Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten patients underwent resection of primary or secondary cardiac tumor. Two-dimensional transthoracic echocardiography per se accurately located the endoluminal cardiac mass in nine patients, and transesophageal echocardiography demonstrated a right atrial tumor in the tenth case. The indications for urgent surgery included prior embolic events (3 cases), syncopal attacks (2) or echocardiographic evidence of a multilobulated mass (2 cases). The operative strategy was standardized for atrial tumors, but for malignant myocardial neoplasm both the anatomic site and the extent of tumor growth determined the surgical procedure. Histologic examination showed myxoma in seven cases, fibroma in one and metastases of malignant melanoma in two cases. The course after resection of endoluminal benign tumor was uneventful apart from transient atrial fibrillation in four cases. Follow-up echocardiography (after 4-28 months) showed no recurrent growth. In both cases of intracardiac metastases there was recurrence within 6 to 8 months after resection of the growth.
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PMID:Urgent indications for surgery in primary or secondary cardiac neoplasm. 274 6

The testicular carcinoma serially transplanted in nude mice with BALB/c genetic background was used for experimental chemotherapy. A stable growth and a high production of alpha-fetoprotein (AFP) were observed in this tumor line. The effect and side effect of Cis-platinum (CDDP) and other anticancer agents on this tumor line in nude mice were studied by the chemotherapy with single administration of CDDP 2 mg/kg, 4 mg/kg, 6 mg/kg and 8 mg/kg, and the combination chemotherapy with CDDP, Vinblastine (VBL) 0.1 mg/kg, Bleomycin (BLM) 0.5 mg/kg and Cyclophosphamide (CTX) 2 mg/kg. The body weight of the tumor bearing nude mice, the tumor size (length X breadth) and serum AFP level were measured every week up to 10 weeks after inoculation of the tumor mass. Six weeks after administration of these anticancer agents, the tumor mass was removed out and examined histologicaly. The effects of CDDP and other anticancer agents were observed as inhibition of the tumor growth and regression of the tumor mass. In the groups treated by the combination chemotherapy with either CDDP + VBL + BLM or CDDP + VBL + CTX, the most remarkable inhibition and regression were observed. The AFP levels were remarkably decreased in contrast with those of the control group. The changes of serum AFP levels were reflected in the tumor growth. The serum AFP levels fell down to normal level, however, the tumor mass was clearly recognized. The tumor tissue was damaged histologicaly by the single administration of CDDP. The most remarkable change was shown in the group treated by the combination chemotherapy CDDP 4mg/kg + VBL + BLM. The tumor cells were arranged one or two layers like the epithelium. This histological findings suggested that the malignant tumor could be differentiated to benign tumor. The side effect of CDDP and other anticancer agents was observed as a loss of weight. All of mice treated by the single administration at a dose of CDDP 6 mg/kg and 8 mg/kg died of the side effect of CDDP.
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PMID:[Experimental chemotherapy of human testicular carcinoma transplanted in nude mice]. 619 80

Levels of circulating immune complexes (IC) in the sera of 87 patients with brain tumor were measured by Raji cell radioimmunoassay and Clq binding assay. The control samples were obtained from 40 healthy blood donors and 40 cerebrovascular patients. The patients with glial tumor had a high incidence of elevated level of IC than patients with non-glial benign tumor, elevated level of IC than patients with non-glial benign tumor, cerebrovascular disease and normal controls. There was a significant association between these Clq binding activity and Raji cell binding activity in the sera of glial tumor patients. As regards the sensitivity, high IC levels are more frequent among Raji cell assay than Clq binding assay. The level of IC was found to be higher in patients with recurrent glial tumor than in those with primary tumors. However, the level of IC in the sera from patients with glial tumor did not always decrease during remission after successful treatment. Our data indicate that the measurement of IC may prove useful in the management of patients with brain tumor, in particular, to detect recurrence or progression of tumor growth.
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PMID:[Detection and clinical significance of immune complexes in the sera of brain tumor patients]. 630 40

Subarachnoid hemorrhage attributable to brain tumor, particularly due to benign tumor, is not common. A case of subependymoma in the lateral ventricle, which manifested itself with an episode of subarachnoid hemorrhage was reported. A 33-year-old woman was admitted to our hospital because of severe headache and transient loss of consciousness, but neurological examination revealed no abnormality except for slight disturbance of consciousness and nuchal rigidity. Lumbar puncture showed an opening pressure over 350mmH2O and grossly bloody CSF. CT scan revealed an enhanced mass occupying the left ventricular trigone. Angiography, however, demonstrated no tumor stain or other vascular abnormality. Preoperative diagnosis was an intraventricular tumor of benign nature. A soft tumor arose from the lateral wall of the trigone was removed subtotally by paramedian parieto-occipital approach. Histology of the tumor was of typical subependymoma with scanty vascularity. Intraventricular or subarachnoid hemorrhage from cerebral neoplasm reported so far, is mostly due to a highly vascularized tumor. Subependymoma is of benign nature with poor vascularity, and therefore, intraventricular hemorrhage from the subependymoma was rarely reported in the literature. On the basis of the findings of angiography, serial CT scans and histological examination, it is reasonable to assume that intraventricular bleeding in our case is not attributed to the tumor per se, but to tearing of subependymal or ependymal veins extremely extended by the tumor growth.
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PMID:[A case of subependymoma in the lateral ventricle with intraventricular hemorrhage]. 646 67

A prospective study was undertaken to assess the value of ultrasonography in the clinical monitoring of angiomyolipomas. 26 patients with angiomyolipomas as diagnosed by sonography and verified by computerized tomography (CT) were followed up by sonographic monitoring over a mean period of 45 months. One case was associated with tuberous sclerosis. Inclusion criteria for conservative management had been clinically asymptomatic angiomyolipomas smaller than 5 cm. Significant tumor growth and a change of the sonographic pattern during follow-up was seen in 2 patients. After renewed follow-up CT scanning failed to reveal negative density values, both patients were nephrectomized. Histologic examination showed hemorrhage in the tumor. The remaining 24 patients (92%) showed no changes in the sonographic patterns. Minor tumor growth of 0.5 cm on average was seen in 6 patients over a mean follow-up period of 52 months. Surgical intervention was refrained from in these 24 patients due to the consistent sonographic pattern and the absence of clinical symptoms. Once the angiomyolipoma is verified by CT, sonographic monitoring suffices if the sonostructure remains unchanged. Minor asymptomatic angiomyolipomas today no longer require surgical intervention as this benign tumor has a pathognomonic sonographic appearance.
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PMID:Value of routine sonography in the diagnosis and conservative management of renal angiomyolipoma. 837 45

Acinic cell carcinoma of the salivary glands is a rare cancer representing a low grade malignancy. The recurrence of a tumor is sometimes encountered, usually within 5 years of initial operation. We describe an unusual recurrence after a long interval following primary surgery. In 1987, a 60-year-old woman underwent excision of a mass in the superficial lobe of the right parotid gland under the preoperative diagnosis of a benign tumor. A histologic diagnosis of acinic cell carcinoma was made by examining sections from the resected mass. The patient noted several small nodules in the right parotid region in 1995, but she did not visit our clinic until 1998 when tenderness developed. A locally recurrent tumor and cervical lymph nodes containing metastases were resected and postoperative radiotherapy was given 11 years after the first operation. At least 10 years of follow-up may be necessary for patients with acinic cell carcinoma because of slow-tumor growth.
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PMID:Late recurrence of acinic cell carcinoma of the parotid gland. 1068 18

We assessed diagnostic criteria among 38 spindle cell tumors of the urinary bladder and obtained follow-up in 36 patients. Patients comprised 28 males and 10 females aged 2.5 months to 87 years. Hematuria was the commonest presenting symptom (27 patients). After review and immunohistochemical workup, 17 patients had inflammatory pseudotumor (myofibroblastic tumor), 4 postoperative spindle cell nodule, 1 leiomyoma, 13 sarcoma (7 low-grade; 6 high-grade), and 3 carcinoma. Mean age was 38 years for pseudotumor (range 15 to 74), 65 for postoperative spindle cell nodule, 51 for sarcoma, and 76 for carcinoma. Size of pseudotumor averaged 4.4 +/- 0.7 cm (range 1.5 to 13.0), similar to sarcoma, 4.0 +/- 0.6 cm (range 0.5 to 7.0). Similar proportions of benign tumors and sarcomas had muscularis propria invasion. The criteria that best differentiated sarcoma from inflammatory pseudotumor were presence of necrosis at the tumor-detrusor muscle interface in muscle-invasive cases, and nuclear atypia. Sarcoma also had less prominent microvasculature, less variable cellularity, consistently > or =1 mitotic figure per 10 high-power fields, and predominant acute inflammation without plasma cells. p53 protein nuclear immunostaining was moderate, unlike the rare to absent staining in pseudotumors. Because all 12 sarcomas were desmin-negative, we did not call them leiomyosarcoma; they overlapped with benign tumor in epithelial, mesenchymal, and actin immunostaining. Among 12 sarcoma patients, 2 died of tumor (at 3 months). Two of four experienced tumor recurrence after partial cystectomy (2 and 26 months). No pseudotumors recurred after transurethral resection or partial cystectomy, although one patient, 5 months after transurethral resection, had histologically identical pseudotumor that the surgeon considered residual. Another patient with pseudotumor, not a candidate for tumor ablation after transurethral resection, had continued tumor growth and he died of urosepsis. In conclusion, inflammatory pseudotumor, although overlapping with sarcoma in presentation, age range, and size, does not metastasize and remains histologically distinct from low-grade sarcoma.
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PMID:Inflammatory pseudotumor and sarcoma of urinary bladder: differential diagnosis and outcome in thirty-eight spindle cell neoplasms. 1159 76

Tumor-stroma interactions play a significant role in tumor development and progression. Alterations in the stromal microenvironment, including enhanced vasculature (angiogenesis), modified extracellular matrix composition, inflammatory cells, and dys-balanced protease activity, are essential regulatory factors of tumor growth and invasion. Differential modulation of stromal characteristics is induced by epithelial skin tumor cells depending on their transformation stage when grown as surface transplants in vivo. Tumor cells can regulate the development of a "tumor-stroma" via the aberrant expression of growth factors or induction of growth factor receptors in the stromal compartment. In this context, secretion of the hematopoietic growth factors G-CSF and GM-CSF, constituitively expressed in enhanced malignant tumors, may be good candidates for induction of a tumor stroma through their effect on inflammatory cells. Upon its induction, the tumor stroma will reciprocally influence the differentiation status of tumor cells resulting in a normalization of benign tumor epithelia and the maintenance of a malignant phenotype, respectively. In the HaCaT model for squamous cell carcinoma of the skin, stromal activation and angiogenesis are transient in pre-malignant transplants, however they remain persistent in malignant transplants where progressive angiogenesis is closely correlated with tumor invasion. While continued expression of VEGF and PDGF are associated with benign tumor phenotypes, activation of VEGFR-2 is a hallmark of malignant tumors and accompanies ongoing angiogenesis and tumor invasion. As a consequence the inhibition of ongoing angiogenesis by blocking VEGFR-2 signalling resulted in dramatically impaired malignant tumor expansion and invasion. Comparably, tumor vascularization and invasion was blocked by disturbing the balance of matrix protease activity caused by a lack of PAI-1 in the stromal cells of the knockout mouse hosts. A similar inhibition of tumor vascularization was caused by TSP-1 over-expression in skin carcinoma cells, which also blocked tumor invasion and expansion. On the other hand, when granulation tissue and angiogenesis were only transiently activated as a result of stable transfection of PDGF into non-tumorigenic HaCaT cells, the target cells formed benign, but not malignant, tumors. Collectively, these data show that tumor vascularization, providing intimate association of blood vessels with tumor cells, is a prerequisite for tumor invasion. A potential mechanism for this interrelationship may be the differential regulation of MMP-expression in tumors of different grades of malignancy. In vitro MMP expression did not discriminate between benign and malignant tumor cells unless they were co-cultured with stromal fibroblasts. However, in vivo regulation of MMP expression was clearly dependent on tumor phenotype. While MMP-1 and MMP-13 were down-regulated in benign transplants, they were persistently up-regulated in malignant ones. A tight balance between proteases and their inhibitors is crucial for both the formation and infiltration of blood vessels and for tumor cell invasion, thus again emphasizing the importance of the stromal compartment for the development and progression of carcinomas.
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PMID:Tumor-stroma interactions directing phenotype and progression of epithelial skin tumor cells. 1249 91

Tumor growth and progression are critically controlled by alterations in the microenvironment often caused by an aberrant expression of growth factors and receptors. We demonstrated previously that tumor progression in patients and in the experimental HaCaT tumor model for skin squamous cell carcinomas is associated with a constitutive neoexpression of the hematopoietic growth factors granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF), causing an autocrine stimulation of tumor cell proliferation and migration in vitro. To analyze the critical contribution of both factors to tumor progression, G-CSF or GM-CSF was stably transfected in factor-negative benign tumor cells. Forced expression of GM-CSF resulted in invasive growth and enhanced tumor cell proliferation in a three-dimensional culture model in vitro, yet tumor growth in vivo remained only transient. Constitutive expression of G-CSF, however, caused a shift from benign to malignant and strongly angiogenic tumors. Moreover, cells recultured from G-CSF-transfected tumors exhibited enhanced tumor aggressiveness upon reinjection, i.e., earlier onset and faster tumor expansion. Remarkably, this further step in tumor progression was again associated with the constitutive expression of GM-CSF strongly indicating a synergistic action of both factors. Additionally, expression of GM-CSF in the transfected tumors mediated an earlier recruitment of granulocytes and macrophages to the tumor site, and expression of G-CSF induced an enhanced and persistent angiogenesis and increased the number of granulocytes and macrophages in the tumor vicinity. Thus both factors directly stimulate tumor cell growth and, by modulating the tumor stroma, induce a microenvironment that promotes tumor progression.
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PMID:Cooperative autocrine and paracrine functions of granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor in the progression of skin carcinoma cells. 1552 Jan 86

The cells of a weakly tumorigenic and non-metastatic murine fibrosarcoma (QR-32) are converted into highly malignant tumors (acquiring metastatic potential) once they have grown in vivo after being co-implanted with gelatin sponge which induces inflammation. In the present study, we examined whether nitric oxide (NO) is involved in the inflammation-based tumor progression by administrating a specific inhibitor to inducible nitric oxide synthase, aminoguanidine (AG). First, we co-implanted 1 x 10(5) QR-32 cells with gelatin sponge (10 x 5 x 3 mm piece) into a subcutaneous space in C57BL6 mice. Administration of AG in drinking water (1%) had started 2 days before the tumor implantation and continued until the termination of the experiment. The incidence of tumor formation and the tumor growth did not differ between AG-treated group and -untreated group. On day 28, we excised the arising tumors to establish culture cell lines for evaluation of their acquisition of metastatic phenotype in other normal mice. Metastasis incidence and the number of metastatic colonies were significantly reduced in the tumor cell lines obtained from AG-treated mice compared to those from non-treated mice (p < 0.05). Immunohistochemical analysis demonstrated that inducible nitric oxide synthase and nitrotyrosine in the inflamed lesion were reduced in the AG-administered mice. However, intensity of 8-hydroxy-2-deoxyguanosine was not different between the groups. These results showed that nitric oxide and its reactive nitrogen oxide species cooperatively play a pivotal role in the progression of benign tumor cells in inflamed lesions.
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PMID:Involvement of reactive nitrogen oxides for acquisition of metastatic properties of benign tumors in a model of inflammation-based tumor progression. 1612 21


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