer exposed to magnetic fields of 1G and
electrical fields or 3O0mA/m2. West et al [31] showed enhanced
growth of mouse JB6 cells exposed to magnetic fields of 10G. The
results of the cell proliferation aspect of the study reported
here, measured by 3H-thymidine uptake of exposed cells, showed
similar increases in growth rates. These findings suggest that
the cellular mechanisms controlling cell proliferation and those
determining invasive capacity and tumor size may be mediated in
separate fashions. There is support for this concept.
Mahnensmith and Aronsan [] identified the role of the Na+/H+
plasma membrane antiporter in mammalian cells. Grinstein and
Rothstein [] as well as the work of Rozengurt and Mendoza [] and
that of Moolenaar et al [] lucidated the regulation of that
exchanger. L'Alleman et al [] demonstrated the blockade of the
antiport will
shut dawn DNA synthesis and cell proliferation in fibroblasts.
Cell invasion and metastasis, on the other hand, have been
clearly shown to be controlled by the activation of plasminogen
to surface bound plasmin by the autocrine binding of urokinase
plasminogen activator to its receptor (uPA/uPAR). These actions
initiate the proteolytic cascade required for tumor cell
invasion and metastasis. Separate effects of EMF exposure on the
Na+/H+ antiport from those on the uPA/uPAR ligand may well
explain the apparent paradox of reduced cellular invasiveness
and smaller tumor production in the face of increased cell
proliferation and growth resultant from the same
stimulus.Studies designed to demonstrate effects on growth,
embryonic development, organ system function as well as
cytogenetics have been carried out on avian, mammalian and
bacterial species have again yielded variable results
[32.33.34.35.36.37.38.39.40.41.42]. Through the comparisons of
these similar studies which have produced conflicting or even
contradictory results there emerges a strong suggestion of
specificity of exposure effect. The variations of length,
intensity and frequency of exposures have been offered as
explanations of conflicting results.
The results of
the present study, showing variable levels of response to
changes in the length and duration of exposures, are supportive
of this concept.
Both electrical
and magnetic fields singly imposed on MATB rat mammary cancer
cells produced significant inhibition of tumor growth and cell
invasiveness. Combined electric and magnetic field exposures
produced the most profound change. EMF exposure of identical
cells at identical energy levels which demonstrated decreased
cell invasiveness and tumor growth provoked seemingly
incongruent increase in cell growth and proliferation. These
results are consistent with the current understanding of the
regulatory pathways of cell proliferation vs those of invasion
and metastasis.
The disparate findings of increased cell growth in the face of
diminished tumor mass and cell invasiveness may be the result of
the response of separate regulatory devices to the same
stimulus. Further inquiry into the mechanisms involved in the
responses found in this report are currently the subject of
further inquiry. Comparison of the range of response to the
varying exposure levels utilized in this study to the existing
literature supports the concept of specificity of field strength
and exposure duration on the effects produced.
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