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Optimal therapy for pancreatic adenocarcinoma requires surgical removal with tumor-free margins. Superior outcomes have been reported for high-volume centers incorporating a multidisciplinary approach. Postoperative ("adjuvant") chemotherapy and radiation should be considered in patients with successfully resected primary tumors. Combined modality treatment with chemotherapy and radiation should be considered for locally advanced, unresectable tumors. Gemcitabine can provide symptom relief and a modest improvement in survival for patients with metastatic disease. Strict attention to relief of symptoms such as pain, depression, anorexia/cachexia, and jaundice is essential in all patients with pancreatic cancer. All patients with pancreatic cancer should be encouraged to enter clinical trials of new therapies, given that long-term survival for all stages remains poor.
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PMID:Pancreatic cancer. 1205 45

3,3'-Dimethylbenzidine dihydrochloride is one of five chemicals being evaluated in 2-year carcinogenicity and toxicity studies as part of the NTP's Benzidine Dye Initiative. This Initiative was designed to evaluate representative benzidine congeners, benzidine congener-derived dyes, and benzidine-derived dyes. 3,3'-Dimethylbenzidine dihydrochloride was nominated for study because of the potential for human exposure during production of bisazobiphenyl dyes and because benzidine, a structurally related chemical, is a known human carcinogen. Toxicology and carcinogenesis studies were conducted by administering 3,3'-dimethylbenzidine dihydrochloride (approximately 99% pure) in drinking water to groups of F344/N rats of each sex for 14 days, 13 weeks, or 9 or 14 months. The 14-month exposures were planned as 24-month exposures but were terminated early because of rapidly declining animal survival, due primarily to neoplasia. These studies were performed only in rats because similar studies were being performed in mice at the National Center for Toxicological Research (NCTR). Hematologic and serum chemical analyses and thyroid hormone determinations were conducted in conjunction with the 13-week and 9-month studies. Genetic toxicology studies were conducted in Salmonella typhimurium, Chinese hamster ovary (CHO) cells, and Drosophila melanogaster. 14-Day Studies: Rats were exposed to 3,3'-dimethylbenzidine dihydrochloride in drinking water at doses ranging from 600 to 7,500 ppm. All five males and one female in the 7,500 ppm group and 1/5 males in the 5,000 ppm group died. Final mean body weights were decreased in males receiving 1,250 ppm or more and in all exposed females, and final mean body weights of animals receiving 2,500 ppm or more were lower than initial weights. Water consumption decreased with increasing chemical concentration. Compound-related effects observed in rats receiving 5,000 ppm or more included minimal to slight hepatocellular necrosis, accumulation of brown pigment (presumably bile) in individual hepatocytes, increased severity of nephropathy relative to controls, and severe lymphocytic atrophy of the thymus. Treated animals also showed an increased severity of atrophy of the bone marrow relative to controls, varying degrees of lymphocytic atrophy of the mandibular and mesenteric lymph nodes and spleen, increased vacuolization and necrosis of cells of the adrenal cortex, focal acinar cell degeneration in the pancreas, and, in males, increased immature sperm forms in the testis and epididymis. 13-Week Studies: 3,3'-Dimethylbenzidine dihydrochloride was administered in drinking water at doses of 300, 500, 1,000, 2,000, and 4,000 ppm. All rats receiving 4,000 ppm and 4/10 males and 1/10 females receiving 2,000 ppm died before the end of the studies. Depressions in final mean body weight relative to controls ranged from 12% to 48% for males and from 9% to 42% for females. Water consumption decreased with increasing dose. At compound concentrations of 300 to 2,000 ppm, mean water consumption was 29% to 83% of control values. Compound-related effects included an increase in the severity of nephropathy relative to controls; hepatocellular necrosis and accumulation of brown pigment (presumably bile) in sinusoidal lining cells; lymphocytic atrophy of the thymus, spleen, and mandibular and mesenteric lymph nodes; atrophy of the bone marrow in the higher-dose groups; degeneration of pancreatic acinar cells; and, in males, immature sperm forms in the testis and epididymis. Decreases in serum triiodothyronine (T3) values were observed in exposed females, and decreases in mean thyroxin (T4) concentrations in exposed males and females; no significant changes were observed in thyroid stimulating hormone (TSH) levels in exposed rats. Based on the decreased survival, reductions in water consumption and body weight gain, and chemical-induced hepatocellular and renal lesions observed in the 13-week studies, the doses selected for the 9- and 14-month drinking water studies of 3,3'-dimethylbenzidine dihydrochloride were 0, 3 3,3'-dimethylbenzidine dihydrochloride were 0, 30, 70, and 150 ppm. Seventy rats of each sex were used in the control group, 45 in the low-dose group, 75 in the mid-dose group, and 70 in the high-dose group. 9-Month Studies: Ten rats of each sex in the control and 150 ppm dose groups were evaluated after 9 months. Chemical-related effects observed in exposed animals included alveolar/bronchiolar carcinoma in one male, basal cell carcinoma of the skin in one male, a squamous cell carcinoma of the oral cavity in one female, preputial gland carcinoma in two males, clitoral gland carcinoma in three females, adenocarcinoma of the small intestine in two males, Zymbal's gland carcinoma in two males and three females, hepatocellular carcinoma in two males, and adenomatous polyps of the large intestine in three males. Other effects seen in dosed rats included focal cellular alteration in the liver, lymphoid atrophy in the spleen, and increased severity of nephropathy relative to controls. An increase in serum T3 values was observed in exposed males, and a decrease in mean T4 concentrations in exposed males and females. TSH concentrations were increased in exposed male and female rats. Body Weights and Survival in the 14-Month Studies: The average amount of 3,3'-dimethylbenzidine dihydrochloride consumed per day was approximately 1.8, 4.0, or 11.2, mg/kg for low-, mid-, or high-dose male rats and 3.0, 6.9, or 12.9 mg/kg for low-, mid-, or high-dose female rats. The mean body weight of high-dose males was about 85&percnt; of the control value by week 28. By the end of the study, mean body weights of low-, mid-, and high-dose males were 97&percnt;, 92&percnt;, and 70&percnt; of the control values, respectively. Mean body weights of high- and mid-dose females were about 85&percnt; of the control values at week 32 and week 44, respectively. At the end of the study, mean body weights of exposed females were about 94&percnt;, 81&percnt;, and 74&percnt; of the control values for low-, mid-, and high-dose groups, respectively. Because of extensive neoplasia, many exposed males and females were dying or were sacrificed moribund in the first year, and all high-dose males died by week 55. The studies were terminated at weeks 60 to 61, at which time the group survivals were male: control, 60/60, low dose, 41/45; mid dose, 50/75; high dose, 0/60; female: 59/60; 39/45; 32/75; 10/60. Nonneoplastic Effects in the 14-Month Studies: Increases in nonneoplastic lesions in dosed rats included cystic degeneration and foci of cellular alteration in the liver; exacerbation of nephropathy; and focal or multifocal hyperplasia of the Zymbal's gland, preputial and clitoral glands, and alveolar epithelium. Neoplastic Effects in the 14-Month Studies: Neoplasms were observed in exposed rats at many sites: skin, Zymbal's gland, preputial and clitoral glands, liver, oral cavity, small and large intestine, mammary gland, lung, brain, and mesothelium. The incidence of these neoplastic effects in male and female rats is summarized in the table at the end of this section (see page 8 of the Technical Report). Genetic Toxicology: 3,3'-Dimethylbenzidine dihydrochloride was mutagenic in Salmonella typhimurium strain TA98 with exogenous metabolic activation; it was not mutagenic in strains TA100, TA1535, or TA97 with or without activation. 3,3'-Dimethylbenzidine dihydrochloride induced sister-chromatid exchanges (CHO) and chromosomal aberrations in CHO cells in the absence of exogenous metabolic activation; these effects were not evident in test with S9 activation. Sex-linked recessive lethal mutations were induced in germ cells of adult male Drosophila melanogaster administered 3,3'-dimethylbenzidine dihydrochloride in feed or by injection. No reciprocal translocations occurred in D. melanogaster germ cells following exposure to 3,3'-dimethylbenzidine dihydrochloride. Conclusions: Under the conditions of these 14-month drinking water studies, there was clear evidence of carcinogenic activity of 3,3'-dimethylbenzidine dihydrochloride for male F344/N rats, as indicated by benign and malignant neoplasms of the skin, Zymbal's gland, preputial gland, liver, oral cavity, small and large intestine, lung, and mesothelium. Increased incidences of neoplasms of the brain may have been related to chemical administration. There was clear evidence of carcinogenic activity for female F344/N rats, as indicated by benign and malignant neoplasms of the skin, Zymbal's gland, clitoral gland, liver, oral cavity, small and large intestine, mammary gland, and lung. Increased incidences of neoplasms of the brain and mononuclear cell leukemia may have been related to chemical administration. Synonyms: o-tolidine dihydrochloride; 3,3'-dimethylbiphenyl-4,4'-diamine dihydrochloride; 3,3'-dimethylbiphenyl-4,4'-biphenyldiamine dihydrochloride; 4,4'-diamino-3,3'-dimethylbiphenyl dihydrochloride
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PMID:NTP Toxicology and Carcinogenesis Studies of 3,3'-Dimethylbenzidine Dihydrochloride (CAS No. 612-82-8) in F344/N Rats (Drinking Water Studies). 1263 69

Toxicology and carcinogenesis studies of d-limonene, a naturally occurring monoterpene found in many volatile oils, especially in citrus oils, were conducted because of its widespread use as a flavor and fragrance additive for food and household cleaning products and its increasing use as an industrial solvent. The d-limonene used in these studies was more than 99% pure and was administered in corn oil by gavage. Short-term studies were conducted in F344/N rats and B6C3F1 mice to identify toxic effects and affected sites and to help establish doses for the 2-year studies. Genetic toxicology studies were conducted in Salmonella typhimurium, mouse L5178Y cells, and Chinese hamster ovary (CHO) cells. The doses selected for the 16-day studies ranged from 413 to 6,600 mg/kg for both rats and mice; deaths and reduction in body weight gain occurred at the two highest doses. No compound-related clinical signs or histopathologic lesions were observed in any of the surviving dose groups. In the 13-week studies, doses of d-limonene ranged from 150 to 2,400 mg/kg for rats and from 125 to 2,000 mg/kg for mice. Deaths occurred in the high dose group of each species and sex. Greater than 10% reductions in body weight gain were observed in the two highest dose groups of male rats and male mice and the high dose female rats. Rough hair coats and decreased activity were observed at the two highest doses in both rats and mice. There were no chemical-related histopathologic lesions in female rats or in mice of either sex. A compound-related increased severity of nephropathy was observed in the kidney of male rats. This lesion was characterized by degeneration of epithelial cells in the convoluted tubules, granular casts in the outer stripe of the outer medulla, and epithelial regeneration. These lesions have been described as reasonably characteristic of the hyaline droplet nephropathy that is associated with an accumulation of liver-generated a2u-globulin in the cytoplasm of tubular epithelial cells. Two-year studies of d-limonene were conducted by administering 0, 75, or 150 mg/kg d-limonene in corn oil by gavage to groups of 50 F344/N male rats, 5 days per week for 103 weeks; groups of 50 female F344/N rats were administered 0, 300, or 600 mg/kg. These doses were selected based on compound-related, potentially life-threatening kidney lesions observed in males at 300 mg/kg and higher and on the large number of deaths of female rats at 2,400 mg/kg. Groups of 50 male B6C3F1 mice were administered 0, 250, or 500 mg/kg according to the same schedule; groups of 50 female B6C3F1 mice were administered 0, 500, or 1,000 mg/kg. These doses were selected based on the deaths observed for both male and female mice at 2,000 mg/kg during the 13-week studies and the body weight depression in male mice at 1,000 mg/kg and higher. Mean body weights of rats dosed with d-limonene were similar to those of vehicle controls throughout the studies. Survival of the high dose female rats after week 39 and of the vehicle control male rats after week 81 was significantly reduced (survival at week 104-- male: vehicle control, 29/50; low dose, 33/50; high dose, 40/50; female: 42/50; 40/50; 26/50). Mean body weights of dosed and vehicle control male mice were similar throughout the studies. Mean body weights of high dose female mice were notably lower than those of the vehicle controls after week 28. Survival of the low dose group of male mice was significantly lower than that of vehicle controls at the end of the study (33/50; 24/50; 39/50). No difference in survival was observed between vehicle control and dosed female mice (43/50; 44/50; 43/50). In the 2-year studies, the kidney was confirmed as the primary target organ for chemically related lesions. No lesions were observed in female rats. For males, the nonneoplastic lesions included exacerbation of the age-related nephropathy, linear deposits of mineral in the renal medulla and papilla, and focal hyperplasia of the transitional epithelium overlying the renal papilla. Uncommon tubular cell adenomas and adenocarc and adenocarcinomas of the kidney also occurred in dosed male rats, and this effect was supported by a dose-related increased incidence of tubular cell hyperplasia, as shown in the table below. INCIDENCES OF MALE RATS WITH RENAL LESIONS IN THE TWO-YEAR GAVAGE STUDY OF d-LIMONENE Site/Lesion Vehicle Control 75 mg/kg 150 mg/kg Renal papilla Mineralization 7/50 43/50 48/50 Epithelial hyperplasia 0/50 35/50 43/50 Kidney Tubular cell hyperplasia 0/50 4/50 7/50 Tubular cell adenoma 0/50 4/50 8/50 Tubular cell adenocarcinoma 0/50 4/50 3/50 In subsequent 21-day studies, male and female F344/N rats were administered d-limonene at doses ranging from 75 to 1,200 mg/kg. Microscopic examination of the kidney sections from these rats indicated a compound-related increase in intracytoplasmic granules in the proximal convoluted tubules of dosed male rats but not of female rats. The granules were shown to contain a2u-globulin by an immunohistochemical strain. a2u-Globulin was shown to be increased in kidney homogenates from dosed male rats by an ELISA test. In mice, no chemically related increases in neoplasms were observed. The incidence of neoplasms of the anterior pituitary gland in high dose female mice was lower than that in vehicle controls (adenomas or carcinomas, combined:vehicle control, 12/49; high dose, 2/48). Cells with an abnormal number of nuclei (8/49; 32/50) and cytomegaly (23/49; 38/50) were observed in the liver of high dose male mice. Genetic Toxicology: d-Limonene was not mutagenic in four strains of S. typhimurium (TA98, TA100, TA1535, or TA1537), did not significantly increase the number of trifluorothymidine (Tft)-resistant cells in the mouse L5178Y/TK± assay, and did not induce chromosomal aberrations or sister chromatid exchanges (SCEs) in cultured CHO cells. All assays were conducted in the presence and absence of exogenous metabolic activation. Conclusions: Under the conditions of these 2-year gavage studies, there was clear evidence of carcinogenic activity of d-limonene for male F344/N rats, as shown by increased incidences of tubular cell hyperplasia, adenomas, and adenocarcinomas of the kidney. There was no evidence of carcinogenic activity of d-limonene for female F344/N rats that received 300 or 600 mg/kg. There was no evidence of carcinogenic activity of d-limonene for male B6C3F1 mice that received 250 or 500 mg/kg. There was no evidence of carcinogenic activity of d-limonene for female B6C3F1 mice that received 500 or 1,000 mg/kg. An increased severity of spontaneous nephropathy, increased incidences of linear mineralization of the renal medulla and papilla, and hyperplasia of the transitional epithelium of the renal papilla were present in dosed male rats. Synonyms: cyclohexene; 4-isopropenyl-1-methyl; 1-methyl-4-(1-methylethenyl)cyclohexene; p-mentha-1,8-diene; carvene; cinene; cajeputene
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PMID:NTP Toxicology and Carcinogenesis Studies of d-Limonene (CAS No. 5989-27-5) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1270 37

Benzyl acetate, a water-white liquid with a pear-like odor, is a natural constituent of several essential oils and flower absolutes extracted from jasmine, hyacinth, gardenia, tuberose, ylang-ylang, cananga, and neroli. Commercial benzyl acetate, a liquid prepared synthetically from benzyl chloride, acetic acid, and triethylamine is used primarily as a component of perfumes for soaps and as a flavoring ingredient. This compound is practically insoluble in water but is miscible in alcohol and ether and soluble in benzene and chloroform. Toxicology and carcinogenesis studies of benzyl acetate (>99% pure) were conducted by administering benzyl acetate in corn oil gavage to groups of 50 male and 50 female F344/N rats at doses of 0, 250, or 500 mg/kg body weight and to groups of 50 male and 50 female B6C3F1 mice at doses of 0, 500, or 1,000 mg/kg once daily five days per week for 103 weeks. Dose selection for the 2-year study was based on mean body weight gain depression and decreased survival observed at higher doses in 13 week studies. The absence of any observable adverse effect of benzyl acetate on the survival or mean body weight gains of the rats or mice in the 2-year studies suggests that both the rats and the mice of each sex could have tolerated higher doses. An infection in the genital tract was probably responsible for the deaths of 26/35 control, 14/32 low-dose, and 8/20 high-dose female mice before the end of the study. Acinar-cell adenomas in the pancreas of male rats occurred with a positive trend (P<0.01), and the incidence in the high-dose group (37/49, 76%) was significantly (P<0.01) higher than in the vehicle controls (22/50, 40%). The incidence of these tumors in the low-dose group (27/50, 54%) was comparable to that in the gavage controls. Acinar-cell hyperplasia of the pancreas was observed in 37/50 control, 34/50 low-dose, and 36/49 high-dose male rats. No acinar-cell hyperplasia or adenoma of the pancreas was observed in female rats. The incidence of retinopathy and cataracts in the high-dose male rats was increased compared with the controls (retinopathy: 1/50; 0/50; 20/50; cataracts: 0/50; 0/50; 13/50). Low-dose female rats had an increased incidence of retinopathy (18/50). Retinopathy and cataracts in rats have been associated with proximity to fluorescent light in this and previous studies. Preputial gland neoplasms occurred with a positive trend (P<0.05) in male rats (cystadenocarcinoma: 0/50; 0/50; 3/50; all adenocarcinoma: 0/50; 1/50; 4/50; adenocarcinoma or carcinoma combined: 1/50; 1/50; 6/50). However, the incidence of all preputial gland tumors was not significantly elevated (2/50; 1/50; 6/50). For female rats the incidence of clitoral gland neoplasms was marginally increased (2/50; 0/50; 5/50). Hepatocellular adenomas occurred in mice of each sex with statistically positive trends (males: 0/50; 5/49; 13/50; females: 0/50; 0/50; 6/50), and the incidences in the high-dose groups were greater than those in the controls (males: P<0.001; females: P<0.05). Hepatocellular carcinomas were marginally elevated in dosed male and high-dose female mice (males: 10/50; 14/49; 12/50; females: 1/50; 0/50; 4/50). Squamous cell papillomas or carcinomas of the forestomach (uncommon neoplasms) occurred with a positive trend (P<0.05) in male mice (4/49; 4/48; 11/49). The incidence of these tumors was also marginally (P=0.054) increased in the high-dose female mice (0/50; 0/50; 4/48). The incidences of these tumors in both the high-dose male and the high-dose female mice were considerably higher than the historical corn oil gavage control rates at this laboratory (males, 2/296, 0.7%; females, 2/297, 0.7%) and throughout the program (males, 14/1,070, 1.3%; females, 3/1,073, 0.3%). Forestomach hyperplasia occurred at increased incidences in dosed mice of either sex (males: 1/49, 7/48, 22/49; females: 1/50, 6/50, 17/48). The neoplasms and hyperplasia of the forestomach were probably related to administration of benzyl acetate. In a separate metabolism study, benzyl acetate was absorbed from the gastrointestinal traolism study, benzyl acetate was absorbed from the gastrointestinal tract of rats and mice, with approximately 90&percnt; of the administered dose recovered as various metabolites in the urine within 24 hr. The primary metabolite was hippuric acid, with minor amounts of a mercapturic acid, and one or more unidentified metabolites. This capacity for absorption, metabolism, and disposition was unaffected by the amount or number of doses administered. Benzyl acetate was not mutagenic in strains TA100, TA98, TA135, or TA137 of Salmonella typhimurium in the presence or absence of Aroclor 1254-induced Sprague-Dawley rat or Syrian hamster S9 when tested according to the preincubation protocol. Benzyl acetate did not induce sister-chromatid exchanges or chromosomal aberrations in Chinese hamster ovary cells in the presence or absence of Aroclor 1254-induced Sprague-Dawley rat liver S9. Benzyl acetate was mutagenic in the mouse lymphoma L5178Y/TK± assay in the presence, but not in the absence, of Aroclor 1254-induced Fisher 344 rat liver S9. An audit was conducted on the experimental data and the draft technical report for these 2-year studies on benzyl acetate. Based on the results of this audit additional pathology examinations were conducted on all target organs in male rats and male and female mice. The Technical Report reflects these final pathology evaluations. The overall conclusions regarding the toxicology and carcinogenicity of benzyl acetate did not change as a result of this evaluation. Under the conditions of these gavage studies, benzyl acetate increased the incidence of acinar-cell adenomas of the exocrine pancreas in male F344/N rats; the gavage vehicle may have been a contributing factor. There was no evidence of carcinogenicity for female F344/N rats. For male and female B6C3F1 mice there was some evidence of carcinogenicity in that benzyl acetate caused increased incidences of hepatocellular adenomas and squamous cell neoplasms of the forestomach. Synonyms: alpha-acetoxytoluene; benzyl ethanoate; acetic acid, benzyl ester
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PMID:NTP Toxicology and Carcinogenesis Studies of Benzyl Acetate (CAS No. 140-11-4) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1274 78

A 12-year-old male cat with depression and dyspnoea was presented for investigation. Radiography and computed tomography revealed hydrothorax and solid masses involving the sternum, ribs and thoracic vertebrae. The cat died two days after first presentation, and postmortem examination revealed lung masses and proliferative bony lesions. Histologically, a neoplastic proliferation of epithelial cells was seen in the lungs, with a large amount of collagen and deposits of cholesterin. The bone lesions were also composed of neoplastic epithelial cells and abundant calcified osteoid, without atypia. A diagnosis of pulmonary adenocarcinoma with osteoblastic bone metastases was made. This is the first reported case of osteoblastic metastases in the cat.
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PMID:Pulmonary adenocarcinoma with osteoblastic bone metastases in a cat. 1458 62

The aims of this study were to prospectively evaluate gastric function in esophageal cancer patients after chemoradiotherapy and following surgery, using cutaneous electrogastrography (EGG). Twenty-three patients with esophageal adenocarcinoma were recruited to the study. A subset of patients (n = 11) underwent neoadjuvant chemoradiotherapy and were also studied at 14 days after treatment. All patients underwent EGG studies prior to and following surgery, at 3 months postoperatively. Ten of these patients were also studied at medians of 6 months and 12 months after surgery. Twenty normal volunteers were used as controls. Post-operative EGG studies were monitored with a modified technique; the electrodes being placed in the subscapular region in the area of the transposed stomach. Following neoadjuvant treatment there was a significant increase in abnormal gastric myoelectrical activity involving changes in tachygastrias and decreased motility as measured by power ratio. Post-operatively there was a significant increase in bradygastria which persisted at 6 months but not at 12 months. There was a corresponding decrease in normogastria which persisted at 6 months and to a lesser extent at 12 months. Dominant frequency remained significantly depressed at 3, 6 and 12 months. Gastric myoelectrical activity is normal in untreated esophageal cancer. Neoadjuvant chemoradiotherapy causes a disruption to normal myoelectrical activity involving reduced motility and tachygastrias. Surgery causes a depression in dominant frequency with a reduced incidence of normogastria at 3 months and 6 months but with a tendency towards normality at 12 months.
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PMID:Gastric myoelectrical activity post-chemoradiotherapy and esophagectomy: a prospective study using subscapular surface recording. 1520 46

We report a case of advanced colon cancer which was supposed to have arisen from a hyperplastic polyp in a 68-year-old man. Colonoscopy revealed a depressed reddish area with a surrounding elevated lesion that was of a faded color compared with the normal mucosa. After the mucosal surface had been sprayed with crystal violet dye, magnifying colonoscopy showed an amorphous area in the central depression and the surrounding, slightly elevated lesion had an asteroid pattern. The depressed area was therefore considered to be a colonic cancer surrounded by a hyperplastic polyp. Endoscopic ultrasonography showed that the lesion was infiltrating further than the deep submucosal layer and it was therefore decided to treat the patient by laparoscopically assisted right hemicolectomy. The depressed lesion was found to be a well-differentiated adenocarcinoma invading the muscularis propria (diagnosed as IIc + IIa-like advanced adenocarcinoma). The surrounding flat elevated lesion was found to be hyperplastic mucosa. No adenomatous lesions were found. There have been few reported cases in which a preoperative diagnosis of carcinoma in a hyperplastic polyp has been made, but the possibility of carcinogenesis from hyperplastic polyps has come under consideration recently. This case was considered to be important because it raises the possibility that nonpolypoid cancer can develop from a hyperplastic polyp.
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PMID:Small invasive colonic cancer occurring in a hyperplastic polyp. 1532 79

Muscle protein degradation is thought to play a major role in muscle atrophy in cancer cachexia. To investigate the importance of the ubiquitin-proteasome pathway, which has been suggested to be the main degradative pathway mediating progressive protein loss in cachexia, the expression of mRNA for proteasome subunits C2 and C5 as well as the ubiquitin-conjugating enzyme, E2(14k), has been determined in gastrocnemius and pectoral muscles of mice bearing the MAC16 adenocarcinoma, using competitive quantitative reverse transcriptase polymerase chain reaction. Protein levels of proteasome subunits and E2(14k) were determined by immunoblotting, to ensure changes in mRNA were reflected in changes in protein expression. Muscle weights correlated linearly with weight loss during the course of the study. There was a good correlation between expression of C2 and E2(14k) mRNA and protein levels in gastrocnemius muscle with increases of 6-8-fold for C2 and two-fold for E2(14k) between 12 and 20% weight loss, followed by a decrease in expression at weight losses of 25-27%, although loss of muscle protein continued. In contrast, expression of C5 mRNA only increased two-fold and was elevated similarly at all weight losses between 7.5 and 27%. Both proteasome functional activity, and proteasome-specific tyrosine release as a measure of total protein degradation was also maximal at 18-20% weight loss and decreased at higher weight loss. Proteasome expression in pectoral muscle followed a different pattern with increases in C2 and C5 and E2(14k) mRNA only being seen at weight losses above 17%, although muscle loss increased progressively with increasing weight loss. These results suggest that activation of the ubiquitin-proteasome pathway plays a major role in protein loss in gastrocnemius muscle, up to 20% weight loss, but that other factors such as depression in protein synthesis may play a more important role at higher weight loss.
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PMID:Expression of the ubiquitin-proteasome pathway and muscle loss in experimental cancer cachexia. 1616 Jun 95

Early duodenal carcinoma is a rare entity. Most duodenal carcinomas are diagnosed at a more advanced stage. This report describes the case of a 59-year-old lady with an early duodenal adenocarcinoma diagnosed at check-up gastroduodenoscopy in an outpatient clinic who was referred to us for further investigation and management. The initial upper endoscopy at our department revealed a type IIa+c lesion in the proximal duodenum (10 - 12 mm diameter, flat elevated lesion with central depression). Using chromoendoscopy and magnification endoscopy the lesion could be well demarcated and neoplastic changes in the architecture of the intestinal villi could be detected. After submucosal epinephrine-saline injection, the lesion was removed by endoscopic resection without complications. Histopathological examination revealed the rare entity of an early duodenal carcinoma arising from incomplete-type gastric metaplasia in the duodenum. In summary, the presented paper describes a case of successful endoscopic treatment of an early duodenal carcinoma arising from incomplete gastric metaplasia.
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PMID:[Early duodenal adenocarcinoma arising in gastric metaplasia treated by endoscopic resection]. 1662 61

A 17-year-old Quarter horse mare was referred to Cornell University for postmortem examination after 72 hours of encephalopathy that consisted of depression, mania, and blindness. A plasma sample and cerebral spinal fluid demonstrated hyperammonemia. Gross necropsy examination findings included the following: mild icterus, a transmural mass in the glandular portion of the gastric fundus, multiple masses throughout the liver, and a large tumor thrombus in the portal vein. Microscopically, the gastric mass, hepatic masses, and portal vein thrombus were composed of similar neoplastic epithelial cells that formed variably sized acini and branching cords separated by a dense desmoplastic stroma. Throughout the cerebral frontal cortex were numerous Alzheimer type II astrocytes. Hepatic encephalopathy was caused by gastric adenocarcinoma, with metastasis to the liver and the portal vein. The clinical and pathologic lesions from this unique case, as well as hyperammonemia and portal vein thrombosis in the pathogenesis of hepatic encephalopathy, are discussed.
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PMID:Gastric adenocarcinoma in a horse with portal vein metastasis and thrombosis: a novel cause of hepatic encephalopathy. 1684 2

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