==================================CMR52==================================
52. Relationships between dietary fat and breast cancer. Qualitative
effects of dietary lipids and breast cancer. Unsaturated vs.
saturated fats. Including epidemiological studies, clinical trials,
and animal models.
1
UI - 87092476
AU - Pariza MW
TI - Calorie restriction, ad libitum feeding, and cancer.
AB - The inhibition of cancer by calorie restriction was discovered
over 50 years ago. By 1950 it had been well characterized and
there existed sufficient data to propose a mechanism of action.
For reasons that remain unclear, but are probably related to the
perception of the calorie restricted rodent as "small: and the ad
libitum feeding regimen as more "normal,: the concept of calorie
restriction has been largely ignored by investigators after this
time. Hence, despite the fact that calorie restriction is one of
the oldest, best-documented, and most effective ways known to
reduce cancer risk in rodents, it has had little impact on modern
cancer research. In this report the history of calorie
restriction is briefly reviewed, and a mechanism of action is
proposed that involves increased production of ACTH and decreased
production of gonadotrophins. It is further proposed that these
changes may come about in part from the restriction of the time
during which feeding is permitted as well as from the restriction
of food per se. There is renewed interest in calorie restriction
due in part to the growing recognition that there are differences
in the efficiency of utilization of various sources of energy, in
particular that fat calories are utilized more efficiently and
provide more usable energy than carbohydrate calories. New data
are presented indicating that the apparent enhancement by dietary
fat of mammary cancer in rats is really a manifestation of the
caloric effect. Further, the effect is abolished by moderate
calorie restriction of only 15-20%. The application of these
findings to the prevention of cancer in humans is considered.
MH - Adrenocorticotropic Hormone/BIOSYNTHESIS ; Animal ; Body Weight ;
Caloric Intake ; Dietary Carbohydrates/METABOLISM ; Dietary Fats/
METABOLISM ; *Eating ; Energy Metabolism ; *Food Deprivation ;
Mammary Neoplasms, Experimental/ETIOLOGY/METABOLISM ; Neoplasms,
Experimental/ETIOLOGY/*PREVENTION & CONTROL ; Review ; Support,
Non-U.S. Gov't ; Support, U.S. Gov't, Non-P.H.S. ; Support, U.S.
Gov't, P.H.S.
SO - Proc Soc Exp Biol Med 1986 Dec;183(3):293-8
2
UI - 87085852
AU - Clinton SK ; Alster JM ; Imrey PB ; Nandkumar S ; Truex CR ;
Visek WJ
TI - Effects of dietary protein, fat and energy intake during an
initiation phase study of 7,12-dimethylbenz[a]anthracene-induced
breast cancer in rats.
AB - A factorial experiment was conducted to examine the effects of
dietary protein (8, 16, 32% of energy from casein) and dietary
fat (12, 24, 48% of energy from corn oil) on the initiation of
7,12-dimethylbenz[a]anthracene (DMBA)-induced breast
carcinogenesis in rats. Forty weanling female Sprague-Dawley rats
were assigned to each of nine diets fed ad libitum. After 4 wk
each rat received DMBA (20 mg/kg) via gastric intubation. For an
additional 22 wk after carcinogen administration all rats
consumed a diet containing 16% of dietary energy from protein and
24% from fat. Dietary fat, protein and ad libitum energy
consumption exhibited statistically significant effects on final
tumor prevalence, but interactive effects were not found. At
necropsy, rats fed corn oil at 12, 24 and 48% of energy prior to
DMBA administration showed tumor prevalences of 58, 58 and 85%
with 116, 153 and 231 total tumors, respectively. The data
indicate a significant nonlinear effect of dietary fat.
Corresponding numbers for rats fed casein at 8, 16 and 32% of
energy prior to DMBA were prevalences of 79, 65 and 59%, with
total tumor counts of 194, 144 and 162. Higher dietary protein
during the initiation phase was associated with a significant
reduction in tumor prevalence, which was most striking between 8
and 16% of energy from protein. In addition, results of multiple
logistic regression showed that tumorigenesis was increased with
greater ad libitum energy intake. The odds of a tumor at necropsy
were multiplied by 1.19 for each kilocalorie increase in ad
libitum energy intake averaged over the post-DMBA phase of the
experiment. An additional six weanling rats fed each diet for 4
wk were killed for assay of hepatic carcinogen metabolizing
enzymes at the time corresponding to DMBA administration in the
initiation experiment. Both protein and fat showed independent
effects on the activity of several enzymes. However, enzyme
activity did not suggest a unifying mechanism whereby these
nutrients influence DMBA-induced mammary carcinogenesis.
MH - Adenocarcinoma/ETIOLOGY ; Adenoma/ETIOLOGY ; Animal ; *Caloric
Intake ; Carcinogens/METABOLISM ; Dietary Fats/*ADMINISTRATION &
DOSAGE/PHARMACODYNAMICS ; Dietary Proteins/*ADMINISTRATION &
DOSAGE/PHARMACODYNAMICS ; Female ; Mammary Neoplasms,
Experimental/*ETIOLOGY/PREVENTION & CONTROL ; Microsomes, Liver/
DRUG EFFECTS/ENZYMOLOGY ; Rats ; Rats, Inbred Strains ; Support,
U.S. Gov't, P.H.S. ; *9,10-Dimethyl-1,2-Benzanthracene
SO - J Nutr 1986 Nov;116(11):2290-302
3
UI - 87067576
AU - Hawrylewicz EJ
TI - Fat-protein interaction, defined 2-generation studies.
AB - Mammary tumor burden, in rats fed either normal or high fat diets
related positively to the level of protein in the diet. This
relationship existed with either a direct (NMU) or indirect
carcinogen (DMBA). Significant differences in body growth, sexual
maturation, morphologic structures in the mammary duct, and
hormone activities during the estrous cycle probably contributed
to lower tumor burden in the low protein-normal fat (LP-NF)
group. Animals fed a high protein-normal fat (HP-NF) diet
throughout their entire life have, with the exception of early
sexual maturation, no distinctive characteristics compared to the
control group. Inspite of these physical and physiologic
similarities, increased dietary protein enhanced the effect of
administered carcinogens. Animals fed a high protein-high fat
(HP-HF) diet were compared to rats fed a normal protein-high fat
(NP-HF) diet. Increased dietary protein further enhanced the
effect of the high fat diet resulting in an increased
carcinogen-induced tumor burden. These studies indicate that the
design of the animal model, i.e. age of initiation of a test
diet, appears to have a significant bearing on mammary tumor
development. The biologic mechanisms which respond to diet
modifications and which may influence breast tumor growth have
not been thoroughly elaborated and require additional study.
MH - Animal ; Body Weight ; Cell Transformation, Neoplastic/DRUG
EFFECTS ; Cocarcinogenesis ; Dietary Fats/ADMINISTRATION & DOSAGE/
*METABOLISM ; Dietary Proteins/ADMINISTRATION & DOSAGE/
*METABOLISM ; Disease Models, Animal ; Eating ; Epidemiologic
Methods ; Mammae/DRUG EFFECTS ; Mammary Neoplasms, Experimental/
ETIOLOGY ; Methylnitrosourea ; Prolactin/BLOOD ; Review ;
Thymidine/METABOLISM ; 9,10-Dimethyl-1,2-Benzanthracene
SO - Prog Clin Biol Res 1986;222:403-33
4
UI - 87030455
AU - Elegbede JA ; Elson CE ; Qureshi A ; Dennis WH ; Yatvin MB
TI - Increasing the thermosensitivity of a mammary tumor (CA755)
through dietary modification.
AB - Disruption of the integrity of tumor cellular membranes has been
proposed as an initiating event in hyperthermic cell death.
Thermosensitivity measured by the shift in the harmonic mean of
tumor regrowth delay of CA755 mammary adenocarcinomas grown in
the hind legs of male BDF1, mice increased 22% when the hosts
were fed a diet enriched in polyunsaturated fatty acids. Although
the diet elicited the anticipated increase in tumor membrane
phospholipid polyunsaturated fatty acids, the proportion of total
unsaturated fatty acids decreased and the proportion of
membrane-rigidifying saturated fatty acids increased.
Concomitantly, the concentrations of cholesterol and phospholipid
phosphorus increased and the ratio of phosphatidylethanolamine to
phosphatidylcholine decreased, presumably to counter the effect
of the change in the fatty acid pattern. In host liver membranes,
the diet-mediated increase in proportion of polyunsaturated fatty
acids was not accompanied by an increase in the proportion of
rigidifying saturated fatty acids. Instead, the homeoviscous
adaptation consisted of decreases in monounsaturated fatty acids
and cholesterol concentration and an increase in the
phosphatidylethanolamine-phosphatidylcholine ratio. Addition of a
natural inhibitor of cholesterol biosynthesis to the
polyunsaturated fatty acid enriched-diet reversed the
diet-mediated increase in the
phosphatidylethanolamine-phosphatidylcholine ratio of host liver
membranes. Tumor membrane lipids from hosts fed the combined
dietary factors were characterized by the formentioned
rigidifying increase in saturated fatty acids and compensatory
decrease in the phosphatidylethanolamine-phosphatidylcholine
ratio. The inhibitor reversed the compensatory increases in
cholesterol and phospholipid phosphorus concentrations. As a
consequence the thermosensitivity of tumors bearing this
perturbed membrane was increased.
MH - Adenocarcinoma/PHYSIOPATHOLOGY ; Animal ; Anticholesteremic
Agents/PHARMACODYNAMICS ; Body Weight ; Cell Survival ;
Cholesterol/BLOOD ; *Dietary Fats ; Fatty Acids, Unsaturated ;
*Heat ; Liver/PATHOLOGY ; Mammary Neoplasms, Experimental/
METABOLISM/*PHYSIOPATHOLOGY ; Membrane Lipids/METABOLISM ; Mice ;
Mice, Inbred Strains ; Organ Weight ; Phospholipids/METABOLISM ;
Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S.
SO - Eur J Cancer Clin Oncol 1986 May;22(5):607-15
5
UI - 87027938
AU - Rose DP ; Boyar AP ; Wynder EL
TI - International comparisons of mortality rates for cancer of the
breast, ovary, prostate, and colon, and per capita food
consumption.
AB - The 1978-1979 mortality rates for cancers of the breast,
prostate, ovary, and colon in 26 to 30 countries were related to
the average 1979-1981 food availability data published by the
United Nations. The previously described relationship between
breast cancer mortality rates and animal fat consumption
continues to be evident, and applies also to the other three
tumor types. The correlation with breast cancer was particularly
strong in postmenopausal women. Since 1964, particularly notable
increases in both breast cancer mortality rate and dietary fat
intake have occurred in those countries with a relatively low
breast cancer risk. The international comparisons support
evidence from animal experiments that diets in which olive oil is
a major source of fat are associated with reduced breast cancer
risk. The excess in mortality rates for breast and ovarian cancer
in Israel relative to the national animal fat consumption may be
due to the mixed ethnic origin of the Israeli population.
Positive correlations between foods and cancer mortality rates
were particularly strong in the case of meats and milk for breast
cancer, milk for prostate and ovarian cancer, and meats for colon
cancer. All four tumor types showed a negative correlation with
cereal intake, which was particularly strong in the case of
prostate and ovarian cancer. Although, in general, there was a
good positive correlation between prostate and breast cancer
mortality rates and between prostate cancer and animal fat,
discrepancies in national ranking indicate the operation of other
etiologic factors that modify risk. The observed positive
correlations between the four cancer mortality rates and caloric
intake from animal sources, but negative correlations for
vegetable-derived calories, suggest that, of the two, animal fat
and not energy is the major dietary influence on cancer risk.
MH - Adult ; Breast Neoplasms/*MORTALITY ; Caloric Intake ; Colonic
Neoplasms/*MORTALITY ; Comparative Study ; *Diet ; Dietary Fats ;
Female ; Human ; Male ; Menopause ; Middle Age ; Ovarian
Neoplasms/*MORTALITY ; Plant Oils ; Prostatic Neoplasms/
*MORTALITY ; Support, U.S. Gov't, P.H.S. ; World Health
SO - Cancer 1986 Dec 1;58(11):2363-71
6
UI - 87004446
AU - Pariza MW ; Hargraves WA ; Benjamin H ; Christou M ; Jefcoate CR
; Storkson J ; Albright K ; Kraus D ; Sharp P ; Boissonneault GA
; et al
TI - Modulation of carcinogenesis by dietary factors.
AB - The purpose of this report is to present recent data on two
modulating factors of carcinogenesis that are found in
Western-type diets: a beef-derived mutagenesis modulator that has
been shown to inhibit the initiation of epidermal carcinogenesis
in mice, and the possible role of net energy rather than dietary
fat per se in the enhancement of rat mammary carcinogenesis.
MH - Animal ; *Carcinogens ; Cattle ; *Diet/ADVERSE EFFECTS ; Dietary
Fats/ADVERSE EFFECTS ; Energy Metabolism ; Female ; Mammary
Neoplasms, Experimental/ETIOLOGY ; Meat ; Mice ; Mutation ; Rats
; Rats, Inbred F344 ; Skin Neoplasms/PREVENTION & CONTROL ;
Support, Non-U.S. Gov't ; Support, U.S. Gov't, Non-P.H.S. ;
Support, U.S. Gov't, P.H.S.
SO - Environ Health Perspect 1986 Aug;67:25-9
7
UI - 87001945
AU - Wynder EL ; Rose DP ; Cohen LA
TI - Diet and breast cancer in causation and therapy.
AB - The major macronutrient associated with increased breast cancer
risk is dietary fat. Evidence for this association is based on
epidemiologic, clinical, and laboratory animal studies. In
addition, there is suggestive epidemiologic evidence that
differences in postmastectomy survival rates in Japan and the
United States may be attributable to differences in dietary fat
intake. The importance of the type of fat consumed, as well as
its amount, has emerged as an issue of major importance. Some
oils, including those rich in monounsaturates, medium chain fatty
acids, or omega-3 (n-3) fatty acids appear to lack
tumor-promoting effects despite their presence in the diet at
high levels. Possible mechanisms by which dietary fat may exert
its effects could be either direct or indirect. Direct mechanisms
involve dietary modification of membrane structure and function;
indirect mechanisms involve alterations in the endocrine system,
and/or the metabolism of essential fatty acids to biologically
active eicosanoids such as prostaglandins, and suppression of
immune responses. Dietary guidelines and dietary intervention
trials for the primary and secondary prevention of breast cancer
are discussed.
MH - Animal ; Breast Neoplasms/BLOOD/*ETIOLOGY/OCCURRENCE ;
Comparative Study ; Dietary Fats/*ADVERSE EFFECTS ; Female ;
Hormones/BLOOD ; Human ; Japan ; Male ; Mammary Neoplasms,
Experimental/ETIOLOGY ; Mice ; Prostatic Neoplasms/ETIOLOGY/
OCCURRENCE ; Rats ; Support, U.S. Gov't, P.H.S. ; United States
SO - Cancer 1986 Oct 15;58(8 Suppl):1804-13
8
UI - 86229821
AU - Rogers AE ; Conner B ; Boulanger C ; Lee S
TI - Mammary tumorigenesis in rats fed diets high in lard.
AB - Studies were performed to examine the effect of a lard diet on
tumorigenesis by 7,12-dimethylbenzanthracene (DMBA), given
parenterally rather than by gavage, to eliminate any effect of
the high lard diet on carcinogen absorption. In addition, the
effect of low dietary levels of the antioxidants butylated
hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) in the
tumor model was evaluated. The lards fed were analyzed for fatty
acid composition and content of certain potential contaminants.
DMBA induced tumors when given by intravenous or subcutaneous
injection. The high lard diet appeared to enhance tumorigenesis
in rats given a dose of 0.25 mg (10% of the gavage dose) by
injection into the mammary gland, although the effect was not
statistically significant. In other experiments using lard from
different sources and DMBA given by gavage, significant
enhancement of tumorigenesis was limited to groups fed the high
lard diets throughout the experiment or beginning after DMBA
exposure. In contrast to earlier results, there was no
demonstrable effect of feeding the high lard diets before DMBA
administration. Addition of BHA and BHT to the lard at the
concentration assayed in commercial lard samples or at the
maximum concentration permitted did not influence the
tumorigenesis. In groups in which tumorigenesis was enhanced by
the high lard diet, the incidence of malignant, invasive tumors
was higher than in other groups.
MH - Animal ; Comparative Study ; Dietary Fats/*ADVERSE EFFECTS ;
Female ; Mammary Neoplasms, Experimental/ETIOLOGY/*PATHOLOGY ;
Rats ; Rats, Inbred Strains ; Support, U.S. Gov't, P.H.S. ; Time
Factors ; 9,10-Dimethyl-1,2-Benzanthracene
SO - Lipids 1986 Apr;21(4):275-80
9
UI - 86228507
AU - Gabor H ; Abraham S
TI - Effect of dietary menhaden oil on tumor cell loss and the
accumulation of mass of a transplantable mammary adenocarcinoma
in BALB/c mice.
AB - A reduction in the size of transplantable mammary adenocarcinoma
IX was achieved when female BALB/c mice were fed isocaloric 10%
fat diets containing either hydrogenated cottonseed oil (HCTO) or
menhaden oil (MO) as opposed to those mice fed corn oil (CO).
Indeed, CO increased the size of the neoplasms when fed alone at
5 or 1% of the diet, although such diets contained less fat
calories than did the 10% fat diets containing the other two
oils. At the 10% level of dietary fat, enhanced accumulation of
tumor mass was observed even when 7.5, 5.0, and 2.5% CO was
administered in combination with either HCTO or MO. Although this
effect of CO could not be inhibited when nine times as much HCTO
was added to the diet, such growth enhancement was abolished when
the diet contained nine times as much MO. Hence these experiments
emphasized the importance of the type rather than the amount of
dietary fat. Whereas MO contained polyunsaturated fatty acids
(PUFA's) [approximately 1% as linoleic acid, approximately 16% as
5,8,11,14,17-eicosapentaenoic acid (EPA), approximately 11% as
4,7,10,13,16,19-docosahexaenoic acid (DHA)], HCTO contained none
and CO had about 60% of its constituent fatty acids in the form
of linoleic acid. The rate of tumor cell loss, determined by the
[125I]5-iodo-2'-deoxyuridine method, in the 10% MO-fed or the 10%
HCTO-fed mice (54 or 45%, respectively) was more than twice that
observed for tumors from the 10% CO-fed mice (22%). These
observations were discussed in terms of the influence of the
dietary PUFA linoleic acid [C 18:2 (No. of carbons:No. of double
bonds), n-6], the PUFA EPA (C 20:5, n-3), and the PUFA DHA (C
22:6, n-3) on the size of mammary tumors and on the involvement
of prostaglandins in this process.
MH - Adenocarcinoma/METABOLISM/*PATHOLOGY ; Animal ; Body Weight ;
Cottonseed Oil/PHARMACODYNAMICS ; Dietary Fats/*PHARMACODYNAMICS
; Fatty Acids/ANALYSIS ; Female ; Linoleic Acids/METABOLISM ;
Mammary Neoplasms, Experimental/METABOLISM/*PATHOLOGY ; Mice ;
Mice, Inbred BALB C ; Neoplasm Transplantation ; Oils/
*PHARMACODYNAMICS ; Prostaglandins/BIOSYNTHESIS ; Support,
Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S.
SO - JNCI 1986 Jun;76(6):1223-9
10
UI - 86308830
AU - L:e MG ; Moulton LH ; Hill C ; Kramar A
TI - Consumption of dairy produce and alcohol in a case-control study
of breast cancer.
AB - In a French case-control study of 1,010 breast cancer cases and
1,950 controls with nonmalignant diseases, the risk of breast
cancer was found to be positively associated with frequency of
cheese consumption and the level of fat in the milk consumed. A
negative association was found between frequency of yogurt
consumption and the risk of breast cancer. No association was
found between the consumption of butter and the risk of breast
cancer. The positive association between a daily consumption of
alcohol and the risk of breast cancer previously reported was not
altered when dairy produce consumption was taken into account.
MH - Aged ; *Alcohol Drinking ; Breast Neoplasms/*ETIOLOGY ; Cheese/
ADVERSE EFFECTS ; Dairy Products/*ADVERSE EFFECTS ; Dietary Fats/
ADVERSE EFFECTS ; Female ; Human ; Lactobacillus Acidophilus ;
Middle Age ; Risk ; Support, Non-U.S. Gov't
SO - JNCI 1986 Sep;77(3):633-6
11
UI - 86308825
AU - Lubin F ; Wax Y ; Modan B
TI - Role of fat, animal protein, and dietary fiber in breast cancer
etiology: a case-control study.
AB - A case-control study of 818 breast cancer (BC) patients and 2
matched control groups, surgical controls (SCs) and neighborhood
controls (NCs), was undertaken in Israel between 1975 and 1978.
The interview schedule included a detailed dietary history based
on the frequency of consumption of 250 food items, which were
grouped according to their principal nutrient component. The
average frequency of consumption of each food item in each
nutrient group was computed. Medical, demographic, hormonal, and
parity histories were also obtained. Risks associated with fat,
animal protein, and fiber consumption were evaluated. Two types
of analysis were performed [in 2 age groups (less than 50 yr and
greater than or equal to 50 yr)], using the conditional logistic
method: evaluating the risk attributable to nutrition only and
controlling for nondietary confounding factors as well. When no
adjustment for nondietary confounding factors was made, the risk
increased with fat intake in both age groups [one-tailed P-value
for linear trend = .08 and .07 in age less than 50 and .01 and
.10 for the greater than or equal to 50 age category for the BC
case (BCC)-SC and BCC-NC comparisons, respectively]. Increased
fiber intake decreased the risk in the younger age group
(one-tailed P-value for linear trend = .06 and .07 for the BCC-SC
and BCC-NC comparisons, respectively), while in the 50-or-over
age category the trend was inconsistent. The risk associated with
animal protein was much less clear. For women in the highest
quartiles of fat and animal protein intake and the lowest
quartiles of fiber intake, risk was about twice as high as that
for women in the lowest quartiles of fat and animal protein
intake and in the highest quartile of fiber intake (one-tailed
P-value for linear trend = .04 and .08 for age less than 50 and
.08 and .09 for the age category greater than or equal to 50
BCC-SC and BCC-NC comparisons, respectively). When hormonal and
demographic confounding factors were controlled for, this pattern
persisted but it remained significant for 1 control only. Power
increased when cases were analyzed against both controls
simultaneously (one-tailed P-value for linear trend = .10 for age
less than 50 and .02 for age greater than or equal to 50). Thus a
higher fat-animal protein and lower fiber diet is associated with
increased cancer risk, but this relationship needs to be studied
further.
MH - Adult ; Age Factors ; Aged ; Breast Neoplasms/*ETIOLOGY ; Dietary
Fats/*ADMINISTRATION & DOSAGE ; Dietary Fiber/*ADMINISTRATION &
DOSAGE ; Dietary Proteins/*ADMINISTRATION & DOSAGE ; Female ;
Human ; Middle Age ; Risk ; Support, U.S. Gov't, P.H.S.
SO - JNCI 1986 Sep;77(3):605-12
12
UI - 86307146
AU - Horwitt MK
TI - The promotion of vitamin E.
AB - Investigations that have influenced the promotion of vitamin E
supplementation are reviewed. The various forms of vitamin E
found in foods and the composition of synthetic vitamin E in
common use are described with note of a frequent error of
identification made in reports of studies on vitamin E. Recent
communications on the use of antioxidants to delay carcinogenesis
in animals and in humans are discussed. The publicity given the
reports of cancer prevention by antioxidants will probably
increase self-supplementations. It is therefore necessary to
understand the pharmacological limits of such supplementation
with vitamin E. Daily supplementation of adults with about 200 mg
of d-alpha-tocopherol equivalents per day has not been proven to
be harmful, but the effects of ingestion of more than 800 mg a
day have not been studied sufficiently. Special precautions
should be taken in administering emulsified vitamin E
preparations intravenously to premature infants.
MH - Animal ; Antioxidants ; Breast Neoplasms/BLOOD ; Chemistry ;
Dietary Fats/ADMINISTRATION & DOSAGE/ADVERSE EFFECTS ; Female ;
Human ; Infant ; Infant, Premature ; Lipid Peroxides/METABOLISM ;
Male ; Mammary Neoplasms, Experimental/ETIOLOGY/PREVENTION &
CONTROL ; Neoplasms, Experimental/PREVENTION & CONTROL ;
Nomenclature ; Nutrition ; Nutritional Requirements ; Review ;
Support, Non-U.S. Gov't ; Vitamin E/ADMINISTRATION & DOSAGE/
ADVERSE EFFECTS/BLOOD/*PHYSIOLOGY/THERAPEUTIC USE ; Vitamin E
Deficiency/DRUG THERAPY
SO - J Nutr 1986 Jul;116(7):1371-7
13
UI - 86286734
AU - Boylan ES ; Cohen LA
TI - The influence of dietary fat on mammary tumor metastasis in the
rat.
AB - Young, virgin female Fischer 344 rats bearing the 13762
transplantable mammary tumor were fed diets containing either 5%
(low-fat group) or 23% (high-fat group) corn oil for five weeks
before and six weeks after tumor implantation. Animals in the two
diet groups gained weight at comparable rates throughout the
experiment. There was no significant difference between the
low-fat and high-fat groups with respect to average tumor
diameter measured twice per week for six weeks. At the time of
death (6 weeks after tumor implantation), the lungs of all rats
in both diet groups contained some metastatic tumor deposits; the
volume of the metastases in the lungs varied widely in both
groups. Numbers of metastases to regional lymph nodes and kidneys
appeared unaffected by the fat content of the diet. Thus, both
growth of the 13762 mammary tumor itself and metastatic spread
from the tumor were comparable whether the young rats were fed a
high-fat or a low-fat diet.
MH - Animal ; Comparative Study ; Dietary Fats/*ADMINISTRATION &
DOSAGE ; Female ; Lung Neoplasms/PATHOLOGY/SECONDARY ; Mammary
Neoplasms, Experimental/*PATHOLOGY ; *Neoplasm Metastasis ;
Neoplasm Transplantation ; Oils/ADMINISTRATION & DOSAGE ; Rats ;
Rats, Inbred F344 ; Support, Non-U.S. Gov't ; Support, U.S.
Gov't, P.H.S.
SO - Nutr Cancer 1986;8(3):193-200
14
UI - 86271915
AU - Hislop TG ; Coldman AJ ; Elwood JM ; Brauer G ; Kan L
TI - Childhood and recent eating patterns and risk of breast cancer.
AB - A case-control study was done to examine the relationship between
childhood and recent eating practices and risk of breast cancer.
Eight hundred forty-six cases and 862 controls returned
questionnaires indicating their menopausal status. In
premenopausal women, breast cancer risk was increased with recent
consumption of foods high in fat content (gravy, beef, pork) and
reduced with foods low in fat content (fish); in postmenopausal
women, risk was increased with pork consumption only. Regarding
carotene sources, risk was reduced with carrot consumption in
postmenopausal women only. Similar trends in risk were not found
for childhood eating practices. Body weight influenced the breast
cancer risk differently for pre- and postmenopausal women:
Heavier weight in childhood and teens reduced the risk of
premenopausal breast cancer, and heavier weight in adulthood
increased the risk of postmenopausal breast cancer. We conclude
that fat consumption is associated with breast cancer, especially
in premenopausal women.
MH - Adult ; Body Height ; Body Weight ; Breast Neoplasms/*ETIOLOGY ;
Child ; *Diet ; Dietary Fats ; Female ; Human ; Menopause ;
Middle Age ; Obesity/COMPLICATIONS ; Questionnaires ; Risk ;
Support, Non-U.S. Gov't
SO - Cancer Detect Prev 1986;9(1-2):47-58
15
UI - 86271709
AU - Hawrylewicz EJ ; Huang HH ; Liu JM
TI - Dietary protein, enhancement of N-nitrosomethylurea-induced
mammary carcinogenesis, and their effect on hormone regulation in
rats.
AB - The effect of supplemental dietary protein (casein) fed with high
fat diets was investigated using the N-nitrosomethylurea-induced
mammary tumor model. Isocaloric diets containing casein and corn
oil at 19 and 15% (normal protein-high fat) or 33 and 15% (high
protein-high fat) were fed ad libitum to Sprague-Dawley mother
rats. Female offspring continued on the diet. Food consumption
and growth curves were similar over the entire growth period.
N-Nitrosomethylurea (50 mg/kg body weight) or saline was
administered at 7 and 8 weeks of age via the tail vein. Dietary
protein had no effect on serum prolactin or growth hormone
throughout the estrous cycle: Prior to carcinogen administration,
at 7 weeks old, proestrus at 5 p.m., serum prolactin was 231.6
+/- 141.0 (SE) ng/ml (12 rats) versus 292.2 +/- 141.0 (13 rats)
for normal versus high protein diet groups, respectively. No
difference was noted after carcinogen injection at 9, 13, 28, and
33 weeks of age. Similarly no effect was noted on serum growth
hormone activity. Tumor latency was 7 weeks and incidence was
100% in normal protein (24 rats) and high protein (39 rats)
groups 28 weeks after carcinogen treatment. The number of tumors
per rat (4.38 +/- 0.37 versus 2.87 +/- 0.35, P less than 0.002)
and average tumor weight (17.97 +/- 2.63 versus 9.94 +/- 2.92 g)
were significantly greater in the high protein group. Study
indicates that diet or carcinogen treatment did not alter hormone
regulation during the estrous cycle. However, supplemental
dietary protein increased the effect of high fat diets enhancing
the mammary tumor burden.
MH - Animal ; Body Weight ; Caloric Intake ; Dietary Fats/PHYSIOLOGY ;
Dietary Proteins/*PHYSIOLOGY ; Estrus ; Female ; Mammary
Neoplasms, Experimental/CHEMICALLY INDUCED/*ETIOLOGY ;
Methylnitrosourea ; Methyltyrosines/PHARMACODYNAMICS ; Prolactin/
BLOOD ; Rats ; Somatotropin/BLOOD ; Support, U.S. Gov't, P.H.S.
SO - Cancer Res 1986 Sep;46(9):4395-9
16
UI - 86264637
AU - Boeryd B ; Hallgren B
TI - The incidence of spontaneous mammary carcinoma in C3H mice is
influenced by dietary fat given from weaning and given to the
mothers during gestation and lactation.
AB - The influence of dietary fat given to breeding C3H female mice
during gestation and lactation on the incidence of spontaneous
mammary carcinoma in the female offspring was studied. EWOS'
commercial diet (E-diet) for mice and two test diets, one
containing 2% soy oil (S-diet) and the other 2% soy oil and 0.1%
methoxy-substituted glycerol ethers (MGE-diet), instead of the
animal fat in the E-diet, were used. The breeding females were
given the S- or MGE-diet during gestation and lactation and the
progeny the S- or E-diet from weaning. The incidence of mammary
carcinoma was studied in the force-bred progeny. The results
disclosed significant correlations between the diets of the
progeny and the number of litters and between the number of
litters and the incidence of breast carcinoma. The results also
indicated a strong influence of the mother's diet on the
incidence of mammary carcinoma in the female progeny.
MH - Age Factors ; Animal ; Dietary Fats/*ADVERSE EFFECTS ; Female ;
Fertility ; Lactation ; Mammary Neoplasms, Experimental/*ETIOLOGY
; Mice ; Parity ; Pregnancy ; Support, Non-U.S. Gov't
SO - Acta Pathol Microbiol Immunol Scand [A] 1986 May;94(3):237-41
17
UI - 86255105
AU - Cohen LA ; Thompson DO ; Choi K ; Karmali RA ; Rose DP
TI - Dietary fat and mammary cancer. II. Modulation of serum and tumor
lipid composition and tumor prostaglandins by different dietary
fats: association with tumor incidence patterns.
AB - For investigation of the role of linoleic acid (LA) and its
biologically significant metabolites in mammary tumor promotion
by dietary fat, a detailed study of the fatty acid group
composition of serum lipids, tumor neutral lipids, tumor
phospholipids, and tumor prostaglandins (PG's) was conducted in
female inbred F344 rats initiated with N-nitrosomethylurea (CAS:
684-93-5) and fed diets containing various types and amounts of
fat. The oils, safflower [23%, high fat (HF); 5%, low fat], corn
(23%, 5%), olive (23%, 5%), and coconut (23%) varied widely with
respect to their LA content and their
polyunsaturate:monounsaturate:saturate ratios (9:1:1, 4.6:2.6:1,
0.6:5.9:1, and 0.008:0.05:1, respectively, for safflower, corn,
olive, and coconut oils). A modified hexane-based technique was
used for extraction of serum and tumor lipids. Total tumor lipids
ranged from a low of 5 to a high of 228 mg/g (wet wt) with no
differences found among the 7 dietary groups. The phospholipid
content of the tumors ranged from 27 to 47% of total tumor lipid,
again with no differences seen among dietary groups. Total serum
lipids varied from a low of 3.77 mg/ml (safflower oil, 23%) to a
high of 6.11 mg/ml (coconut oil, 23%), and an overall inverse
trend was observed between total serum lipids and tumor incidence
for the 4 HF diet groups. Serum cholesterol levels were
significantly depressed in the HF safflower oil and corn oil
groups compared to those in all other dietary groups and, in
general, varied inversely with respect to mammary tumor
incidence. Serum and tumor neutral fatty acid profiles closely
reflected those of the diet, while tumor phospholipids appeared
more resistant to diet-induced changes. Olive oil-fed animals
exhibited high levels of oleic acid in both serum and tumor
lipids. The levels of the major metabolite of LA, arachidonic
acid (AA), in tumor phospholipids were highly variable and did
not equate with dietary or serum LA levels. A positive
association was found among dietary LA, tumor PGE2, and mammary
tumor incidence among the 4 HF groups; however, no association
was found between tumor AA levels and either tumor PGE2 levels or
mammary tumor incidence. The results of this study suggest that
dietary LA may exert its effects on mammary tumor promotion by
virtue of its role as a PG precursor; but the precise steps in
this sequence and possible competitive interactions between
essential fatty acids, monoenes, and saturates and the
PG-synthesizing system remain to be determined.
MH - Animal ; Cholesterol/BLOOD ; Cocarcinogenesis ; Comparative Study
; Dietary Fats/ADVERSE EFFECTS/*METABOLISM ; Fatty Acids/
METABOLISM ; Female ; Mammary Neoplasms, Experimental/ETIOLOGY/
*METABOLISM/PATHOLOGY ; Methylnitrosourea/TOXICITY ; Oils/ADVERSE
EFFECTS/*METABOLISM ; Phospholipids/METABOLISM ; Prostaglandins/
*METABOLISM ; Prostaglandins E/METABOLISM ; Prostaglandins F/
METABOLISM ; Radioimmunoassay ; Rats ; Rats, Inbred F344 ;
Support, U.S. Gov't, P.H.S. ; Triglycerides/BLOOD
SO - JNCI 1986 Jul;77(1):43-51
18
UI - 86255104
AU - Cohen LA ; Thompson DO ; Maeura Y ; Choi K ; Blank ME ; Rose DP
TI - Dietary fat and mammary cancer. I. Promoting effects of different
dietary fats on N-nitrosomethylurea-induced rat mammary
tumorigenesis.
AB - The promoting effects of diets varying both in type and amount of
fat on N-nitrosomethylurea [(NMU) CAS: 684-93-5]-induced mammary
tumorigenesis were assessed in female inbred F344 rats. Two seed
oils (safflower and corn) and two fruit oils (olive and coconut),
varying widely in their diene, monoene, and saturated fatty acid
ratios, were fed in the casein-based AIN-76A diets at 23%
[high-fat (HF) diet] and 5% [low-fat (LF) diet] by weight, with
the exception of coconut oil which was fed only at 23%. The
predominant fatty acid in safflower and corn oils was linoleic
acid (82 and 56%, respectively), while the predominant fatty
acids in olive and coconut oils were oleic (79%) and myristic
(54%), respectively. The test diets were fed beginning 2 days
after administration of NMU and continued until termination of
the experiment at 22 weeks post NMU administration. Analysis of
tumor incidence, latency, and multiplicity data obtained from the
7 experimental groups indicated that animals fed the HF safflower
and corn oil diets exhibited enhanced mammary tumor yields when
compared to animals fed HF olive or coconut oil diets or their LF
counterparts. Since weight gains and total caloric intake were
similar in all 4 HF groups, the results of this study indicate
that the tumor-promoting properties of HF diets are more of a
function of differences in fatty acid composition than of fat
content per se or of total caloric intake.
MH - Animal ; Body Weight ; Cocarcinogenesis ; Dietary Fats/*ADVERSE
EFFECTS/ANALYSIS ; Fatty Acids/ANALYSIS ; Female ; Mammary
Neoplasms, Experimental/BLOOD/*ETIOLOGY/PATHOLOGY ;
Methylnitrosourea/*TOXICITY ; Oils/*ADVERSE EFFECTS/ANALYSIS ;
Rats ; Rats, Inbred F344 ; Statistics ; Support, U.S. Gov't,
P.H.S. ; Time Factors
SO - JNCI 1986 Jul;77(1):33-42
19
UI - 86229823
AU - Braden LM ; Carroll KK
TI - Dietary polyunsaturated fat in relation to mammary carcinogenesis
in rats.
AB - High fat diets promote the development of mammary tumors induced
in rats by 7,12-dimethylbenz(a)anthracene (DMBA), and
polyunsaturated fats are more effective than saturated fats. This
difference is related to the linoleic acid content of
polyunsaturated vegetable oils, but the amount of linoleate
required for maximum tumor promotion appears to be higher than
indicated by earlier experiments. Comparison of the effects of a
polyunsaturated vegetable oil (corn oil) containing linoleate
with a fish oil (menhaden oil) containing polyunsaturated fatty
acids derived from linolenic acid showed that higher dietary
levels of corn oil increased the yield of DMBA-induced mammary
tumors, while corresponding levels of menhaden oil had an
inhibitory effect. This is further evidence that promotion of
mammary tumorigenesis by polyunsaturated vegetable oils may be
mediated by prostaglandins or other biologically active
eicosanoids derived from n-6 fatty acids.
MH - Animal ; Comparative Study ; Dietary Fats/*ADVERSE EFFECTS ;
Fatty Acids/ANALYSIS ; Fatty Acids, Unsaturated/*ADVERSE EFFECTS
; Female ; Mammary Neoplasms, Experimental/*PATHOLOGY ; Oils/
ADVERSE EFFECTS ; Rats ; Rats, Inbred Strains ; Support, Non-U.S.
Gov't ; 9,10-Dimethyl-1,2-Benzanthracene
SO - Lipids 1986 Apr;21(4):285-8
20
UI - 86229820
AU - Kritchevsky D ; Weber MM ; Buck CL ; Klurfeld DM
TI - Calories, fat and cancer.
AB - The experiments reported are part of our effort to dissociate the
tumor-enhancing effects of dietary fat and high caloric intake.
Rats either were fed ad libitum diets containing 4% corn oil or
their calories were restricted by 40% and their diets contained
13.1% corn oil. Incidence of 7,12-dimethylbenz(a)anthracene
(DMBA)-induced mammary tumors was 80% in rats fed ad libitum and
20% in those fed the calorie-restricted diets. Incidence of
1,2-dimethylhydrazine (DMH)-induced colon tumors was 100% in rats
fed ad libitum and 53% in those whose caloric intake was
restricted by 40%. The tumor yield (tumors per tumor-bearing rat)
was significantly lower in rats on caloric restriction. In
another series, rats were fed diets containing 5, 15 or 20% corn
oil ad libitum or were fed calorie-restricted (by 25%) diets
which provided 20 or 26.6% corn oil (therefore, the same absolute
amount of fat was consumed in each of the pair-fed groups). Tumor
incidence and tumor yield in the two calorie-restricted groups
were similar to those seen in the rats fed 5% fat ad libitum;
tumor burden (total g of tumor) was 45-65% lower in the
calorie-restricted rats. The data suggest that caloric intake is
a more stringent determinant of tumor growth than fat intake.
MH - Animal ; Caloric Intake ; Colonic Neoplasms/*ETIOLOGY/PATHOLOGY ;
Comparative Study ; *Diet ; Diet, Reducing ; Dietary Fats/
*ADVERSE EFFECTS ; Female ; Male ; Mammary Neoplasms,
Experimental/*PATHOLOGY ; Rats ; Rats, Inbred F344 ; Rats, Inbred
Strains ; Support, Non-U.S. Gov't ; Support, U.S. Gov't, P.H.S. ;
9,10-Dimethyl-1,2-Benzanthracene
SO - Lipids 1986 Apr;21(4):272-4
21
UI - 86213772
AU - Cohen LA ; Choi K ; Weisburger JH ; Rose DP
TI - Effect of varying proportions of dietary fat on the development
of N-nitrosomethylurea-induced rat mammary tumors.
AB - The influence of diets varying in their relative proportions of
dietary fat on N-nitrosomethylurea (NMU)-induced mammary
tumorigenesis, was assessed. Animals were initiated on day 50 of
age with 25 mg/kg NMU and then placed on casein-based AIN-76A
diets containing 5, 10, 16 and 23% corn oil (wt/wt). There were
30 animals/group and the experiment was terminated 22 weeks
post-NMU. It was found that animals fed diets containing 16 and
23% corn oil exhibited tumor incidences between 2 and 3 times
that of animals fed diets containing 5 and 10% corn oil. No
differences in tumor incidence could be detected between the 5
and 10% groups or the 16 and 23% groups, suggesting that a
threshold occurs at some point between 10 and 16% fat (or 20 and
33% of total calories as fat). The results of this study suggest
that the tumor-promoting effects of dietary fat are manifested in
terms of a threshold, rather than a linear dose-response effect.
MH - Animal ; Breast Neoplasms/PREVENTION & CONTROL ; Cocarcinogenesis
; Dietary Fats/*ADMINISTRATION & DOSAGE ; Female ; Human ;
Mammary Neoplasms, Experimental/*CHEMICALLY INDUCED ;
Methylnitrosourea ; Mice ; Rats ; Rats, Inbred F344 ; Risk ;
Support, U.S. Gov't, P.H.S.
SO - Anticancer Res 1986 Mar-Apr;6(2):215-8
22
UI - 86189494
AU - Ip C ; White G
TI - BCG-modulated mammary carcinogenesis is dependent on the schedule
of immunization but is not affected by dietary fat.
AB - The present study was designed to study the effect of dietary fat
intake on the modulation of dimethylbenz[a]anthracene
(DMBA)-induced mammary carcinogenesis in rats injected with the
methanol extract residue of Bacillus Calmette-Guerin (MER-BCG).
Rats were maintained on either a 5% or a 20% corn oil diet for
the entire duration of the experiment. When MER-BCG was
administered 2 and 3 weeks before DMBA, mammary tumorigenesis was
suppressed in the 2 dietary groups with different levels of fat
intake. This was in contrast to when MER-BCG was administered 3
and 5 weeks after DMBA; in this case the development of mammary
tumors was noticeably enhanced regardless of the fat intake of
the host. The magnitude of inhibition or increase by MER-BCG was
similar in animals fed either fat level, although a high fat diet
consistently stimulated mammary tumorigenesis in the 2
experiments. In vitro assays on T cell mitogen-induced
blastogenesis and natural killer cell activity in splenocytes
isolated from the untreated rats showed that dietary fat failed
to elicit any differential response in these immune functions.
MH - Animal ; BCG Vaccine/*ADMINISTRATION & DOSAGE ; *Dietary Fats ;
Female ; Killer Cells, Natural/IMMUNOLOGY ; Lymphocyte
Transformation ; Mammary Neoplasms, Experimental/CHEMICALLY
INDUCED/IMMUNOLOGY/*PREVENTION & CONTROL ; Rats ; Rats, Inbred
Strains ; Spleen/IMMUNOLOGY ; Support, U.S. Gov't, P.H.S. ;
9,10-Dimethyl-1,2-Benzanthracene
SO - Cancer Lett 1986 Apr;31(1):87-96
23
UI - 86183757
AU - Newman SC ; Miller AB ; Howe GR
TI - A study of the effect of weight and dietary fat on breast cancer
survival time.
AB - Female breast cancer patients who had participated in a
case-control study conducted during 1973-1975 were followed up,
using record linkage to the Statistics Canada mortality data
base, to the end of 1980. A number of variables recorded for the
case-control study, in particular body weight and daily intake of
dietary fat near the time of diagnosis, were examined to see if
they had any bearing on breast cancer mortality. The data were
analyzed using the methods of Mantel and Cox. Dietary fat was not
found to be related to patient survival. However, cases with
greater than average body weight experienced a shortened survival
time.
MH - Adult ; Aged ; Body Weight ; Breast Neoplasms/*MORTALITY ; Death
Certificates ; Diet Surveys ; Dietary Fats/*ADVERSE EFFECTS ;
Epidemiologic Methods ; Female ; Human ; Medical Record Linkage ;
Middle Age ; Prognosis ; Statistics ; Support, Non-U.S. Gov't ;
Time Factors
SO - Am J Epidemiol 1986 May;123(5):767-74
24
UI - 86166145
AU - Bieber MA
TI - Lack of oestrogen-like activity in commercially refined vegetable
oils.
AB - Commercially refined corn, safflower, sunflower and soya-bean
oils, as well as well as lard and beef tallow, were fed to
pre-pubertal female mice at a level of 5 or 20% of a
semi-synthetic diet to assess whether they exhibited any
oestrogen-like activity, as measured by changes in uterine weight
or in the ratio of uterine weight to body weight. No measurable
oestrogen-like activity was observed, in contrast to the effects
in positive-control animals treated with 5, 10 or 15 ppb
diethylstilboestrol. This finding contradicts an earlier report
in the literature. It also shows that oestrogen-like activity in
a commercially refined oil is not likely to be a variable in the
complex mechanism of the dietary modulation of induced
breast-tumour growth.
MH - Animal ; Breast Neoplasms/ETIOLOGY ; Dietary Fats/ADVERSE EFFECTS
; Estrogens/*PHARMACODYNAMICS ; Female ; Mice ; Mice, Inbred ICR
; Oils/*PHARMACODYNAMICS ; Organ Weight/DRUG EFFECTS ; Uterus/
DRUG EFFECTS
SO - Food Chem Toxicol 1986 Mar;24(3):251-3
25
UI - 86165888
AU - Bauer RL
TI - Office techniques to maintain the health of aging patients.
AB - The fecal occult blood test is safe and inexpensive; however,
diet, medications, desiccation of the sample, and delay in
developing the specimen may affect results. If the test is used,
six separate samples, two from each of three consecutive bowel
movements, should be examined to obtain optimum results. Serum
cholesterol need not be assessed routinely in geriatric patients.
Dietary restriction of fats is a necessity only in the context of
a weight reduction diet.
MH - Accident Prevention ; Aged ; Antihypertensive Agents/THERAPEUTIC
USE ; Breast Neoplasms/PREVENTION & CONTROL ; Cerebrovascular
Disorders/PREVENTION & CONTROL ; Cervix Neoplasms/PREVENTION &
CONTROL ; Cholesterol, Dietary/METABOLISM ; Clinical Trials ;
Colonic Neoplasms/PREVENTION & CONTROL ; Coronary Disease/
PREVENTION & CONTROL ; Female ; *Geriatrics ; Human ;
Hypertension/DRUG THERAPY/PREVENTION & CONTROL ; Influenza
Vaccine/THERAPEUTIC USE ; Lung Neoplasms/PREVENTION & CONTROL ;
Male ; Middle Age ; Occult Blood ; Pneumonia/PREVENTION & CONTROL
; Pneumonia, Lobar/PREVENTION & CONTROL ; *Preventive Medicine ;
Prostatic Neoplasms/PREVENTION & CONTROL ; Sigmoidoscopy ;
Smoking/PREVENTION & CONTROL
SO - Geriatrics 1986 May;41(5):91-2, 96-102, 106-7
26
UI - 86133205
AU - Leung KH ; Ip MM
TI - Effect of dietary polyunsaturated fat and
7,12-dimethylbenz(a)-anthracene on rat splenic natural killer
cells and prostaglandin E synthesis.
AB - Dietary polyunsaturated fat has been shown to stimulate mammary
tumorigenesis induced in rats by 7,12-dimethylbenz(a)anthracene
(DMBA). Studies were undertaken to investigate the effect of
polyunsaturated fat and DMBA on splenic natural killer (NK)
activity and prostaglandin E (PGE) synthesis. In a first
experiment, splenic NK activity at 33, 55, 75, and 110 days of
age was measured in Sprague-Dawley rats fed 0.5% low fat (LF), 5%
normal fat (NF), or 20% high fat (HF) corn oil diets from 23 days
of age. At 55 days of age, half of the rats from the 75 and 110
day age groups were given 5 mg DMBA. Ten days after the
initiation of the diets splenic NK activity against YAC-1
lymphoma was decreased from 50% cytotoxicity in rats fed NF diet
to 21% cytotoxicity in rats fed HF diet, but was not affected by
LF feeding. No difference in NK activity was observed among the
groups at the later time periods. DMBA had no effect on NK
activity at 20 or 55 days after its administration. In a second
experiment, where DMBA (15 mg/rat) was given to half of the rats
at 50 days of age and NF or HF diets were started 3 days later,
NK activity was 35% in rats fed NF diet and 21% in rats fed HF
diet, 5 days after the diets were started. No difference in NK
activity in rats fed either diet was observed at later time
periods. DMBA decreased both NK activity and spleen cellularity
transiently. In both experiments, PGE synthesis by spleen cells
cultured for 18 h was not affected by dietary fat intake, but was
slightly increased 3 days after DMBA administration. Results from
these experiments suggest that the stimulation of DMBA-induced
mammary tumorigenesis by polyunsaturated fat and by DMBA itself
may possibly be mediated by a transient decrease in splenic NK
cell activity.
MH - Animal ; Dietary Fats/*ADVERSE EFFECTS ; Fatty Acids, Unsaturated/
*ADVERSE EFFECTS ; Female ; Killer Cells, Natural/DRUG EFFECTS/
*IMMUNOLOGY ; Mammary Neoplasms, Experimental/*CHEMICALLY INDUCED/
IMMUNOLOGY ; Prostaglandins E/*BIOSYNTHESIS ; Rats ; Spleen/
CYTOLOGY/IMMUNOLOGY ; Support, U.S. Gov't, P.H.S. ;
9,10-Dimethyl-1,2-Benzanthracene/*PHARMACODYNAMICS
SO - Cancer Immunol Immunother 1986;21(2):161-3
27
UI - 86127279
AU - Wysowski DK ; Goldberg EL ; Comstock GW ; Diamond EL
TI - A study of a possible association between breast cancer and
gallbladder disease.
AB - Because gallstones and breast cancer were reported to have
several of the same risk factors, a study was conducted in
Washington County, Maryland to determine if women with breast
cancer have an increased risk of prior gallbladder disease.
Living white female breast cancer cases (n = 133), who were
diagnosed from 1973 to 1983, were identified from the county's
cancer registry and interviewed along with an equal number of
sex-, race-, and age-matched controls about a history of
gallbladder disease and other risk factors. Medical records were
used to verify a history of gallbladder disease in interviewed
cases and controls and to search for a diagnosis of gallbladder
disease in 52 white female breast cancer cases who were diagnosed
and died between 1974 and 1983, and 52 matched controls. No
difference was found in gallbladder disease frequency among
living or deceased cases and their matched controls. The results
confirm the known association of several risk factors with breast
cancer and with gallbladder disease, but most of the risk factors
hypothesized to be the same for the two diseases were not the
same. However, an unexpectedly strong association was found
between gallbladder disease and history of myocardial infarction;
this result deserves further study.
MH - Aged ; Breast Neoplasms/*COMPLICATIONS/MORTALITY ; Cholecystitis/
COMPLICATIONS/OCCURRENCE ; Cholelithiasis/COMPLICATIONS/
OCCURRENCE ; Dietary Fats/ADMINISTRATION & DOSAGE ; Female ;
Gallbladder Diseases/*COMPLICATIONS/OCCURRENCE ; Human ;
Interviews ; Maryland ; Middle Age ; Myocardial Infarction/
COMPLICATIONS ; Obesity/COMPLICATIONS ; Registries ; Risk
SO - Am J Epidemiol 1986 Mar;123(3):532-43
28
UI - 86116250
AU - Aylsworth CF ; Cullum ME ; Zile MH ; Welsch CW
TI - Influence of dietary retinyl acetate on normal rat mammary gland
development and on the enhancement of
7,12-dimethylbenz[a]anthracene-induced rat mammary tumorigenesis
by high levels of dietary fat.
AB - The effect of high levels of dietary fat and retinyl acetate
(ROA) on 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat
mammary tumor development and growth was examined. Female
Sprague-Dawley rats, 51-53 days of age, were treated ig with 5 mg
DMBA. At 55-57 days of age, the animals were divided into the
following dietary treatment groups: A) 4.5% fat [control fat
(CF)]; B) CF + 1.0 mmol ROA/kg diet (CF + ROA); C) 20.0% fat
[high fat (HF)]; and D) HF + ROA. HF diets significantly
increased mammary tumor multiplicity, with or without ROA, but
did not significantly influence mammary tumor growth. ROA
treatment reduced mammary tumor multiplicity regardless of the
level of dietary fat and inhibited mammary tumor growth in the
presence of normal levels of dietary fat. High levels of dietary
fat did not significantly influence normal mammary gland growth
and development. ROA significantly decreased normal mammary gland
growth and development regardless of the level of dietary fat.
Blood retinoids in rats fed ROA were primarily in the form of
retinyl esters, i.e., retinyl linoleate, retinyl
palmitate-oleate, and retinyl stearate. Free retinol levels in
blood were not significantly influenced by ROA feeding. Blood
retinyl ester levels were lower in rats fed the HF + ROA diet as
compared to rats fed the CF + ROA diet.
MH - Animal ; Body Weight/DRUG EFFECTS ; Cocarcinogenesis ; Dietary
Fats/*ADMINISTRATION & DOSAGE/PHARMACODYNAMICS ; Female ; Mammae/
*DRUG EFFECTS/GROWTH & DEVELOPMENT ; Mammary Neoplasms,
Experimental/*CHEMICALLY INDUCED/PATHOLOGY ; Rats ; Rats, Inbred
Strains ; Retinoids/BLOOD ; Support, U.S. Gov't, Non-P.H.S. ;
Support, U.S. Gov't, P.H.S. ; Time Factors ; Vitamin A/*ANALOGS &
DERIVATIVES/BLOOD/PHARMACODYNAMICS ;
*9,10-Dimethyl-1,2-Benzanthracene
SO - JNCI 1986 Feb;76(2):339-45
29
UI - 86116249
AU - Boissonneault GA ; Elson CE ; Pariza MW
TI - Net energy effects of dietary fat on chemically induced mammary
carcinogenesis in F344 rats.
AB - The effect of net energy, as distinct from kilocalorie intake or
the percent of fat in the diet, on 7,12-dimethylbenz[a]anthracene
[(DMBA) CAS: 57-97-6]-induced mammary tumorigenesis in female
inbred F344 rats was investigated. Rats were fed a 5% corn oil
diet from weaning until DMBA administration, when they were
switched to one of three dietary regimens: 5% corn oil diet,
low-fat diet fed ad libitum (LF); 30% corn oil diet, high-fat
diet fed ad libitum (HF); or 30% corn oil diet fed at a level
providing a calculated net energy equivalent to the group on LF
[high-fat diet fed at a restricted level (HF-R)]. Calculated
relative net energy values of the amounts of diet actually
consumed by the groups on HF-R, LF, and HF were, respectively,
0.90, 1.00, and 1.07 (kcal equivalent to 34.1, 42.2, and 40.8,
respectively). Weight gain for the groups on LF and HF-R was the
same throughout the experiment (24 wk), while rats on HF weighed
significantly more at 6 weeks and thereafter. Body composition
analyses at 24 weeks established that the groups on HF and HF-R
were equivalent in fat: protein ratio, whereas the group on LF
had about 35% less body fat and 15% more body protein. Carcass
energy was in the following order for rats in these diet groups:
HF greater than HF-R greater than LF. At 24 weeks, tumor
incidences for the groups on HF, LF, and HF-R were, respectively,
73, 43, and 7%. These data indicated that tumor appearance does
not depend on the percent fat in the diet per se but rather on a
complex interaction involving energy intake, energy retention,
and body size.
MH - Animal ; Body Composition ; Body Weight ; Caloric Intake ;
Cocarcinogenesis ; Dietary Fats/*METABOLISM/PHARMACODYNAMICS ;
Energy Metabolism ; Female ; Mammary Neoplasms, Experimental/
*CHEMICALLY INDUCED/METABOLISM ; Rats ; Rats, Inbred F344 ;
Support, Non-U.S. Gov't ; Support, U.S. Gov't, Non-P.H.S. ;
Support, U.S. Gov't, P.H.S. ; Time Factors ;
9,10-Dimethyl-1,2-Benzanthracene
SO - JNCI 1986 Feb;76(2):335-8
30
UI - 86079172
AU - Sylvester PW ; Ip C ; Ip MM
TI - Effects of high dietary fat on the growth and development of
ovarian-independent carcinogen-induced mammary tumors in rats.
AB - This study examined the influence of high dietary fat intake on
the development of ovarian-independent mammary tumors in both
vehicle-treated controls and rats made deficient in estrogen and
prolactin during tumor induction. The majority of
7,12-dimethylbenz(a) anthracene (DMBA)-induced mammary tumors in
rats are dependent on estrogen and prolactin for growth, and
suppression of prolactin and estrogen at the time of tumor
initiation causes a reduction in tumor incidence and increase in
tumor latency. However, the majority of mammary tumors which do
develop in these animals exhibit ovarian-independent growth.
Sprague-Dawley rats were given 7.5 mg DMBA p.o. at 57 days of
age. Starting 1 day prior to and continuing for 7 days after DMBA
administration, rats were given daily injection of vehicle or the
combination of tamoxifen (20 micrograms/rat) plus bromocryptine
(5 mg/kg). At the end of drug treatment, rats in each treatment
group were equally divided and placed on normal fat (5% corn oil)
or high fat (20% corn oil) diets for the duration of the
experiment. Vehicle-treated rats were ovariectomized 27 wk and
drug-treated rats 47 wk after DMBA administration to determine
tumor ovarian dependency. Vehicle-treated rats fed high fat diets
showed significant increases in mammary tumor incidence and
number as compared to similarly treated rats fed a normal fat
diet, with approximately 80% of the tumors in each group being
ovarian dependent. Likewise, tamoxifen-bromocryptine-treated rats
fed a high fat diet showed a significant enhancement in mammary
tumor number, although not incidence, as compared to similarly
treated rats fed a normal diet. Tumors in these drug-treated
groups displayed essentially the same incidence of ovarian
dependence (23%). Tamoxifen-bromocryptine-treated groups
displayed a 2-fold increase in latency of tumor appearance as
compared to vehicle-treated controls; however, this long latency
was not reduced when these rats were fed a high fat diet. These
results demonstrate that high dietary fat stimulates
ovarian-dependent and -independent mammary tumorigenesis in rats
but does not influence the hormonal responsiveness of these
tumors.
MH - Animal ; Bromocriptine/PHARMACODYNAMICS ; Dietary Fats/*ADVERSE
EFFECTS ; Estrogens/PHYSIOLOGY ; Female ; Mammary Neoplasms,
Experimental/*CHEMICALLY INDUCED ; Ovariectomy ; Ovary/PHYSIOLOGY
; Prolactin/PHYSIOLOGY ; Rats ; Support, U.S. Gov't, P.H.S. ;
Tamoxifen/PHARMACODYNAMICS ; 9,10-Dimethyl-1,2-Benzanthracene
SO - Cancer Res 1986 Feb;46(2):763-9
31
UI - 86079171
AU - Sylvester PW ; Russell M ; Ip MM ; Ip C
TI - Comparative effects of different animal and vegetable fats fed
before and during carcinogen administration on mammary
tumorigenesis, sexual maturation, and endocrine function in rats.
AB - The purpose of this investigation was to determine whether diets
high in animal or vegetable fat affected mammary tumorigenesis
when fed to rats only prior to and during the initiation phase of
carcinogenesis. Weanling 21-day-old female Sprague-Dawley rats
were divided into different dietary treatment groups and were
allowed to feed and libitum on one of the following diets: 5%
(normal fat) corn oil; 20% (high fat) corn oil; 20% palm oil; 20%
beef tallow; or 20% lard. At 52 days of age, all rats were given
p.o. 7.5 mg 7,12-dimethylbenz(a)anthracene (DMBA). One week
following DMBA administration, all rats were switched to the 5%
corn oil control diet and were maintained on this diet for the
duration of the experiment. Rats fed a 20% lard diet during the
treatment period showed a significant increase in mammary tumor
incidence and number 19 weeks after DMBA administration, when
compared to all other dietary treatment groups. Rats fed a 20%
beef tallow diet during this same time period also demonstrated
enhanced mammary tumor development, during the 10- to 19-week
time period after DMBA. Mammary tumor development in rats fed 20%
corn oil or palm oil diets during this treatment period was
similar to that of normal fat controls. Estrogens are potent
stimulators of mammary tumor growth and development in rats.
Because mammary tumorigenesis was enhanced in rats fed high
animal, but not vegetable fat diets, it was possible that
estrogens present in animal fat might be responsible for this
stimulation. Further studies demonstrated however, that increased
mammary tumorigenesis in rats fed diets high in animal fat could
not be explained on the basis of endocrine stimulation. Average
day of vaginal opening for all groups fed 20% fat diets was
similar and occurred earlier than in normal fat controls. In
addition, 50- to 65-day-old rats in the different dietary
treatment groups showed no differences in basal or surge levels
of serum prolactin, luteinizing hormone, or estradiol. Rat
diestrus uterine weight also showed no significant differences
among dietary treatment groups. Thus diets containing high levels
of animal fat caused little if any increased estrogenic activity
in rats. In conclusion, high dietary intake of lard and beef
tallow, but not vegetable fat, fed from weaning until only 1 week
after DMBA administration, significantly enhances mammary
tumorigenesis in rats. The mechanism(s) by which animal fat
induces this stimulation is not clear, but it does not appear to
result from endogenous or exogenous endocrine stimulation.
MH - Animal ; Dietary Fats/*ADVERSE EFFECTS ; Estrus ; Female ;
Mammary Neoplasms, Experimental/CHEMICALLY INDUCED ; Neoplasms,
Experimental/*CHEMICALLY INDUCED ; Prolactin/*BLOOD ; Rats ; *Sex
Maturation ; Support, U.S. Gov't, P.H.S. ; Time Factors
SO - Cancer Res 1986 Feb;46(2):757-62