Suppression of mouse mammary tumor proviral DNA and protooncogene expression: association with nutritional regulation of mammary tumor development.

Chen, Rou-Fuie; Good, Robert A.; Engelman, Robert W.; Hamada, Nobuyuki; Tanaka, Akiko; Nonoyama, Meihan; Day, Noorbibi K.

doi:10.1073/pnas.87.7.2385

Cited by 31 publications

(34 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…ICR mice had the lowest tumor incidence and number of MTs per tumor-bearing mouse. Furthermore, these findings are consistent with several earlier publications, which reported that intermittent fasting/refeeding interventions prevented spontaneous MT development in rodents (46,(48)(49)(50). Somewhat different results have been reported for the consequences of ICR interventions using chemical carcinogen models when the feeding regimen is initiated at the time of carcinogen administration.…”

Section: Discussionsupporting

confidence: 82%

Serum Insulin-like Growth Factor-I and Mammary Tumor Development inAd libitum–Fed, Chronic Calorie–Restricted, and Intermittent Calorie–Restricted MMTV-TGF-α Mice

Rogozina

Bonorden

Grande

et al. 2009

Cancer Prevention Research

View full text Add to dashboard Cite

The effect of chronic (CCR) and intermittent (ICR) caloric restriction on serum insulin-like growth factor (IGF)-I levels and mammary tumor (MT) development was investigated. Tenweek-old MMTV-TGF-α female mice were assigned to ad libitum-fed (AL; AIN-93M diet), ICR [3-week 50% caloric restriction using AIN-93M-mod diet, 2× protein, fat, vitamins, and minerals followed by 3 weeks of daily 100% AL consumption of AIN-93M (∼75% of AL for each 6-week cycle)], and CCR (calorie and nutrient intake matched for each 6-week ICR cycle) groups. Half of the mice from each group were sacrificed at 79 (end of restriction) or 82 (end of refeeding) weeks of age. Serum was obtained at euthanasia and in cycles 1, 3, 5, 8, and 11. MT incidence was 71.0%, 35.4%, and 9.1% for AL, CCR, and ICR mice. ICRRestricted mice had significantly lower terminal serum IGF-I and IGF-I/IGF binding protein-3 (IGFBP-3) ratio than CCR, ICR-Refed, and AL mice. There were no differences in terminal IGFBP-3. Final body, internal, and mammary fat pad weights correlated positively with IGF-I and negatively with IGFBP-3. Few changes were found for protein expression of IGF-IRα and IGFBP-3 in mammary tissue and MTs. During the study, IGF-I levels of ICR-Restricted mice were reduced, whereas refeeding allowed partial recovery. For all groups, elevated IGF-I levels preceded MT detection, although not all values were significant versus mice without MTs. However, the specific role of IGF-I in the protective effect of calorie restriction remains to be determined. These results confirm that ICR prevents MT development to a greater extent than CCR.Worldwide, each year, approximately 1 million women are newly diagnosed with breast cancer (1). This malignancy is second only to lung cancer as a cause of cancer death in women (2). Searching for new ways of prevention and early detection and for physiologic and (or) pathophysiologic markers of breast malignances is a prevalent area of current medical-biological studies.Insulin-like growth factor (IGF)-I is a peptide growth factor with demonstrated roles in mammary gland development (3, 4). Both IGF-I and its primary signaling receptor, IGF-IR, are present in the developing mammary gland (5-8). Additionally, the high-affinity IGF binding protein-3 (IGFBP-3; ref. 9) is also found in this tissue and its expression correlates with specific stages of the progression of mammary epithelial growth and maturation (10). In particular, IGF-I and its signaling pathway (s) have important roles in regulating cellular proliferation, growth, and apoptosis, resulting in interest of this regulatory system to mammary tumorigenesis (11-13).It is interesting to note that laboratory investigation of the relation of IGF-I to mammary/breast cancer was motivated by epidemiologic/clinical research (14). These studies have generally supported an increased risk of breast cancer in association with elevated serum levels of IGF-I in premenopausal women but not in those women who are postmenopausal as summarized in several recent meta-analyse...

show abstract

Section: Discussionsupporting

confidence: 82%

Serum Insulin-like Growth Factor-I and Mammary Tumor Development inAd libitum–Fed, Chronic Calorie–Restricted, and Intermittent Calorie–Restricted MMTV-TGF-α Mice

Rogozina

Bonorden

Grande

et al. 2009

Cancer Prevention Research

View full text Add to dashboard Cite

show abstract

“…The other studies used purified 20,22,35,36 or semi-purified diets. 21,23,24,42 Given the strong and consistent effect of energy restriction on cancer prevention in experimental animals, it is clearly possible that the balance between energy consumption, retention and expenditure, perhaps in combination with frequency and length of fasting periods between meals, represents an underlying and central link in the relationship between diet, nutrition and cancer in Western society. 43 Future dietary cohort studies and intervention trials are needed to get insight into the effects of energy and/or fat restriction on human breast cancer development.…”

Section: Discussionmentioning

confidence: 99%

Energy restriction and the risk of spontaneous mammary tumors in mice: A meta‐analysis

Dirx

Zeegers

Dagnelie

et al. 2003

Intl Journal of Cancer

139

View full text Add to dashboard Cite

Our meta-analysis was aimed at providing a systematic review of the literature regarding the effect of energy restriction on spontaneous mammary tumors in mice and at providing a more precise pooled (summary) estimate of the risk of mammary tumors. A sensitivity analysis was conducted to obtain insight in potential heterogeneity between the animal studies. A literature search was conducted with the following terms to identify relevant articles: animal studies, mammary tumors, fat restricted, dietary carbohydrates, energy restriction and calorie restriction. A criteria list for the assessment of quality items (i.e., study characteristics) in animal experiments was developed that was intended to quantitatively assess potential factors that underlie heterogeneous results of different animal experiments. Incidence figures were used to calculate the risk difference. The pooled risk difference was calculated by random effects meta regression analysis. Fourteen animal experiments were included in this metaanalysis. Publication bias could not be identified. The pooled risk difference for the 14 studies was ؊0.55 with a narrow 95% confidence interval (؊0.69; ؊0.41), implying that the energy-restricted animal groups developed 55% less mammary tumors than the control groups. No heterogeneity could be detected between the studies based on study characteristics that included the age of mice at the start of intervention, duration of intervention, allocation of the mice, use of ad libitum control group, fertility of the mice and the type of energy-providing nutrient (fat, carbohydrate or protein). This meta-analysis confirms that energy restriction in itself consistently protects against the development of mammary tumor in mice, irrespective of the type of restricted nutrient or other study characteristics. © 2003 Wiley-Liss, Inc. Key words: energy restriction; mammary tumors; mice; meta-analysisWorldwide, breast cancer is the most frequent cancer in women and is one of the main causes of death in women today. 1,2 It is important to understand more about the etiology and possibilities for prevention of breast cancer. The hypothesis that high fat intake will increase the risk of breast cancer has often been examined in human studies. Although epidemiological studies in humans suggested that diet (energy and fat) is related to the incidence of breast cancer, 3-5 the results are not consistent. A pooled analysis of the results of several cohort studies yielded no evidence of a positive association between total dietary fat intake and the risk of breast cancer. 6 To clarify the role of dietary factors in the etiology of breast cancer, much research has been conducted in rodents, especially regarding the effect of dietary fat-intake and energy (i.e., caloric) restriction on breast cancer risk. Energy restriction has been suggested to be a very effective way of reducing the incidence of mammary tumors in rodents. 7,8 The animal experimental data supports the hypothesis that, in mammary tumor development, there is a specific enhancin...

show abstract

“…Our findings showed that CEIR can modulate mouse mammary tumor virus (MMTV) proviral expression at the mRNA level, delay protooncogene activation, and abrogate the development of breast tumors (6,14,15). In the current study, we show that the protective influences of CEIR can be imposed in an organ site of retrovirus-induced tumorigenesis other than the breast by demonstrating that calorie restriction can significantly impair retrovirus-induced lymphomagenesis in AKR mice.…”

mentioning

confidence: 99%

“…The preparation and composition of the two semipurified diets used have been described in detail (6,14) (Table 1). All dietary constituents were obtained from ICN.…”

mentioning

confidence: 99%

“…Prehybridization (duration, 8-24 hr) and hybridization (8)(9)(10)(11)(12)(13)(14)(15)(16) hr) were at 420C in buffer containing 5 x SSC (1x SSC is 0.15 M NaCl/15 mM trisodium citrate), 50%6 formamide (deionized), denatured salmon sperm DNA (60 ,ug/ml), yeast tRNA (37 jg/ml), 0.4% sodium dodecyl sulfate (SDS), 50 mM sodium phosphate (pH 7; prepared from 1 M stocks of mono-and dibasic sodium phosphate), 0.1% sodium pyrophosphate and 2x Denhardt's solution (lx is 0.02% Ficoll 400/0.02% polyvinylpyrrolidone/0.02% bovine serum albumin).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Calorie restriction suppresses subgenomic mink cytopathic focus-forming murine leukemia virus transcription and frequency of genomic expression while impairing lymphoma formation.

Shields

Engelman

Fukaura

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

View full text Add to dashboard Cite

Calorie restriction suppresses mammary proviral mRNA expression and protooncogene activation in breast tumor-prone C3H/Ou mice while inhibiting tumor formation.To determine whether the beneficial effects of chronic energyintake restriction (CEIR) can be extended to an organ site of retrovirus-induced tumorigenesis where the dynamics of growth and sexual maturity are not paramount as they are in breast tissue, calorie restriction of 40% was imposed on thymic lymphoma-prone AKR mice when 4 weeks old. Recombination between various murine leukemia virus (MuLV) mRNAs, resulting in the generation of an 8.4-kilobase genomic-length transcript with mink cytopathic focus-forming (MCF) characteristics, is considered the proximal retroviral event in AKR lymphomagenesis. Thymic expression of subgenomic MCF MuLV mRNA was uniformly suppressed among 6-and 8-weekold CEIR mice (P < 0.02). This suppression of MuLV transcription preceded a 25% reduction in the appearance of genomic-length MCF transcripts among CEIR mice and a 28% reduction in cumulative lymphoma mortality. The latency to median tumor incidence was extended >3 months by calorie restiction, and median lifespan was extended -50%. Survival curves for the full-fed and CEIR dietary cohorts were found to be signiflcantiy different (P < 0.0001), with full-fed mice experiencing a 3 times greater risk of lymphoma mortality.These frndings extend the known range of pathologic states influenced by CEIR in inbred mice and show that retroviral mechanisms involved in generation of lymphold malignancy can be signlfcantly impaired by calorie restriction.Chronic energy-intake restriction (CEIR) without essential nutrient deficiency extends the latency to onset and reduces the frequency of neoplastic and non-neoplastic disease in inbred mice. Diseases delayed or prevented by calorie restriction include the systemic amyloidosis of senescenceaccelerated mice (1), the systemic lupus erythematosus-like syndrome of B/W F1 mice (2, 3), the breast cancer of C3H mice (4-6), the nephrophthisis of kd/kd mice (7), and the lymphoproliferative syndrome of autoimmune-prone MRL mpj lpr/lpr mice (8, 9).The influences ofcalorie restriction on leukemogenesis and formation of lymphoma have been inferred from disease pattern surveys of large populations of outbred rats (10) and long-lived inbred (11) and hybrid (12) mice fed semipurified diets. In these surveys, cumulative frequencies of mortality due to lymphoma among calorie-restricted cohorts were lower and maximum longevities were extended. Further evidence that CEIR can regulate leukemogenesis is implied by an early report (13) of the stringent underfeeding of a nonpurified diet to inbred, lymphoma-prone AK mice. In that study, food restriction was severe enough to produce adult mean body weights of <17 g, organ underdevelopment, and high mortality attributable to causes other than lymphoma, but this restriction also lowered the incidence and delayed the onset of lymphoma (13).That calorie restriction can influence mechanisms of retrovirus-i...

show abstract

Suppression of mouse mammary tumor proviral DNA and protooncogene expression: association with nutritional regulation of mammary tumor development.

Cited by 31 publications

References 26 publications

Serum Insulin-like Growth Factor-I and Mammary Tumor Development inAd libitum–Fed, Chronic Calorie–Restricted, and Intermittent Calorie–Restricted MMTV-TGF-α Mice

Serum Insulin-like Growth Factor-I and Mammary Tumor Development inAd libitum–Fed, Chronic Calorie–Restricted, and Intermittent Calorie–Restricted MMTV-TGF-α Mice

Energy restriction and the risk of spontaneous mammary tumors in mice: A meta‐analysis

Calorie restriction suppresses subgenomic mink cytopathic focus-forming murine leukemia virus transcription and frequency of genomic expression while impairing lymphoma formation.

Contact Info

Product

Resources

About