Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report two cases of periosteal osteosarcoma of the jaws, a tumour which is one of the two variants of juxtacortical osteosarcoma. Periosteal osteosarcoma involving the jaw bones is extremely rare. Because of its chondroblastic differentiation, sometimes predominant, this tumour may pose some problems of differential diagnosis with chondrosarcoma or pleomorphic adenoma: immunochemistry may be necessary. This localization does not change the clinical, radiologic, histologic and prognostic features of periosteal osteosarcoma.
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PMID:[Periosteal osteosarcoma of the jaw. Apropos of 2 cases]. 781 Nov 21

We report a rare case of carcinosarcoma of parotid gland in a pleomorphic adenoma. The tumor showed two distinct heterologous components, a ductal carcinoma and an osteosarcoma. The latter has not been described so far in such tumors arising in pleomorphic adenoma of parotid gland.
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PMID:Carcinosarcoma of parotid gland having osteosarcoma as sarcomatous component: a case report. 815 25

The antiproliferative action of 1,25-dihydroxyvitamin D3 in osteosarcoma, breast carcinoma, and colon carcinoma cell lines has been described. In this study, the level of vitamin D receptor was analyzed in a panel of colon adenoma and adenocarcinoma cell lines and the receptor level was correlated with the response to treatment with 1,25-dihydroxyvitamin D3. Ribonuclease protection and ligand-binding assays quantitated the level of vitamin D receptor mRNA expression and the level of functional receptors, respectively. The more well-differentiated cell lines, such as VACO 330, showed higher levels of vitamin D receptor than less-differentiated cell lines, such as SW620. Proliferation assay, clonogenic assay, and growth curve study in HT29 and SW620 cell lines assessed the antiproliferative effect of 1,25-dihydroxyvitamin D3 at concentrations ranging from 10(-11) to 10(-6) M. HT29 showed significant (P < 0.05) growth inhibition at 10(-9) to 10(-6) M concentrations, but growth of SW620 remained unchanged. The amount of vitamin D receptor in 12 malignant colonic tumors was compared with that of adjacent normal tissue, and in 9 cases, the tumor expressed a lower vitamin D receptor level. Our results suggest that the level of vitamin D receptor correlates with the degree of differentiation in human colon cancer cell lines and may serve as a useful biological marker in predicting clinical outcome in patients.
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PMID:1,25-Dihydroxyvitamin D3 receptor as a marker of human colon carcinoma cell line differentiation and growth inhibition. 839 79

A rapidly growing mandibular tumor occurred in a 17 month old female infant. Tumor outgrowth showing a periosteal reaction was radiographically seen on the lower surface (base) of the mandible. Under the biopsy diagnosis of osteosarcoma, high-dose chemotherapy with methotrexate was performed, resulting in little effect. The right hemimandibulectomy specimen disclosed intraosseous infiltrative growth of pleomorphic adenoma of salivary gland type, associated with chondroid stroma and reactive bone formation. The highly proliferative small-sized cells retained immunohistochemical features of myoepithelial cells, with positive reactivity of cytokeratin, vimentin, S-100 protein, alpha-smooth muscle actin, epithelial membrane antigen, CA15-3, type IV collagen, laminin and p53 protein. No heterotopia of the salivary gland was identified within the bone tissue. The tumor recurred 2 months later. Due to uncontrollable local growth, the patient died 8 months after operation. At autopsy, reactive ossification was closely associated with malignant myoepithelial proliferation. No distant metastasis was noted. This osteosarcoma-like tumor can be regarded as myoepithelial carcinoma in pleomorphic adenoma, originating from intramandibular heterotopic salivary gland tissue.
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PMID:Myoepithelial carcinoma in pleomorphic adenoma of salivary gland type, occurring in the mandible of an infant. 854 41

The expression of Bfl-1 gene, a novel Bcl-2 related gene, was determined by Northern blot analysis using a radiolabeled cDNA specific for Bfl-1 gene in 82 surgically resected tissue specimens of 28 gastric cancers, 15 colon cancers, nine breast cancers, eight bone and soft tissue sarcomas, five ovarian cancers, nine colon adenomas and eight gastric adenomas. A high rate of expression was observed in gastric and colon cancer, at 86 and 93%, respectively. In breast cancer, bone and soft tissue sarcoma and ovarian cancer, the expression rate was 33, 25 and 40%, respectively. In stomach cancer, the expression rate of Bfl-1 gene in metastatic lymph nodes was 82%, which was higher than 50% of the primary sites (p < 0.02). The intensity of RNA bands of the gastric cancer specimens was compared according to the stage, demonstrating that there was no difference in the expression levels of Bfl-1 gene between the stages in both primary sites and metastatic lymph nodes. Bfl-1 gene was expressed in three (33%) out of nine adenomas of the colon, while it was not detected in all eight gastric adenomas, We also examined the RNA expression of Bfl-1 gene in 22 human cancer cell lines consisting of five stomach cancer, four squamous cell carcinoma, three lung cancer, three cervical cancer, two colon cancer, two brain cancer, two leukemia and one osteosarcoma cell lines. Bfl-1 gene band was detected in one (5%) cervical cancer cell line, SiHa. The results of cancer tissue specimens indicate that Bfl-1 gene may play an important role in carcinogenesis of human cancers and may be involved in a relatively early phase of the adenoma-carcinoma sequence in colon cancer development. However, the mechanism responsible for the very low rate of expression in established cell lines is not clearly understood and further investigation is necessary to clarify the mechanism involved.
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PMID:Expression of a novel Bcl-2 related gene, Bfl-1, in various human cancers and cancer cell lines. 949 79

Manifesting a putative origin from a pleomorphic adenoma, carcinosarcoma of the salivary gland is a heterologous neoplasm in which a sarcomatous and a carcinomatous component coexist. We present a parotid gland carcinosarcoma in a 77-year-old man with peculiar morphological findings. Fine-needle aspiration cytology allowed a preoperative diagnosis of poorly differentiated carcinoma. At histologic examination, the tumor showed biphasic differentiation with an epithelial component made up of well-differentiated keratinizing squamous carcinoma and ductal-type adenocarcinoma, and a mesenchymal component, revealing focal areas of osteosarcoma and myoepithelial malignant proliferation. Carcinosarcoma is a very rare malignant neoplasm, accounting for 0.16% of malignant salivary gland tumors: only 60 cases have been reported, some of which arose "de novo", i.e., without clinico-pathologic evidence of a pre- or co-existing pleomorphic adenoma.
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PMID:Carcinosarcoma of the parotid gland: cytological, clinicopathological and immunohistochemical study of a case. 1092 29

True malignant mixed tumor (carcinosarcoma) of the salivary gland is an extremely rare tumor. By definition, it is composed of both malignant epithelial and malignant mesenchymal elements. The most common type of the former is squamous cell carcinoma or adenocarcinoma and the most common type of the latter is chondrosarcoma, followed in frequency by fibrosarcoma, leiomyosarcoma, osteosarcoma, and in rare instances liposarcoma. We report a case of true malignant mixed tumor of the parotid gland in association with a pleomorphic adenoma in a 47-year-old man that contained a very unusual type of malignant mesenchymal component, rhabdomyosarcoma. Cytologic and histologic features and immunohistochemical results are presented. In addition, the literature is reviewed, and the possible histogenesis and pathogenesis of malignant mixed tumor of the salivary gland are briefly discussed.
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PMID:True malignant mixed tumor (carcinosarcoma) of parotid gland with unusual mesenchymal component: a case report and review of the literature. 1137 Dec 38

Neurofibromatosis type 1 (NF 1) is a syndrome with a predisposition for benign and malignant tumor development. Of the malignant neoplasms, osteogenic sarcomas are rare but have been described. There are some reports of patients with neurofibromatosis type 1 with a parathyroid adenoma and hyperparathyroidism. Also, there are studies that imply that the parathyroid hormone plays a role in the regulation and modulation of oseogenic sarcomas in vitro. We report about a 50-year-old female suffering from neurofibromatosis type 1, with a 3-year documented history of untreated hyperparathyroidism and a parathyroid adenoma. The patient developed a mandibular osteogenic sarcoma. To our knowledge, this is the first reported case occurring in the mandible. The unusual tumor site for a patient with neurofibromatosis type 1, the conjugation with hyperparathyroidism and the rapid growth of an osteogenic sarcoma are intriguing.
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PMID:Neurofibromatosis type 1, hyperparathyroidism, and osteosarcoma: interplay? 1243 89

A 69-year-old woman was diagnosed with a malignant tumor of the right proximal femur. She had primary hyperparathyroidism and chronic elevation of parathyroid hormone levels (PTH > 1,000 pg/ml). She underwent resection of the bone lesion; histological analysis showed a high-grade fibroblastic osteosarcoma. In addition, she underwent curative resection of a large left superior parathyroid adenoma. To our knowledge, this is the third reported clinical case of osteosarcoma arising in association with hyperparathyroidism.
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PMID:Osteosarcoma of bone in apatient with primary hyperparathyroidism: a case report. 1251 Aug 19

Nitrofurantoin was studied and evaluated because of its widespread use as a drug for treating urinary tract infections in humans, its structural relationship to known carcinogenic 5-nitrofuran compounds, and the lack of adequate studies to assess its carcinogenicity. Toxicology and carcinogenesis studies of nitrofurantoin were conducted by administering nitrofurantoin (greater than 99% pure) in feed to groups of F344/N rats and B6C3F1 mice of each sex for 14 days, 13 weeks, or 2 years. Fourteen-Day and Thirteen-Week Studies: None of the rats (at dietary concentrations up to 20,000 ppm) died before the end of the 14-day studies. Rats that received 5,000, 10,000, or 20,000 ppm lost weight. Four of five male and 4/5 female mice that received 10,000 ppm and 1/5 females that received 5,000 ppm nitrofurantoin died before the end of the studies. Mice that received 5,000 ppm and male mice that received 10,000 ppm lost weight. In the 13-week studies, final mean body weights of rats that received 2,500, 5,000, or 10,000 ppm were 10%, 34%, or 47% lower than that of the controls for males and 15%, 31%, or 41% lower for females. Feed consumption by dosed and control rats was generally similar. Degeneration of the germinal epithelium of the seminiferous tubules of the testis was observed in male rats that received 2,500 to 10,000 ppm nitrofurantoin. Necrosis of the ovarian follicles was observed in 8/10 female rats that received 10,000 ppm, in 3/10 females that received 5,000 ppm, and in 1/10 that received 2,500 ppm. For mice, final mean body weights of the 5,000-ppm groups were 13% lower than that of the controls for males and 15% lower for females. Two of 10 male mice that received 5,000 ppm and 1/10 males that received 300 ppm died before the end of the 13-week studies. Estimated feed consumption was similar for dosed and control groups. Degeneration of the germinal epithelium of the testis was observed in males that received 1,300 to 5,000 ppm; necrosis of the ovarian follicles was observed in females that received 5,000 ppm but not in the lower dose groups. Necrosis of the renal tubular epithelium was observed in 2/9 males that received 5,000 ppm. Based on these results, 2-year studies of nitrofurantoin were conducted by feeding diets containing 0, 1,300, or 2,500 ppm nitrofurantoin to groups of 50 male F344/N rats and to groups of 50 male and female B6C3F1 mice for 103 weeks. Groups of 50 female F344/N rats were fed diets containing 0, 600, or 1,300 ppm nitrofurantoin on the same schedule. Body Weight and Survival in the Two-Year Studies: Mean body weight and average daily feed consumption of dosed male and female rats were similar to those of the controls throughout the studies. The average amount of nitrofurantoin consumed per day was estimated to be 60 and 110 mg/kg for low and high dose male rats and 30 and 60 mg/kg for low and high dose female rats. No significant differences in the number of rats surviving to the end of the studies were observed between any groups of rats of either sex (male: control, 24/50; low dose, 27/50; high dose, 26/50; female: 25/50; 26/50; 31/50). Mean body weights of high dose male and female mice were up to 12% lower than those of the controls throughout most of the studies. The average daily feed consumption by dosed mice ranged from 93% to 100% that by controls. The average amount of nitrofurantoin consumed per day was estimated to be 280-300 mg/kg and 570-580 mg/kg for low and high dose mice. The survival of the control group of female mice was lower than that of the dosed groups (control, 19/50; low dose, 37/50; high dose, 37/50). The decrease in survival was most likely related to the increase in microbial infection in the reproductive tract observed in the controls. Groups of male mice had similar survival (28/50; 29/50; 34/50). Nonneoplastic and Neoplastic Effects in the Two-Year Studies: Organs showing toxicity from nitrofurantoin exposure identified in the short-term studies were the testis in male rats and mice, the ovary in female rats and mice, and the kidney in male mice. Lesions oband mice, the ovary in female rats and mice, and the kidney in male mice. Lesions observed in the 2-year studies were in the testis in male rats and mice, ovary in female mice, and kidney in male rats. Chronic nephropathy was observed in nearly all rats, but the severity of the lesions was judged to be greater in dosed male rats. Hyperplasia of the transitional cell epithelium (control, 0/50; low dose, 5/50; high dose, 2/50) and hydronephrosis of the renal pelvis (0/50; 5/50; 2/50) were also observed in dosed male rats. In the standard single sections of the left and right kidney from each rat, tubular cell adenomas were observed in one low dose and two high dose males; a tubular cell carcinoma was observed in another high dose male. Because the number of renal tubular cell neoplasms identified by standard procedures in the dosed male rats was low, additional step-sections of the kidney were evaluated. The incidences of tubular cell adenomas derived from the step-sections and original sections (combined) were significantly increased in dosed male rats (adenomas: 3/50; 11/50; 19/50); tubular cell carcinomas occurred in two high dose males only. Lesions considered to be associated with the nephropathy and nitrofurantoin exposure were observed in male rats and included hyperplasia of the parathyroid glands (3/49; 18/47; 23/49), fibrous osteodystrophy of the bone (0/50; 5/50; 5/50), and mineralization of the glandular stomach (1/49; 8/50; 14/50). Atypical cells of the epididymis (0/50; 0/50; 12/50) and degeneration of the testis (0/50; 0/50; 36/50) were observed in high dose male rats. Fibrinoid necrosis of arterioles (1/50; 8/50; 15/50) and perivascular infiltration of mononuclear cells (3/50; 9/50; 19/50) were also observed in the testis of male rats. Interstitial cell adenomas of the testis occurred with a negative trend (47/50; 45/50; 21/50), and no adenomas or carcinomas of the preputial gland were seen in high dose male rats (12/48; 11/50; 0/47). The incidence of clitoral gland neoplasms was increased in low dose female rats (5/44; 10/38; 4/42). Osteosarcomas were observed in the bone of one low dose and two high dose male rats. The historical incidence of osteosarcomas in untreated male F344/N rats is 8/1,937 (0.4&percnt;). The incidences of subcutaneous tissue neoplasms in dosed male rats were greater than that in the controls (1/50; 7/50; 5/50). No neoplastic lesions in dosed female rats or male mice were considered to be compound related at the doses of nitrofurantoin administered. For female mice, ovarian atrophy was observed in 48/50 low dose and 49/50 high dose mice but not in controls. Tubular cell adenomas of the ovary (0/50; 0/50; 5/50), benign mixed tumors (tubular and stromal) (0/50; 0/50; 4/50), and granulosa cell tumors (0/50; 3/50; 2/50)) were observed in dosed female mice. One granulosa cell tumor in the high dose group was malignant. Ovarian abscesses (18/50) and suppurative inflammation of the uterus (11/50) were observed in control female mice but not in dosed female mice and are believed to be related to indigenous microbial infections and most likely were the cause of early deaths in this group. Adenocarcinomas of the uterus were seen in one low dose and in one high dose mouse. Testicular aspermatogenesis (1/49; 1/49; 16/50), degeneration of the germinal epithelium (0/49; 3/49; 23/50), and atypical cells (0/50; 0/49; 26/50) and depletion (1/50; 1/49; 15/50) of the epididymis were observed at increased incidences in high dose male mice. Spindle cell hyperplasia of the adrenal cortex was observed in dosed female mice (3/50; 41/50; 45/50). A spindle cell adenoma (adrenal capsule adenoma) was seen in one low dose female mouse, and a spindle cell carcinoma (adrenal capsule carcinoma) was seen in one low dose male mouse. Mineralization of the renal medulla (male: 0/50; 0/50; 17/50; female: 0/50; 0/50; 7/50) and dilatation of the renal tubules (male: 0/50; 0/50; 14/50) were observed in high dose mice. Hepatocellular neoplasms (adenomas or carcinomas, combined) were observed at an increased incidence in high dose female mice (2/50; 2/50; 8/50). An Ito cell tumor of the liver was observed in one low dose and one high dose female mouse. Malignant lymphomas occurred in female mice (12/50; 19/50; 24/50). Genetic Toxicology: Nitrofurantoin was mutagenic in Salmonella typhimurium strains TA98 and TA100, with and without metabolic activation, but was not mutagenic for strains TA1535 or TA1537. Nitrofurantoin induced forward mutations at the TK+/- locus of L5178Y mouse lymphoma cells in the absence of metabolic activation (it was not tested with activation). Nitrofurantoin induced increased numbers of sister chromatid exchanges and chromosomal aberrations in cultured Chinese hamster ovary cells with and without metabolic activation. Results of the sex-linked recessive lethal assay in Drosophila were negative after administration of nitrofurantoin by feeding or by injection. Conclusions: Under the conditions of these 2-year feed studies, there was some evidence of carcinogenic activity of nitrofurantoin for male F344/N rats as shown by increased incidences of uncommon kidney tubular cell neoplasms. Uncommon osteosarcomas of the bone and neoplasms of the subcutaneous tissue were observed in dosed male rats. Incidences of interstitial cell adenomas of the testis and neoplasms of the preputial gland were decreased in the 2,500-ppm group of male rats. There was no evidence of carcinogenic activity of nitrofurantoin for female F344/N rats fed diets containing 600 ppm or 1,300 ppm for 2 years. Female rats may have been able to tolerate higher doses. There was no evidence of carcinogenic activity of nitrofurantoin for male B6C3F1 mice fed diets containing 1,300 ppm or 2,500 ppm for 2 years. There was clear evidence of carcinogenic activity of nitrofurantoin for female B6C3F1 mice as shown by increased incidences of tubular adenomas, benign mixed tumors, and granulosa cell tumors of the ovary. Nonneoplastic lesions considered related to nitrofurantoin exposure were chronic nephropathy and associated lesions (hyperplasia of the parathyroid gland, fibrous osteodystrophy of the bone, and mineralization of the glandular stomach) in male rats and testicular degeneration in male rats and mice. Ovarian atrophy and hyperplasia of the adrenal cortex spindle cells were observed in dosed female mice. Synonyms: 1-(((5-nitro-2-furanyl)methylene)amino-2,4-imidazolidinedione); 1-(5-nitro-2-furfurylideneamino)-hydantoin; N-(5-nitro-2-furfurlidene)-1-aminohydantoin; 1-((5-nitrofurfurylidene)amino)hydantoin Trade Names: Benkfuran; Benkfurin; Chemiofuran; Cyantin; Dantafur; Furadantin; Furadantine; Furadantoin; Furadonin; Furadonine; Furantoin; Furatoin; Furobactina; Ituran; Macrodantin; Nifurantin; NSC 2107; N-Toin; Orafuran; Parafuran; Urizept; USAF EA-2; Welfurin; Zoofurin
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PMID:NTP Toxicology and Carcinogenesis Studies of Nitrofurantoin (CAS No. 67-20-9) in F344/N Rats and B6C3F1 Mice (Feed Studies). 1272 84


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