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Malignant tumors of the eyelid: a population-based study of non-basal cell and non-squamous cell malignant neoplasms.

OBJECTIVE: To determine the relative frequencies, average annual incidences, and patient characteristics of non-basal cell and non-squamous cell malignant neoplasms of the eyelid in a defined geographic population. DESIGN AND SETTING: A retrospective study using the Florida Cancer Data System to identify malignant tumors of the eyelid, except for basal cell and squamous cell carcinomas, from 1981 through 1994. Cases were limited to persons who resided within Florida. MAIN OUTCOME MEASURE: Incidence of histologically confirmed malignant eyelid tumors. RESULTS: Two hundred six primary malignant eyelid tumors were identified. The 3 most common, in order of frequency, were melanoma, sebaceous carcinoma, and lymphoma. The median age at diagnosis for all patients was 73 years. Only 3 of the 206 malignant neoplasms occurred in blacks. The annual incidence of eyelid melanoma and sebaceous carcinoma in whites older than 20 years was 0.6 and 0.5 per million, respectively. Kaposi sarcoma was the most common type of mesenchymal tumor. Eleven different histologic types of lymphoma were found in the eyelid. Only 2 of 27 lymphomas had T-cell lineage. CONCLUSIONS: Malignant tumors of the eyelid other than basal cell and squamous cell carcinoma are uncommon and usually occur in elderly white persons. Primary eyelid tumors of any type are rare in blacks. The risk of a non-basal cell and non-squamous cell malignant neoplasm of the eyelid in Florida is 6.4 times greater for whites than for blacks (95% confidence interval [CI], 2.1-20.2). A variety of B-cell lymphomas can be manifested as primary eyelid tumors.

Adenocarcinoma, Sebaceous↗

Deletion mapping of chromosome 3p and 13q and preliminary analysis of the FHIT gene in human nonmelanoma skin cancer.

Loss of heterozygosity of chromosomes 3p and 13q occurs frequently in human cutaneous squamous cell neoplasms, suggesting the presence of one or more tumor suppressor genes on these chromosome arms that may be involved in the pathogenesis of this tumor type. To date there is no clear evidence in cutaneous tumors where these putative genes are located. In this study we have analyzed 20 squamous cell neoplasms that show allelic loss at chromosome 13q, and 22 squamous cell neoplasms that show allelic loss at chromosome 3p, in an attempt to define the smallest area of deletion. One commonly deleted region was identified on chromosome 13 that centred around 13q13, and two commonly deleted regions were identified on chromosome 3 that mapped to 3p24-pter and 3p12-p14.1. Our findings suggest the presence of at least one tumor suppressor gene on chromosome 13 and two tumor suppressor genes on chromosome 3p that may be involved in the progression of these neoplasms. Deletions within the Fragile Histidine Triad gene, located at 3p14.2, have been reported in several tumors, leading to the suggestion that this gene is involved in tumor development. To evaluate the role of the Fragile Histidine Triad gene in nonmelanoma skin cancer, we have used reverse transcriptase polymerase chain reaction analysis to screen for deletions in 16 tumors (five basal cell carcinomas, five squamous cell carcinomas, five actinic keratoses, and one case of Bowen's disease) and HaCaT and A431 cell lines. A normal transcript was found to be expressed in 14 of 16 tumors and both cell lines. This suggests that the Fragile Histidine Triad gene is not a common target for deletion in Bowen's disease and the cell lines HaCaT and A431.

Acid Anhydride Hydrolases↗

Basal cell carcinomas and squamous cell carcinomas of human skin show distinct patterns of chromosome loss.

Although basal cell carcinomas and squamous cell carcinomas are clinically and pathologically distinct, the molecular basis for these differences is not clear. We have used polymorphic microsatellite markers to determine the pattern and extent of chromosome losses in a series of 44 basal cell carcinomas and 47 squamous cell neoplasms of the skin. Basal cell carcinomas showed a distinctive allelotype with chromosome loss largely confined to a single chromosome arm, 9q (26 of 44 informative tumors). In contrast to the predominance of loss on a single chromosome arm in basal cell carcinomas, squamous cell neoplasms showed more widespread loss with loss of heterozygosity of markers from 35 of 39 chromosome arms in one or more of the tumors studied. The pattern of loss was also different from basal cell carcinomas with frequent loss of heterozygosity of markers from 9p (41%), 13q (46%), 17p (33%), 17q (33%), and 3p (23%) in squamous cell neoplasms. The frequent loss of markers from these chromosome arms relative to other chromosome losses suggests that these arms may contain genes important in the development of cutaneous squamous cell carcinomas.

Basal Cell Carcinoma↗

[Prognostic significance of DNA analysis in neoplastic cells of patients with squamous cell lung neoplasms treated surgically].

The aim of our study was the assessment of the ploidia and its influence on the remission time and the survival of surgically treated patients with squamous cell lung cancer. The results were then related to the clinical staging, grading, size and localization of the tumor. The tissue samples (n = 60) of squamous cell lung carcinoma resected between 1995-1996 at the Department of Thoracic Surgery at University of Medical Sciences in Poznań were prepared using modified Hedley's method. The measurement was done in Cytoron Absolute flow cytometer. The abnormal DNA (aneuploid) was found in 40% of tumors. In two-year observation period more patients died with aneuploid tumors (54.6% deaths) than with diploid tumors (35.2% deaths). No significant correlation was found between the ploidy and frequency of metastasis to regional lymph nodes, tumor size, localization and grading. The estimation of the DNA content in the cancer cells seems to be a significant and valuable prognostic factor. The measurement of the DNA content can be useful in patients to estimate risk of recurrence after surgery.

Adult↗

NTP Toxicology and Carcinogenesis Studies of Iodinated Glycerol (Organidin(R).) (CAS No. 5634-39-9) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

Toxicology and carcinogenesis studies of iodinated glycerol (Organidin(R)., a complex mixture prepared by the reaction of iodine with glycerol and found to contain 33% 3-iodo-1,2-propanediol as the major component) were conducted because of human exposure to iodinated glycerol as an expectorant and its possible relationship to the formation of alkyl iodides, e.g., methyl iodide, a suspected animal carcinogen. These studies were conducted by giving iodinated glycerol in water by gavage (5 days per week) to groups of F344/N rats and B6C3F1 mice for 16 days, 13 weeks, or 2 years. Genetic toxicology studies were conducted with iodinated glycerol in Salmonella typhimurium, mouse L5178Y lymphoma cells, Chinese hamster ovary (CHO) cells, and B6C3F1 mice (in vivo bone marrow micronucleus test). Also, 3-iodo-1,2-propanediol was tested in S. typhimurium and B6C3F1 mice (in vivo micronucleus assay). Sixteen-Day and Thirteen-Week Studies: Sixteen-day studies were conducted by giving iodinated glycerol at doses up to 1,000 mg/kg to rats and up to 500 mg/kg to mice. All female rats and 4/5 male mice in the highest dose group died before the end of the studies; there were no dose-related effects on body weights of male or female rats or male mice at the end of the studies. The forestomach of 2/5 female mice that received 500 mg/kg was thickened and granular. Thirteen-week studies were conducted by administering iodinated glycerol at doses up to 500 mg/kg to rats and mice. During these studies, 3/10 female rats and 1/10 female mice that received 500 mg/kg died. Final mean body weights of rats and mice that received 500 mg/kg were 4% lower than those of vehicle controls for males and 6%-7% lower for females. Kidney tubular cell lesions, including cortical necrosis, regeneration, and calcification, were observed at increased incidences in the highest dose group of female rats. Lymphoid hyperplasia of the stomach was observed in dosed male and female rats. Kidney tubular cell regeneration was also observed in dosed female mice. Inflammation or abscesses of mild-to-moderate severity and hyperplasia, acanthosis, and/or hyperkeratosis of mild-to-moderate severity were observed in the forestomach of the highest dosed group of female mice. Body Weight and Survival in the Two-Year Studies: Two-year studies were conducted by administering 0, 125, or 250 mg/kg iodinated glycerol in deionized water by gavage, 5 days per week for 103 weeks, to groups of 50 male F344/N rats and 50 male B6C3F1 mice. Groups of 50 female F344/N rats and 50 female B6C3F1 mice were administered iodinated glycerol on the same schedule at lower doses of 0, 62, or 125 mg/kg because of the increased severity of kidney and stomach lesions in the 13-week studies. Mean body weights of high dose male rats were 5%-10% lower than those of vehicle controls from week 43 to week 68 and 10%-13% lower from week 72 to the end of the studies. Mean body weights of low dose male rats and high dose female rats were 4%-9% lower than those of vehicle controls from week 88 to the end of the studies. The survival of the high dose group of male rats was considerably lower than that of the vehicle controls after week 86. No other significant differences in survival were observed between any groups of rats of either sex (male: vehicle control, 28/50; low dose, 20/50, high dose, 2/50; female: 31/50; 30/50; 27/50). Mean body weights of dosed and vehicle control male mice were similar. Mean body weights of high dose female mice were 6%-8% lower than those of vehicle controls from week 40 to week 64 and were 9%-13% lower thereafter. No significant differences in survival were observed between any groups of mice of either sex (male: 36/50; 40/50; 32/50; female: 40/50; 33/50; 38/50). Nonneoplastic and Neoplastic Effects in the Two-Year Studies: The incidence of mononuclear cell leukemia were increased in dosed male rats (vehicle control, 14/50; low dose, 29/50; high dose, 24/50). Follicular cell carcinomas of the thyroid gland in male rats occurred at an increased incidence in low dose male rats (0/49; s of the thyroid gland in male rats occurred at an increased incidence in low dose male rats (0/49; 5/49; 1/49). Reduced survival of high dose male rats may have been responsible for the decreased tumor incidence in this group relative to that in the low dose group. Follicular cell carcinomas were observed in one low dose and one high dose female rat. Follicular cell carcinomas of the thyroid gland have been observed in 3/293 water gavage vehicle control male F344/N rats and in 10/1,904 untreated control male F344/N rats. Adenomas of the nasal cavity were observed in two high dose male rats. Adenomas of the nasal cavity have not been observed in 300 water gavage vehicle control male F344/N rats or in 1,936 untreated control male F344/N rats. Squamous metaplasia and focal atrophy of the salivary glands were observed at increased incidences in dosed rats (squamous metaplasia--male: 0/48; 47/50; 48/49; female:1/49; 48/50; 49/50; focal atrophy--male: 1/48; 10/50; 30/49; female: 0/49; 4/50; 11/50). In dosed female mice, adenomas of the anterior pituitary gland were increased (10/47; 15/45; 24/46). The incidences of adenomas of the harderian gland in dosed female mice were increased (6/50; 8/40; 13/50). A carcinoma of the harderian gland was observed in another high dose female mouse. Dilatation of the thyroid gland follicle and follicular cell hyperplasia were observed at increased incidences in dosed mice (dilatation--male: 0/48; 28/50; 32/50; female: 4/48; 11/48; 10/48; hyperplasia--male: 3/48; 46/50; 34/50; female: 2/48; 25/48; 35/48). The incidences of follicular cell adenomas were 3/48, 6/50, and 0/50 for males and 2/48, 3/48, and 4/48 for females. Hyperkeratosis and acanthosis of the forestomach were observed at increased incidences in high dose male mice (hyperkeratosis: 0/49; 0/49; 5/50; acanthosis: 0/49; 1/49; 5/50). Squamous cell papillomas were observed in female mice (1/49; 2/50; 5/49). The historical incidence of forestomach squamous cell neoplasms is 4/339 (1.2%) in water gavage vehicle control female B6C3F1 mice and is 18/1,994 (0.9%) in untreated control female B6C3F1 mice. Squamous cell neoplasms were not observed in male mice. Genetic Toxicology: Treatment of the base-substitution mutant S. typhimurium strains TA100 and TA1535 with iodinated glycerol in a preincubational protocol with and without S9 resulted in a dose-related increase in the number of revertant colonies; no increase in revertants was observed with the frame-shift mutant strains TA98 or TA1537. 3-Iodo-1,2-propanediol was also mutagenic in TA100 with or without S9; it was not mutagenic in TA98. Iodinated glycerol increased the number of trifluorothymidine-resistant cells in mouse lymphoma L5178Y/TK± assay in the absence of exogenous metabolic activation; it was not tested with activation. Iodinated glycerol induced sister chromatid exchanges (SCEs) and chromosomal aberrations in CHO cells without S9; with S9, the frequency of SCEs was increased more than without S9 but no chromosomal aberrations were induced. No increase in micronucleated polychromatic erythrocytes was observed in the bone marrow of B6C3F1 mice after injection with either iodinated glycerol or 3-iodo-1,2-propanediol. Conclusions: Under the conditions of these 2-year gavage studies, there was some evidence of carcinogenic activity for male F344/N rats administered iodinated glycerol, as indicated by increased incidences of mononuclear cell leukemia and follicular cell carcinomas of the thyroid gland. Adenomas of the nasal cavity in two high dose male rats may have been related to the administration of iodinated glycerol. There was no evidence of carcinogenic activity for female F344/N rats administered 62 or 125 mg/kg iodinated glycerol by gavage for 103 weeks. There was no evidence of carcinogenic activity for male B6C3F1 mice administered 125 or 250 mg/kg iodinated glycerol by gavage for 103 weeks. There was some evidence of carcinogenic activity for female B6C3F1 mice administered iodinated glycerol, as indicated by increased incidences of adenomas of the anterior pituitary gland and neoplasms of the harderian gland. Squamous cell papillomas of the forestomach may have been related to the administration of iodinated glycerol. Significant nonneoplastic lesions considered related to exposure of iodinated glycerol were squamous metaplasia and focal atrophy of the salivary gland in male and female rats. Dilatation of the thyroid gland follicle and follicular cell hyperplasia were observed in male and female mice. Synonyms or Trade Names: Organidin®.; iodopropylidene glycerol

Journal Article↗

Two distinct p53 immunohistochemical patterns in human squamous-cell skin cancer, precursors and normal epidermis.

Specimens of squamous-cell neoplasms (81 invasive cancers, 36 in situ cancers, 70 dysplasias, 5 keratoacanthomas, 19 papillomas) and normal skin were immunostained with p53 antibody. Nuclear accumulation of p53 was visualized as following 2 distinct patterns: dispersed or compact. The former is interpreted as a reversible reaction to sunlight, whereas the latter, after microdissection and sequencing of DNA, has been shown to reflect clonal multiplication of keratinocytes with mutated p53. The dispersed pattern was diffusely distributed and usually only involved a small proportion of epidermal cells. The compact pattern was characterized as a contiguous area of homogeneously stained cells sharply demarcated from its surroundings. It involved patches of normal epidermis or large areas of dysplastic or malignant squamous epithelium. Immature cells were always stained, whereas immunoreactivity was variably present in differentiating keratinocytes. Dispersed patterns occurred in 94.7% of strongly UV-exposed skin (mainly face) and to a lesser extent in less exposed parts of the body. It showed no correlation to the age of the individual. About two-thirds of biopsies from individuals over age 50 displayed compact patterns in sun-exposed, otherwise normal, epidermis. About 65% of pre-malignant and malignant squamous-cell neoplasms had a compact pattern. The presence of p53 immunoreactivity as a compact pattern supports the idea that mutations of the p53 gene are early events in the sequence from dysplasia to invasive squamous-cell cancer of the skin. Also, even in the absence of cellular atypia, patches of epidermal cells can accumulate p53 in a way that is indistinguishable from that of cancer and pre-cancer.

Carcinoma, Squamous Cell↗

Myxoid liposarcoma of the oral cavity with involvement of the periodontal tissues.

BACKGROUND, AIMS: Liposarcoma is the 2nd most frequent soft tissue sarcoma in adults, but it is extremely rare in the head and neck and, particularly, in the oral cavity. We report on a 25-year-old female who presented with a periodontal mass, extended from the right upper 3rd molar to the right upper 2nd premolar, covered by intact oral mucosa. The clinical differential diagnosis included peripheral giant cell granuloma, salivary gland neoplasms, squamous cell carcinoma of the gingiva, sarcoma and malignant lymphoma. METHODS: To accurately plan subsequent treatment, an excisional biopsy was performed and a myxoid liposarcoma was diagnosed. Consequently, the patient underwent wide excision of the neoplasm with maxillary en-block resection. RESULTS: The post-operative course was uneventful and the patient is alive and well 8 years after the original diagnosis. The authors stress the importance of considering soft tissue sarcomas in the diagnostic approach to patients with unusual periodontal neoplasms and to plan adequate surgical sampling of the lesion (i.e. excisional biopsy). CONCLUSIONS: This appears of pivotal importance as more limited specimens may result in inaccurate pre-operative diagnosis.

Adult↗

Benzyl acetate carcinogenicity, metabolism, and disposition in Fischer 344 rats and B6C3F1 mice.

Carcinogenesis studies of benzyl acetate (a fragrance and flavoring agent) were conducted in F344 rats and B6C3F1 mice. The chemical was given in corn oil by gavage once daily, 5 days/week for 103 weeks, to groups of 50 animals of each sex and species. For rats the doses were 0, 250, and 500 mg/kg body weight and for mice the doses were 0, 500, and 1000 mg/kg. Mean body weights of control and dosed rats and mice were not affected adversely by benzyl acetate. The survival of control and low dose female mice was lower than that of the high dose group. A genital tract infection may have contributed to the reduced survival. No other significant difference in survival was observed for dosed rats or mice. Benzyl acetate was absorbed from the gastrointestinal tract of rats and mice, with approximately 90% of the administered dose recovered as various metabolites in the urine within 24 h. 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. Under the conditions of these studies, benzyl acetate administration was associated with an increased incidence of acinar cell adenoma of the exocrine pancreas in male F344/N rats. No evidence of carcinogenicity was found for female F344/N rats. For male and female B6C3F1 mice there was evidence of carcinogenicity, in that benzyl acetate caused an increased incidence of hepatocellular neoplasms (particularly adenomas) and squamous cell neoplasms of the forestomach.

Absorption↗

NTP Toxicology and Carcinogenesis Studies of C.I. Disperse Blue 1 (A commercial dye containing approximately 50% 1,4,5,8-tetraaminoanthraquinone, and 20% water) (CAS No. 2475-45-8) in F344/N Rats and B6C3F1 Mice (Feed Studies).

C.I. Disperse Blue 1, a component of several semipermanent hair dyes, was studied as a commercial-grade product (minus lignosulfonate dispersants) containing approximately 50% 1,4,5,8-tetraaminoanthraquinone, 30% other compounds structurally related to 1,4,5,8-tetraaminoanthraquinone, and 20% water. C.I. Disperse Blue 1 was studied for toxicity and carcinogenicity in single-administration gavage, 14-day feed, 13-week feed, and 104-week feed studies. All studies used F344/N rats and B6C3F1 mice. In the single-administration gavage studies, no deaths occurred within 14 days at doses up to 3,000 mg/kg C.I. Disperse Blue 1 in rats or up to 2,000 mg/kg in mice. In the 14-day studies, rats and mice received dietary concentrations of up to 50,000 ppm. All male rats survived, and 2/5 female rats in the 50,000-ppm group died. All mice receiving 25,000 ppm or more died. Three of five males and 2/5 female mice in the 12,500-ppm groups died. In the 13-week studies, diets containing concentrations up to 20,000 ppm C.I. Disperse Blue 1 were fed to rats, and diets containing concentrations up to 10,000 ppm were fed to mice. No compound-related deaths of rats occurred; however, pathologic changes occurred at 2,500 ppm and higher and included urinary tract calculi, urinary bladder inflammation, hyperplasia of the urinary bladder transitional epithelium, and nephrosis, Compound-related deaths occurred at 10,000 ppm in mice of each sex. Pathologic changes included chronic inflammation and hyperplasia of the urinary bladder transitional epithelium and urinary tract calculi at dietary concentrations of 2,500 ppm and higher and nephrosis, myocardial necrosis, and testicular degeneration at 10,000 ppm. The renal lesions at 5,000 ppm were considered to be potentially life threatening. These composite findings from the short-term studies were used to identify target organs and to help select dietary concentrations for the longer term studies. In the 2-year studies in rats, groups of 50 animals of each sex were administered C.I. Disperse Blue 1 at dietary concentrations of 0, 1,250, 2,500, or 5,000 ppm. These dietary concentrations corresponded to 0, 45, 95, and 217 mg/kg per day for males and 0, 56, 111, and 240 mg/kg per day for females. Survival of males and females in the 5,000 ppm groups and males in the 2,500-ppm group was significantly reduced. Final body weights, as percent of controls, were: male-- low dose 100%; mid dose, 94%; high dose, 85%; female-- low dose, 99%; mid dose, 94%; high dose, 87%. Compound-related effects of feeding diets containing C.I. Disperse Blue 1 for 104 weeks to F344/N rats included urinary bladder neoplasms and calculi at the incidences noted in the table. Positive statistical associations existed between the presence of calculi and transitional cell neoplasms of the urinary bladder in male and female rats, leiomyomas or leiomyosarcomas (combined) in female rats, and squamous cell neoplasms in male rats. The increased incidence of pancreatic islet cell adenomas or carcinomas (combined) in high dose male rats was significant by survival-adjusted analyses (overall incidences: control, 1/49; low dose, 2/50; mid dose, 5/50; high dose, 3/50). In the 2-year studies in mice, 50 animals of each sex were administered diets containing C.I. Disperse Blue 1 at 0, 600, 1,200, or 2,500 ppm. These dietary concentrations corresponded to doses of 0, 112, 239, and 540 mg/kg per day for males and 0, 108, 235, and 520 mg/kg per day for females. Survival was comparable among control and dosed male or female mice. Final body weights, as percent of controls, were as follows: male-- low dose, 97%; mid dose, 98%; high dose, 101%; female-- low dose, 110%; mid dose, 104%; high dose, 91%. The incidences of hepatocellular adenomas or carcinomas (combined) were increased for dosed male mice (9/50; 21/50; 16/50) and for low dose female mice (3/50; 13/49; 3/50; 4/50). Alveolar/bronchiolar adenomas or carcinomas (combined) occurred with an increased incidence in high dose male mice (4/50; 9/49; 5/50; 11/50). Several nonneoplastic effects were increased incidence in high dose male mice (4/50; 9/49; 5/50; 11/50). Several nonneoplastic effects were detected in the kidneys of mid dose and high dose male and high dose female rats and of all dosed groups of male and female mice. These effects on the kidney included calculi, hydronephrosis, and epithelial hyperplasia in rats and casts and renal tubular degeneration in mice. C.I. Disperse Blue 1 was studied for mutagenicity in Salmonella typhimurium in the presence or absence of Aroclor 1254-induced male Sprague-Dawley rat or male Syrian hamster liver S9. C.I. Disperse Blue 1 was mutagenic in strain TA1535 in the presence of S9 and in strains TA97 and TA98 in the presence or absence of S9; it was not mutagenic in strain TA100. An audit of the experimental data was conducted for the 2-year toxicology and carcinogenesis studies of C.I. Disperse Blue 1. No data discrepancies were found that influenced the final interpretations. Under the conditions of these feed studies of C.I. Disperse Blue 1, there was clear evidence of carcinogenicity for male and female F344/N rats as shown by the increased occurrence of transitional cell papillomas and carcinomas, of leiomyomas and leiomyosarcomas, and of squamous cell papillomas and carcinomas of the urinary bladder. Urinary bladder calculi were observed in the groups of rats in which urinary bladder neoplasms were increased. Positive associations existed between the presence of calculi and transitional cell neoplasms in male and female rats, leiomyomas or leiomyosarcomas (combined) in female rats, and squamous cell neoplasms in male rats. A marginally increased occurrence of pancreatic islet cell adenomas or carcinomas (combined) was observed in male rats exposed to C.I. Disperse Blue 1. There was equivocal evidence of carcinogenicity of C.I. Disperse Blue 1 in male B6C3F1 mice as shown by marginally increased incidences of hepatocellular adenomas or carcinomas (combined) in dosed male mice and a marginally increased occurrence of alveolar/bronchiolar adenomas or carcinomas (combined) in high dose male mice. There was no evidence of carcinogenicity of C.I. Disperse Blue 1 in female B6C3F1 mice. Synonyms: C.I. 64500; 1,4,5,8-tetraamino-9,10-anthracenedione; 1,4,5,8-tetraaminoanthraquinone

Journal Article↗

Two-year evaluation of misoprostol for carcinogenicity in CD Sprague-Dawley rats.

The carcinogenic potential of misoprostol, a synthetic prostaglandin E1 analogue with anti-ulcer potential, was evaluated in CD Sprague-Dawley rats. The compound was given daily by gavage at 24, 240, and 2,400 micrograms/kg, up to 150 times the daily human dose for 2 years. Necropsies were done on all animals and the incidences of non-neoplastic and neoplastic changes analyzed for significance by life table methods. The only statistically significant non-neoplastic finding was epithelial hyperplasia and hyperkeratosis of the gastric mucosa. These changes, which are characteristic of some prostaglandins, were expected. Other non-neoplastic findings were typical of known spontaneous conditions in this strain of rats. The most frequent neoplasm was the pituitary adenoma, followed by the mammary fibroadenoma, mammary adenoma, mammary adenocarcinoma, and thyroid C-cell adenoma. A rare neoplasm, squamous cell carcinoma of the ovary was found in two rats. There was no evidence that misoprostol is carcinogenic for CD Sprague-Dawley rats.

Alprostadil↗

The 1998 Pan American Lecture. Intraocular invasion of conjunctival squamous cell carcinoma in five patients.

PURPOSE: To report five patients with intraocular invasion of conjunctival squamous cell carcinoma and to make recommendations regarding clinical recognition and treatment of this condition. METHODS: The authors reviewed the clinical records and pathology slides on five patients who had intraocular invasion of conjunctival squamous cell carcinoma, and they describe the presenting features and histopathology in these cases. RESULTS: Intraocular invasion of conjunctival squamous cell carcinoma occurred in older patients who had one or more recurrences of a previously excised conjunctival epithelial tumor located near the comeoscleral limbus. The intraocular recurrence often was heralded by the onset of low-grade inflammation and secondary glaucoma, simulating a granulomatous iridocyclitis. A white mass generally was observed in the anterior chamber angle. Histopathologic examination revealed an ingrowth of malignant epithelial cells through the limbus with diffuse involvement of the anterior segment of the eye. The reported patients were managed by modified enucleation (standard enucleation with excision of affected conjunctival tissue). Metastatic disease did not develop in any of the patients. CONCLUSIONS: The onset of signs of uveitis and glaucoma and a white mass in the anterior chamber angle in a patient with prior excision of a conjunctival squamous cell neoplasm tumor should raise suspicion of intraocular recurrence of conjunctival squamous cell carcinoma. Most affected patients require enucleation or subtotal orbital exenteration. The prognosis is good.

Aged↗

Muco-cutaneous changes during long-term therapy with hydroxyurea in chronic myeloid leukaemia.

Hydroxyurea is an antimetabolite agent used in the treatment of myeloproliferative disorders and sickle cell anaemia. Although hydroxyurea is relatively well tolerated, adverse effects often involve skin and mucous membrane during long-term therapy. A group of 510 patients affected by chronic myeloid leukaemia from 1977 to 1998 has been considered. Only 158 patients were treated with hydroxyurea and fulfilled inclusion/exclusion criteria of this study. A spectrum of severe cutaneous and mucosal changes (inflammatory and neoplastic) was seen in about 13% of patients (21 patients out of 158) and was studied in detail. Cutaneous and mucosal atrophy were observed in all 21 patients. Skin atrophy was often characterized by numerous telangiectases, especially on legs and on sun-exposed sites (16/21). Cutaneous, mucosal and nail hyperpigmentation was evident, albeit with variable extent, in 10 of the 21 patients. Severe stomatitis and glossitis with flattening of papillae were another common finding. Five patients, who received a particularly long treatment with hydroxyurea, developed squamous-cell neoplasms on sun-exposed sites (both squamous-cell carcinomas and keratoacanthomas). Acral changes were characteristic and constant, including acral erythema (21/21), dermatomyositis-like changes on the dorsa of hands (7/21), ulcers localized on acral areas of legs, on genitalia and oral mucosae (20/21). The frequency and the variety of these muco-cutaneous changes are reported and the mechanisms by which hydroxyurea may induce this muco-cutaneous syndrome-like group of changes, are proposed.

Adult↗

The influence of carcinogenic dosage and of sex on the induction of epitheliomas and sarcomas in the dorsal skin of rats.

The effect of varying the numbers (4, 5, 10, 20 and 40) of weekly applications of DMBA to the dorsal skin of intact and castrate male and female rats on the induction of basal and squamous celled epitheliomas and of sarcomas has been investigated.Basal celled tumours originate mainly in hair follicles and squamous celled neoplasms in the interfollicular regions of the epidermis and differ in their progression to malignancy. Penetration of the panniculus carnosus is neither a sufficient nor necessary criterion of malignancy since growing hair follicles pass through the muscle layer and carcinomas and sarcomas which are still confined to the dermis, spread along the perineural lymphatics and metastasise to the lungs.Sex and castration do not affect carcinogenesis of epitheliomas in the dorsal skin at any dose level. Significantly more sarcomas result from 20 weekly paintings in male than in female or castrate rats.The induction period for all tumour types is shortened in sensitive individuals only by an increase from 5 to 10 weekly applications. For less sensitive animals the rate of oncogenesis is accelerated with number of administrations up to 20, but slowed down from this level by 40 paintings. The optimal dose for speed of induction of all tumour types, for maximal yield of basal celled epitheliomas and for that of sarcomas in male rats is 20 weekly applications.THE PROGRESSION TO MALIGNANCY VARIES WITH TUMOUR TYPE: it is fast for sarcomas and slow for basal celled neoplasms. Of the 336 rats at risk only 1% have fibromas or other precursor lesions, while 40% have sarcomas; animals with squamous celled papillomas account for 12%, but those with carcinomas for 66%; there are, however, 64% of rats with basal celled papillomas and only 9% with carcinomas.The optimal dose phenomenon in carcinogenesis is discussed.

Animals↗

[Double adenoid cystic and squamous cells carcinoma of the hypopharynx and larynx. A contribution to the issue of multicomponent neoplasms].

Bicomponent cancer of the piriform fossa and larynx of 55 years old man has been described. The patient was treated surgically and by radiotherapy. The performance of laryngectomy and partial pharyngectomy with conservative bilateral neck dissection was used as surgical treatment. In histopathological findings of postoperative specimens two types of neoplasms: squamous cells and adenoid-cystic cancers were stated. The authors presented opinions on the affection arising of multicomponent tumours of the aerodigestive truct.

Carcinoma, Adenoid Cystic↗

NTP Toxicology and Carcinogenesis Studies of C.I. Direct Blue 218 (CAS No. 28407-37-6) in F344/N Rats and B6C3F1 Mice (Feed Studies).

C.I. Direct Blue 218 is a copper chelated dye used for cellulose, acetate, nylon, silk, wool, tissue, papers, and textile goods with a urea-formaldehyde finish. C.I. Direct Blue 218 is one of five chemicals/dyes that are part of the National Toxicology Program's Benzidine Dye Initiative, established to determine the toxicity and carcinogenicity of representative benzidine congeners, congener-derived dyes, and benzidine-derived dyes. Industrial grade C.I. Direct Blue 218 was selected for study because of its widespread use. Because of the high salt content, the dye was desalted prior to use. Toxicology and carcinogenesis studies were conducted by administering C.I. Direct Blue 218 in feed to groups of male and female F344/N rats and B6C3F1 mice for 14 days, 13 weeks, and 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, cultured Chinese hamster ovary cells, and Drosophila melanogaster. 14-DAY STUDY IN RATS: Groups of five male and five female F344/N rats were fed diets containing 0, 1,000, 3,000, 7,000, 15,000, or 30,000 ppm C.I. Direct Blue 218. All rats survived until the end of the study. Rats receiving 30,000 ppm lost weight, and the mean body weight gain of males receiving 15,000 ppm was significantly lower than that of the controls. Feed consumption by rats receiving 30,000 ppm was lower than that by the controls. Decreased organ weights at the 30,000 ppm level were related to the decreased body weights at this exposure level. 14-DAY STUDY IN MICE: Groups of five male and five female mice were fed diets containing 0, 1,000, 3,000, 7,000, 15,000, or 30,000 ppm C.I. Direct Blue 218. All mice survived until the end of the study. The final mean body weight of males receiving 30,000 ppm was 25% lower than that of controls and that of 30,000 ppm females was 20% lower than that of controls. Feed consumption by exposed and control groups was similar except for the 15,000 and 30,000 ppm groups. Feed spillage, due to reduced palatability, precluded the accurate determination of feed consumption by these two groups. Male and female mice receiving 30,000 ppm appeared hyperactive and emaciated during the last week of the study. Decreased organ weights were noted at 30,000 ppm and were attributed to the decreased mean body weights at this exposure level. 13-WEEK STUDY IN RATS: Groups of 10 male and 10 female rats were fed diets containing 0, 3,000, 10,000, or 20,000 ppm C.I. Direct Blue 218. All male and female rats survived until the end of the study. Rats exposed to 3,000,10,000, or 20,000 ppm C.I. Direct Blue 218 received approximate daily doses of 200, 600 or 1,300 mg dye/kg body weight (males) and 200, 800, or 1,400 mg/kg (females). The final mean body weight of male rats receiving 20,000 ppm was 24% lower than that of the controls and the final mean body weight of female rats receiving 20,000 ppm was 15% lower than that of the controls. Feed consumption by exposed and control groups was similar except in the 20,000 ppm groups where feed spillage was noted. Absolute and relative kidney weights of rats receiving 10,000 or 20,000 ppm were significantly greater than those of controls. Significantly decreased organ weights were noted, particularly in the 20,000 ppm groups, and were attributed to the lower mean body weights at this exposure level. The hematocrit, hemoglobin, mean erythrocyte volume, and mean erythrocyte hemoglobin values in male and female rats receiving 10,000 and 20,000 ppm were significantly lower than those of controls. Serum levels of alanine aminotransferase and sorbitol dehydrogenase in male and female rats receiving 20,000 ppm were significantly higher than those of controls, which is consistent with hepatocellular injury. Male rats receiving 10,000 ppm and male and female rats receiving 20,000 ppm had hepatic lesions consisting of intracytoplasmic pigment in periportal Kupffer cells, minimal to mild individual hepatocyte necrosis, increased numbers of binucleated and multinucleated hepatocytes, and minimal bile duct hyperplasia. Male and female rats receiving 20,000 ppm had ys receiving 20,000 ppm had yellow-green pigment within the cytoplasm of proximal convoluted tubules of the kidney. Microconcretions of mineral were observed along the corticomedullary junction of the kidney in most female rats, but the numbers of microconcretions in kidney sections were increased in females that received 20,000 ppm. 13-WEEK STUDY IN MICE: Groups of 10 male and 10 female B6C3F1 mice were fed diets containing 0, 3,000, 10,000, or 20,000 ppm C.I. Direct Blue 218. There were no deaths attributed to C.I. Direct Blue 218. Mice exposed to 3,000, 10,000, or 20,000 ppm C.I. Direct Blue 218 received approximate daily doses of 400, 1,500, or 3,600 mg dye/kg body weight (males) and 400, 1,800, or 4,000 mg/kg (females). The final mean body weight of males that received 20,000 ppm was 24% lower than that of the controls, and the final mean body weight of females that received 20,000 ppm was 14% lower than that of controls. Feed consumption by exposed mice was similar to that by controls except in the 20,000 ppm groups where feed spillage was noted. Significant differences in organ weights were noted at 20,000 ppm which were attributed primarily to the lower mean body weights in these exposure groups. The hematocrit, hemoglobin, mean erythrocyte volume, and mean erythrocyte volume, and mean erythrocyte hemoglobin values were significantly lower in males and females receiving 10,000 and 20,000 ppm. Serum levels of alanine aminotransferase and sorbitol dehydrogenase in male and female mice receiving 10,000 and 20,000 ppm were significantly higher than those of controls, indicating hepatic injury. Male and female mice receiving 20,000 ppm had hepatic lesions consisting of centrilobular hepatocyte hypertrophy and karyomegaly, multifocal individual hepatocyte necrosis, oval cell proliferation, and periportal Kupffer cells with intracytoplasmic pigment. Males and females receiving 20,000 ppm also had increased numbers of pigmented macrophages within the red pulp of the spleen. 2-YEAR STUDY IN RATS: The doses selected for the 2-year study of C.I. Direct Blue 218 were based on the lower final mean body weights and the occurrence of hepatic lesions in the 20,000 ppm groups in the 13-week study. Groups of 60 male and 60 female rats were fed diets containing 0, 1,000, 3,000, or 10,000 ppm C.I. Direct Blue 218 for 103 weeks. Nine or 10 rats from each group were evaluated after 15 months. Survival, Body Weights, Feed and Compound Consumption, and Clinical Findings: Survival of female rats receiving 10,000 ppm was slightly, but not significantly, lower than that of the controls. Mean body weights of male and female rats in the 10,000 ppm groups were approximately 5% to 14% lower than those of the controls after week 15, and the final mean body weights of male and female rats at this level were 11% and 9% lower than those of the controls, respectively. Feed consumption by exposed male and female rats was similar to that by the controls and was estimated to deliver daily doses of 40, 120, and 440 mg dye/kg body weight to males and 50, 140, and 470 mg/kg to females. No chemical-related clinical signs of toxicity were noted. Hematology and Clinical Chemistry: The hematocrit, hemoglobin, mean erythrocyte volume, and mean erythrocyte hemoglobin values in 10,000 ppm female rats were significantly lower than those of controls, while in males only the mean erythrocyte hemoglobin value was significantly lower. Serum levels of alanine aminotransferase and sorbitol dehydrogenase in male and female rats receiving 10,000 ppm were significantly higher than those of the controls at the 15-month interim evaluation. Pathology Findings: Squamous cell papillomas of the oral mucosa (pharynx) occurred in five males receiving 10,000 ppm but not in the lower exposure groups or in controls. A squamous cell carcinoma occurred in one 10,000 ppm male and a benign basosquamous tumor was observed in another. The incidence of oral mucosal neoplasms in the 10,000 ppm males was significantly greater than that in controls and exceeded the range observed in untreated historical controls (lO/l,253, 0.8%; range 0%-4%). These neoplasms were considered chemical related. Administration of C.I. Direct Blue 218 to rats produced significantly increased incidences of forestomach basal cell hyperplasia in males receiving 3,000 or 10,000 ppm (0 ppm, 0/50; 1,000 ppm, 2/50; 3,000 ppm, 10/50;10,000 ppm, 19/50) and in females receiving 10,000 ppm (1/50, 1/49, 5/50, 11/49). Further, there were marginal increased incidences of focal squamous hyperplasia in the 3,000 and 10,000 ppm males (1/50,1/50, 6/50, 4/50). Squamous cell papillomas of the forestomach were seen in two 3,000 ppm males and in one 10,000 ppm male; no papillomas were observed in the controls. A squamous cell carcinoma was also seen in one 3,000 ppm male. Because of the uncommon occurrence of forestomach neoplasms in untreated control male rats (4/1,253, 0.3%; range 0%-2%) and the slight increase in the incidence of focal hyperplasia, these neoplasms may have been chemical related. The incidence of uterine endometrial stromal polyps in each exposed group of female rats was significantly greater than that of the controls (1/50,12/50,10/50, 10/50). Because the incidences in the exposed groups did not increase in a dose-related manner and the incidence in the controls was unusually low (historical incidence: 205/1,251,16.4%; range 2%-30%), the higher incidence of stromal polyps in the exposed groups was not considered chemical related. 2-YEAR STUDY IN MICE: The dose selection for the 2-year study was based on the lower final mean body weights and the liver lesions observed at the 20,000 ppm level in the 13-week study. Groups of 60 male and 60 female mice were fed diets containing 0, 1,000, 3,000, or 10,000 ppm C.I. Direct Blue 218 for 103 weeks. Nine or 10 mice from each exposure group were evaluated after 15 months. Survival, Body Weights, Feed and Compound Consumption, and Clinical Findings: Survival of exposed male and female mice was similar to that of the controls. Mean body weights of male and female mice receiving 10,000 ppm were 10% to 29% lower than those of the controls during most of the study, and the final mean body weights in these groups were 19% lower than that of the controls for males and 27% lower than that of the controls for females. Feed consumption by exposed mice was similar to that by controls and the diets were estimated to deliver daily doses of approximately 120, 360, and 1,520 mg of dye/kg body weight to males and 140, 470, and 2,050 mg/kg to females. No chemical-related clinical signs of toxicity were noted. Hematology and Clinical Chemistry: Hematocrit, hemoglobin, and mean erythrocyte volume values in males and females receiving 10,000 ppm were significantly lower than those of the controls. Serum levels of alanine aminotransferase and/or sorbitol dehydrogenase values in male and female mice that received 10,000 ppm were significantly higher than those of controls, which is consistent with hepatocellular damage. Pathology Findings: The administration of C.I. Direct Blue 218 to mice produced significantly increased incidences of hepatocellular adenoma (0 ppm, 16/50; 1,000 ppm, 19/50; 3,000 ppm, 17/50; 10,000 ppm, 40/50) and hepatocellular carcinoma (7/50, 3/50, 8/50,17/50) in males receiving 10,000 ppm, and a significantly increased incidence of hepatocellular adenoma in females receiving 3,000 or 10,000 ppm (7/49, 12/50, 17/49, 41/49). In females that received 10,000 ppm, the incidence of hepatocellular carcinoma was marginally increased. Consistent with these findings, the incidence of hepatocellular foci of cytologic alteration, a preneoplastic lesion, was also increased in males and females in the 10,000 ppm groups. The increased incidences of hepatocellular foci, adenomas, and carcinomas were considered chemical related. Uncommon renal tubule neoplasms also occurred at low incidences in male mice receiving C.I. Direct Blue 218, but not in controls. Renal tubule adenomas were seen in two males receiving 1,000 ppm, one male receiving 3,000 ppm, and one male receiving 10,000 ppm. A renal tubule carcinoma was also seen in one male that received 1,000 ppm. Because renal tubule neoplasms are uncommon in male mice (4/1,366, 0.3%; range 0%-2%), these neoplasms may have been chemical related. Carcinomas of the small intestine occurred in four male mice receiving 10,000 ppm. One was observed at the 15-month interim evaluation, while the other three were observed in mice at the end of the study. One control male mouse also had a carcinoma of the small intestine. Because of the uncommon occurrence of small intestine neoplasms in untreated male mice (12/1,374, 0.9%; range 0%-4%), the slightly higher incidence of these neoplasms in males receiving 10,000 ppm may have been chemical related. Carcinomas of the small intestine also occurred in one 3,000 ppm and one 10,000 ppm female, but the low incidences precluded drawing an association with chemical administration. GENETIC TOXICOLOGY: C.I Direct Blue 218 was not mutagenic in Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537 tested with and without exogenous metabolic activation (S9). It was also tested in a modified Salmonella test protocol which employed reductive metabolism supplied by flavin mononucleotide or rat cecal bacteria, followed by oxidative metabolism; results of this test using strain TA1538 were also negative. C.I. Direct Blue 218 induced a small but significant increase in sister chromatid exchanges in Chinese hamster ovary cells at the highest dose tested without S9. No increase in chromosomal aberrations were observed in Chinese hamster ovary cells with or without S9. C.I. Direct Blue 218 did not induce sex-linked recessive lethal mutations in germ cells of male Drosophila melanogaster. CONCLUSIONS: Under the conditions of these 2-year feed studies, there was some evidence of carcinogenic activity of C.I. Direct Blue 218 in male F344/N rats based on the occurrence of pharyngeal neoplasms. Squamous cell neoplasms of the forestomach may have been chemical related. There was no evidence of carcinogenic activity of C.I Direct Blue 218 in female F344/N rats given 1,000, 3,000, or 10,000 ppm. There was clear evidence of carcinogenic activity of C.I. Direct Blue 218 in male and female B6C3F1 mice based on increased incidences of hepatocellular adenomas and carcinomas. The occurrence of a few neoplasms of the kidney and small intestine in male mice may have been related to C.I. Direct Blue 218 treatment. The administration of C.I. Direct Blue 218 produced an increased incidence of forestomach basal cell hyperplasia in rats and hepatocellular foci of cytologic alteration in mice. Synonyms: cuprate(4-), [mu-[(3,3'-dihydroxy[1,1'-biphenyl]-4,4'-diyl)bis[5-amino-4-hydroxy- 2,7-naphthalnedisulfonato]](8-)]]di-, tetrasodium; copper, [tetrahydrogen-3,3'-[(3,3'-dihydroxy-4,4'-biphenylylene)bis(azo)]bis [5-amino-4-hdroxy-2,7-naphthalenedisulfonato](4-)]di-, tetrasodium salt; 1-naphthol-3,6-disulfonic acid, 2,2'-(3,3'-dihydroxy-4,4'-biphenylylenebisazo)bis [8-amino-, dicopper deriv., tetrasodium salt

Journal Article↗

A survey on neoplasia in domestic species over a 40-year period from 1935 to 1974 in the Republic of South Africa. I. Tumours occurring in cattle.

A survey was carried out on all the bovine neoplasms recorded in the registration files of the Section of Pathology of the Veterinary Research Institute, Onderstepoort, Republic of South Africa, over a 40-year period from 1935 to 1974. The 606 neoplasms were divided and tabulated into 20 groups according to body systems or tissue types. Skin, connective tissue, lymphoid tissue and ocular tumours in that order accounted for the majority of neoplasms. Squamous cell carcinoma was the most frequent neoplasm and the 2 main sites for it were the eye and the vulva. Fibromas and fibrosarcomas made up the majority of the connective tissue tumours. The lymphoid tissue tumours, composed almost entirely of lymphosarcomas, were the 3rd most common group of tumours. Penile fibropapillomas and cutaneous papillomas were commonly encountered, and there was also a noteworthy incidence of melanomas, mesotheliomas and neurofibromas. The male and female genital tracts were relatively frequently neoplastic, due principally to the occurrence of penile fibropapillomas, vulvar squamous cell carcinomas and uterine carcinomas. The incidence of respiratory, hepatic and vascular system tumours was moderate, whilst tumours of the endocrine, central nervous, skeletal and muscular systems were rarely encountered.

Animals↗