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Retroperitoneal sarcomas in dogs: 14 cases (1992-2002).

OBJECTIVE: To describe the clinical features, surgical and histologic findings, biological behavior, and outcome of dogs with retroperitoneal sarcomas. DESIGN: Retrospective study. ANIMALS: 14 dogs. PROCEDURES: Medical and pathology records from 1992 to 2002 of dogs with tumors originating in the retroperitoneal space were reviewed. Dogs with retroperitoneal tumors originating from the adrenal glands, kidneys, or ureters were excluded. Inclusion criteria included observation of a tumor arising from the retroperitoneal space during exploratory surgery or necropsy and histologic confirmation of tumor type. Details of clinical signs, diagnostic findings, surgical management, and outcome were determined from medical records and telephone interviews with veterinarians and owners. RESULTS: Retroperitoneal sarcoma was diagnosed in 14 dogs, 2 at necropsy and 12 during exploratory surgery. Hemangiosarcoma was the most common histologic diagnosis. Seven dogs had regional extension of the sarcoma into adjacent organs, and 4 dogs had metastatic disease. Grossly complete resection was possible in 6 dogs. Cytoreductive surgery or incisional biopsy was performed in the remaining dogs. Two dogs were treated with palliative radiation therapy (1 intraoperatively and 1 postoperatively). Three dogs received adjunctive chemotherapy, although none completed the targeted course because of development of local recurrence or metastatic disease. Local recurrence was reported in 2 of 12 dogs and metastasis in 10 of 14 dogs. Thirteen dogs died or were euthanatized as a result of the retroperitoneal sarcoma; 1 dog was alive and disease-free 410 days after surgery. Median survival time was 37.5 days. CONCLUSIONS AND CLINICAL RELEVANCE: In dogs, retroperitoneal sarcomas are aggressive tumors with a high rate of local recurrence and metastasis, and a poor survival time.

Animals↗

Carcinomas and other lesions of the liver in mice ingesting organochlorine pesticides.

Carcinomas of the liver were readily induced in male and female mice given organochlorine pesticides orally. The carcinomas were predominantly hepatocellular, with a few being cholangiocellular, and varied from well differentiated to poorly differentiated to undifferentiated. They are capable of invading, metastasizing, and killing the mice. Hemangiosarcomas, leimyosarcomas, and reticulum cell sarcomas were also occasionally seen in mice receiving these chemicals. Hepatic vein thrombosis and hepatic necrosis was observed in some mice.

Adenoma, Bile Duct↗

Immunogenic properties of a nonproducer malignant tumor induced by murine sarcoma virus.

A cloned cell line H-11 (HP) derived from an MSV-induced neoplasm (a hemangiosarcoma) was found to possess virus-specific tumor rejection antigen(s). The specific nature of the immune response was established through the use of a polyoma virus-induced neoplasm no. 89 both in cross immunization and cross challenge experiments. Virus antigens or surface antigens associated with virus production are not responsible for tumor rejection since virus production could not be detected, nor were any viral fingerprints of MSV found by the several assays used.

Animals↗

Leukoerythroblastosis and normoblastemia in the cat.

Over a six-month period, 6% of 313 cats evaluated hematologically had either leukoerythroblastosis or normoblastemia. Diseases associated with these hematological conditions included haemobartonellosis, hepatic lipidosis, trauma, viral and bacterial infections, myeloproliferative disorders, and hemangiosarcoma. The finding of leukoerythroblastosis or normoblastemia may aid in diagnosing cats presenting with nonspecific signs.

Anemia, Myelophthisic↗

External jugular vein hemangioma occurring as a lateral neck mass.

Hemangioma is an extremely frequent tumor, accounting for 7% of all benign neoplasms. In contrast, hemangioma arising in blood vessels is rare and should be differentiated from other neoplasms of vascular origin, such as hemangioendothelioma, hemangiopericytoma, hemangiosarcoma, and leiomyosarcoma. The case we report has the peculiarity of occurring as a lateral neck mass in which color-coded duplex sonography contributed significantly to diagnosis.

Female↗

Effects of radiation on incidence of primary liver cancer among atomic bomb survivors.

We describe the radiation risk for primary liver cancers between 1958 and 1987 in a cohort of atomic bomb survivors in Hiroshima and Nagasaki, Japan. The analysis is based on a comprehensive pathology review of known or suspected liver neoplasms that generated 518 incident, first primary cases, mostly hepatocellular carcinoma. Excess relative risk from atomic bomb radiation was linear: 0.81 per sievert weighted liver dose (95% CI [0.32, 1.43]; P < 0.001). Males and females had similar relative risk so that, given a threefold higher background incidence in males, the radiation-related excess incidence was substantially higher in males. Excess risk peaked for those with age at exposure in the early 20s; there was essentially no excess risk in those exposed before age 10 or after age 45. Whether this was due to a difference in sensitivity or possible confounding by other factors could not be addressed retrospectively in the full cohort. A paucity of cholangiocarcinoma and hemangiosarcoma cases suggested that they are not significantly associated with whole-body radiation exposure, as they are with the internal alpha-particle-emitting radiological contrast medium Thorotrast. Because most of the radiation-related excess cases occurred among males, it is important to ascertain what factors put men at greater risk of radiation-related liver cancer.

Cohort Studies↗

Inhalation chemotherapy for macroscopic primary or metastatic lung tumors: proof of principle using dogs with spontaneously occurring tumors as a model.

This study represents part of an effort to determine the safety and efficacy of inhaled antineoplastic drugs, using pet dogs with spontaneously arising primary and metastatic lung cancers (including sarcoma, carcinoma, and malignant melanoma) as a model. Dogs received new formulations of either paclitaxel (PTX) or doxorubicin (DOX) by the inhalation route every 2 weeks using a specially designed aerosol device. Response was assessed radiographically using the indices of tumor nodule number and volume measurement of discrete pulmonary nodules. Dogs experiencing progressive disease after two consecutive treatments were crossed over to receive the alternate compound. In 24 dogs, 6 (25%) responses were noted including 5 partial responses (PR) and 1 complete response. These include 4 (22.2%) of 18 responses to DOX and 2 (13.3%) of 15 responses to PTX. Responses were noted with osteosarcoma (including three dogs with metastatic osteosarcoma that had failed prior systemic chemotherapy), liposarcoma, hemangiosarcoma, and undifferentiated sarcoma. One dog with mammary carcinoma experienced a 47% reduction in volume after PTX inhalation, just shy of PR criteria. One dog with liposarcoma is experiencing a long-term (>12 months) stabilization of disease on PTX. To date, no systemic toxicities have been observed with either PTX or DOX inhalations. Local (pulmonary) toxicity was not observed with PTX; however, changes consistent with pneumonitis/fibrosis were observed in some dogs receiving DOX. Only one of these dogs showed clinical signs, which were responsive to steroid and antitussive therapy. These data represent "proof of principle" for the avoidance of systemic toxicity while delivering efficacious local drug levels by the inhalation route.

Administration, Inhalation↗

Noncirrhotic presinusoidal portal hypertension associated with chronic arsenical intoxication.

A 39-year-old male with bleeding esophageal varices due to portal hypertension was observed. The patient had taken an arsenical preparation during a period of 12 yr because of psoriasis and subsequently developed keratotic changes of the palms and soles of his feet and an epithelioma of the scrotum. Physical examination was unremarkable except for splenomegaly and skin lesions. Liver function tests were normal; a needle biopsy of the liver (right lobe) showed nonspecific changes. Combined hepatic and umbilicoportal catheterization revealed, on splenography and portography, huge esophageal varices and patent portal vein; dilation, distortion, and cut-off of many intrahepatic portal branches were found. A marked gradient existed between the free portal venous pressure (25 mm Hg) and the wedged hepatic venous pressure (9.5 mm Hg). Hepatic blood flow, portal PO2, cardiac output, cardiac index, and blOOD volume were within normal range. Arteriographies did not reveal arteriovenous shunts in the splanchnic or splenic vessels. A splenorenal shunt were performed and a wedged biopsy of the liver (left lobe) revealed nonspecific changes. Three years later the patient had not experienced any episode of hemorrhage or hepatic encephalopathy but developed an epithelioma of the tongue. No known cause could be incriminated in the pathogenesis of the portal hypertension. However, there was unequivocal chronic arsenic intoxication. Toxic hepatitis, cirrhosis, noncirrhotic portal hypertension, and hemangiosarcoma of the liver have been reported with the intake of arsenicals. Thus, it is suggested that in this patient, presinusoidal portal hypertension was secondary to chronic arsenical intake associated with marked intrahepatic vascular changes seen on portography.

Adult↗

[Littoral hemangioma of the spleen].

The authors report a rare case of littoral hemangioma of the spleen (LHS) accompanied by a revision of the literature on the argument. A male 65-year-old patient was referred to their attention with suspected ultrasonographic diagnosis of lymphoma with a splenic localisation. The complete CT diagnosis led to suspected splenic angioma. During surgery, anatomopathological analysis of the biopsy revealed LHS. The pathological anatomy showed lesions ranging in size from small foci to large nodules which almost completely replaced the splenic parenchyma. These areas were made up of vascular canals or axes that imitate splenic sinuses and have irregular lumen, often appearing as papillary projections and cyst-like spaces; they are bordered by high (cylindrical) endothelial cells that project into the vascular lumen and reveal hemophagocytosis; there is very little mitotic activity. The patient was discharged 7 days after surgery. The authors underline the extreme rarity of this neoplasm and the virtual absence of symptoms, although some cases report signs of hypersplenism, including platelet deficiency and anemia. The diagnostic iter must take care to exclude other pathologies affecting the spleen, including lymphoma, metastases and primary malignant splenic tumours. Lastly, a differential diagnosis must be made with the malignant variant, littoral hemangiosarcoma of the spleen.

Aged↗

Impact of ionizing radiation and genetic background on mammary tumorigenesis in p53-deficient mice.

Loss of p53 function is known to compromise cell cycle regulation, inductionof apoptosis, and DNA damage repair and can facilitate neoplastic transformation of cells. Mutations in the p53 gene are identified frequently in breast carcinomas. Li-Fraumeni patients inheriting a mutant p53 allele have an increased risk for developing tumors including breast cancer. Although mouse lines carrying mutations in the p53 gene have been generated, they die primarily of lymphoma and thus to date provide a limited model for the study of this disease and the role of p53 in nonfamilial breast cancer. An increasing body of literature suggests that the incidence of various tumors is determined largely by the genetic background on which mutations are studied. In addition, population studies and studies in animals suggest that environmental factors, together with genetic factors, determine overall risk for development of specific types of tumors. We therefore examined the impact of genetic background together with exposure to ionizing radiation on the development of tumors, particularly mammary tumors, in p53-deficient animals. We report here that modifier alleles present in the BALB/c strain increase the incidence of hemangiosarcomas [15 of 53 (28.3%); P = 0.0007] in p53(-/-) mice above rates reported previously in p53(-/-) mice on a mixed background as compared to the incidence observed in DBA/p53(-/-) mice. However, no increase in the frequency of mammary tumors is seen in these mice or in p53(-/-) DBA/2 animals, nor was an increase in mammary tumors observed in the DBA/2 p53(+/-) mice, even after exposure to 5 Gy of whole-body ionizing radiation. In contrast, a significant increase in the incidence of mammary tumors was observed in similarly treated BALB/c p53(+/-) mice (37.3% versus 6.8%; P = 0.0007). This was accompanied by a comparable decrease in the incidence of lymphomas. These results show that environmental agents together with genetic factors can increase the frequency and decrease the latency of mammary tumors, leading to an incidence similar to that observed in Li-Fraumeni syndrome. Furthermore, it suggests that the risk of development of a particular type of tumor by individuals deficient in p53 after exposure to damaging agents can be influenced by modifier alleles.

Alleles↗

[Intravascular papillary endothelial hyperplasia: multiple lesions appearing in the course of treatment with interferon beta].

INTRODUCTION: Intravascular papillary endothelial hyperplasia is a benign and rare vascular lesion. We report a case of multiple vascular lesions of the hand following 3 months treatment with beta-interferon injections for multiple sclerosis. OBSERVATION: A 50 year-old man had multiple vascular nodules of the hands. He was treated with beta interferon injections for multiple sclerosis for 3 months. Histology showed typical changes of intravascular papillary endothelial hyperplasia: papillary endothelial proliferation in a dilated cavity associated with thrombosis. DISCUSSION: Intravascular papillary endothelial hyperplasia is a benign and rare vascular lesion usually presenting as a simple nodule. It may be painful. Diagnosis is histologic, characterized by papillary endothelial proliferation associated with a thrombus within a vessel. It may be confused with hemangiosarcoma. Treatment is surgical and recurrence after treatment is rare. Intravascular papillary endothelial hyperplasia is generally considered as an unusual form of thrombus organization. Intravascular papillary endothelial hyperplasia is divided into two groups: a pure form occurring within a dilated vessel and a mixed form appearing in benign vascular lesions. The originality of this case is the rarity and the multiplicity of the lesions. The possible pathogenesis of interferon-induced cutaneous vascular lesions is discussed.

Cell Division↗

Loss of Bax alters tumor spectrum and tumor numbers in ARF-deficient mice.

p19(ARF) is a key regulator of the p53-mediated apoptotic and tumor suppressor pathway. The proapoptotic Bax gene is a transcription target of p53, yet genetic studies in some animal models have suggested that Bax and p53 loss may cooperate in tumorigenesis. ARF-deficient mice are tumor prone, and to determine whether Bax loss could cooperate in the development of these tumors, we generated mice null for both ARF and Bax. The tumor latency of Bax+/+ARF-/-, Bax+/-ARF-/- and Bax-/-ARF-/- mice was similar with a mean survival of 48.9, 48.1, and 47.6 weeks, respectively. In Bax+/+ARF-/- mice, the predominant tumor type was B- and T-cell lymphoma followed by sarcomas and a lack of carcinomas. However, the frequency of lymphoma development dramatically decreased, whereas that of sarcomas and carcinomas increased, in a gene dosage-dependent manner in Bax+/-ARF-/- and Bax-/-ARF-/- mice. Furthermore, uncommon tumors of ARF-/- mice (osteosarcoma and hemangiosarcoma) were observed in Bax/ARF-double null mice, and tumor types not described previously in ARF-null mice (mixed germ cell tumor, Triton tumor, and histiocytic sarcoma) also developed in Bax-/-ARF-/- animals. Importantly, multiple primary malignant tumors of different lineage arose in 25% of the Bax-/-ARF-/- mice, whereas only one tumor type per animal was observed in Bax+/+ARF-null littermates. Finally, the wild-type Bax allele was retained in tumors arising in Bax+/-ARF-/- mice. Thus, Bax appears to function as a tumor modifier rather than as a classic tumor suppressor, and the combined loss of Bax and the ARF allows for the emergence of multiple malignant tumor types, an alteration of the tumor spectrum, and tumors not observed previously in ARF-null mice.

Animals↗

The multiple tumor syndrome. Personal experience.

The multiple tumor syndrome is an unusual pathologic condition, which consists in association of multiple malignancies in the same patient. Seven cases are discussed: two women, five men, aged 32-70 years. The period between the two neoplasias was 2-23 years (in 6 cases). In one case the two malignancies appeared concomitantly. The hematological malignancies were: multiple myeloma: 2 cases; chronic granulocytic leukemia: 2 cases; chronic lymphatic leukemia: 3 cases. In four cases, the solid tumor followed the hematological malignancy at variable periods (2 and 4 years). In other two cases, the solid tumors preceded the hematological malignancy with 2 years, 23 years respectively. The solid tumors were genital cancers, malignant melanoma, spino-cellular carcinoma, thyroid cancer, hemangiosarcoma. In a single case the second tumor was a hematological malignancy too (NHL-diffuse lymphocytic lymphoma). Possible implications of previous therapy and environmental factors are discussed.

Adult↗

NTP Toxicology and Carcinogenesis Studies of 2-Amino-4-Nitrophenol (CAS No. 99-57-0) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

2-Amino-4-nitrophenol is used to color semipermanent hair dyes and in the manufacture of mordant dyes for leather, nylon, silk, wool, and fur. 2-Amino-4-nitrophenol was nominated by the National Cancer Institute for toxicology and carcinogenesis studies because of widespread human exposure associated with its manufacture and use. Toxicology and carcinogenesis studies were conducted by administering 2-amino-4-nitrophenol (98% pure) in corn oil by gavage, 5 days per week, to groups of F344/N rats and B6C3F1 mice of each sex in 15-day, 13-week, and 2-year studies. Fifteen-Day and Thirteen-Week Studies: During the 15-day studies, rats and mice received doses of 0, 313, 625, 1,250, 2,500, or 5,000 mg/kg. All rats that received 2,500 or 5,000 mg/kg and all female rats that received 1,250 mg/kg died before the end of the studies. Final mean body weights of chemically exposed rats surviving to the end of the studies were comparable to those of vehicle controls. Diarrhea was observed in all groups of exposed rats except those receiving 313 mg/kg. All mice that received 2,500 or 5,000 mg/kg, 2/5 males and all females that received 1,250 mg/kg, and 1/5 females that received 313 mg/kg died before the end of the studies. Final mean body weights of exposed mice surviving until the end of the studies were comparable to those of vehicle controls. In 13-week studies, F344/N rats and B6C3F1 mice of each sex received 2-amino-4-nitrophenol at doses of 0, 62.5, 125, 250, 500, or 1,000 mg/kg. All rats that received 1,000 mg/kg and 2/10 males and 2/10 females that received 500 mg/kg died before the end of the studies. The final mean body weight of male rats that received 500 mg/kg was reduced 10% compared with that of vehicle controls; final mean body weights of all other surviving exposed rat groups were comparable to those of vehicle controls. Diarrhea and lethargy were observed for rats that received 500 or 1,000 mg/kg. All male mice and most females that received 1,000 mg/kg and 4/10 females that received 500 mg/kg died before the end of the studies. Final mean body weights of chemically exposed mice were comparable to those of vehicle controls. No compound-related clinical signs were observed in mice during the studies. Mineralization of the renal cortex and degeneration of the renal tubular epithelium were observed in male and female rats that received 1,000 mg/kg and in males that received 500 mg/kg. Degeneration and necrosis of the renal tubular epithelium was observed in 5/10 male and 3/10 female mice that received 1,000 mg/kg. Body Weight and Survival in the Two-Year Studies: In the 2-year studies, rats and mice received 2-amino- 4- nitrophenol at doses of 0, 125, or 250 mg/kg. Mean body weights of male rats that received 250 mg/kg were 8%-10% lower than those of vehicle controls throughout most of the 2-year study. Mean body weights of female rats were comparable to those of vehicle controls. Soft stools and occasional diarrhea were observed in chemically exposed rats starting 6 months after the beginning of the studies. Survival of male rats that received 250 mg/kg was markedly lower than that of vehicle controls after week 89 (final survival: vehicle control, 32/50; 125 mg/kg group, 24/50; 250 mg/kg group, 10/50). Survival of female rats was comparable among all groups (final survival: 25/50; 27/50; 31/50). Mean body weights of male and female mice that received 250 mg/kg were comparable to those of vehicle controls; the mean body weights of female mice that received 125 mg/kg were as much as 17% greater than that of vehicle controls. Survival of all mouse groups was comparable during the 2-year studies (final survival: male-- 28/50; 29/50; 23/50; female--28/50; 31/50; 30/50). Nonneoplastic and Neoplastic Effects in the Two-Year Studies: Pigmentation of the small and large intestines was present in exposed rats but not in vehicle controls. Ulcers and erosive lesions of the digestive tract were observed in male rats that received 250 mg/kg and to a lesser extent in male rats that received 125 mg/kg. A carcinoma of the colon occurrkg. A carcinoma of the colon occurred in one male rat that received 250 mg/kg; no other neoplasms were observed in the gastrointestinal tract of rats. No pigmentation, ulcers, or erosive lesions were found in the digestive tract of mice. The severity of nephropathy was markedly greater in exposed male rats than in vehicle controls. Associated with the nephropathy were nonneoplastic lesions indicative of reduced renal function and secondary hyperparathyroidism, including parathyroid hyperplasia, mineralization of various organs, and fibrous osteodystrophy. Renal tubular cell hyperplasia (1/50; 4/48; 5/50) and renal cortical (tubular cell) adenomas (0/50; 1/48; 3/50) occurred in male rats. Renal cortical adenomas are infrequently observed in male F344/N rats (historical incidence, 0.5&percnt;). More preputial gland adenomas or carcinomas (combined) were observed in low dose male rats than in vehicle controls (3/50; 10/48; 3/50), whereas the incidences of clitoral gland neoplasms were decreased in dosed female rats (9/50; 6/50; 1/49). Hemangiomas or hemangiosarcomas (combined) occurred in male mice that received 2-amino-4-nitrophenol (0/50; 1/50; 5/50); each tumor was present at a different site. The historical control incidence is 11&percnt; at the study laboratory and 6&percnt; in 2-year NTP studies. Genetic Toxicology: 2-Amino-4-nitrophenol was mutagenic in Salmonella typhimurium strains TA98 and TA100 with metabolic activation. 2-Amino-4-nitrophenol was not mutagenic in strains TA1535 or TA1537. 2-Amino-4-nitrophenol was mutagenic in the mouse lymphoma L5178Y/TK&plusmn; assay without metabolic activation. It was not tested with activation. 2-Amino-4-nitrophenol induced sister chromatid exchanges (SCEs) and chromosomal aberrations in Chinese hamster ovary cells in the presence and absence of metabolic activation. Audit: The data, documents, and pathology materials from the 2-year studies of 2-amino-4-nitrophenol were audited at the NTP Archives. The audit findings show that the conduct of the studies is documented adequately and support the data and results given in this Technical Report. Conclusions: Under the conditions of these 2-year gavage studies, there was some evidence of carcinogenic activity of 2-amino-4-nitrophenol for male F344/N rats, as shown by increased incidences of renal cortical (tubular cell) adenomas. The incidences of renal tubular cell hyperplasia were also increased in male rats exposed to 2-amino-4-nitrophenol. The survival of male rats that received 2-amino-4-nitrophenol was reduced compared with survival of vehicle control male rats. There was no evidence of carcinogenic activity of 2-amino-4-nitrophenol for female F344/N rats or for male or female B6C3F1 mice that received 125 or 250 mg/kg per day.

Journal Article↗

NTP Toxicology and Carcinogenesis Studies of Tris(2-ethylhexyl)phosphate (CAS No. 78-42-2) In F344/N Rats and B6C3F1 Mice (Gavage Studies).

Tris(2-ethylhexyl)phosphate is one of a family of triakyl phosphates that have been widely used as fire retardants and plasticizers. Another triakyl phosphate, tris(2,3-dibromopropyl)phosphate (Tris-BP), once used as a flame retardant in children's sleepwear, has been shown to be carcinogenic, but tris(2-ethylhexyl)phosphate has not been previously studied. Tris(2-ethylhexyl)phosphate, a clear, viscous liquid, is used as a component of vinyl stabilizers, grease additives, and flame-proofing compositions; however, it is used primarily as a plasticizer for vinyl plastic and synthetic rubber compounds. In 1974, approximately 3 million pounds of tris(2-ethylhexyl)phosphate was produced in the United States; imports during that year were negligible. Substantial human exposure probably occurs during production of tris(2-ethylhexyl)phosphate and during the manufacture and use of products containing it, but data on the magnitude of exposure are not available. Two-year toxicology and carcinogenesis studies of tris(2-ethylhexyl)phosphate were conducted by administering the test chemical in corn oil by gavage, 5 days per week for 103 weeks, to groups of 50 male and 50 female F344/N rats and B6C3F1 mice. Male rats received doses of 2,000 or 4,000 mg/kg body weight, female rats received 1,000 or 2,000 mg/kg, and male and female mice received 500 or 1,000 mg/kg. Fifty vehicle control animals of each sex and species received 10 ml/kg body weight (rats) or 3.3 ml/kg (mice) corn oil by gavage on the same schedule. Inflammation of the gastric mucosa in mice and mild weight depression in rats and mice were the only dose-related effects observed in the preliminary studies. In the 2-year studies, survival rates and mean body weight gains of dosed female rats and dosed mice were comparable to those of their perspective controls. Survival rates of dosed male rats were comparable to that of the vehicle controls, but body weight gains were depressed. One nonneoplastic lesion, follicular cell hyperplasia of the thyroid, was observed at increased incidences in dosed male and female mice. Two compound-related increased incidences of neoplasms could not be discounted. In male rats, the incidence of pheochromocytoma of adrenal glands increased with dose (2/50, 4%; 9/50, 18%; 12/50, 24%). There were also two additional malignant pheochromocytomas in the high dose group. However, the incidence of adrenal pheochromocytoma in vehicle controls of this study (2/50, 4%) was low compared with the 25% incidence observed in two previous studies in this laboratory or the overall historical incidence of 18% observed throughout the Program, and thus the evidence of carcinogenicity was considered to be equivocal. In female mice, the incidence of hepatocellular carcinoma (0/48; 4/50; 7/50) in high dose animals (1,000 mg/kg) was significantly increased relative to that of the vehicle controls. Decreased incidences were observed for acinar cell adenomas of the pancreas in dosed male rats (14/50, 28%; 5/48, 10%; 2/49, 4%) and for fibroadenomas of the mammary glands in low dose female rats (11/50, 22%; 2/50, 4%; 7/50, 14%). Hemangiosarcomas of the circulatory system in male mice (7/50, 14%; 0/50; 1/49, 2%) and lymphomas of the hematopoietic system in female mice (14/49, 29%; 10/50, 20%; 6/50, 12%) were decreased compared with vehicle controls. A decrease in the incidence of lymphomas and an increased incidence of carcinomas of the liver in female mice (both seen in this study) were observed in studies of di(2-ethylhexyl)adipate. Increased incidences of liver carcinomas and decreased incidences of mammary fibroadenomas were observed also in female rats in the di(2-ethylhexyl)phthalate studies. A possible link among these three chemicals may be metabolic conversion to 2-ethylhexanol. Tris(2-ethylhexyl)phosphate was not mutagenic in Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537 in the presence or absence of 9000 x g (S9) fractions from Aroclor 1254-induced Sprague-Dawley rat or Syrian hamster liver. An audit of the experimental data from these carcinogeneoclor 1254-induced Sprague-Dawley rat or Syrian hamster liver. An audit of the experimental data from these carcinogenesis studies was conducted by the National Toxicology Program. No data discrepancies were found that significantly influenced the final interpretations of these experiments. Under the conditions of these studies, a comparison of concurrent and historical controls indicated that there was equivocal evidence of carcinogenicity in male F344/N rats receiving 2,000 and 4,000 mg/kg tris(2-ethylhexyl)phosphate, as evidenced by increased incidences of pheochromocytomas of the adrenal glands. There was no evidence of carcinogenicity in female F344/N rats or in male B6C3F1 mice receiving tris(2-ethylhexyl)phosphate. There was some evidence of carcinogenicity in female B6C3F1 mice that received 1,000 mg/kg tris(2-ethylhexyl)phosphate, as shown by an increased incidence of hepatocellular carcinoma. Tris(2-ethylhexyl)phosphate was associated with increased incidences of follicular cell hyperplasia of the thyroid gland in male and female B6C3F1 mice. Synonyms and Trade Names: TOF; trioctyl phosphate; phosphoric acid tri(2-ethylhexyl) ester; Flexolreg. TOF; Kronitexreg.

Journal Article↗

NTP Toxicology and Carcinogenesis Studies of Propylene (CAS No. 115-07-1) in F344/N Rats and B6C3F1 Mice (Inhalation Studies).

Propylene is used as a starting material in the production of polypropylene plastics and various other chemicals, including acrylonitrile, isopropyl alcohol, propylene oxide, butyraldehyde, cumene, dodecane, nonene, and allyl chloride. The major derivatives are polypropylene (25%), acrylonitrile (15%), isopropyl alcohol (10%), and propylene oxide (10%). It is also a valuable feed-stock chemical for the production of gasoline. Other miscellaneous applications include use as a starting material for polymerization reactions to form vinyl chloride copolymers and low-molecular-weight homopolymers that are used as additives in lubricating oils and in the manufacture of hydroquinone. The chemical is also used as an aerosol propellant or component. The major end uses of propylene are in the production of fabricated plastics (50%) and fibers (15%). Toxicology and carcinogenesis studies of propylene (greater than 99% pure) were conducted by exposing groups of 50 F344/N rats and 49 or 50 B6C3F1 mice of each sex to propylene in air by inhalation at concentrations of 5,000 or 10,000 ppm, 6 hours per day, 5 days per week, for 103 weeks. Other groups of 50 rats and 50 mice of each sex in chambers received air only on the same schedule and served as chamber controls. The highest concentration of propylene that was considered safe for these studies was 10,000 ppm because of the risk of explosion that can occur at higher concentrations. The survival of exposed and control rats and mice was comparable. Throughout most of the studies, mean body weights of exposed male and female rats were slightly lower (0%-5%) than those of the controls, but the decrements were not concentration related. After week 59 of the study, mean body weights of 10,000-ppm male mice were usually slightly lower (5%) than those of the controls, whereas those in other exposed groups of male and female mice were generally comparable with those of the controls. No compound-related adverse clinical signs were observed in either species. An increased incidence of squamous metaplasia of the nasal cavity was observed in female rats exposed at the 5,000-ppm and 10,000-ppm concentrations (control, 0/49; low, 15/50; high, 6/50) and in male rats exposed at 5,000 ppm (2/50; 19/50; 7/50). Epithelial hyperplasia of the nasal cavity was increased in female rats exposed at the 10,000-ppm concentration (0/49; 4/50; 9/50); the incidences in male rats were 2/50, 2/50, and 5/50. Inflammation of the nasal cavity, characterized by an influx of lymphocytes, macrophages, and granulocytes into the submucosa and by granulocytes into the lumen, occurred at increased incidences in low concentration and high concentration male rats and in high concentration female rats. Chronic focal inflammation of the kidneys occurred at an increased incidence in low concentration and high concentration mice of each sex. Hemangiosarcomas were found in one low dose male mouse (liver), two high dose male mice (spleen), and three high dose female mice (subcutis, spleen, and uterus). Hemangiomas were found in one low dose and in one high dose female mouse (liver). Vascular tumors were not found in control mice of either sex. The low incidences of vascular tumors and their occurrence in a variety of organs suggest that they are not related to administration of propylene. The occurrence of uterine endometrial stromal polyps in female mice showed a positive trend (P<0.05; 0/47; 0/47; 3/48); the incidence in the 10,000-ppm group was not significantly greater than that in the concurrent control group, but the incidence was higher than the mean historical control rate (22/2,411, 0.9%) and was within the range (0%-6%) observed in studies throughout the Carcinogenesis Program. The occurrence of endometrial stromal polyps in three high concentration female mice was not considered to be clearly related to exposure to propylene. The incidence of male mice with alveolar/bronchiolar adenomas or carcinomas (combined) occurred with a negative trend (P<0.05; 16/50; 4/49; 7/50), and the reduced incidences in both exposed groups wegative trend (P<0.05; 16/50; 4/49; 7/50), and the reduced incidences in both exposed groups were less (P<0.05) than that in the control group. The control incidence of these tumors in an inhalation study conducted concurrently at the same laboratory was similar (15/50), suggesting a possible exposure-related decrease. The biologic significance of this decrease in male mice is difficult to assess; the incidences seen in these control and exposed animals are within the range of incidences (2&percnt;-34&percnt;; mean, 16.7&percnt;) observed in control male mice in other studies throughout the Carcinogenesis Program. An audit of the experimental data was conducted for these carcinogenesis studies on propylene. No data discrepancies were found that influenced the final interpretations. Under the conditions of these studies, there was no evidence of carcinogenicity in male and female F344/N rats or in male and female B6C3F1 mice exposed to propylene by inhalation at concentrations of 5,000 or 10,000 ppm for 103 weeks. In the nasal cavity, propylene induced squamous metaplasia of the respiratory epithelium in male and female rats and epithelial hyperplasia in female rats. Synonyms: propene; methylethylene; methylethene

Journal Article↗

NTP Toxicology and Carcinogenesis Studies of 3-Chloro-2-methylpropene (Technical grade containing 5% dimethylvinyl chloride) (CAS No. 563-47-3) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

Toxicology and carcinogenesis studies of technical-grade 3-chloro-2-methylpropene (containing 5% dimethylvinyl chloride), a widely used insecticide and a chemical intermediate, were performed on F344/N rats and B6C3F1 mice. In the 13-week studies, 50%-100% mortality occurred in groups of male and female rats receiving 400 mg/kg, male rats receiving 300 mg/kg, and male and female mice receiving 500-1,250 mg/kg. Inflammation and necrosis of the liver were seen in rats and mice, and necrosis of cortical tubules of the kidney was seen in mice. Based on these observations, groups of 50 male and 50 female rats were administered 3-chloro-2-methylpropene in corn oil by gavage at doses of 0, 75, or 150 mg/kg body weight, 5 days per week for 103 weeks, and groups of 50 male and 50 female mice received 3-chloro-2-methylpropene at 0, 100, or 200 mg/kg on the same schedule. In the 2-year studies, the mean body weight of high dose male rats was consistently 10%-15% lower than that of the vehicle control group, and late in the study there was a marginal reduction in survival of high dose male rats. Mean body weights and survival in low dose male rats and in both dosed groups of female rats were comparable to those of their vehicle control groups. Mean body weights of high dose male mice and of both dosed groups of female mice were slightly (5%-9%) lower than those of the vehicle controls, whereas survival in both male and female mice was not affected by 3-chloro-2-methylpropene administration. Dose-related increases in the incidence of forestomach inflammation were observed in male and female mice (male: vehicle control, 0/49; low dose, 9/49; high dose, 7/49; female: vehicle control, 2/50; low dose, 3/48; high dose, 9/44). Increased incidences of forestomach basal cell hyperplasia were observed in rats and mice of each sex. 3-Chloro-2-methylpropene induced forestomach squamous cell papillomas and squamous cell carcinomas in rats and mice as shown in the table. Invasion or metastasis of the squamous cell carcinomas to other organs was observed in two low dose male, three high dose male, and one high dose female mice. Renal tubular cell adenocarcinomas (1/49), renal transitional cell carcinomas (1/49), and transitional cell papillomas (1/49) of the urinary bladder were observed in high dose male rats, and renal tubular cell adenomas (1/50) and renal tubular cell adenocarcinomas (1/50) were seen in low dose male rats. These urinary tract neoplasms were not observed in vehicle controls. The incidences of inflammation of the nasal cavity and of nephropathy/nephrosis were greater in the two dosed groups than in the vehicle control groups of rats and mice of each sex. Negative trends or lower incidences of pheochromocytomas of the adrenal gland and C-cell adenomas or carcinomas (combined) of the thyroid gland were observed in dosed male rats. Negative trends were observed in the incidences of hepatocellular adenomas or carcinomas (combined) in dosed male mice and of hemangiomas or hemangiosarcomas (combined) in dosed female mice. 3-Chloro-2-methylpropene was weakly mutagenic in Salmonella typhimurium strain TA1537 with 10% rat liver S9; results in strain TA100 with 10% Syrian hamster liver S9 or with 10% or 30% rat liver S9 were judged equivocal. Mutagenicity tests with S. typhimurium strains TA1535 and TA98 were negative with or without metabolic activation. 3-Chloro-2-methylpropene was mutagenic in the mouse lymphoma L5178/TK+/- forward mutation assay without exogenous metabolic activation. Cytogenetics tests with cultured Chinese hamster ovary cells were positive for induction of chromosomal aberrations and sister-chromatid exchanges (SCE's) in the absence of rat liver S9. With metabolic activation, SCE levels remained significantly elevated, but the number of chromosomal aberrations was reduced. An audit of the experimental data was conducted for these 2-year carcinogenesis studies on 3-chloro-2-methylpropene. No data discrepancies were found that influenced the final interpretations. Under the conditions of these 2-year gavage studies, d the final interpretations. Under the conditions of these 2-year gavage studies, there was clear evidence of carcinogenicity for 3-chloro-2-methylpropene as shown by the increased incidences of squamous cell neoplasms in the forestomach of male and female F344/N rats and of male and female B6C3F1 mice. Synonyms: 2-methallyl chloride; methyl allyl chloride; b-methallyl chloride; pi-chloroisobutylene; isobutenyl chloride; 3-chloro-2-methyl-1-propene; 2-methyl-2-propenyl chloride

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NTP Toxicology and Carcinogenesis Studies of n-Butyl Chloride (CAS No. 109-69-3) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

Toxicology and carcinogenesis studies of n-butyl chloride (greater than 99.5% pure), a solvent as well as an alkylating agent, were conducted by exposing groups of F344/N rats and B6C3F1 mice to n-butyl chloride in corn oil by gavage for 14 days, 13 weeks, and 2 years. In the 14-day studies, no compound-related gross pathologic effects were observed in groups of five male or female rats or mice administered doses of up to 3,000 mg/kg body weight. However, deaths occurred in the groups administered 750, 1,500, or 3,000 mg/kg. Tremors and convulsions following gavage administration were observed. In the 13-week studies, groups of 10 male and 10 female rats were administered up to 500 mg/kg n-butyl chloride, and similar groups of mice received up to 1,000 mg/kg, Three of 10 male rats in the 500 mg/kg dose group and one female mouse in the 120 mg/kg dose group died before the end of the studies. Mild to moderate extramedullary hematopoiesis was observed in 3/10 male rats receiving 500 mg/kg. Mean body weights of male and female rats receiving 250 or 500 mg/kg were lower than those of the vehicle controls. Convulsions were observed in male and female rats receiving 250 mg/kg or higher and in 2/10 female mice receiving 1,000 mg/kg. Based on these results, 2-year toxicology and carcinogenesis studies of n-butyl chloride were conducted by administering doses of 0, 60, or 120 mg/kg in corn oil by gavage to groups of 50 male and 50 female rats and doses of 0, 500, or 1,000 mg/kg to groups of 50 male and 50 female mice. In the 2-year studies, survival relative to that of vehicle controls was significantly lower in high dose male rats (40/50 vs 17/50) and high dose female rats (35/50 vs 11/50) and in male mice receiving 1,000 mg/kg (33/50 vs 10/50). Due to excessive mortality in the 1,000 mg/kg female mice, the group was terminated in the 45th week and a second series of 2-year studies in mice of each sex was started at concentrations of 0 and 250 mg/kg. Male mice in the 1,000 mg/kg group had 10% lower mean body weights than the vehicle control group. No adverse effects on survival or body weights in other dosed groups of rats and mice were observed. Convulsions were observed before or after gavage administration on several occasions during the rat studies. These observations were noted primarily in the high dose groups (male: vehicle control, 1/50; low dose, 3/50; high dose, 27/50; female: vehicle control, 0/50; low dose, 7/50; high dose, 45/50). Hemorrhage of the brain and alveoli were observed primarily in high dose male and female rats dying from convulsions. Lymphoid depletion of the spleen and splenic hemosiderosis were also observed inthese animals. In mice, convulsions were observed only in the first studies (in the high dose female mice that were terminated early and in 6/50 high dose male mice). Pheochromocytomas of the adrenal gland occurred at marginally increased incidence in low dose female rats (1/50; 6/50; 1/49). Hyperplasia was observed in 3/50 vehicle controls, 7/50 low dose females, and 4/49 high dose females. The incidence of pheochromocytomas was low, not dose related, and not seen in males, and thus it was not considered to be compound related. Cytoplasmic vacuolization of the adrenal cortex occurred at increased incidences in males (5/50; 10/50; 20/50) but not in female rats. Nephropathy of the kidney occurred at increased incidences in female rats (13/50; 25/50; 20/50) but not in male rats. Additional nonneoplastic lesions such as congestion, inflammation, or nephrosis were not present to any degree in either vehicle control or dosed female rats. An increased incidence of alveolar/bronchiolar adenomas or carcinomas (combined) was observed in the 500 mg/kg group of female mice (3/50 vs 9/50), but little effect was seen in the 250 mg/kg group (6/50 vs 8/50). The incidences of adenomas or carcinomas (combined) in dosed female mice were not significantly different from that in the pooled vehicle control group from the first and second studies (pooled controls, 9/100; 250 mg/kg, 8/50; 500 mg/kg, 9/50). The lack o0). The lack of hyperplasia in female mice and the negative trend in male mice suggest that these marginal effects were probably not related to the administration of n-butyl chloride. An increased incidence of hepatocellular adenomas or carcinomas (combined) was observed in the 500 mg/kg dose group of female mice (3/50 vs 8/50) but not in the 250 mg/kg dose group (9/50 vs 7/50). An increased incidence of hemangiosarcomas was observed in male mice in the first study (1/50; 3/50; 4/50) but not in the second study (4/50 vs 2/50). Neither of these marginal effects was regarded as compound related. n-Butyl chloride was not mutagenic in Salmonella typhimurium strains TA98, TA1535, or TA1537 in the presence or absence of Aroclor 1254-induced male Sprague-Dawley rat liver S9 or in the presence of male Syrian hamster liver S9. n-Butyl chloride was mutagenic in the mouse lymphoma L5178Y/TK&plusmn; assay in the absence of Aroclor-induced male rat liver S9 and was not tested in the presence of S9. n-Butyl chloride did not induce sister-chromatid exchanges or chromosomal aberrations in Chinesehamster ovary cells in the presence or absence of Aroclor-induced male rat liver S9. An audit of the experimental data was conducted for the 2-year studies of n-butyl chloride. No data discrepancies were found that influenced the final interpretations. Under the conditions of these 2-year gavage studies, there was no evidence of carcinogenicity of n-butyl chloride for male and female F344/N rats at daily doses of 60 or 120mg/kg, for male B6C3F1 mice at doses of 250, 500, or 1,000 mg/kg, or for female B6C3F1 mice at doses of 250 or 500 mg/kg. Chemical-induced toxicity in high dose rats (primarily females) reduced the sensitivity of the study for determining carcinogenicity. Synonyms: 1-chlorobutane; butyl chloride; n-propylcarbinyl chloride

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