Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 53-year-old female was admitted with apathy, left sensory and motor disturbance, left homonymous hemianopsia, and dressing apraxia. Computed tomography and magnetic resonance imaging showed a huge mass markedly enhanced in and around the right trigone. Cerebral angiography revealed rich vascularity of the tumor mainly fed by the right anterior choroidal artery. The feeding vessel was embolized with microfibrillar collagen after superselective catheterization. Seven days later, the tumor was totally removed with low blood loss. The histological diagnosis was fibroblastic meningioma. She was discharged without neurological deficit, except for left homonymous hemianopsia.
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PMID:Giant meningioma fed by the anterior choroidal artery: successful removal following embolization--case report. 128 Mar 43

The nitrosourea-induced rat glioma clone RG2 was tested for its capacity to form multicellular tumor spheroids (MTS's). Resulting spheroids were investigated by light and electron microscopy with regard to their proliferation patterns and morphological features. Using microsurgical techniques and avoiding mechanical injury of the brain tissue, the authors successfully transplanted avascular MTS's under the dura of the cerebellum, above the vermis, in 43 adult syngeneic Fischer CD rats. The rate of tumor establishment was 93%, and the tumors that were solid and spheroid in shape grew exponentially. Neovascularization could be observed at 3 days after implantation, and invasion of the cerebellum occurred by 3 to 5 days. Neurological deterioration, including ataxia, impairment of walking, and apathy, could be observed after 10 days. The mean survival time was approximately 16 days. The subdural cerebellar tumors were studied by histological techniques, and two morphometric methods were applied to check the growth of implanted spheroids. All tumors were deeply stained with the Evans blue dye-albumin complex, demonstrating disturbance of the blood-brain barrier. The easy accessibility of the cerebellar vermis in rats, the microsurgical implantation of glioma spheroids under the dura avoiding nerve tissue disruption, and the high percentage of reproducible establishment of tumors favor this experimental brain-tumor model. This should be an excellent model for study of experimental therapies.
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PMID:RG2 glioma growth in rat cerebellum after subdural implantation. 242 62

The author studied the medical records of 133 patients who underwent surgery for adenocarcinoma of the colon or rectum in the Metropolitan Hospital Complex Arnulfo Arias Madrid from June 1972 to July 1992. In 9 (6.7%) the tumor was staged as Dukes A, in 49 (36.8%) as Dukes B; in 60 (43.1%) as Dukes C and in 10 (16.7%) as Dukes D. The anatomical location of the tumor was the cecum in 9 (6.7%), the ascending colon in 3 (2.3%), the sigmoid colon in 44 (33%) and the rectum in 41 (31.6%). Of the rectal carcinomas 24 (58.5%) were in the inferior one third, 10 (24.3) were in the middle and 7 (17%) in the superior third. It is evident that nearly two thirds of the tumors were within reach of the digital rectal examination of the sigmoidoscopic examination. The parents ranged from 21 to 89 years of age and their median age was 63 years. 73 patients were women and 60 were men. 60.5% of the women and 39.5% of the men had carcinoma of the colon. The sexual prevalence of carcinoma of the rectum was different: 5% were in men and 43% were in women. 2.2% of the tumors were synchronous and 4% were metachronous. The author discusses the number, type and indications for the surgical procedures used. There were no perioperative deaths. The 5 year survival for adenocarcinomas of the colon was 100% for those patients with tumors staged as Dukes A, 78.5% for the Dukes B, 61.1% for the Dukes C and 0% for those staged as Dukes D. For the rectal adenocarcinomas the 5 year survival was 100% for those patients with tumors in Stage Dukes A, 57.1%, for those in Dukes B, 33.3 for those in Dukes C and 0% in those in Dukes D. These results indicate that these patients are seen in an advanced stage and point to the urgent need to make the diagnosis in early, curable stages. The low incidence of tumors in stage Dukes A indicates an indifference of the patients and/or the doctors to the symptoms and signs of this disease. The most frequent symptoms, in descending order were: bleeding on defecation (all types), change in bowel habits (diarrhea or constipation), abdominal pains, tenesmus and anemia (with its different clinical manifestations). Other symptoms were a palapable abdominal mass, feces with bloody mucus and rectal prolapse on defecation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Colorectal cancer. A study of 133 surgical cases]. 847 34

There are two broad categories of drug resistance encountered during cancer chemotherapy, i.e. intrinsic and acquired. They are observed in virtually every type of tumor with every known anticancer chemotherapeutic drug. As such there is an urgent need to develop innovative approaches of preventing or reversing these types of resistance. One strategy to do so is to develop completely new drugs which may be resistance free, such as direct acting angiogenesis inhibitors (T. Boehm, J. Folkman, T. Browder, M.S. O'Reilly, Antiangiogenic therapy of experimental cancer does not induce acquired drug resistance, Nature 390 (1997) 404-407; R.S. Kerbel, Inhibition of tumor angiogenesis as a strategy to circumvent acquired resistance to anti-cancer therapeutic agents, BioEssays 13 (1991) 31-36; R.S. Kerbel, A cancer therapy resistant to resistance, Nature 390 (1997) 335-336). Another is to devise methods which will improve significantly the effectiveness of those conventional drugs already in use, such as adriamycin, cyclophosphamide and taxol. We have directed efforts towards the latter. They depend on the discovery of a new class of chemosensitizers which act as antiadhesive agents rendering solid tumors more susceptible to such conventional cytotoxic therapeutic drugs. Examples of this concept are illustrated with bovine testicular hyaluronidase and a mouse mammary tumor called EMT-6. When this enzyme preparation is used to treat intact multicellular spheroids of the EMT-6 tumor, the spheroids are substantially disaggregated. Dispersed spheroids are more susceptible to the cytotoxic effects of cyclophosphamide than intact spheroids. Moreover, this antiadhesive chemosensitizing effect can actually be reproduced in BALB/c mice when EMT-6 cells are grown intraperitoneally as an ascites tumor (consisting mostly of multicellular aggregates) and the mice are given injections of hyaluronidase and cyclophosphamide. In a similar fashion, the indifference of P-glycoprotein-positive multidrug-resistant EMT-6 spheroids to the P-glycoprotein reversal agent PSC-833 (a cyclosporin A analogue) can be reversed by disaggregation of the intact spheroids by hyaluronidase. This renders the treated cells highly sensitive to a combination of adriamycin and PSC-833 in a manner similar to the striking chemosensitization effects commonly observed in monolayer culture systems. Thus, hyaluronidase has the potential to reverse forms of both intrinsic and acquired drug resistance in solid tumors, such as EMT-6, which are sensitive to its antiadhesive effects.
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PMID:Reversal of intrinsic and acquired forms of drug resistance by hyaluronidase treatment of solid tumors. 983 18

The authors present the case of a patient treated in the Department of Infectious Diseases at CMUJ in Cracow. The patient's full clinical picture suggested the possibility of the development of neuroborreliosis and disguised the symptoms of a developing intracranial tumor. Neuroborreliosis was suspected due to epidemiologic history (a tick bite, erythema migrans), general symptoms (fatigue, hypersomnia, apathy, dysmnesia, concentration disorders) and neurological symptoms, seropositive tests for Borrelia burgdorferi in serum and cerebrospinal fluid (IgG), increased protein concentration in cerebrospinal fluid. Owing to the fact that the serologic criteria of neuroborreliosis were not fulfilled, and other symptoms (loss of consciousness) appeared, CT was done. The CT showed the presence of a tumor in the longitudinal fissure of the brain, which, after intraoperative and histopathological examination, was defined as meningioma.
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PMID:[The coexistence of an intracranial tumor and a positive epidemiologic history of Lyme borreliosis as the reason for diagnostic problems--case report]. 1069 87

A 72-year-old man was referred for geriatric evaluation with a view toward placement in institutional care. He presented originally to an internal medicine team with a six-month history of weight loss, constipation, generalized weakness, and apathy; investigations to rule out an underlying neoplasm were negative. Interdisciplinary assessment revealed coexisting dementia, myopathy, and oropharyngeal dysphagia. These findings prompted further diagnostic evaluation and a diagnosis of inflammatory myopathy with associated oropharyngeal dysphagia and dementia was made. The dementia, myopathy, and oropharyngeal dysphagia responded to steroids and rehabilitation and the patient regained his independence.
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PMID:Dementia with oropharyngeal dysphagia and myopathy. 1145 67

Hexachlorocyclopentadiene is an intermediate used in the manufacture of flame retardants, resins, and chlorinated cyclodiene pesticides. Toxicology and carcinogenesis studies were conducted by exposing male and female F344/N rats and B6C3F1 mice to atmospheres containing hexachlorocyclopentadiene (approximately 98% pure) for 6 hours per day, 5 days per week, for 13 weeks or 2 years. A stop-exposure evaluation was conducted in male B6C3F1 mice to determine the influence of exposure level and exposure duration on the development of nonneoplastic lesions of the respiratory tract and on their regression or progression after exposure was stopped. Genetic toxicology studies were conducted in Salmonella typhimunum, cultured Chinese hamster ovary cells, Drosophila melanogaster, and mouse peripheral blood samples were analyzed for frequency of micronucleated normochromatic erythrocytes. 13-WEEK STUDY IN RATS: Groups of 10 male and 10 female rats were exposed to atmospheres containing 0, 0.04, 0.15, 0.4, 1, or 2 ppm (equivalent to 0, 0.45, 1.67, 4.46, 11.14, and 22.28 mg/m(3)) hexachlorocyclopentadiene. Additional rats were exposed to 0, 0.04, 0.4, or 2 ppm hexachlorocyclopentadiene and evaluated for differences in clinical pathology parameters. All rats in the 1 and 2 ppm groups died during the first 4 weeks of the study. The final mean body weight and mean body weight gain of males exposed to 0.4 ppm were significantly lower than those of the controls. Listlessness was observed in 2 ppm rats from week 1, in 1 ppm rats from week 2, and in 0.4 ppm rats during week 3. Rats exposed to 1 or 2 ppm also experienced respiratory distress. No chemical-related differences in hematology, clinical chemistry, or urinalysis parameters were observed in male or female rats. Absolute and relative lung weights of 0.4 ppm males were significantly greater than those of the controls. Inflammation (necrotizing, chronic, or suppurative) of the nose, larynx, trachea, and lung was observed in 0.4, 1, and 2 ppm males and females. Squamous metaplasia of the epithelial lining of the nose of 0.4 ppm males and 1 and 2 ppm males and females was also observed. 13-WEEK STUDY IN MICE: Groups of 10 male and 10 female mice were exposed to atmospheres containing 0, 0.04, 0.15, 0.4, 1, or 2 ppm (equivalent to 0, 0.45, 1.67, 4.46, 11.14, and 22.28 mg/m(3)) hexachlorocyclopentadiene. Additional mice were exposed to 0, 0.04, 0.4, or 2 ppm and evaluated for differences in clinical pathology parameters. All 2 ppm mice died during the first week of exposure. All 1 ppm mice died during the first 5 weeks of exposure. Five males and two females in the 0.4 ppm group died during the first 2 weeks of exposure. Deaths in the other groups were not related to hexachlorocyclopentadiene exposure. Final mean body weights of males exposed to 0.15 and 0.4 ppm and the body weight gain of 0.4 ppm males were significantly lower than those of the controls. Treatment-related clinical findings included listlessness in 0.4 and 1 ppm males and females. No chemical-related differences in hematology, clinical chemistry, or urinalysis parameters were observed in male or female mice. Necrosis or inflammation of the nose, larynx, trachea, or lung occurred in mice exposed to 0.4,1, and 2 ppm hexachlorocyclopentadiene. Squamous metaplasia of the larynx or trachea was observed in 0.15, 0.4, and 1 ppm males and in 0.4 and 1 ppm females. 2-YEAR STUDY IN RATS: Survival, Body Weights, Clinical Findings, and Urinalysis Groups of 60 male and 60 female rats were exposed to atmospheres containing 0, 0.01, 0.05, or 0.2 ppm (equivalent to 0, 0.11, 0.56, and 2.28 mg/m(3)) hexachlorocyclopentadiene. Survival rates and mean body weights of exposed rats were similar to those of the controls. No chemical-related clinical findings were observed in male or female rats during the 2-year study. No differences in urinalysis parameters at the 15-month interim evaluation could be attributed to exposure to hexachlorocyclopentadiene. Pathology Findings: No increases in neoplasm incidences could be attributed to hexachlorocyclorocyclopentadiene. Toxicity was limited to the respiratory tract and included an increase in the incidence of pigmentation of the respiratory epithelium of the nose, trachea, and the bronchi and bronchioles of the lung in both males and females. Exposure to hexachlorocyclopentadiene also caused an increase in the incidence of squamous metaplasia of the laryngeal epithelium of exposed females; the incidences in 0.01 and 0.2 ppm females were significantly greater than that of the controls. The severity of squamous metaplasia was minimal in all exposed and control females. 2-YEAR STUDY IN MICE: Survival, Body Weights, Clinical Findings, and Urinalysis Groups of 60 male and 60 female mice were exposed to atmospheres containing 0, 0.01, 0.05, or 0.2 ppm (equivalent to 0, 0.11, 0.56, and 2.28 mg/m(3)) hexachlorocyclopentadiene. The 2-year survival rate of female mice in the 0.2 ppm group was marginally lower than that of the controls due to a higher incidence of ovarian inflammation in 0.2 ppm females. Mean body weights of 0.2 ppm males (weeks 62 to 103) and females (throughout the study) were lower than those of the controls. No clinical findings in male or female mice were attributed to chemical exposure during the 2-year study. There were no chemical-related differences in urinalysis parameters at the 15-month interim evaluation. Pathology Findings: The site of toxicity of hexachlorocyclopentadiene exposure in mice in the 2-year study was the respiratory tract. Chemical-related pigmentation of the respiratory epithelium of the nose, trachea, and lung and suppurative inflammation of the nose were observed. No increased neoplasm incidences in males or females could be attributed to hexachlorocyclopentadiene exposure. STOP-EXPOSURE EVALUATION: Survival, Body Weights, and Clinical Findings Groups of male mice were exposed to atmospheres containing 0.2 ppm hexachlorocyclopentadiene for 33 or 66 weeks or 0.5 ppm for 26 or 42 weeks followed by exposure to air until the end of the study. Fifty male mice from each stop-exposure group were evaluated at 2 years. Two-year survival rates of stop exposure groups were similar to that of the controls. Final mean body weights of stop-exposure groups were similar to that of the controls. No chemical related clinical findings were observed. Pathology Findings: Nonneoplastic respiratory tract lesions similar to those observed in the core study were observed in males in the stop-exposure groups. Chemical-related pigmentation and inflammation of the respiratory epithelium were persistent as indicated by their presence in many male mice after recovery periods of 62 to 78 weeks, and the incidence and severity of the lesions were related to exposure concentration and duration. GENETIC TOXICOLOGY: Hexachlorocyclopentadiene was not mutagenic in Salmonella typhimurium strains TA98, TA100, TA1535, and TA1537 when tested with and without S9. Hexachlorocyclopentadiene did induce sister chromatid exchanges and chromosomal aberrations in cultured Chinese hamster ovary cells, with and without S9. No induction of sex-linked recessive lethal mutations was observed in male Drosophila melanogaster treated with hexachlorocyclopentadiene by feeding or injection, and no increase in the frequency of micronucleated erythrocytes was seen in male or female B6C3F1 mice exposed to hexachlorocyclopentadiene by inhalation for 13 weeks. CONCLUSIONS: Under the conditions of these 2-year studies, there was no evidence of carcinogenic activity of hexachlorocyclopentadiene in male or female F344/N rats or B6C3F1 mice exposed to 0.01, 0.05, or 0.2 ppm. Exposure of rats to hexachlorocyclopentadiene produced pigmentation of the respiratory epithelium of the nose, trachea (males), and bronchi and bronchioles of the lung. Squamous metaplasia of the laryngeal epithelium occurred in female rats exposed to hexachlorocyclopentadiene. Suppurative inflammation of the nose as well as pigmentation of the respiratory mucosal epithelium occurred in mice exposed to hexachlorocyclopentadiene. Synonyms: Perchlorocyclopentadiene, hexachloro-1,3-cyclopentadiene, HEX, HCPD, HCCP, HCCPD Trade Name: C-56-Graphlox
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PMID:NTP Toxicology and Carcinogenesis Studies of Hexachlorocyclopentadiene (CAS No. 77-47-4) in F344/N Rats and B6C3F1 Mice (Inhalation Studies). 1259 26

An adenocarcinoma in the seminal vesicles of a 15-month-old male Wistar rat from a 30-month inhalation study is described. The rat was killed because of cachexia, apathy and a large palpable mass in the abdominal cavity. Macroscopic examination of the abdominal cavity revealed a 3.8 cm x 3.2 cm yellow-grey to pink mass, firm to soft in consistency. The cut section revealed cystic spaces. Histologically, the mass consisted of epithelial cells arranged in glandular and solid patterns with abundant amounts of connective tissue. Epithelial tumour cells were round-to-cylindrical with round-to-oval basophilic nuclei and one or two prominent nucleoli and a distinct eosinophilic cytoplasm. The glandular structure contained clusters of macrophages in their lumen with eosinophilic cytoplasm and indented nuclei. Extensive necrosis and reactive inflammation were present. The histological features of the small nodules in the pancreas and on the surface of the liver, rectum and urinary bladder resembled those of the primary tumour in the seminal vesicles. Based on these criteria, the neoplasm (mass) was diagnosed as an adenocarcinoma of the seminal vesicles. The immunohistological examination confirmed the diagnosis, i.e. immunostaining was positive for cytokeratins (4, 7, 14, 15, 18, and 19), vimentin, PCNA, and ED(1).
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PMID:Metastasizing seminal vesicle adenocarcinoma in a Wistar rat. 1583 44

Groups of six BALB/c mice each were intravenously inoculated with lethal doses of Ba-P210 (B210) or 12B1 cells and examined by autopsy, histology, special staining methods, enzyme histochemistry and immunohistochemistry. Clinical symptoms related to neoplasia consisted of a poor nutritional state, anaemia, mild to moderate dehydration and apathy. Paresis was apparent in three mice inoculated with 12B1 cells. Necropsy revealed splenomegaly in all animals. Sporadic haemorrhages in the lungs and enlargement of some lymph nodes were seen in some of the animals. Histological examination showed neoplastic cells in the spleen, in the bone marrow of the sternum, in the lung interstitium and in sinusoids of the liver in all mice. In six of nine brains examined, mild to moderate infiltration by neoplastic cells was observed. In all but two mice mild infiltration of the kidneys was found. The enlargement of lymph nodes was caused by an accumulation of neoplastic cells. The paresis was due to neoplastic infiltration of the vertebra, epidural space and spinal roots. Staining with Sudan black revealed cytoplasmic granules in neoplastic cells; however, the peroxidase reaction was negative. Numerous neoplastic cells disseminated in the red pulp of the spleen were reactive with CD3, CD79beta, CD11b and with neutrophil antibodies. We classified the disease induced by both of the cell lines as acute myeloid undifferentiated leukaemia (AML MO).
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PMID:Characteristics of two mouse bcr-abl-transformed cell lines. II. Pathological lesions induced in mice. 1618 May 44

The authors presented a patient with metastatic brain tumor originating from urachal carcinoma. A 64-year-old female was admitted to our hospital with complaints of memory disturbance, indifference and apathy of 3 months duration. Head CT and MRI on admission showed a round mass with perifocal edema in the right frontal lobe. After administration of Gd-DTPA, the mass lesion showed ringed enhancement effect. Pelvic MRI scan revealed a bladder tumor, which was diagnosed as urachal carcinoma. The brain lesion was suspected to have metasta sized metastatic from urachal carcinoma, and was excised by craniotomy. Histology of the brain tumor was identical to that of urachal carcinoma. Postoperatively the patient received local radiation therapy, but died of multiple metastasis to lung and local recurrence, 18 months later. Urachal carcinoma is an extremely rare tumor, comprising 0.17-0.34% of all bladder tumors. Though this rare tumor carries a poor prognosis, it may be effective for longer survival of a patient to treat the metastatic brain lesion with surgery and radiation.
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PMID:[Metastatic brain tumor originating from urachal carcinoma: case report]. 1622 81


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