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PubMed2005

U.S. EPA's IRIS assessment of 2-butoxyethanol: the relationship of noncancer to cancer effects.

U.S. EPA's integrated risk information system (IRIS) assessment of 2-butoxyethanol (EGBE) indicates that the human carcinogenic potential of EGBE cannot be determined at this time, but that "suggestive evidence" for cancer exists from laboratory animal studies (hemangiosarcoma of the liver in male mice and forestomach squamous cell papilloma or carcinoma in female mice [National Toxicology Program (NTP), 2000a. Toxicology and carcinogenesis studies of 2-butoxyethanol (CAS no. 111-76-2) in F344/N rats and B6C3F1 mice (inhalation studies). National Toxicology Program Technical Report Series No. 484. U.S. Department of Health and Human Services, National Institutes of Health, Washington, DC]). Since the last EGBE IRIS assessment, a number of studies have provided evidence that the carcinogenic effects observed in mice are nonlinear in their mode of action and may be dependent on threshold events such as EGBE-induced hemolytic effects. EPA is in the process of considering several questions relating to this issue. First, can a plausible mode of action be determined for the two types of tumors observed in mice? Second, are the mechanisms involved applicable to humans? If so, should the mode of action be considered to result in a linear or nonlinear dose-response? These questions will be addressed within the context of the agency's new cancer guidelines and with regard to how the answers might affect a revised IRIS assessment for EGBE.

Animals↗
PubMed1992

Hereditary renal cell carcinoma in the Eker rat: a rodent familial cancer syndrome.

A rodent model of hereditary cancer in which a single gene mutation predisposes rats to bilateral multicentric renal cell carcinoma (RCC) is described. This rat hereditary cancer syndrome shares certain similarities with von Hippel-Lindau disease (VHLD). In addition to the early development of renal epithelial tumors with morphologic similarity to human RCC, rats which bear the RCC gene are predisposed to the development of secondary primary cancers later in life. Splenic vascular proliferative lesions, including hemangiosarcoma, were seen in 23% of 14-month-old rats of both sexes that had renal tumors. At fourteen months of age, 62% of female rats with renal cell tumors had sarcomas of the lower reproductive tract of probable smooth muscle origin. Non-carrier siblings of affected animals did not have renal, reproductive, or splenic neoplasia. The finding of a specific constellation of familial neoplasms, including multicentric bilateral renal cell carcinoma, in this autosomal dominant disorder of rats suggests that this syndrome is analogous to human VHLD. In addition to its usefulness for studies of the biochemical and molecular mechanisms of renal carcinogenesis, this animal model will provide a unique tool to investigate how cancer susceptibility genes interact with environmental risk factors such as chemical carcinogens.

Animals↗
PubMed2003

Mechanisms of anticancer drug resistance.

Chemotherapy agents are extremely important in the treatment of liquid malignancies, such as lymphoma, myeloma, and chronic lymphocytic leukemia. In addition, chemotherapy agents have proven effective in the adjuvant treatment of solid tumors, such as osteosarcoma, hemangiosarcoma, transitional cell carcinoma, and others. Unfortunately, chemotherapy resistance in these situations is the most significant cause of treatment failure. Therefore, the ability to predict, treat, or circumvent resistance is extremely likely to improve clinical outcomes. This article has reviewed the most widely investigated forms of chemotherapy resistance, such as reduced drug accumulation, increased DNA damage repair, decreased apoptosis, and others; however, new mechanisms are being found at an alarming pace. In addition, investigations to date have routinely centered on single-cell mechanisms of drug resistance, and cancer is truly a three dimensional disease. The elucidation of mechanisms surrounding (1) how tumors interact with their normal microenvironment, (2) how tumors interact in a three-dimensional environment, and (3) a better understanding of basic tumor physiology and biology may supersede in importance those previously elucidated single-cell mechanisms of chemoresistance.

Animals↗
PubMed1997

Radiation therapy in the management of bone tumors.

Radiation therapy is used in the management of both primary and metastatic bone tumors. The most common primary bone tumor in dogs and cats is osteosarcoma of the appendicular skeleton. A number of other primary bone tumors occur at a much lower rate in both species and include chondrosarcoma, fibrosarcoma, hemangiosarcoma, multiple myeloma, and lymphoma. This article reviews the results of published reports on the utility of radiation therapy in the treatment of primary and metastatic bone tumors of companion animals.

Animals↗
PubMed2003

Carcinogenic potential of o-nitrotoluene and p-nitrotoluene.

The potential of o-nitrotoluene and p-nitrotoluene to cause cancer in mammalian species was studied in male and female F344/N rats and B6C3F1 mice. These chemicals are on the EPA list of high production chemicals and there is potential for human exposure (High Production Volume Chemical List (2000) http://oaspub.cpa.gov/opptintr/chemrtk/volchall.htm.). o-Nitrotoluene, administered in the feed for up to 2 years, caused clear evidence for cancer at multiple sites in rats and mice. Male rats, receiving o-nitrotoluene in the feed ( approximately 0, 25, 50, or 90 mg/kg per day), developed treatment-related mesotheliomas, subcutaneous skin neoplasms, mammary gland fibroadenomas, and liver neoplasms. By 2 years, mesotheliomas, skin, liver, mammary gland and liver tumors also occurred in 'stop-study' male rats that received o-nitrotoluene at 125 or 315 mg/kg per day for only the first 3 months of study. These 'stop-studies' showed that the critical events leading to tumor formation occurred after 3 months of dosing, and these events were irreversible and eventually led to cancer at multiple sites. o-Nitrotoluene given in the feed to female rats (approximately 0, 30, 60, or 100 mg/kg per day) and to male and female mice (approximately 0, 150, 320, or 700 mg/kg per day) also caused a carcinogenic response. In female rats, treatment-related subcutaneous skin neoplasms and mammary gland fibroadenomas occurred. Hemangiosarcomas and carcinomas of the large intestine (cecum) were seen in treated male and female mice. In contrast to o-nitrotoluene, p-nitrotoluene given in the feed over approximately the same exposure levels caused only equivocal evidence of carcinogenic activity in male rats (subcutaneous skin neoplasms); some evidence of carcinogenic activity in female rats (clitoral gland neoplasms); equivocal evidence of carcinogenic activity in male mice (lung neoplasms); and no evidence of carcinogenic activity in female mice. Differences in the o-nitrotoluene and p-nitrotoluene carcinogenic activity may be due to differences in the metabolism of the parent compound to carcinogenic metabolites.

Animals↗
PubMed1999

Heterozygous p53-deficient mice are not susceptible to 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) carcinogenicity.

2-Amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) is a very potent mutagen which induces tumors in the liver, lung and hematopoietic system of CDF1 mice and the liver, Zymbal gland and skin in F344 rats. The recent development of transgenic knockout mice allows their introduction for sensitive screening of environmental carcinogens due to the rapid development of tumors. P53 gene deficient mice (p53-/-) were found to spontaneously develop malignant lymphoma and hemangiosarcoma, whereas heterozygotes (p53+/-) mice display a high incidence of tumors of the urinary bladder when treated with N-butyl-N-(4-hydroxybutyl)nitrosamine. In the present study, to determine whether p53 gene knockout mice can be utilized in a short-term assay model for the screening of heterocyclic amines (HCAs), the effects of MeIQx, as a representative compound, at low doses were examined. Male and female p53+/- mice and wild type littermates (p53+/+) were continuously given diets containing 0, 0.1, 1, 10 and 100 ppm MeIQx for 1 year. No significant difference in tumor induction was observed other than an increase in liver adenomas in males receiving 10 ppm MeIQx treatment. The results indicate that p53+/- mice have no practical advantages for use in short-term carcinogenicity tests of HCAs.

Alleles↗
PubMed1998

Validation of transgenic mice harboring the human prototype c-Ha-ras gene as a bioassay model for rapid carcinogenicity testing.

Studies were conducted to validate the transgenic (Tg) mice harboring human prototype c-Ha-ras gene, namely the rasH2 mice (CB6F1), as a model for rapid carcinogenicity testing. Short-term (26 weeks) carcinogenicity testing of 18 mutagenic (Salmonella) trans-species carcinogens, two mutagenic single-species (mouse-only) carcinogens, six non-mutagenic trans-species carcinogens, one non-mutagenic single-species (mouse-only) carcinogen, four mutagenic non-carcinogens and four non-mutagenic non-carcinogens were completed. The studies revealed that the Tg mice are able to detect various types of mutagenic carcinogens and may also detect various non-mutagenic carcinogens within 26 weeks. Dose-dependent tumor responses were observed with various carcinogens except for a few equivocal cases. The validation studies also revealed that the Tg mice are generally much more susceptible to both mutagenic and non-mutagenic carcinogens than control non-Tg mice. Most of the malignant tumors were observed in the carcinogen-treated Tg mice and only very few or none in the corresponding non-Tg mice. Most of the carcinogens tested induced some of the target organ tumors observed in B6C3F1 mice in a 2-year bioassay as well as certain types of tumors specific to the Tg mice, i.e. lung alveolar epithelial tumors, spleen hemangiosarcomas, forestomach squamous cell tumors. No significant tumor induction has been observed in the Tg mice either with mutagenic or non-mutagenic non-carcinogens. Although further validation studies are still required, the rasH2 mouse seems to be a promising candidate as an animal model for the development of a rapid carcinogenicity testing system.

Animals↗
PubMed2001

Primary chest wall tumors: early and long-term results of surgical treatment.

OBJECTIVES: A retrospective study of primary chest wall tumors (PCWTs/CWTs) was conducted to review their clinical, radiological and pathological features, as well as the early and long-term results of surgical management. MATERIALS AND METHODS: From 1986 through 1996, 41 patients (18/44% male, 23/56% female, aged 15-78 years) with PCWTs were treated in our department. RESULTS: Twenty-three patients (nine male, 14 female, mean age 36 years) had a benign CWT: enchondroma, five patients; fibrous dysplasia, four patients; neurilemmoma, three patients; osteochondroma, two patients; granular cell tumor, two patients; fibroma, two patients; lipoma, two patients; fibrolipoma, one patient; eosinophilic granuloma, one patient; aneurysmal bone cyst, one patient. Eighteen patients (nine male, nine female, mean age 59 years) had a malignant CWT: plasmacytoma, five patients; chondrosarcoma, two patients; osteosarcoma, two patients; fibrosarcoma, two patients; desmoid tumor, two patients; leiomyosarcoma, one patient; malignant fibrous histiocytoma, one patient; tendon sheath sarcoma, one patient; hemangiosarcoma, one patient; neurinosarcoma, one patient. The ribs were involved in 21 patients, the sternum in five patients, and the soft tissue in 17 patients. Distinction between benign and malignant CWT was not possible using radiographic criteria alone, and diagnosis was always confirmed histologically. Surgical treatment consisted of wide resection in 29 patients (15 benign/14 malignant CWTs), with the use of synthetic mesh in five cases, and excisional or incisional biopsy in 12 patients. There was no perioperative mortality. Two patients with a benign CWT (fibroma, one patient; neurilemmoma, one patient) had a local recurrence at 13 and 26 months after resection, respectively, and underwent wide resection (recurrence rate 8.7%). Follow-up at 3-13 years revealed one non-tumor-related death in patients with benign CWT (overall mortality rate 4.3%) and no other local recurrence. The overall 5- and 10-year survival in patients with malignant CWT was 33.3%. CONCLUSIONS: We believe that all CWTs should be considered malignant until proven otherwise. Wide resection with tumor-free margins is required in order to provide the best chance for cure in both benign and malignant lesions.

Adolescent↗
PubMedDate not supplied

Masson's pseudoangiosarcoma, alias intravascular papillary endothelial hyperplasia, in dissecting aortic aneurysm caused by cystic medionecrosis.

This report describes a 25-year-old man who died due to extensive cystic medionecrosis of the aortic wall complicated by both an acute and an ancient dissection. The very unusual finding of an intravascular papillary endothelial hyperplasia, also known as Masson's pseudoangiosarcoma, in the dissected wall is reported given its resemblance to a hemangiosarcoma.

Adult↗
PubMed2001

Oncogenic transformation induced by membrane-targeted Akt2 and Akt3.

The kinases Akt2, Akt3 and their myristylated variants, Myr-Akt2 and Myr-Akt3 were expressed by the RCAS vector in chicken embryo fibroblasts (CEF). Myr-Akt2 and Myr-Akt3 were strongly oncogenic, inducing multilayered foci of transformed cells. In contrast, wild-type Akt2 and Akt3 were only poorly transforming, their efficiencies of focus formation were more than 100-fold lower; foci appeared later and showed less multilayering. Addition of the myristylation signal not only enhanced oncogenic potential but also increased kinase activities. Myr-Akt2 and Myr-Akt3 also induced hemangiosarcomas in the animal, whereas wild type Akt2 and Akt3 were not oncogenic in vivo. Furthermore, Akt2, driven by the lck (lymphocyte specific kinase) promoter in transgenic mice, induced lymphomas. The oncogenic effects of Akt2 and Akt3 described here are indistinguishable from those of Akt1. The downstream targets relevant to oncogenic transformation are therefore probably shared by the three Akt kinases.

Animals↗
PubMed2005

Therapeutic pericardiocentesis in the dog and cat.

Pericardial effusion is a potentially life-threatening problem leading to a rise in the intrapericardial pressure resulting in varying degrees of hemodynamic compromise. Cardiac tamponade occurs when the intrapericardial pressure equals or exceeds right ventricular diastolic filling pressures leading to a decreased cardiac output. In dogs, the most common causes of pericardial effusion that require pericardiocentesis are cardiac neoplasia and idiopathic pericardial effusion (IPE). The incidence of cardiac neoplasia in dogs is low, and it is rare in cats. In dogs, hemangiosarcoma and chemodectoma are the two most common types of cardiac neoplasia. In cats, lymphosarcoma is the most common form of cardiac neoplasia, but they are more likely to develop pericardial effusion secondary to congestive heart failure or feline infectious peritonitis. Common histories include lethargy, dyspnea, anorexia, collapse, and abdominal distension. Pericardiocentesis is used to stabilize animals with life-threatening cardiac tamponade, relieve the pressure leading to right-sided heart failure, and obtain fluid samples for diagnostic evaluation. The fluid should be quantified and characterized. Serious complications associated with pericardiocentesis are rare. Complications include cardiac puncture, arrhythmias, and laceration of a tumor or coronary artery resulting in intrapericardial hemorrhage or sudden death.

Animals↗
PubMed2003

Pericardiocentesis and principles of echocardiographic imaging in the patient with cardiac neoplasia.

Ultrasonography is a safe, noninvasive, sensitive, and specific tool for evaluation of the heart and pericardium in patients with cardiac neoplasia. In small animals, the incidence of cardiac neoplasia is low. In dogs, hemangiosarcoma and chemocdectoma are the two most common types of cardiac neoplasia. In cats, lymphosarcoma is the most common form of cardiac neoplasia. Pericardial effusion is a common and potentially life-threatening consequence of cardiac neoplasia. Pericardial effusion leads to a rise in the intrapericardial pressure, resulting in varying degrees of hemodynamic compromise. Cardiac tamponade occurs when the intrapericardial pressure equals or exceeds right ventricular diastolic filling pressures, leading to a decreased cardiac output. Pericardiocentesis is used to stabilize animals with life-threatening cardiac tamponade, and to obtain fluid samples for diagnostic evaluation. The fluid should be quantified and characterized. If the etiology of the effusion is not known, then a sample of the fluid should be submitted for fluid analysis and cytology. Serious complications associated with pericardiocentesis are rare. Complications include cardiac puncture, arrhythmias, and laceration of the tumor or coronary artery, resulting in intrapericardial hemorrhage.

Animals↗
PubMed2003

Transfusion issues in the cancer patient.

Blood transfusions are a lifesaving but transient therapy used to correct deficiencies of blood cells and coagulation factors that occur in cancer patients. Anemia can occur in cancer patients as a result of hemolysis, blood loss, or bone marrow failure. The blood component most commonly recommended for the treatment of anemia is packed red blood cells. Coagulation disorders are common with hemangiosarcoma and diffuse hepatic tumors. Fresh frozen plasma is used as a source for replacement coagulation factors for the treatment of disseminated intravascular coagulation or other cancer-associated coagulopathies. Although thrombocytopenia and neutropenia can be the result of bone-marrow failure from tumor infiltration, chemotherapy, or radiation therapy, these platelets and neutrophils are rarely transfused to veterinary cancer patients. Pretransufsion testing consists of blood typing in cats, and cross matching in dogs and cats if the dog has previously been transfused. Cancer patients receiving transfusions should be monitored on a continual basis during and immediately following the transfusion to enable early identification of an adverse event, allowing the transfusion to be discontinued.

Anemia↗
PubMed2003

Small-bowel tumors diagnosed by wireless capsule endoscopy: report of five cases.

Tumors of the small bowel, both benign and malignant, are relatively uncommon. As the symptoms are vague and conventional diagnostic tests are unsatisfactory, these tumors often present a clinical, radiological, and endoscopic challenge. We report here on five patients in whom small-bowel tumors were diagnosed using wireless capsule endoscopy. The indications for capsule endoscopy were: obscure gastrointestinal bleeding in four patients (one jejunal capillary hemangioma, one ileal hemangiosarcoma, and two jejunal gastrointestinal stromal tumors) and chronic abdominal pain in one patient (ileal carcinoid). Wireless capsule endoscopy, a new endoscopic method, promises to improve the diagnosis of deep small-bowel pathology.

Aged↗
PubMed2000

Phosphatidylinositol 3-kinase signaling mediates angiogenesis and expression of vascular endothelial growth factor in endothelial cells.

Phosphatidylinositol 3-kinase (PI 3-kinase) is a signaling molecule that controls numerous cellular properties and activities. The oncogene v-p3k is a homolog of the gene coding for the catalytic subunit of PI 3-kinase, p110alpha. P3k induces transformation of cells in culture, formation of hemangiosarcomas in young chickens, and myogenic differentiation in myoblasts. Here, we describe a role of PI 3-kinase in angiogenesis. Overexpression of the v-P3k protein or of cellular PI 3-kinase equipped with a myristylation signal, Myr-P3k, can induce angiogenesis in the chorioallantoic membrane (CAM) of the chicken embryo. This process is characterized by extensive sprouting of new blood vessels and enlargement of preexisting vessels. Overexpression of the myristylated form of the PI 3-kinase target Akt, Myr-Akt, also induces angiogenesis. Overexpression of the tumor suppressor PTEN or of dominant-negative constructs of PI 3-kinase inhibits angiogenesis in the yolk sac of chicken embryos, suggesting that PI 3-kinase and Akt signaling is required for normal embryonal angiogenesis. The levels of mRNA for vascular endothelial growth factor (VEGF) are elevated in cells expressing activated PI 3-kinase or Myr-Akt. VEGF mRNA levels are also increased by insulin treatment through the PI 3-kinase-dependent pathway. VEGF mRNA levels are decreased in cells treated with the PI 3-kinase inhibitor LY294002 and restored by overexpression of v-P3k or Myr-Akt. Overexpression of VEGF by the RCAS vector induces angiogenesis in chicken embryos. These results suggest that PI 3-kinase plays an important role in angiogenesis and regulates VEGF expression.

Animals↗
PubMedDate not supplied

The Tg rasH2 mouse in cancer hazard identification.

The Tg rasH2 transgenic mouse has been developed as an altemative to the lifetime mouse bioassay to predict the carcinogenic potential of chemicals. Unlike the p53+/- mouse, the Tg rasH2 mouse is sensitive to both genotoxic and nongenotoxic carcinogens. The Tg rasH2 mouse, officially designated CB6F1-TgN (RasH2), contains multiple copies of the human c-Ha-ras oncogene and promoter within its genome. These mice develop spontaneous andchemically inducedneoplasms earlierin life and in greaternumbersthan wild-type mice, reflectingtheirenhanced sensitivity to neoplasia. The most common spontaneous neoplasms in control Tg rasH2 mice 8 to 9 months of age are lung adenomas and carcinomas (7.4% incidence), splenic hemangiomas and hemangiosarcomas (5.4%), forestomach squamous cell papillomas and carcinomas (2.4%), and skin neoplasms (1.2%). Simulations have demonstrated that 20 to 25 mice/sex/treatment group are required to provide the assay with adequate statistical power. Four of 6 known or suspected human carcinogens tested in Tg rasH2 mice were positive in this assay. For 19 nonmutagenic agents testing positive in conventional rodent bioassays, 7 chemicals were positive, 10 chemicals were negative, and 2 were equivocal. None of the 10 nonmutagenic rodent carcinogens that were negative in the Tg rasH2 mouse model are considered to be human carcinogens. All nonmutagenic chemicals that were negative in the conventional rodent bioassays were also negative in the Tg rasH2 model. Results for 15 of 18 mutagenic chemicals tested in Tg rasH2 mice agreed with the results of conventional rodent bioassays, and 3 results were equivocal. The Tg rasH2 mouse model appears to predict known or suspected human carcinogens as well as the traditional mouse bioassay, but with fewer positive results for nongenotoxic compounds that are not considered human carcinogens. The Tg rasH2 mouse model is the most thoroughly tested in vivo altemative to the lifetime mouse bioassay for nongenotoxic compounds administered by oral or parenteral routes. The U.S. FDA Carcinogenicity Assessment Committee has determined that the Tg rasH2 model has been adequately evaluated for consideration for carcinogenicity testing of pharmaceutical candidates and its use could contribute to the weight of evidence for carcinogenicity assessment. The FDA will consider proposals to replace lifetime mouse carcinogenicity studies with 6-month Tg rasH2 mouse studies to support pharmaceutical registration on a case-by-case basis.

Animals↗
PubMed1988

Studies on the mechanism of the acute and carcinogenic effects of N-nitrosodimethylamine on mink liver.

Outbreaks of liver necrosis and liver hemangiosarcoma were detected in a mink breeding colony in Argentina. Analysis of the Minks' food revealed the presence of 2.6 ppm dimethylnitrosamine (NDMA) in it, apparently as a result of the addition of nitrite as preservative. Previous studies gave evidence of the particular susceptibility of minks to NDMA and other hepatic insults. We have determined several biochemical parameters known to correlate with NDMA hepatotoxic effects and compared them with those in rat liver. NDMA administration to both species resulted in the formation of reactive metabolites able to interact with liver DNA to give N7-methylguanine and O6-methylguanine adducts. Biotransformation of NDMA by liver slices to CO2 was significantly lower in the mink than in the rat, whereas the covalent binding (CB) to nucleic acids was slightly lower than in in the rat. Aminopyrine N-demethylase activity was also significantly less in mink than in rat liver. The CB of NDMA reactive metabolites to microsomal proteins was not significantly lower in mink as compared to the rat, and the same holds true for the biotransformation of NDMA to formaldehyde by microsomal preparations. Results suggest that the high susceptibility of minks to NDMA might be partially due to a decreased ability to detoxicate NDMA but also to a higher intrinsic susceptibility of their liver cells to a given chemical insult.

Animals↗
PubMed2005

Magnetic resonance imaging and characterization of spontaneous lesions in a transgenic mouse model of tuberous sclerosis as a model for endothelial cell-based transgene delivery.

Tuberous sclerosis (TSC) is an autosomal dominant genetic disorder characterized by abnormalities in cellular migration, proliferation, and differentiation in many tissues. Benign hamartomas develop in multiple organs, believed to be caused by somatic mutation in addition to germ line mutation to cause loss of both alleles of either the TSC1 or TSC2 tumor suppressor gene, with resultant dysregulated growth due to loss of hamartin or tuberin function, respectively. This study focuses on detecting spontaneous lesions in a knockout mouse model of TSC2 by magnetic resonance imaging (MRI) and exploring the efficiency of introducing gene products into lesions, using transduced endothelial cells as gene vehicles. MRI was shown to be effective in detecting spontaneous lesions in multiple tissues as a means of assessing the prevalence of tumors. Tsc(2+/) heterozygous mice were screened at 12-24 months of age. MRI detected 100% of the renal lesions (cystadenomas, renal cell carcinomas) and 75% of the hepatic lesions (hemangiosarcomas), later identified by histology. Cell-mediated gene delivery was evaluated by immunohistochemical analysis of renal, hepatic, and lung lesions after intravenous delivery of MS1 mouse endothelial cells, transduced to express an enhanced form of green fluorescent protein (EGFP). Preliminary immunohistochemical analysis, using a polyclonal antibody to EGFP and a horseradish peroxidase-diaminobenzidine detection system, revealed these cells throughout liver, kidney, and lung sections from injected animals, organs that are frequently affected in TSC2 patients, as well as within the lesions themselves.

Animals↗