Inflammatory Breast Cancer: the Immune Perspective

Total Page:16

File Type:pdf, Size:1020Kb

Inflammatory Breast Cancer: the Immune Perspective The Texas Medical Center Library DigitalCommons@TMC The University of Texas MD Anderson Cancer Center UTHealth Graduate School of The University of Texas MD Anderson Cancer Biomedical Sciences Dissertations and Theses Center UTHealth Graduate School of (Open Access) Biomedical Sciences 5-2013 Inflammatory Breast Cancer: The Immune Perspective Evan N. Cohen Follow this and additional works at: https://digitalcommons.library.tmc.edu/utgsbs_dissertations Part of the Immunity Commons, and the Medical Sciences Commons Recommended Citation Cohen, Evan N., "Inflammatory Breast Cancer: The Immune Perspective" (2013). The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access). 369. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/369 This Dissertation (PhD) is brought to you for free and open access by the The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences at DigitalCommons@TMC. It has been accepted for inclusion in The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access) by an authorized administrator of DigitalCommons@TMC. For more information, please contact [email protected]. Inflammatory Breast Cancer: The Immune Perspective by Evan Nathaniel Cohen, B.S., B.A. APPROVED:!!!! ______________________________! James M. Reuben, Ph.D., M.B.A. Supervisory Professor ______________________________! Bradley McIntyre, Ph.D. ______________________________! Naoto T. Ueno, M.D., Ph.D. ______________________________! Stephen E. Ullrich, Ph.D. ______________________________! Wendy A. Woodward, M.D., Ph.D. APPROVED:!!!!____________________________ Dean, The University of Texas Graduate School of Biomedical Sciences at Houston Inflammatory Breast Cancer: The Immune Perspective Presented to the Faculty of The University of Texas Health Science Center at Houston and The University of Texas MD Anderson Cancer Center Graduate School of Biomedical Sciences in Partial Fulfillment of the Requirements for the Degree of DOCTOR OF PHILOSOPHY by Evan Nathaniel Cohen, B.S., B.A. Houston, Texas May, 2013 DEDICATION This dissertation is dedicated to my parents, Stephen and Marin Cohen, and the patients of the Morgan Welch Inflammatory Breast Cancer Research Program and Clinic at the University of Texas MD Anderson Cancer Center. In memory of Marilyn Kretzer ACKNOWLEDGEMENTS This study was funded in part by the following grants: Assessment of Circulating Breast Cancer Stem Cells To Predict Recurrent Disease, W81XWH-09-1-0031 01, DOD (Evan N. Cohen), Cancer Center Support Grant, NIH/NCI; State of Texas Rare and Aggressive Breast Cancer Research Program (Naoto T. Ueno); Human Breast Cancer Stem Cell Surrogates, CA138239-02, NIH/NCI (James Reuben and Wendy Woodward). I would like to thank my parents who have supported me at every step. My parents and sister have given me their unequivocal support and inspiration throughout, as always, for which my mere expression of thanks does not suffice. It would not have been possible to write this doctoral thesis without the help and support of the kind people around me, to only some of whom it is possible to give particular mention here. First and foremost, I would like to thank my advisor, James Reuben. I could not have asked for a more supportive advisor. I appreciate all his contributions of time, ideas, and funding to make my Ph.D. experience productive and stimulating. The joy and enthusiasm he has for research was contagious and motivational for me, even during tough times in the Ph.D. pursuit. I am also thankful for the excellent example he has provided as a genuinely good person and professor. Above all, he made me welcomed as a friend, which I appreciate from my heart. The members of the Dr. Reuben’s lab have contributed immensely to my personal and professional time at MD Anderson. The group has been a source of friendships as well as good advice and collaboration. I cannot imagine how I would have survived these last years without the help and friendship of Hui Gao. Hui has taught me most of iv what I learned in the lab through grad school and certainly everything about flow cytometry. Most importantly, she has been a true friend and I cannot possibly thank her properly. This thesis is a compilation of massive amounts of data that has been amassed by a wonderful team of dedicated people. Sanda Tin was responsible for coordinating the LAB08-199 protocol within the lab that is the basis for many of the patient data presented here. Summer Jackson, Juanita Lara, and Charla Parker were responsible for recruiting the patients. Qiong Wu and YingDong Li diligently processed the samples. Raul “Josh” Garza and Matt Galland analyzed many of the serum samples. Antonio Giordano has lent his clinical expertise to put our blood samples into context. Simone Anfossi and Hyun-Jun “Robert” Park, my fellow travelers through this education, helped me learn RT-PCR and countless other assays. Gail Hammond helped with all the little and not so little things I seem incapable of doing. As mentioned above, Hui Gao’s careful eye was always present at every step. Under Dr. Reuben, we have been more than co-workers. I think of these people as my extended family. Additionally over the years, I have had the unique privilege to work with a number of post-docs and fellows that have come through the lab. First, I would like to thank Bang-Ning Lee who helped guide me through my early days in the lab. And Carolina Gutierrez, who I don’t think taught me anything about science, but so much about medicine and even more about life. We were all most saddened when Michal Mego, who developed the test we used for circulating tumor cells in EMT with Prof. Sendurai Mani, returned to his home in Slovakia. We miss him as much as he misses his hair. Perhaps one of the greatest experiences of my time at MD Anderson was the ability to work with and guide some truly outstanding high school and college students v including Nicole Kruijs, Grant Dougherty, Thomas Yang, Lilly Zhang, Albert Huang and Ken Tong. Meshaal Nadeem spent several of her summers and winters with us. If her work here is any indication, I have been very fortunate to meet her so early in her career. I am also grateful I had the opportunity to work with Xiaoyan “Sunny” Wang, Changping Li, Mario Giuliano, De-Yu Shen, “Jessica” Li Li, Gracie Rodriguez, Monica Martinez, Ugo de Giorgi, Paloma “Jimena” de Andres, Laura Camacho, Karin Görner, Zarixia Zavala and her student Amilcar Rivera, Tiffany LaFortune, Ujjwala Warwdekar, Lamees Ali Aziz Alsayed Atteya, Neslihan Duzkale, Tamer Fouad, Sriram Yennu and countless other fellows that Dr. Reuben has hosted. This institution has been a wonderful opportunity to meet people from a variety of fields. I am especially grateful to Prof. Gabriel Lopez-Berestein in Experimental Therapeutics and Prof. Val Johnson in Statistics who hosted me in first year rotations. These were valuable experience that broadened my horizons. Through Dr. Reuben, I also had the opportunity to collaborate with Prof. Charles Cleeland in Symptom Research and Prof. Sriram Yennu in Palliative Care and Rehabilitative Medicine. I would like to thank Neelima G Reddy from Prof. Raja Luthra’s lab for helping with the Fluidigm experiments and Bisrat Debeb from Dr. Woodward’s lab who helped with the mammosphere experiments. In addition, the members of Hematopatholgy, Breast Medical Oncology and the Morgan Welch Inflammatory Breast Cancer Research Program and Clinic have all been very supportive; providing know-how, reagents, sounding boards, guidance and advice. I particularly need to thank Dave Imperial, Nikhil Chari, Hatice Duzkale, and Archie Tamayo in HemPath and Lara C. Alvarez de Lacerda in BMO. I have been fortunate to have the guidance of a wonderful committee. I would like to thank Drs. Massimo Cristofanilli, Bradley McIntye, Fredika Robertson, Naoto T. vi Ueno, Stephen Ullrich, and Wendy Woodward for their time, interest, helpful comments and insightful questions. Their support has truly enriched my time and experience here. Finally, I wish to thank the patients of the MD Anderson Nellie B. Connally Breast Center and Morgan Welch Inflammatory Breast Cancer Research Program and Clinic who eagerly await answers. vii Inflammatory Breast Cancer: The Immune Perspective Publication No.________ Evan Nathaniel Cohen, PhD Supervisory Professor: James M. Reuben, Ph.D. ABSTRACT Inflammatory breast cancer (IBC) is the most insidious form of locally advanced disease. Although rare and less than 2% of all breast cancer, IBC is responsible for up to 10% of all breast cancer deaths. Despite the name, very little is known about the role of inflammation or immune mediators in IBC. Therefore, we analyzed blood samples from IBC patients and non-IBC patients, as well as healthy donor controls to establish an IBC- specific profile of peripheral blood leukocyte phenotype and function of T cells and dendritic cells and serum inflammatory cytokines. Emerging evidence suggests that host factors in the microenviromement may interact with underlying IBC genetics to promote the aggressive nature of the tumor. An integral part of the metastatic process involves epithelial to mesenchymal transition (EMT) where primary breast cancer cells gain motility and stem cell-like features that allow distant seeding. Interestingly, the IBC consortium microarray data found no clear evidence for EMT in IBC tumor tissues. It is becoming increasingly evident that inflammatory factors can induce EMT. However, it is unknown if EMT-inducing soluble factors secreted by activated immune cells in the IBC microenvironment can" account for the absence of viii EMT in studies of the tumor cells themselves. We hypothesized that soluble factors from immune cells are capable of inducing EMT in IBC. We tested the ability of immune conditioned media to induce EMT in IBC cells.
Recommended publications
  • The Snf1-Related Kinase, Hunk, Is Essential for Mammary Tumor Metastasis
    The Snf1-related kinase, Hunk, is essential for mammary tumor metastasis Gerald B. W. Wertheima, Thomas W. Yanga, Tien-chi Pana, Anna Ramnea, Zhandong Liua, Heather P. Gardnera, Katherine D. Dugana, Petra Kristelb, Bas Kreikeb, Marc J. van de Vijverb, Robert D. Cardiffc, Carol Reynoldsd, and Lewis A. Chodosha,1 aDepartments of Cancer Biology, Cell and Developmental Biology, and Medicine, Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, PA 19104-6160; bDepartment of Diagnostic Oncology, The Netherlands Cancer Institute, Antoni van Leeuwenhoek Hospital, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands; cCenter for Comparative Medicine, University of California, County Road 98 and Hutchison Drive, Davis, CA 95616; and dDivision of Anatomic Pathology, Mayo Clinic, Rochester, MN 55905 Communicated by Craig B. Thompson, University of Pennsylvania, Philadelphia, PA, July 27, 2009 (received for review April 22, 2009) We previously identified a SNF1/AMPK-related protein kinase, Hunk, Results from a mammary tumor arising in an MMTV-neu transgenic mouse. Hunk Is Overexpressed in Aggressive Subsets of Human Cancers. To The function of this kinase is unknown. Using targeted deletion in investigate its role in human tumorigenesis, we cloned the human mice, we now demonstrate that Hunk is required for the metastasis homologue of Hunk from a fetal brain cDNA library. Sequence of c-myc-induced mammary tumors, but is dispensable for normal analysis yielded a composite cDNA spanning an ORF of 714 amino development. Reconstitution experiments revealed that Hunk is suf- acids (GenBank accession #NM࿝014586). Review of this sequence ficient to restore the metastatic potential of Hunk-deficient tumor and of human genome data indicated that a single Hunk isoform cells, as well as defects in migration and invasion, and does so in a exists that is 92% identical to murine Hunk at the amino acid level manner that requires its kinase activity.
    [Show full text]
  • Surgically-Induced Multi-Organ Metastasis in an Orthotopic Syngeneic Imageable Model of 4T1 Murine Breast Cancer
    ANTICANCER RESEARCH 35: 4641-4646 (2015) Surgically-Induced Multi-organ Metastasis in an Orthotopic Syngeneic Imageable Model of 4T1 Murine Breast Cancer YONG ZHANG1, NAN ZHANG1, ROBERT M. HOFFMAN1,2 and MING ZHAO1 1AntiCancer, Inc., San Diego, CA, U.S.A.; 2Department of Surgery, University of California, San Diego, CA, U.S.A. Abstract. Background/Aim: Murine models of breast cancer When implanted orthotopically, 4T1 has been shown to with a metastatic pattern similar to clinical breast cancer in metastasize to organs similarly to clinical breast cancer in humans would be useful for drug discovery and mechanistic humans, including to lungs, liver, brain and bone (3-6). Tao studies. The 4T1 mouse breast cancer cell line was developed et al. transformed the 4T1 cell line to express luciferase for by Miller et al. in the early 1980s to study tumor metastatic longitudinal detection of primary growth and metastases (7). heterogeneity. The aim of the present study was to develop a In their study, metastasis at high rates, including the lungs, multi-organ-metastasis imageable model of 4T1. Materials and liver and bone, occurred in most animals within six weeks Methods: A stable 4T1 clone highly-expressing red fluorescent with lower frequency of metastasis to brain and other sites. protein (RFP) was injected orthotopically into the right second This imageable model is limited by the weak signal of mammary fat pad of BALB/c mice. The primary tumor was luciferase which requires photon-counting of anesthetized resected on day 18 after tumor implantation, when the average animals. The weak signal of luciferase cannot produce a true tumor volume reached approximately 500-600 mm3.
    [Show full text]
  • Canine Mammary Carcinoma
    Oncology Services Lloyd Veterinary Medical Center Hixson-Lied Small Animal Hospital Canine Mammary Carcinoma What is a canine mammary carcinoma? Tumors of the mammary gland develop when the cells associated with the mammary gland become cancerous and grow uncontrollably. In dogs, approximately 50% of mammary tumors are malignant (have the potential to spread to other areas of the body). The other half are considered to be benign. The most common type of malignant mammary tumor is a carcinoma. What are the clinical signs of a mammary tumor? This tumor is often identified during a routine physical exam, or you may notice it at home. They usually manifest as a swelling of the mammary gland or the nearby tissues/skin. They can be firm or soft. How is a mammary tumor diagnosed? Biopsy is required to diagnose a mammary gland tumor. Prior to making definitive treatment options, full staging with an abdominal ultrasound, chest x-rays, and evaluation of the local lymph nodes are recommended to look for any spread of disease. How is a mammary tumor treated? Treatment of mammary tumors is aimed at both local control (removing the primary tumor and minimizing the likelihood of local recurrence) and systemic control (delaying the onset of spread of disease). Each tumor should be removed with a wide band of normal tissue around the tumor to result in the best possible outcome. If this type of surgery is not possible, a combination of surgery and radiation therapy may be discussed. Based on the type of tumor, and several factors evaluated on biopsy, chemotherapy may be recommended in addition to surgical removal.
    [Show full text]
  • Suppression Ofautochthonous Grafts Ofspontaneous Mammary Tumor by Induced Allogeneic Graft Rejection Mechanism
    [CANCER RESEARCH 33, 645-647, April 1973] Suppression of Autochthonous Grafts of Spontaneous Mammary Tumor by Induced Allogeneic Graft Rejection Mechanism Reiko Tokuzen and Waro Nakahara National Cancer Center Research Institute, Tsukiji 5-chome, Chuo-ku, Tokyo, Japan SUMMARY existing between the allogeneic and autochthonous grafts are involved in determining the different susceptibilities to the Autochthonous grafts of spontaneous mammary adenocar- host-mediated antitumor effect of plant polysaccharides. cinoma of mice give 100% takes with no spontaneous More recently, we examined local cellular reactions around regression. However, the growth of these autografts was Sarcoma 180 grafts during the process of regression under markedly inhibited with a high rate of complete regression polysaccharide treatment, and we found a massive outpouring when the grafts were mixed with ascitic Sarcoma 180 and of lymphoid cells 1 week after tumor implantation. No such implanted under i.p. treatment with lentinan. Lentinan is one cellular reaction was noted in untreated controls or in mice of the so-called antitumor-active plant polysaccharides; it treated with inactive polysaccharides. Similarly, autoch strongly inhibits Sarcoma 180 but has no effect on thonous grafts of spontaneous mammary tumors, not at all autochthonous grafts. Without the lentinan treatment, the inhibited by polysaccharides, called forth no local lymphoid mixed autografts and Sarcoma 180 or Sarcoma 180 alone cell infiltration. constantly produced large tumors. These results indicate that a The question arose as to what would happen to autoch local rejection mechanism against allogeneic tumor (Sarcoma thonous grafts if such local cell reaction were induced around 180), induced by injections of lentinan, failed to recognize them as in that which occurred around Sarcoma 180 under autografts as "self and destroyed them along with the polysaccharide treatment.
    [Show full text]
  • Understanding the Etiology of Inflammatory Breast
    UNDERSTANDING THE ETIOLOGY OF INFLAMMATORY BREAST CANCER by Lauren M. Shuman A thesis submitted to the Faculty of the University of Delaware in partial fulfillment of the requirements for the degree of Master of Science in Biological Sciences Spring 2015 © 2015 Lauren M. Shuman All Rights Reserved ProQuest Number: 1596894 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a complete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. ProQuest 1596894 Published by ProQuest LLC (2015). Copyright of the Dissertation is held by the Author. All rights reserved. This work is protected against unauthorized copying under Title 17, United States Code Microform Edition © ProQuest LLC. ProQuest LLC. 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, MI 48106 - 1346 UNDERSTANDING THE ETIOLOGY OF INFLAMMATORY BREAST CANCER by Lauren M. Shuman Approved: ____________________________________________________ Kenneth L. van Golen, Ph.D. Professor in charge of thesis on behalf of the Advisory Committee Approved: ____________________________________________________ Robin W. Morgan, Ph.D. Chair of the Department of Biological Sciences Approved: ____________________________________________________ George H. Watson, Ph.D. Dean of the College of Arts and Sciences Approved: ____________________________________________________ James G. Richards, Ph.D. Vice Provost for Graduate and Professional Education ACKNOWLEDGMENTS First and foremost, I would like to thank Dr. Kenneth van Golen for a list of things, but namely for the opportunity to work in this lab that gave me my first experience in cancer research.
    [Show full text]
  • Control of Mammary Tumor Differentiation by SKI-606 (Bosutinib)
    Oncogene (2011) 30, 301–312 & 2011 Macmillan Publishers Limited All rights reserved 0950-9232/11 www.nature.com/onc ORIGINAL ARTICLE Control of mammary tumor differentiation by SKI-606 (bosutinib) L Hebbard1,7,9, G Cecena1,7, J Golas2,8, J Sawada3,7, LG Ellies4, A Charbono1,7, R Williams1,7, RE Jimenez5, M Wankell1,7, KT Arndt2,8, SQ DeJoy2,8, RA Rollins2,8, V Diesl2,8, M Follettie2,8, LChen2,8, E Rosfjord2,8, RD Cardiff6, M Komatsu3,7, F Boschelli2,8 and RG Oshima1,7 1Cancer Research Center, Sanford-Burnham Medical Research Institute, La Jolla, CA, USA; 2Center for Integrative Biology and Biotherapeutics, Pfizer Research, Pearl River, NY, USA; 3Sanford-Burnham Medical Research Institute, Lake Nona, FL, USA; 4Pathology Department, University of California, San Diego, CA, USA; 5Biomedical Science Program, University of California, San Diego, La Jolla, CA, USA and 6Center for Genomic Pathology University of California, Davis, CA, USA C-Src is infrequently mutated in human cancers but it Introduction mediates oncogenic signals of many activated growth factor receptors and thus remains a key target for cancer In breast cancer, Src is of particular interest as it is therapy. However, the broad function of Src in many cell activated by both steroid hormone receptors and ErbB types and processes requires evaluation of Src-targeted family growth factor receptors and activates transcrip- therapeutics within a normal developmental and immune- tion factors such as STAT3, STAT5 and b-catenin by competent environment. In an effort to understand the direct phosphorylation (Silva and Shupnik, 2007; Kim appropriate clinical use of Src inhibitors, we tested an Src et al., 2009).
    [Show full text]
  • Clinicopathological Diversity of Canine Mammary Gland Tumors in Sri Lanka: a One-Year Survey on Cases Presented to Two Veterinary Practices
    veterinary sciences Article Clinicopathological Diversity of Canine Mammary Gland Tumors in Sri Lanka: A One-Year Survey on Cases Presented to Two Veterinary Practices Harsha Ariyarathna 1, Niranjala de Silva 2, Danielle Aberdein 1, Dayananda Kodikara 3, Manjula Jayasinghe 2, Ranjith Adikari 2 and John S. Munday 1,* 1 School of Veterinary Science, Massey University, Palmerston North 4442, New Zealand; [email protected] (H.A.); [email protected] (D.A.) 2 Faculty of Veterinary Medicine and Animal Science, University of Peradeniya, Peradeniya 20400, Sri Lanka; [email protected] (N.d.S.); [email protected] (M.J.); [email protected] (R.A.) 3 New Animal Clinic, 132/B, S. De. S. Jayasinghe Mawatha, Kohuwala, Nugegoda 10250, Sri Lanka; [email protected] * Correspondence: [email protected]; Tel.: +64-6-356-9099 (ext. 85172) Received: 19 February 2018; Accepted: 24 April 2018; Published: 27 April 2018 Abstract: Mammary gland tumors (MGTs) are one of the most common neoplasms among dogs in Sri Lanka. However, the clinicopathological diversity of MGTs in Sri Lanka is largely unknown, impeding accurate diagnosis and effective treatment of the disease. The present study investigated the clinicopathological features of MGTs in 74 dogs presented to two veterinary practices in Sri Lanka treated surgically, over a one-year period. Information regarding the patient signalment, clinical presentation, and reproductive history were collected, and each neoplasm was examined histologically. Forty-one (54.4%) dogs were primarily presented for mammary neoplasia, while a MGT was an incidental finding in 33 (44.6%) dogs. The majority of tumors were histologically malignant (n = 65, 87.8%), and 18 malignant tumor sub-types were identified.
    [Show full text]
  • Electrochemotherapy Modulates Mammary Tumor Growth in Rats on a Western Diet Supplemented with Curcumin
    biomedicines Article Electrochemotherapy Modulates Mammary Tumor Growth in Rats on a Western Diet Supplemented with Curcumin Raji Sundararajan 1,*, Lakshya Mittal 1 and Ignacio G. Camarillo 2,3 1 School of Engineering Technology, Purdue University, West Lafayette, IN 47907, USA; [email protected] 2 Department of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA; [email protected] 3 Purdue Center for Cancer Research, Purdue University, West Lafayette, IN 47907, USA * Correspondence: [email protected] Received: 25 September 2020; Accepted: 10 November 2020; Published: 13 November 2020 Abstract: In the US, every 12 min, six women are diagnosed with breast cancer and one dies. This highlights a critical need for developing alternate therapies using natural compounds, which are cost effective and with less side effects. Curcumin, the yellow pigment of turmeric has been found to suppress initiation, progression, and metastasis of a variety of tumors. Multiple clinical trials highlight the efficacy of curcumin in treating breast cancer and other diseases. Our in vitro studies have demonstrated that the electrical pulse (EP) application can further enhance the effectiveness of curcumin against breast cancer cells in a therapy called electrochemotherapy (ECT). In a direct extension of these results, we studied the effect of ECT coupled with intratumoral curcumin administration (EP+Cur) on N-methyl-N-nitrosourea (MNU) induced mammary tumors in female Sprague Dawley rats. Beginning at the weaning and throughout the study, rats were fed either western diet (West) or western diet, supplemented with 1% curcumin (W+Cur). Our results showed that EP+Cur treatment led to a reduced growth rate in rats fed with W+Cur diet compared to West diet (57.14% vs.
    [Show full text]
  • Spontaneous Malignant Mixed Tumors of the Rat, and the Successful Transplantation and Separation of Both Components from a Mammary Tumor Wilhelmina F
    Spontaneous Malignant Mixed Tumors of the Rat, and the Successful Transplantation and Separation of both Components from a Mammary Tumor Wilhelmina F. Dunning, Ph.D., Maynie R. Curtis, Ph.D.,* and Mark E. Maun, M.D. (Department o/ Pathology, Wayne University College o/ Medicine in co-operation with the Detroit Institute o/ Cancer Research, Detroit 26, Michigan) (Received for publication June 1, 1945) Malignant mixed tumors in man are relatively rare, comas and 1 a mixed tumor. Loeb (14) reported the but their occurrence has occasioned considerable dis- transplantation of an adenocarcinoma of the sub- cussion of their probable histogenesis. In 1937, Raso maxillary gland of a mouse, which developed into (16) reported an osteoid chondrosarcoma of the breast mixed tumors and spindle cell sarcomas in the first and collected from the literature, dating from 1835, transplanted generation. A transplantable mixed tumor 74 mammary tumors containing bone and cartilage, of the fowl was reported by Foulds (10). The primary but only 5 were considered to be true mixed tumors. growth, which appeared to be a carcinoma of the ovi- Saphir and Vass (17), in 1938, reviewed 153 cases of duct, was transplanted for 12 generations with varying "carcinosarcoma," excluding any tumors containing success into the pectoral muscles of fowls of the same large amounts of cartilage and bone that might be in- and different breeds. Bone and cartilage were found terpreted as teratomas. They concluded from the mor- in growths of the first and succeeding generations of phology of these neoplasms that in all but 3 or 4 cases transplantation.
    [Show full text]
  • Mammary Tumours in Dogs and Its Treatment Option- a Review
    Review Article ISSN: 2574 -1241 DOI: 10.26717/BJSTR.2020.30.004980 Mammary Tumours in Dogs and its Treatment Option- A Review Haben Fesseha* Haben Fesseha, School of Veterinary Medicine, Wolaita Sodo University, Ethiopia *Corresponding author: Haben Fesseha, School of Veterinary Medicine, Wolaita Sodo University, Ethiopia ARTICLE INFO ABSTRACT Received: September 11, 2020 Mammary tumors are the most common type of tumors in intact female dogs. Several epidemiologic studies have been conducted over the years and provide an estimate of Published: September 22, 2020 the incidence of canine mammary gland tumors. This type of treatment recommendation may also be made in dogs based on recognized, well-accepted prognostic factors such as tumor size, stage, type, and histologic differentiation. Based on the limited clinical Citation: Haben Fesseha. Mammary information available in veterinary medicine, the drugs that are effective in human breast Tumours in Dogs and its Treatment Option- A Review. Biomed J Sci & Tech Res in the treatment of malignant mammary gland tumors in dogs. The treatment of canine 30(4)-2020. BJSTR. MS.ID.004980. mammarycancer, such gland as cyclophosphamide, tumors will be based 5-fluorouracil, on the individual and doxorubicin, oncologist’s may understanding also have a role of Keywords: Neoplasm; Tumor Disease; Hyperplastic Lesions; Mammary Adenoma; tumor biology, experience, interpretation of the available studies, and a little bit of gut- Fibrothecoma; Glandular Epithelium chemotherapy in dogs with high-risk mammary
    [Show full text]
  • Pursuing Drugs for Mammary Cancer So You Want to Add One More Caot?
    ® Expert information on medicine, behavior and health from a world leader in veterinary medicine 'Tail Vaccinations Save Lives' 2 Pursuing Drugs for Mammary Cancer New research finds that they make it easier to deal with sarcomas. Cornell researchers identify an inhibitor that seems to The Power ofTouch 2 Stroking anxious shelter cats can kill cancer cells while leaving healthy cells unaffected ease their stress and increase immunity. How to Handle a Fainting Episode 3 n esearchers studying feline Baker Institute for Animal Health, An immediate veterinary visit is a ftmammary cancer at Cornell have identified a promising chemical, must to uncover the underlying cause. University College of Veterinary BB-CI-amidine, that seems to kill off Should Their (at Drink Milk? 8 Medicine have set an ambitious feline mammary cancer cells while They may love it, but it offers few agenda. They hope that their leaving healthy cells unaffected. benefits and some potential harm. ongoing work will lead to better diagnosis. treatment and preven­ Malignant Tumors. The chemi­ IN THE NEWS ••• tion of breast tumors in cats and cal inhibits certain enzymes, Raising Awareness About humans. Much of their interest called peptidylarginine deimi­ Obesity's Risks and Solutions lies in how a novel class of drugs nase (PAD), which tend to be Despite the potential con­ affects breast cell tumors. over expressed (increased) in sequences of obesity, up to 59 In a study funded by the Cor­ feline mammary tumors. The percent of cats are overweight, nell Feline Health Center. As­ ~- majority 0 f t hese tumors are .2> according to the American sistant Professor Gerlinde Van '" malignant, and they're the Anima l Hospital Association.
    [Show full text]
  • Epidemiological Studies on Canine Mammary Tumour and Its Relevance for Breast Cancer Studies
    IOSR Journal of Pharmacy Vol. 2, Issue 2, Mar.-Apr, 2012, pp. 322-333 Epidemiological Studies on Canine Mammary Tumour and its Relevance for Breast Cancer Studies Kuldip Gupta1, Naresh Kumar Sood1, Sanjeev Kumar Uppal2, Jitender Mohindroo3, Shashikant Mahajan3, M Raghunath3 and Kiranjeet Singh3 1Department of Veterinary Pathology, 2.Department of Veterinary Medicine and 3.Department of Veterinary of Surgery and Radiology, College of Veterinary Science, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana-141 004, Punjab, India. ABSTRACT Breast cancer is the most common cancer in women. Its incidence is rising globally and more so in the developing countries. There is a need to look for suitable animal model for biomedical research and pharmaceutical trails for this dreadly disease. In this pursuit, huge naturally occurring resource of canine mammary tumour may provide valid answer to impending questions in a shorter time frame. However, the epidemiology of canine mammary tumour (CMT) is poorly documented, especially in India. The present review deals with global and Indian scenario related to epidemiology of canine mammary tumour and its relevance as a model for human breast cancer. Keywords: Animal model, Breast cancer, Canine mammary tumour, Epidemiology, Incidence 1. INTRODUCTION Breast cancer is the most frequent malignant tumor in human females and morbidity and mortality due to it continue to increase, despite remarkable progress in the field of early diagnosis and adjuvant therapy (Raica et al 2009). Mammary neoplasms in dogs are the second most common neoplasms after skin tumors (Rezia et al 2009). Nearly 41% to 53% of the mammary tumors that occur in the bitch are malignant (Misdorp 2002).
    [Show full text]