Incidence Of Mammary Gland Tumors Research Articles

Research of the New Biomarkers of Mammary Gland Tumors in Domestic Cats

This article presents the results of the clinical significance study of changes in the activity of adenosine deaminase and the content of polyamines in the blood plasma of cats with mammary gland tumors. In our work, we investigated the activity of the adenosine deaminase gene in the tissues of mammary gland tumors in cats and compared the activity of this gene with normal mammary gland tissue. In the course of this work, we also found out the frequency of occurrence of mammary gland tumors in the population of domestic cats in the Rostov region and evaluated the prognosis of survival after surgical treatment of breast cancer. The incidence of mammary gland tumors was detected, which amounted to 0.4% of the domestic cats who have applied to veterinary clinics in Rostov region, where the cats with mammary gland neoplasms amounted to approximately 400 individuals for every 100,000 animals. These data reflect the importance of the problem of mammary gland tumors and emphasize the need to study the pathophysiological foundations of carcinogenesis in order to create molecular genetic approaches for early diagnosis of mammary gland tumors. The results of the studies showed that the level of expression of the adenosine deaminase gene in the tissues of invasive nonspecific carcinoma and in the tissues of fibroepithelial hyperplasia sharply increases compared to the tissue of a healthy mammary gland, 36 times in the tissues of invasive carcinomas and 131 times in the tissues of fibroepithelial hyperplasia. At the same time, there were no significant differences between the activity of adenosine deaminase in the blood plasma of healthy animals and in the blood plasma of animals with malignant neoplasms of the mammary gland. Measurement of the level of polyamines in the blood of animals showed that the content of putrescine in the erythrocytes of the blood of cats with benign and tumor-like neoplasms of the mammary fibroepithelial hyperplasia significantly increased by 5 times compared with the indicators of the control group. In malignant neoplasms of the mammary gland invasive nonspecific carcinoma, the content of putrescine and spermin in the blood significantly exceeded the control values by 6 and 10 times, respectively.

Incidence of mammary tumors in the canine population living in the Veneto region (Northeastern Italy): Risk factors and similarities to human breast cancer

Although mammary gland tumors (MT) are the most-common type of tumor in intact female dogs, there is little information about their incidence in dog population. Data on MT in female dogs was retrieved from the Animal Tumor registry of dogs and cats of Venice and Vicenza provinces during 2005–2013 and was analyzed to visualize crude incidence rates by breed and across age categories. Overall, 2744 mammary tumors were reported accounting for 54% of all tumors in female dogs. The annual incidence rate (IR) was 250 cases per 100,000 dogs. The most frequent malignant tumors were complex carcinomas, consisting of both epithelial and myoepithelial tissues (IR=71.89), and simple carcinomas (IR=62.59). The MT incidence rate increased through the study period; particularly in the last 4 years, and malignant neoplasms occurred more frequently (70%) than the benign counterparts (30%). Seventy-four percent of tumors were diagnosed in intact females, and the mean age at diagnosis was significantly higher for spayed dogs than for intact ones. MT were less frequent in dogs younger than 6 years and increased up to approximately 60% for ages between 8 and 13 years. The purebred dogs had a higher probability to have a malignant neoplasm than mixed-breed dogs, particularly in dogs younger than 7 years, and the Samoyed, Dobermann, Schnauzer and Yorkshire Terrier breeds were more inclined to develop malignant MT. The incidence of MT in dogs is increasing, and IRs are comparable to that in women. The epidemiological similarities between dogs and women support the validity of canine MT as a model for human breast cancer.

Abstract A100: Helicobacter hepaticus contributes to mammary gland carcinogenesis through bacterial translocation and subsequent expansion of cancer-promoting myeloid-derived suppressor cells

Abstract Introduction: Gastrointestinal (GI) tract dysbiosis and resulting inflammation are implicated in breast carcinogenesis. CD11b+GR1+ myeloid- derived suppressor cells (MDSCs) are important drivers of breast cancer. Here we report that in APCMin/+ mice treated with enteric Helicobacter hepaticus (H. hepaticus) MDSCs cells are dramatically expanded and, along with the pathogen H. hepaticus, are directly recruited to mammary gland lymph node, where they suppress anti-carcinogenic cytotoxic T-cells and promote procarcinogenic inflammation, respectively. Methods: In our H. hepaticus and specific pathogen free colony we inoculated female APCMin/+ mice with H. hepaticus and compared neoplastic and inflammatory outcomes to the non-infected controls. Results: Successful infection was confirmed by H. hepaticus specific qPCR and fluorescence in situ hybridization (FISH). H. hepaticus was identified not only within the small intestine but also within the mammary gland lymph node and mammary tumor tissue of the treated group. In APCMin/+ mice treated with chow diet, H. hepaticus-induced procarcinogenic CD11b+GR1+ cells within the lamina propria of the small intestine, the surrounding mesenteric lymph nodes, the spleen, peripheral blood and the mammary gland lymph nodes. In H. hepaticus infected mice, this was accompanied by increased splenic expression of IL-1β, IL-6 and GM-CSF and the increased expression of IL-1β, IL-6 and GM-CSF, IL-23a and IL-17a in the small intestine. Interestingly, adding high fat diet to H. hepaticus infected mice appeared to further promote the trafficking of MDSCs from the spleen into the peripheral blood and regional lymph nodes with increased serum inflammatory cytokines production cytokines, including IL-6. This appears to have been mediated, at least in part, by adipocyte signaling to myeloid precursors. Conclusions: We show the presence of H. hepaticus in mammary gland and intestine, which correlated with mammary gland tumor incidence and increased intestinal tumor multiplicity. The co-existence of enteric H. hepaticus infection appears to promote mammary tumorigenesis through upregulation of IL-1β, IL-6 and GM-CSF and the resulting trafficking of tumor promoting CD11b+GR1+ MDSCs. We are currently examining the route and broader relevance of H. hepaticus extra-intestinal translocation and whether this has direct effects on tumorigenesis, consistent with findings in other Helicobacter spp. Citation Format: Xiaowei Chen, Daniel L. Worthley, Zhongming Ge, Yagnesh Tailor, Christian Kaufman, Lenzie Cheaney, Lesley Kline, Gladys Y. Valeriano, Christoph B. Westphalen, Susan E. Erdman, James G. Fox, Timothy C. Wang. Helicobacter hepaticus contributes to mammary gland carcinogenesis through bacterial translocation and subsequent expansion of cancer-promoting myeloid-derived suppressor cells. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications; Oct 3-6, 2013; San Diego, CA. Philadelphia (PA): AACR; Mol Cancer Res 2013;11(10 Suppl):Abstract nr A100.

Abstract 4303: The Jackson Laboratory Repository: resource for mouse strains modeling cancer

Abstract The Jackson Laboratory Repository is an established resource for the importation, cryopreservation, development, and distribution of mouse strains vital to biomedical research. More than 500 new strains are added annually to the approximately 5,000 strains and stocks of mice currently held in the Repository collection. Newly acquired or developed strains include a model of malignant melanoma and metastasis; a xenotransplant model that provides continuous circulation of human growth factors; a targeted mutation strain for studying myeloproliferative diseases such as chronic myelomonocytic leukemia and Chronic Familial Myelocytic Leukemia-Like Syndrome; and a knock-in strain that mimics the t(9;11)(p22;q23) translocation identified in acute myeloid leukemia. Also under development are a transgenic/targeted mutation strain with increased mammary gland tumor incidence and three targeted mutation strains with increased sensitivity to carcinogens or radiation. The Repository's inducible and conditional mutation mouse strains allow researchers to generate temporal and/or tissue-specific tools for modeling human cancer. New additions to the Repository collection include strains with Cre recombinase expression specific to the colon and rectum, as well as a transgenic strain that can be used as part of a bitransgenic system utilizing the tetracycline-inducible expression of a gene of interest in blood vessel endothelial cells. For non-invasive in-vivo imaging studies, the Repository distributes a xenograft/transplant host with widespread expression of firefly luciferase and enhanced green fluorescence protein. The Repository maintains a searchable on-line resource (www.jax.org) for each strain. Researchers can submit their strains to be considered for inclusion in the Repository by using the on-line form available at The Jackson Laboratory website: http://www.jax.org/grc/index.html. The Jackson Laboratory Repository is supported by the NCRR, The Howard Hughes Medical Institute, The Ellison Medical Foundation and donations from private charitable foundations. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4303. doi:10.1158/1538-7445.AM2011-4303

Ochratoxin a: Its Cancer Risk and Potential for Exposure

Ochratoxin A (OA) is a naturally occurring mycotoxin known to contaminate a variety of foods and beverages. The cancer risk posed by OA was reviewed as relevant to human exposure, regulatory activities, and risk management efforts occurring worldwide, particularly in Europe. OA moves through the food chain and has been found in the tissues and organs of animals, including human blood and breast milk. Results from the National Toxicology Program's rodent bioassays show significantly increased incidence of mammary gland tumors in female rats and kidney tumors in male and female rats given OA orally. Liver tumors in female mice fed OA in the diet have also been observed. In humans, OA exposure has been most often associated with the kidney disease Balkan endemic nephropathy (BEN), symptoms of which include tumors of the kidney and urinary tract. No epidemiological studies have yet adequately evaluated the cancer risk of OA in human populations. Studies have shown OA to be genotoxic as well as immunotoxic, although its mode of action is not fully understood. Organizations and agencies in many countries are currently promulgating standards for OA in foods and beverages. Increased efforts in farm management and food safety are being made to mitigate the risks to public health posed by OA. The U.S. Food and Drug Administration (FDA) is currently evaluating data on OA levels in domestic and imported commodities but has not established official regulations or guidelines for OA in the U.S. food supply. Funding for this work was provided by the US Department of Agriculture Cooperative State Research, Education and Extension Service. Any findings, conclusions or recommendations are those of the authors and do not necessarily reflect the views of the U.S. Department of Agriculture.

Secreted Frizzled Related Protein 2 (sFRP2) Decreases Susceptibility to UV-Induced Apoptosis in Primary Culture of Canine Mammary Gland Tumors by NF-κB Activation or JNK Suppression

Tumor formation can result from a decrease in cell death, as well as an increase in cell proliferation. In spite of the high incidence of mammary gland tumors (MGTs) in female dogs, the understanding of its etiology is still poor. Consistent with several proto-oncogenes (such as Wnt) for the mammary gland, sFRP2 is expressed in canine MGTs which is normally silent in the mammary gland. To elucidate the roles of SFRP2 in the tumorigenesis of MGTs, apoptosis regulation mediated by sFRP2 was investigated by overexpression of sFRP2 in MGT cells. DNA fragmentation and TUNEL assays showed a decreased susceptibility of the cells to UV-induced apoptosis in the context of sFRP2 overexpression. To analyze the pathways through which sFRP2 transduces anti-apoptosis signals, multiple-color immunofluorescence staining, immunoprecipitation, and immunoblotting were carried out. sFRP2 was found co-localized in the extracellular matrix of MGTs and the tyrosine phosphorylation of FAK was enhanced. Moreover, JNK was suppressed and NF-kB was activated in the cells expressing sFRP2 after UV-induced apoptosis analyzed by immunoblotting and electrophoretic mobility shift assay (EMSA). Taken together, these results suggest that sFRP2 exerts its anti-apoptotic function in mammary cancer cells through NF-kappaB activation or JNK suppression.

Amended Final Report on the Safety Assessment of Polyacrylamide and Acrylamide Residues in Cosmetics1

Polyacrylamide is a polymer of controllable molecular weight formed by the polymerization of acrylamide monomers available in one of three forms: solid (powder or micro beads), aqueous solution, or inverse emulsions (in water droplets coated with surfactant and suspended in mineral oil). Residual acrylamide monomer is likely an impurity in most Polyacrylamide preparations, ranging from <1 ppm to 600 ppm. Higher levels of acrylamide monomers are present in the solid form compared to the other two forms. Polyacrylamide is reportedly used in 110 cosmetic formulations, at concentrations ranging from 0.05% to 2.8%. Residual levels of acrylamide in Polyacrylamide can range from <.01% to 0.1%, although representative levels were reported at 0.02% to 0.03%. Because of the large sizes of Polyacrylamide polymers, they do not penetrate the skin. Polyacrylamide itself is not significantly toxic. For example, an acute oral toxicity study of Polyacrylamide in rats reported that a single maximum oral dose of 4.0 g/kg body weight was tolerated. In subchronic oral toxicity studies, rats and dogs treated with Polyacrylamide at doses up to 464 mg/kg body weight showed no signs of toxicity. Several 2-year chronic oral toxicity studies in rats and dogs fed diets containing up to 5% Polyacrylamide had no significant adverse effects. Polyacrylamide was not an ocular irritant in animal tests. No compound-related lesions were noted in a three-generation reproductive study in which rats were fed 500 or 2000 ppm Polyacrylamide in their diet. Polyacrylamide was not carcinogenic in several chronic animal studies. Human cutaneous tolerance tests performed to evaluate the irritation of 5% (w/w) Polyacrylamide indicated that the compound was well tolerated. Acrylamide monomer residues do penetrate the skin. Acrylamide tested in a two-generation reproductive study at concentrations up to 5 mg/kg day(- 1) in drinking water, was associated with prenatal lethality at the highest dose, with evidence of parental toxicity. The no adverse effects level was close to the 0.5 mg/kg day(- 1) dose. Acrylamide tested in a National Toxicology Program (NTP) reproductive and neurotoxicity study at 3, 10, and 30 ppm produced no developmental or female reproductive toxicity. However, impaired fertility in males was observed, as well as minimal neurotoxic effects. Acrylamide neurotoxicity occurs in both the central and peripheral nervous systems, likely through microtubule disruption, which has been suggested as a possible mechanism for genotoxic effects of acrylamide in mammalian systems. Acrylamide was genotoxic in mammalian in vitro and in vivo assays. Acrylamide was a tumor initiator, but not an initiator/promoter, in two different mouse strains at a total dose of 300 mg/kg (6 doses over 2 weeks) resulting in increased lung adenomas and carcinomas without promotion. Acrylamide was tested in two chronic bioassays using rats. In one study, increased incidence of mammary gland tumors, glial cell tumors, thyroid gland follicular tumors, oral tissue tumors, uterine tumors and clitoral gland tumors were noted in female rats. In male rats, the number of tumors in the central nervous system (CNS), thyroid gland, and scrotum were increased with acrylamide exposure. In the second study, using higher doses and a larger number of female rats, glial cell tumors were not increased, nor was there an increase in mammary gland, oral tissue, clitoral gland, or uterine tumors. Tumors of the scrotum in male rats were confirmed, as were the thyroid gland follicular tumors in males and females. Taken together, there was a dose-dependent, but not statistically significant, increase in the number of astrocytomas. Different human lifetime cancer risk predictions have resulted, varying over three orders of magnitude from 2 x 10(- 3) to 1.9 x 10(- 6). In the European Union, acrylamide has been limited to 0.1 ppm for leave-on cosmetic products and 0.5 ppm for other cosmetic products. An Australian risk assessment suggested negligible health risks from acrylamide in cosmetics. The Cosmetic Ingredient Review (CIR) Expert Panel acknowledged that acrylamide is a demonstrated neurotoxin in humans and a carcinogen in animal tests, but that neurotoxic levels could not be attained by use of cosmetics. Although there are mechanisms of action of acrylamide that have been proposed for tumor types seen in rat studies that suggest they may be unique to the rat, the Panel was not convinced that these results could be disregarded as a species-specific finding with no relevance to human health and safety. Based on the genotoxicity and carcinogenicity data, the Panel does not believe that acrylamide is a genotoxic carcinogen in the usual manner and that several of the risk assessment approaches have overestimated the human cancer risk. The Panel did conclude, however, that it was appropriate to limit acrylamide levels to 5 ppm in cosmetic formulations.

Endogenous Mouse Mammary Tumor VirusMtv-17 Is Involved inMtv-2-Induced Tumorigenesis in GR Mice

Mtv-2 is an endogenous mouse mammary tumor virus (MMTV) that is responsible for the induction of mammary gland tumors in the high mammary gland tumor-incidence strain GR. GR animals inherit four different endogenous MMTVs in addition toMtv-2:Mtv-3,Mtv-7,Mtv-8 andMtv-17. In this study we analyzed the involvement of these nonpathogenic endogenous proviruses in the mammary gland tumors caused byMtv-2. We showed thatMtv-17 is expressed in the mammary gland of GR mice, efficiently packaged into virions, and shed into milk. DNA isolated from both mammary gland tumors and the nonmalignant mammary gland tissues of GR mice contained amplified copies of both newly acquiredMtv-2 and recombinant proviruses with theenvgene derived fromMtv-17. A small percentage of these tumors contained predominantly recombinant viruses. These findings suggest a role forMtv-17 in the mammary gland tumors induced byMtv-2 in GR mice.

Modulation of oxidative DNA damage levels by dietary fat and calories.

Decreased dietary intake of fat and/or calories generally results in a lower incidence of mammary gland tumors in rodents. Feeding of either low-fat or calorie-restricted diets to rats also has been shown to result in decreased levels of oxidative DNA damage. Since oxidative DNA damage is suggested to have a role in carcinogenesis, this may be one mechanism by which dietary change can reduce cancer risk. The effects of calorie-restricted diets on both oxidative DNA damage levels and mammary gland tumor incidence are generally more pronounced than that of low-fat diets. There is, however, some difficulty in defining what amount of fat should be used to prepare 'low-fat' and 'high-fat' rodent diets as well as what a suitable fat intake for control diets should be in studies that examine the effects of dietary fat and/or calories on tumorigenesis. In particular, the promoting effects of dietary fat may be exerted only up to a certain level of fat, above which no further effect is observed. Another difficulty in the interpretation of the results is that there may be a time-dependent effect of high fat diets on oxidative damage, with increased damage resulting only when the diets are fed for longer periods of time. The appropriate experimental approach to model human dietary exposures therefore remains to be determined. Although the effects of caloric intake on mammary gland tumorigenesis appear to be more pronounced than that of fat intake, low-fat diets still may be useful as a preventive measure in human populations to reduce breast cancer risk for individuals who cannot safely reduce their caloric intake.

Low-frequency electromagnetic radiation enhances the induction of rat mammary tumors by nitrosomethyl urea

Low-frequency electromagnetic fields enhance the induction of mammary gland tumors in rats using nitrosomethyl urea. The incidence of tumors depended on the duration of exposure to static (dc) and variable (ac) magnetic fields. Variable magnetic fields induced mammary gland cancer much more frequently than static ones. Apart from increasing the incidence of mammary gland tumors, household low-frequency electromagnetic fields reduced the mean latent period of tumor development and led to predominance of malignant tumors in the exposed animals as compared to controls. Mammary gland tumors developed rarely under the effect of static or variable magnetic fields per se, without preliminary administration of a carcinogen. Household low-frequency electromagnetic fields may potentially present an oncogenic hazard for animals and humans.

Carcinogenicity of an oxidation product of p-phenylenediamine.

para-Phenylenediamine (p-PD), a widely used aromatic amine in the preparation of commercial oxidative-type hair dyes, has been previously demonstrated to have neither mutagenic activity to Salmonella typhimurium nor carcinogenic activity in rats and mice. In this study, the mutagenicity of p-PD after an oxidation by hydrogen peroxide towards S. typhimurium TA98 and its carcinogenicity in Wistar rats were examined both by topical application to the shaved skin and by s.c. injection. The oxidation product was found to be strongly mutagenic to the bacterial tester strain in the presence of rat liver S-9 fraction. Interestingly, in female rats, both topical application and s.c. injection for 18 months of oxidized p-PD could induce a statistically significant incidence of mammary gland tumors (greater than 50%, P less than 0.05). In addition, uterine tumors and soft tissue tumors of both malignant and benign types were also significantly induced (43% and 57%, P less than 0.05) in the s.c. injection group. On the other hand, tumors of mammary gland and soft tissue were not observed in male rats under similar experimental conditions. However, tumors of other organs including liver, kidney, adrenal gland, thyroid gland, urinary bladder and lung were occasionally observed in male rats of both groups and might be related to the p-PD treatment.

Effect of ovariectomy on life span and incidence of mammary gland tumors in irradiated rats

Effect of ovariectomy on life span and incidence of mammary gland tumors in irradiated rats

Electron-Microscope Examination of Human Milk

CA: A Cancer Journal for CliniciansVolume 1, Issue 6 p. 186-188 ArticleFree Access Electron-microscope examination of human milk First published: September 1951 https://doi.org/10.3322/canjclin.1.6.186AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Reference Bittner, J. J.: Some possible effects of nursing on the mammary gland tumor incidence in mice. Science 84: 162, 1936. Bittner, J. J.: Influence of foster nursing on experimental breast cancer. Tr. & Stud., Coll. Physicians, Philadelphia 9: 129– 143, 1941. Graff, S.; Moore, D. H.; Stanley, W. M.; Randall, H. T., and Haagensen, C. D.: Isolation of mouse mammary carcinoma virus. Cancer 2: 755– 762, 1949. Gross, L.; Gessler, A. E., and McCarty, K. S.: Electron-microscopic examination of human milk particularly from women having family record of breast cancer. Proc. Soc. Exper. Biol. & Med. 75: 270– 276, 1950. Passey, R. D.; Dmochowski, L.; Astbury, W. T.; Reed, R., and Eaves, G.: Electron microscope studies of human breast cancer. Nature, London 167: 643– 644, 1951. Volume1, Issue6September 1951Pages 186-188 ReferencesRelatedInformation

X. Carcinoma of Mammary Gland Following Injection of Methylcholan-threne into Mice of NHO Strain

Summary75 female mice of a total of 125 injected subcutaneously with 1 mg of methyl-cholanthrene at 60 days of age, developed carcinomas of the mammary gland. The mice belonged to the F14-F18 generations of inbreeding. This high incidence of mammary gland tumors was made possible by the suppression of local tumors through the process of genetic selection toward resistance to such local tumors. These induced mammary gland tumors duplicate the series of tumors produced spontaneously in genetic susceptible strains of mice such as the A and the C3H. In addition, however, the tumors arising in genetically resistant female mice of this experiment following the injection of methyl-cholanthrene possess 4 characteristics not present or less pronounced in the tumors of genetically susceptible female mice: (a) they show an increased tendency to undergo squamous metaplasia; (b) many of them (approximately 18%) undergo rather pronounced anaplastic changes, (c) these anaplastic tumors invade surrounding normal tissues ...

Possible Method of Transmission of Susceptibility to Breast Cancer in Mice

A genetic approach to the cancer problem was made possible following the development of inbred strains of mice having a high and a low tumor incidence. On making reciprocal crosses between strains which differed greatly in their incidence of mammary gland tumors, it was observed that when the maternal parents were representatives of the high-tumor stock the first generation females had a high tumor incidence; when the cross was made in the opposite direction the incidence in the hybrid classes approached that of the low-tumor stock (1–14). When the young cast by high-tumor stock females were removed from their own mothers and given to foster mothers of the low-tumor stock, the proportion of the fostered mice developing mammary tumors was reduced to a very low percentage (15–22). This was comparable to the incidence in virgin females of some strains. If, however, there was little difference between the ratios in the breeding and virgin females of a high-tumor strain, the incidence for fostered females used as breeders was reduced considerably below either figure (Bittner and Little, 21; Andervont and McEleney, 22). In the foster-nursing experiments the high-tumor young were permitted to nurse their own high-tumor mothers from the time of birth until they were recorded the following morning. The maximum period was twenty-four hours. In no instance were the nipples sealed to prevent nursing during this interim.

Breast Cancer in Mice

Many of the advances in medical research, especially in the cancer field, may be attributed directly or indirectly to the favorable animal material available for purposes of experimentation. Widely used at the present time are inbred strains of mice developed by various workers, especially Little and Strong. The most exacting physiological tests—the transplantation of normal and neoplastic tissues—have demonstrated the homogeneity of individuals within inbred lines. By using the same stocks, workers in different laboratories have obtained analogous results. A noteworthy example is the extra-chromosomal theory of breast cancer in mice advanced by the members of the staff of the Jackson Memorial Laboratory in 1933 and confirmed by Korteweg in 1934 (1–2). The same stocks were used in each experiment. Results have been published for seven different crosses, all verifying the original observations. In the work with high-tumor and low-tumor stocks of mice it has been assumed in the past that the genetic constitution of the stock determined whether or not the individuals would develop spontaneous tumors of various types. That is, a strain had breast tumors because they had inherited a breast tumor susceptibility. Strong (3), applying the pure-line theory of Johannsen, showed that selection within a high-breast-tumor stock has no influence on the tumor incidence in future generations. Within an inbred line it has been observed by Strong (4) and the author that the incidence of mammary gland tumors is usually as high among the progeny of non-tumor mothers as among those from cancerous mothers.

Some Possible Effects of Nursing on the Mammary Gland Tumor Incidence in Mice

A preliminary report on some possible effects of nursing on the mammary gland tumor incidence in mice is presented. 3 litters of mice from an inbred strain of mice with a mammary gland tumor incidence of 88% were fostered by a strain of mice with a tumor indicence of about 10%. Of the 9 females fostered by the low tumor strain 3 developed mammary gland tumors 4 had primary lung tumors and 2 died nontumorus. Among 40 of their progeny who were fostered 12 developed breast tumors 2 had breast and pulmonary cancers 13 had primary lung tumors and 13 died nontumorus. 10 of the 13 progeny of the fostered females which had breast cancer developed similar growths as compared with 4 of the 24 progeny from fostered females which had lung tumors. The respective proportions were 77% and 17%. These results support the belief in the extrachromosomal influence as a cause in the development of mammary tumor.

Mammary Tumors in Mice in Relation to Nursing

In this report we shall consider in more detail the effects of nursing on mammary gland tumor incidence in mice. Some of the data have been published (Bittner, 1936 c ). Three stocks of mice inbred brother-to-sister have been used in the work. As each strain has been continued by such matings for more than twenty generations, they were considered to be homozygous. The A stock (Bittner, 1931) is descended from a line of albino mice started by Dr. L. C. Strong (1936 a ). It has a high incidence of mammary tumors and a few primary bronchial carcinomas in breeding females (Bittner, 1935 a and b, 1936 b ). The ratios will be given later, as additional observations have been made since the last report. A line of Strong's CBA stock (Strong, 1936 b ) was obtained in 1931. The breast tumor incidence was 13.5 per cent in a total of 125 breeding females at an average age of twenty-one months. Representatives of the C57 Black strain were given to the author by Dr. C. C. Little. The incidence of breast tumors in breeding females of this line is about 1.0 per cent (Cloudman, Bittner and Little, in press). Young born to A stock females were removed as soon as they were recorded (approximately 8:30 each morning) and fostered by females of the CBA or C57 Black stock. These fostered females of the A stock were mated and permitted to nurse their progeny. Thus, only one generation of A stock mice was fostered by low-tumor line females. They are designated as members of the first generation in this report. Mice of subsequent generations were nursed by their A stock mothers.2 The fostered and control or normal mice of the A stock were maintained under identical conditions and received the same diet.

Some Possible Effects of Nursing on the Mammary Gland Tumor Incidence in Mice

Some Possible Effects of Nursing on the Mammary Gland Tumor Incidence in Mice

SOME POSSIBLE EFFECTS OF NURSING ON THE MAMMARY GLAND TUMOR INCIDENCE IN MICE

A preliminary report on some possible effects of nursing on the mammary gland tumor incidence in mice is presented. 3 litters of mice from an inbred strain of mice with a mammary gland tumor incidence of 88% were fostered by a strain of mice with a tumor indicence of about 10%. Of the 9 females fostered by the low tumor strain 3 developed mammary gland tumors 4 had primary lung tumors and 2 died nontumorus. Among 40 of their progeny who were fostered 12 developed breast tumors 2 had breast and pulmonary cancers 13 had primary lung tumors and 13 died nontumorus. 10 of the 13 progeny of the fostered females which had breast cancer developed similar growths as compared with 4 of the 24 progeny from fostered females which had lung tumors. The respective proportions were 77% and 17%. These results support the belief in the extrachromosomal influence as a cause in the development of mammary tumor.