Dog Diseases
Mammary Neoplasms, Experimental
Pancreatic Neoplasms
Neoplasms
Neoplasms, Cystic, Mucinous, and Serous
Neoplasms, Multiple Primary
Neoplasms, Second Primary
Adenocarcinoma, Mucinous
Stimulation of thymidine uptake and cell proliferation in mouse embryo fibroblasts by conditioned medium from mammary cells in culture. (1/4288)
Undialyzed conditioned medium from several cell culture sources did not stimulate thymidine incorporation or cell overgrowth in quiescent, density-inhibited mouse embryo fibroblast cells. However, dialyzed conditioned medium (DCM) from clonal mouse mammary cell lines MCG-V14, MCG-T14, MCG-T10; HeLa cells; primary mouse adenocarcinoma cells; and BALB/c normal mouse mammary epithelial cells promoted growth in quiescent fibroblasts. The amount of growth-promoting activity produced per cell varied from 24% (HeLa) to 213% (MCG-V14) of the activity produced by primary tumor cells. The production of growth-promoting activity was not unique to tumor-derived cells or cells of high tumorigenicity. The amount of growth-promoting activity produced per cell in the active cultures was not correlated with any of the following: tumorigenicity, growth rat, cell density achieved at saturation, cell type, or species of cell origin. It is concluded that transformed and non-transformed cells of diverse origin, cell type, and tumorigenicity can produce growth factors in culture. The growth-promoting potential of the active media from primary tumor cultures accumulated with time of contact with cells and was too great to be accounted for entirely by the removal of low-molecular-weight inhibitors by dialysis. The results are consistent with the hypothesis that conditioned medium from the active cultures contained a dialyzable, growth-promoting activity. Different cell lines exhibited differential sensitivity to tumor cell DCM and fetal bovine serum. Furthermore, quiescent fibroblasts were stimulated by primary tumor cell DCM in the presence of saturating concentrations of fetal bovine serum. These observations support the notion that the active growth-promoting principle in primary tumor cell DCM may not be a serum factor(s). (+info)Isolation and purification of rat mammary tumor peroxidase. (2/4288)
7,12-Dimethylbenz(a)anthracene-induced rat mammary tumors often contain high levels of the enzyme perioxidase, a putative marker of estrogen dependence. This enzyme can be effectively extracted with 0.5 M CaCl2, giving rise to a soluble peroxidase with a molecular weight of about 50,000 as determined by gel filtration. This is the same size as the estrogen-induced peroxidase of rat uterus but smaller than other mammalian peroxidases. Further purification of the rat mammary tumor peroxidase by concanavalin A-Sepharose chromatography and hydrophobic interaction chromatography on phenyl Sepharose provides a 640-fold purification of the enzyme. (+info)Unsaturated fatty acid requirements for growth and survival of a rat mammary tumor cell line. (3/4288)
A cell line, the growth and survival of which is markedly affected by linoleic acid, has been established from a carcinogen-induced rat mammary tumor. The cells have been continuously passaged in 5% rat serum plus 10% fetal calf serum-supplemented medium. The rat serum component was found to be indispensalbe, for when it was omitted the growth rate rapidly declined and the cells died by 5 to 7 days. Removal of the rat serum from the growth medium also resulted in a dramatic loss of Oil Red O-positive droplets in the cells, suggesting that the lipid component of rat serum might be a major growth-promoting principle in rat serum. This is likely since the total lipid fraction, but not the delipidized protein fraction, could largely supplant requirement of the cells for rat serum. Pure linoleic acid was found to be effective in maintaining the cell growth in delipidized serum or in whole fetal calf serum-supplemented medium. Fatty acid analysis revealed a 19-fold higher amount of linoleic acid in rat serum than in fetal calf serum. (+info)Vasopressin stimulation of acetate incorporation into lipids in a dimethylbenz(a)anthracene-induced rat mammary tumor cell line. (4/4288)
In a preliminary report we described the effects of rat prolactin on the incorporation of [14C]acetate into lipids by a cell line from a dimethylbenz(a)anthracene-induced rat mammary tumor. The characteristics of the response to prolactin were very similar to those described for the normal rat mammary gland; namely, insulin was required for full expression of the response, maximal activity was not seen until 36 hr after the addition of the hormones, and growth hormone was able to elicit the same response. However, we were unable to detect binding of 125I-labeled prolactin to these cells, and furthermore, other more purified prolactin preparations were inactive. Upon further investigation we discovered that the activity resided in a low-molecular-weight fraction of the rat prolactin B-1 preparation and was probably either vasopressin or oxytocin or both. These data suggest the possibility that vasopressin may play a role in rodent mammary tumorigenesis. (+info)Glucocorticoid down-regulation of fascin protein expression is required for the steroid-induced formation of tight junctions and cell-cell interactions in rat mammary epithelial tumor cells. (5/4288)
Glucocorticoid hormones, which are physiological regulators of mammary epithelium development, induce the formation of tight junctions in rat Con8 mammary epithelial tumor cells. We have discovered that, as part of this process, the synthetic glucocorticoid dexamethasone strongly and reversibly down-regulated the expression of fascin, an actin-bundling protein that also interacts with the adherens junction component beta-catenin. Ectopic constitutive expression of full-length mouse fascin containing a Myc epitope tag (Myc-fascin) in Con8 cells inhibited the dexamethasone stimulation of transepithelial electrical resistance, disrupted the induced localization of the tight junction protein occludin and the adherens junction protein beta-catenin to the cell periphery, and prevented the rearrangement of the actin cytoskeleton. Ectopic expression of either the carboxyl-terminal 213 amino acids of fascin, which includes the actin and beta-catenin-binding sites, or the amino-terminal 313 amino acids of fascin failed to disrupt the glucocorticoid induction of tight junction formation. Mammary tumor cells expressing the full-length Myc-fascin remained generally glucocorticoid responsive and displayed no changes in the levels or protein-protein interactions of junctional proteins or the amount of cytoskeletal associated actin filaments. However, a cell aggregation assay demonstrated that the expression of Myc-fascin abrogated the dexamethasone induction of cell-cell adhesion. Our results implicate the down-regulation of fascin as a key intermediate step that directly links glucocorticoid receptor signaling to the coordinate control of junctional complex formation and cell-cell interactions in mammary tumor epithelial cells. (+info)Tyrosine kinase inhibitor emodin suppresses growth of HER-2/neu-overexpressing breast cancer cells in athymic mice and sensitizes these cells to the inhibitory effect of paclitaxel. (6/4288)
Overexpression of the HER-2/neu proto-oncogene, which encodes the tyrosine kinase receptor p185neu, has been observed in tumors from breast cancer patients. We demonstrated previously that emodin, a tyrosine kinase inhibitor, suppresses tyrosine kinase activity in HER-2/neu-overexpressing breast cancer cells and preferentially represses transformation phenotypes of these cells in vitro. In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for breast cancer patients. We found that emodin significantly inhibited tumor growth and prolonged survival in mice bearing HER-2/neu-overexpressing human breast cancer cells. Furthermore, the combination of emodin and paclitaxel synergistically inhibited the anchorage-dependent and -independent growth of HER-2/neu-overexpressing breast cancer cells in vitro and synergistically inhibited tumor growth and prolonged survival in athymic mice bearing s.c. xenografts of human tumor cells expressing high levels of p185neu. Both immunohistochemical staining and Western blot analysis showed that emodin decreases tyrosine phosphorylation of HER-2/neu in tumor tissue. Taken together, our results suggest that the tyrosine kinase activity of HER-2/neu is required for tumor growth and chemoresistance and that tyrosine kinase inhibitors such as emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and also sensitize these tumors to paclitaxel. The results may have important implications in chemotherapy for HER-2/neu-overexpressing breast tumors. (+info)Induction of lasting complete regression of preformed distinct solid tumors by targeting the tumor vasculature using two new anti-endoglin monoclonal antibodies. (7/4288)
Endoglin (EDG, CD105) is a proliferation-associated antigen on endothelial cells. In this study, two new anti-EDG monoclonal antibodies (mAbs) Y4-2F1 (or termed SN6j) and P3-2G8 (SN6k) were generated and used for treating distinct preformed tumors. These mAbs, both IgG1-kappa antibodies, cross-reacted weakly with mouse endothelial cells but defined epitopes different from the epitope defined by a previously reported anti-EDG mAb K4-2C10 (B. K. Seon et al., Clin. Cancer Res., 3: 1031-1044, 1997). SN6j and SN6k reacted strongly with human endothelial cells and vascular endothelium of malignant human tissues but showed no significant reactivity with tumor cells per se. The deglycosylated ricin A chain (dgRA) conjugates of the two mAbs showed a weak but specific cytotoxic activity against murine endothelial cells in vitro. In the therapeutic studies, severe combined immunodeficient mice were inoculated s.c. with MCF-7 human breast cancer cells and left untreated until palpable tumors of distinct size (4-6 mm in diameter) appeared. Mice with the distinct tumors were treated by i.v. administration of individual anti-EDG conjugates, unconjugated mAbs, or a control conjugate. Long-lasting complete regression of the tumors was induced in the majority of tumor-bearing mice (n = 8 for each conjugate) when 40 microg of the individual conjugates were administered three times via the tail vein. It is remarkable that the tumors remained regressed without further therapy for as long as the mice were followed (i.e., 100 days). Control conjugate did not induce regression of the tumors in any of the treated mice, although weak nonspecific effects were observed in some of the mice (n = 8). The effects of unconjugated mAbs were small with the dose used, i.e., 34 microg three times. The anti-EDG conjugates showed antiangiogenic activity in the dorsal air sac assay in mice. The results suggest good potential of these conjugates for the clinical application. (+info)Influence of tangeretin on tamoxifen's therapeutic benefit in mammary cancer. (8/4288)
BACKGROUND: Tamoxifen and the citrus flavonoid tangeretin exhibit similar inhibitory effects on the growth and invasive properties of human mammary cancer cells in vitro; furthermore, the two agents have displayed additive effects in vitro. In this study, we examined whether tangeretin would enhance tamoxifen's therapeutic benefit in vivo. METHODS: Female nude mice (n = 80) were inoculated subcutaneously with human MCF-7/6 mammary adenocarcinoma cells. Groups of 20 mice were treated orally by adding the following substances to their drinking water: tamoxifen (3 x 10(-5) M), tangeretin (1 x 10(-4) M), tamoxifen plus tangeretin (3 x 10(-5) M plus 1 x 10(-4) M), or solvent. RESULTS AND CONCLUSIONS: Oral treatment of mice with tamoxifen resulted in a statistically significant inhibition of tumor growth compared with solvent treatment (two-sided P = .001). Treatment with tangeretin did not inhibit tumor growth, and addition of this compound to drinking water with tamoxifen completely neutralized tamoxifen's inhibitory effect. The median survival time of tumor-bearing mice treated with tamoxifen plus tangeretin was reduced in comparison with that of mice treated with tamoxifen alone (14 versus 56 weeks; two-sided P = .002). Tangeretin (1 x 10(-6) M or higher) inhibited the cytolytic effect of murine natural killer cells on MCF-7/6 cells in vitro, which may explain why tamoxifen-induced inhibition of tumor growth in mice is abolished when tangeretin is present in drinking water. IMPLICATIONS: We describe an in vivo model to study potential interference of dietary compounds, such as flavonoids, with tamoxifen, which could lead to reduced efficacy of adjuvant therapy. In our study, the tumor growth-inhibiting effect of oral tamoxifen was reversed upon addition of tangeretin to the diet. Our data argue against excessive consumption of tangeretin-added products and supplements by patients with mammary cancer during tamoxifen treatment. (+info)Mammary neoplasms in animals refer to abnormal growths or tumors that occur in the mammary glands. These tumors can be benign (non-cancerous) or malignant (cancerous). Benign tumors are slow growing and rarely spread to other parts of the body, while malignant tumors are aggressive, can invade surrounding tissues, and may metastasize to distant organs.
Mammary neoplasms are more common in female animals, particularly those that have not been spayed. The risk factors for developing mammary neoplasms include age, reproductive status, hormonal influences, and genetic predisposition. Certain breeds of dogs, such as poodles, cocker spaniels, and dachshunds, are more prone to developing mammary tumors.
Clinical signs of mammary neoplasms may include the presence of a firm, discrete mass in the mammary gland, changes in the overlying skin such as ulceration or discoloration, and evidence of pain or discomfort in the affected area. Diagnosis is typically made through a combination of physical examination, imaging studies (such as mammography or ultrasound), and biopsy with histopathological evaluation.
Treatment options for mammary neoplasms depend on the type, size, location, and stage of the tumor, as well as the animal's overall health status. Surgical removal is often the primary treatment modality, and may be curative for benign tumors or early-stage malignant tumors. Radiation therapy and chemotherapy may also be used in cases where the tumor has spread to other parts of the body. Regular veterinary check-ups and monitoring are essential to ensure early detection and treatment of any recurrence or new mammary neoplasms.
There is no medical definition for "dog diseases" as it is too broad a term. However, dogs can suffer from various health conditions and illnesses that are specific to their species or similar to those found in humans. Some common categories of dog diseases include:
1. Infectious Diseases: These are caused by viruses, bacteria, fungi, or parasites. Examples include distemper, parvovirus, kennel cough, Lyme disease, and heartworms.
2. Hereditary/Genetic Disorders: Some dogs may inherit certain genetic disorders from their parents. Examples include hip dysplasia, elbow dysplasia, progressive retinal atrophy (PRA), and degenerative myelopathy.
3. Age-Related Diseases: As dogs age, they become more susceptible to various health issues. Common age-related diseases in dogs include arthritis, dental disease, cancer, and cognitive dysfunction syndrome (CDS).
4. Nutritional Disorders: Malnutrition or improper feeding can lead to various health problems in dogs. Examples include obesity, malnutrition, and vitamin deficiencies.
5. Environmental Diseases: These are caused by exposure to environmental factors such as toxins, allergens, or extreme temperatures. Examples include heatstroke, frostbite, and toxicities from ingesting harmful substances.
6. Neurological Disorders: Dogs can suffer from various neurological conditions that affect their nervous system. Examples include epilepsy, intervertebral disc disease (IVDD), and vestibular disease.
7. Behavioral Disorders: Some dogs may develop behavioral issues due to various factors such as anxiety, fear, or aggression. Examples include separation anxiety, noise phobias, and resource guarding.
It's important to note that regular veterinary care, proper nutrition, exercise, and preventative measures can help reduce the risk of many dog diseases.
'Mammary neoplasms, experimental' is not a recognized medical term. However, I can provide definitions for the individual terms:
1. Mammary: Pertaining to the breast or mammary glands in females, which are responsible for milk production.
2. Neoplasms: Abnormal growths of tissue, also known as tumors or masses, that can be benign (non-cancerous) or malignant (cancerous).
3. Experimental: Relating to a scientific experiment or study, typically conducted in a controlled setting to test hypotheses and gather data.
In the context of medical research, 'experimental mammary neoplasms' may refer to artificially induced breast tumors in laboratory animals (such as rats or mice) for the purpose of studying the development, progression, treatment, and prevention of breast cancer. These studies can help researchers better understand the biology of breast cancer and develop new therapies and strategies for its diagnosis and management.
Pancreatic neoplasms refer to abnormal growths in the pancreas that can be benign or malignant. The pancreas is a gland located behind the stomach that produces hormones and digestive enzymes. Pancreatic neoplasms can interfere with the normal functioning of the pancreas, leading to various health complications.
Benign pancreatic neoplasms are non-cancerous growths that do not spread to other parts of the body. They are usually removed through surgery to prevent any potential complications, such as blocking the bile duct or causing pain.
Malignant pancreatic neoplasms, also known as pancreatic cancer, are cancerous growths that can invade and destroy surrounding tissues and organs. They can also spread (metastasize) to other parts of the body, such as the liver, lungs, or bones. Pancreatic cancer is often aggressive and difficult to treat, with a poor prognosis.
There are several types of pancreatic neoplasms, including adenocarcinomas, neuroendocrine tumors, solid pseudopapillary neoplasms, and cystic neoplasms. The specific type of neoplasm is determined through various diagnostic tests, such as imaging studies, biopsies, and blood tests. Treatment options depend on the type, stage, and location of the neoplasm, as well as the patient's overall health and preferences.
Neoplasms are abnormal growths of cells or tissues in the body that serve no physiological function. They can be benign (non-cancerous) or malignant (cancerous). Benign neoplasms are typically slow growing and do not spread to other parts of the body, while malignant neoplasms are aggressive, invasive, and can metastasize to distant sites.
Neoplasms occur when there is a dysregulation in the normal process of cell division and differentiation, leading to uncontrolled growth and accumulation of cells. This can result from genetic mutations or other factors such as viral infections, environmental exposures, or hormonal imbalances.
Neoplasms can develop in any organ or tissue of the body and can cause various symptoms depending on their size, location, and type. Treatment options for neoplasms include surgery, radiation therapy, chemotherapy, immunotherapy, and targeted therapy, among others.
Neoplasms: Neoplasms refer to abnormal growths of tissue that can be benign (non-cancerous) or malignant (cancerous). They occur when the normal control mechanisms that regulate cell growth and division are disrupted, leading to uncontrolled cell proliferation.
Cystic Neoplasms: Cystic neoplasms are tumors that contain fluid-filled sacs or cysts. These tumors can be benign or malignant and can occur in various organs of the body, including the pancreas, ovary, and liver.
Mucinous Neoplasms: Mucinous neoplasms are a type of cystic neoplasm that is characterized by the production of mucin, a gel-like substance produced by certain types of cells. These tumors can occur in various organs, including the ovary, pancreas, and colon. Mucinous neoplasms can be benign or malignant, and malignant forms are often aggressive and have a poor prognosis.
Serous Neoplasms: Serous neoplasms are another type of cystic neoplasm that is characterized by the production of serous fluid, which is a thin, watery fluid. These tumors commonly occur in the ovary and can be benign or malignant. Malignant serous neoplasms are often aggressive and have a poor prognosis.
In summary, neoplasms refer to abnormal tissue growths that can be benign or malignant. Cystic neoplasms contain fluid-filled sacs and can occur in various organs of the body. Mucinous neoplasms produce a gel-like substance called mucin and can also occur in various organs, while serous neoplasms produce thin, watery fluid and commonly occur in the ovary. Both mucinous and serous neoplasms can be benign or malignant, with malignant forms often being aggressive and having a poor prognosis.
Skin neoplasms refer to abnormal growths or tumors in the skin that can be benign (non-cancerous) or malignant (cancerous). They result from uncontrolled multiplication of skin cells, which can form various types of lesions. These growths may appear as lumps, bumps, sores, patches, or discolored areas on the skin.
Benign skin neoplasms include conditions such as moles, warts, and seborrheic keratoses, while malignant skin neoplasms are primarily classified into melanoma, squamous cell carcinoma, and basal cell carcinoma. These three types of cancerous skin growths are collectively known as non-melanoma skin cancers (NMSCs). Melanoma is the most aggressive and dangerous form of skin cancer, while NMSCs tend to be less invasive but more common.
It's essential to monitor any changes in existing skin lesions or the appearance of new growths and consult a healthcare professional for proper evaluation and treatment if needed.
Multiple primary neoplasms refer to the occurrence of more than one primary malignant tumor in an individual, where each tumor is unrelated to the other and originates from separate cells or organs. This differs from metastatic cancer, where a single malignancy spreads to multiple sites in the body. Multiple primary neoplasms can be synchronous (occurring at the same time) or metachronous (occurring at different times). The risk of developing multiple primary neoplasms increases with age and is associated with certain genetic predispositions, environmental factors, and lifestyle choices such as smoking and alcohol consumption.
Kidney neoplasms refer to abnormal growths or tumors in the kidney tissues that can be benign (non-cancerous) or malignant (cancerous). These growths can originate from various types of kidney cells, including the renal tubules, glomeruli, and the renal pelvis.
Malignant kidney neoplasms are also known as kidney cancers, with renal cell carcinoma being the most common type. Benign kidney neoplasms include renal adenomas, oncocytomas, and angiomyolipomas. While benign neoplasms are generally not life-threatening, they can still cause problems if they grow large enough to compromise kidney function or if they undergo malignant transformation.
Early detection and appropriate management of kidney neoplasms are crucial for improving patient outcomes and overall prognosis. Regular medical check-ups, imaging studies, and urinalysis can help in the early identification of these growths, allowing for timely intervention and treatment.
A "second primary neoplasm" is a distinct, new cancer or malignancy that develops in a person who has already had a previous cancer. It is not a recurrence or metastasis of the original tumor, but rather an independent cancer that arises in a different location or organ system. The development of second primary neoplasms can be influenced by various factors such as genetic predisposition, environmental exposures, and previous treatments like chemotherapy or radiation therapy.
It is important to note that the definition of "second primary neoplasm" may vary slightly depending on the specific source or context. In general medical usage, it refers to a new, separate cancer; however, in some research or clinical settings, there might be more precise criteria for defining and diagnosing second primary neoplasms.
Adenocarcinoma, mucinous is a type of cancer that begins in the glandular cells that line certain organs and produce mucin, a substance that lubricates and protects tissues. This type of cancer is characterized by the presence of abundant pools of mucin within the tumor. It typically develops in organs such as the colon, rectum, lungs, pancreas, and ovaries.
Mucinous adenocarcinomas tend to have a distinct appearance under the microscope, with large pools of mucin pushing aside the cancer cells. They may also have a different clinical behavior compared to other types of adenocarcinomas, such as being more aggressive or having a worse prognosis in some cases.
It is important to note that while a diagnosis of adenocarcinoma, mucinous can be serious, the prognosis and treatment options may vary depending on several factors, including the location of the cancer, the stage at which it was diagnosed, and the individual's overall health.
Thyroid neoplasms refer to abnormal growths or tumors in the thyroid gland, which can be benign (non-cancerous) or malignant (cancerous). These growths can vary in size and may cause a noticeable lump or nodule in the neck. Thyroid neoplasms can also affect the function of the thyroid gland, leading to hormonal imbalances and related symptoms. The exact causes of thyroid neoplasms are not fully understood, but risk factors include radiation exposure, family history, and certain genetic conditions. It is important to note that most thyroid nodules are benign, but a proper medical evaluation is necessary to determine the nature of the growth and develop an appropriate treatment plan.