UMLS:C0598934 - FACTA Search

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Query: UMLS:C0598934 (tumor growth)
58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CA125 is a new unique tumor marker for epithelial ovarian cancer, and its clinical use has recently increased considerably. We have periodically monitored 14 cases of ovarian cancer (7 cases of serous cystadenocarcinoma, 4 cases of clear cell carcinoma, 1 case of endometrioid carcinoma and 1 case of metastatic ovarian cancer) using CA125, before and after surgery, during chemotherapy, and in follow-up. The serum CA125 was measured with a radioimmunoassay kit. As a result of this monitoring, we have discovered the following facts: The ten cases in which the titer of CA125 dropped to 35U/ml, which is cut off, by 60 days after surgery, when we had finished 2 courses of chemotherapy, showed good progress. In contrast to this, in the other cases, the degree of CA125 was still high 60 days after the surgery and did not drop after that. In these 4 cases, the tumor growth was found. It was therefore concluded that with this method a prognosis could be made much earlier than with the current system, and that relapse could be detected far earlier. We have also examined the mutual relations between CA125 and other tumor markers, IAP, TPA, HBDH, CEA, Ferritin, alpha 1AT, ESR, and LDH. Although we could see some usefulness in periodic monitoring with IAP, unlike CA125 it did not reflect the condition of a disease. The coefficients of correlations between CA125 and other tumor markers are as follows: IAP 0.5268, TPA 0.4541, HBDH 0.4551, CEA 0.2942, Ferritin -0.1005, alpha 1AT 0.5321, ESR -0.0619, LDH 0.5994.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serum CA125 in malignant ovarian tumor--periodical monitoring and correlation with other tumor markers]. 345 77

Immunohistochemical detection of proliferating cell nuclear antigen (PCNA), a cell cycle-related protein used to estimate tumor growth fraction, is variable in formalin-fixed compared with methanol-fixed tissue specimens. This is assumed to result from conformational changes in the antigenic epitope induced by formaldehyde; therefore, to be susceptible to retrieval in archival specimens. In this study, formalin fixation reduced the intensity of staining and the number of positive cells to approximately 25% of those in methanol-fixed material. The washing of tissue specimens prior to methacarn fixation also reduced PCNA staining. Loss of staining was not restored after use of a commercial retrieval kit recommended for PCNA immunohistochemistry. Immunoblotting of formalin fixatives and saline washings after removal of tissue specimens consistently demonstrated the presence of PCNA-like activity in solution. We conclude that the exceptional solubility of PCNA is responsible for reduced immunostaining in formalin-fixed material, that the loss is irreversible, and that methanol or methacarn is the fixative of choice for PCNA immunohistochemistry.
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PMID:Detection of proliferating cell nuclear antigen in paraffin-embedded specimens is dependent on preembedding tissue handling and fixation. 752 64

The response of Ehrlich ascites tumor and the effect on normal tissues (kidney and small intestine) of CD-1 mice were evaluated after intralesional (i.l.) injection of cisplatin dissolved in urografin and lipiodol, which is henceforth termed CUL suspension. The results obtained were compared with the effects of i.p. and i.l. injections of cisplatin dissolved in sterile distilled water. Each of these treatment modalities involves the injection of 10 mg/kg cisplatin. The tumor response was evaluated by tumor growth-delay studies as well as by determining the percentage of cells in the S phase. Toxicity studies were accomplished by evaluation of the change in the body weight of mice and also by S-phase studies. S-phase fraction analyses were done with the use of the Cell Proliferation Kit. This commercial kit was used to measure bromodeoxyuridine (BrdU), a thymidine analogue that is incorporated into cells synthesizing DNA. Tumor, kidney, and small-intestine platinum concentrations were determined by measurement with a flameless atomic absorption spectrophotometer. The results of the tumor growth-delay studies showed that i.p. injection, with water being the drug carrier, produced the weakest antitumor effect, whereas i.l. injection of cisplatin, with lipiodol being the drug carrier, evoked the most enhanced effect. This finding was substantiated by BrdU-uptake analysis of tumor cells, wherein i.p. injections yielded the highest S-phase fraction and CUL treatment gave the lowest. Toxicity studies showed that a very significant decrease in body weight occurred in mice receiving i.p. treatment. No significant decrease in body weight was noted after i.l. treatment. BrdU analysis revealed that DNA synthesis in kidney cells and crypt cells of the small intestine was depressed after i.p. treatment. On the other hand, no significant effect was observed in the kidney or small intestine of CUL-treated mice. A correlation between the effects of the various treatment modalities (on tumors, kidney, and small intestine) and the retention of cisplatin was found.
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PMID:Effects of intralesional injection of cisplatin dissolved in urografin and lipiodol on Ehrlich ascites tumor and normal tissues of CD-1 mice. 803 99

We used retroviral-mediated gene transfer of the human interleukin (IL)-2 gene into murine neuroblastoma cells to investigate whether locally-secreted IL-2 is able to influence the generation of anti-tumor immune responses. Supernatant obtained from cultures of approximately 1 x 10(6) IL-2 gene-transduced, G-418 selected neuro-2a cells was assayed for human IL-2 production by ELISA kit. First, to estimate whether the local secretion of IL-2 from the genetically-modified tumor cells would affect their tumorigenicity in vivo, IL-2-secreting neuro-2a cells were s.c. injected into A/J mice and tumor growth was measured weekly. And to estimate whether IL-2 transfected neuroblastoma cells protect mice from tumor development after wild-type tumor cell challenge, IL-2-secreting neuro-2a cells were s.c. injected into A/J mice. Seven days after IL-2 gene-transfected neuroblastoma cell injection, unmodified neuro-2a cells were s.c. injected into the contralateral site of A/J mice and tumor growth was measured weekly. Finally, to estimate IL-2 effect on pre-established large tumor burdens, IL-2-secreting neuro-2a cells were s.c. injected into A/J mice with established tumor and its growth was measured weekly. The IL-2 gene-transduced neuro-2a clones secreted 120.25-177.3 IU of IL-2 per ml per 10(6) cells during 24 hr. None of the mice injected with IL-2-secreting neuro-2a cells developed tumors within 6 weeks, while all of the mice injected with wild-type neuro-2a cells developed tumors. Immunization of mice with IL-2 gene-transfected, irradiated neuro-2a cells protected these animals against a subsequent challenge with wild-type tumor cells. Finally, the size of large neuroblastomas decreased after IL-2-secreting neuro-2a cell injection into mice. Local secretion of IL-2 gene-transduced tumor cells abrogates their tumorigenicity and induces protective immunity and may inhibit the growth of neuroblastoma.
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PMID:Retroviral-mediated IL-2 gene transfer into murine neuroblastoma. 1073 23

Mild hyperprolactinemia frequently accompanies the hypopituitarism seen in patients with pituitary macroadenomas that do not secrete PRL. Recent data suggested that the hypopituitarism and mild hyperprolactinemia in this setting are largely due to compression of pituitary stalk and portal vessels. Headaches (HAs) are frequently seen in patients with large adenomas and at times in those with microadenomas. Because the walls of the sella turcica are relatively rigid, we postulate that tumor growth within the sella increases intrasellar pressure (ISP), which in turn impairs portal blood flow, resulting in mild hyperprolactinemia and hypopituitarism. We also postulate that increased mean ISP (MISP) contributes to the development of HAs. Normal MISP is not known but is unlikely to exceed normal intracranial pressure of less than 10-15 mm Hg. We determined MISP in 49 patients who had transsphenoidal surgery for pituitary adenomas. MISP was measured using a commonly available intracranial monitoring kit where a fiberoptic transducer was inserted through a 2-mm dural incision at the time of adenomectomy. Patients with deficient FSH, LH, ACTH, or TSH secretion were considered hypopituitary. Data on serum PRL levels were included for analysis only in patients whose adenomas had negative immunostaining for the hormone. MISP measurements ranged from 7-56 mm Hg, with a mean (+/-SD) of 28.8 +/- 13.5 and a median of 26 mm Hg. The pressure measurements were higher in patients with hypopituitarism than in those with normal pituitary function (P = 4.6013 x 10(-6)). Patients presenting with HAs had higher MISP than those who did not (P = 5.44 x 10(-7)), regardless of their pituitary function or tumor sizes. PRL levels correlated positively with MISP values (r = 0.715, P < 0.0001). Tumor size did not correlate with MISP or PRL levels. The findings of increased MISP in hypopituitary patients and the documented correlation with PRL levels, suggest that ISP is a major mechanism involved in the pathogenesis of hypopituitarism and hyperprolactinemia. Similarly, the increased MISP in patients with HAs, irrespective of tumor size or pituitary function, suggest that increased ISP is a major mechanism involved in the pathogenesis of this symptom. The data support the hypothesis that in patients with pituitary adenomas increased ISP is a major mechanism contributing to the development of hyperprolactinemia, hypopituitarism, and HAs. Increased ISP in these patients leads to compression of the portal vessels and the associated interruption of the delivery of hypothalamic hormones to the anterior pituitary. This would explain the reversibility of pituitary function observed in most patients after adenomectomy. However, increased ISP may also lead to decreased blood supply, resulting in ischemic necrosis in some regions of the pituitary. The latter could limit potential recovery of pituitary function after adenomectomy.
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PMID:The dominant role of increased intrasellar pressure in the pathogenesis of hypopituitarism, hyperprolactinemia, and headaches in patients with pituitary adenomas. 1084 53

We tested the effect of different concentrations of ascorbic acid (AA), 50, 100, 250 mg/500 mg/dL) with copper sulfate (CS), 10 mg/dL) on human breast carcinoma (MDA-MB231) cell proliferation in vitro. Cell proliferation was measured using a colori-metric assay (Cell proliferation kit II (XTT), Boehringer, NJ). The results of the mean absorbance of the tissue culture at different AA concentrations and a constant CS concentration were as follow: 0.82 +/- 0.03 (control, mean +/- SE), 0.64 +/- 0.02 (CS above); 0.48 +/- 0.03 (50 mg/dL) AA), 0.21 +/- 0.02 (100 mg/dL), 0.08 +/- 0.01 (250 mg/dL) AA, 0.60 +/- 0.05 (500 mg/dL). These results show that a combination of AA and CS inhibits human breast carcinoma cell proliferation in vitro. This cell proliferation inhibitory effect is directly proportional to the AA concentration with the exception of the 500 mg/dL AA dose. This chemotherapeutic effect was optimally enhanced when AA was added at a concentration of 250 mg/dL. The AA concentrations of 500 mg/dL had a biphasic effect on tumor cell proliferation probably due to back and forth redox reactions between AA and dehydroascorbic acid in a closed system. This study provides preliminary evidence that AA and SC can be used as biological response modifiers (BRM) for tumor growth inhibition.
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PMID:Inhibition of human breast carcinoma cell proliferation by ascorbate and copper. 1201 76

The role of vascular endothelial growth factor (VEGF) during peritoneal dissemination of ovarian carcinoma and the association with tumor microvessel density (MVD) and matrix metalloproteinase (MMP) activity was investigated. To this end, MVD, tumor tissue and ascitic fluid levels of VEGF, and MMP activity of ascitic fluid were examined in patients with ovarian cancer and benign ovarian tumor. The effect of ascites on cell growth, cell invasion activity and angiogenesis was investigated in vitro. Ascitic fluid and tumor tissue samples were obtained from 15 patients with benign ovarian tumor and 24 patients with ovarian carcinoma. Tissue extract and ascitic fluid levels of VEGF were measured using enzyme immunoassay. Tumor microvessels were detected immunohistochemically. MMP activity was measured by gelatin zymography. For the in vitro experiment, the SKOV-3 human ovarian carcinoma cell line was utilized. Cell growth was examined using MTT-assay, cell invasion activity was measured by Matrigel in vitro invasion assay, and neovascularization was assessed using an angiogenesis kit. VEGF levels in tissue extract and ascitic fluid, MVD, expression of active form MMP-2 in ascitic fluid and ascites volume were higher in ovarian cancer patients than in benign ovarian tumor patients. In addition, these were elevated in stage III and IV diseases compared to stage I and II diseases in ovarian cancer patients. MVD and expression of active form MMP-2 in ascitic fluid were closely correlated with VEGF level in tissue extracts, and MVD and ascites volume were closely correlated with VEGF level in ascitic fluid. Cell invasive activity and angiogenesis activity increased when cells were exposed to ascites. These increases were apparent when exposed to ascites obtained from ovarian cancer patients and were related to VEGF concentrations of ascitic fluid and expression of active form MMP-2 in ascitic fluid. The increased VEGF secreted from tumor cells is suggested to enhance tumor growth through angiogenesis, to produce ascites and to elevate ascitic VEGF concentrations and expression of active form MMP-2. The progression of peritoneal involvement may be induced by elevated VEGF and expression of active form MMP-2, followed by increased VEGF in the primary tumor. Control of VEGF in the primary tumor may become an effective strategy against peritoneal dissemination of ovarian carcinoma.
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PMID:Vascular endothelial growth factor activating matrix metalloproteinase in ascitic fluid during peritoneal dissemination of ovarian cancer. 1246 50

n-3 polyunsaturated fatty acids (PUFAs) have been shown to exert beneficial effects in the prevention of cardiovascular disease, inflammation, and on tumor growth. To investigate effects of PUFAs on proliferation and apoptosis in endothelial cells, we tested the n-3 PUFA docosahexaenoic acid (DHA) and the n-6 PUFA arachidonic acid (AA) in human umbilical vein endothelial cells (HUVEC). The mitochondrial membrane potential (MMP) and the production of reactive oxygen species were examined by flow cytometry. Phosphorylation of p53 or p38 MAP kinase, and total levels of p53 were measured by Western blot. DNA binding activity of p53 was analyzed with a TransAM transcription factor assay kit. Tube formation was assessed on Matrigel. In proliferating HUVEC, but not in confluent cells, DHA reduced cell viability and induced apoptosis, as demonstrated by increases in membrane leakage (propidium iodide (PI) staining), Annexin-V binding, sub G(1) phase in the cell cycle, and TUNEL-positive cells. AA had no effect on these parameters. In addition to a reduced MMP and increased reactive oxygen species, phosphorylation of p38 and p53 (serine 15) and impaired DNA binding of p53 were observed. There was no change in total levels of p53. The p38 inhibitor SB203580 had no effect on Annexin V binding. DHA also attenuated HUVEC tube formation. Taken together, DHA induces apoptosis in proliferating, but not in resting HUVEC, potentially via the phosphorylation of p53, resulting in decreased p53 DNA binding. The results suggest that anti-angiogenic effects of DHA may be due to induction of apoptosis in proliferating endothelial cells.
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PMID:Docosahexaenoic acid induces apoptosis in proliferating human endothelial cells. 1579 39

In the present study, we evaluated the effects of a neutralizing anti-Vascular Endothelial Growth Factor (VEGF) polyclonal antibody on murine EAC tumor growth both in vitro and in vivo. Furthermore, we investigated if in the presence of effective VEGF blockade, a conventional chemotherapeutic drug Cisplatin could be effective, and if so would there be an additive effect of the combination regimen. An in vitro cell proliferation assay using MTT kit showed that VEGF antibody alone inhibited proliferation of EAC cells significantly in all the three time intervals (p<0.05). But cisplatin treatment in combination with VEGF antibody resulted in highly significant inhibition (p<0.001) of cell proliferation. Apoptosis assay by FACS analysis showed that VEGF antibody-cisplatin combination treatment induced apoptosis in cultured EAC cells. Intraperitoneal administration of VEGF antibody (100 mug/dose) and cisplatin (0.5 mg/kg/dose) combination was observed to be more effective in reducing tumor burden and increasing life span when compared to VEGF antibody or cisplatin treatment alone in EAC solid tumor bearing mice. In EAC ascites tumor model, all the three types of treatment inhibited tumor burden and increased life span, but the inhibition was less compared to EAC solid tumor bearing mice. VEGF antibody singly and in combination with cisplatin reduced neoangiogenesis and vascular hyperpermeability. However, it is clear from the results that the combination treatment had no additive effect in reducing vascular hyperpermeability. Serum VEGF was not reduced significantly after treatment in EAC ascites tumor bearing mice, whereas in EAC solid tumor bearing mice it was reduced significantly after treatment. The results clearly show that though alone cisplatin showed antitumor efficacy but it had no significant inhibitory effect on neoangiogenesis and vascular hyperpermeability. Thus the present study suggests that anti-VEGF agent can be combined with traditional treatment modalities to ensure more effectiveness.
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PMID:Vascular endothelial growth factor immunoneutralization in combination with cisplatin reduces EAC tumor growth. 1691 27

Hyaluronan (HA) and its major cell surface receptor, CD44, play an important role in tumor growth, proliferation, neovascularization, and invasion. CD44 is an integral transmembrane protein and exists in standard form (CD44s), as well as a myriad of CD44 variants isoforms (CD44v1-v10). Functional fragments of the CD44 can be released from the cell membrane by proteolytic cleavage of extracellular domain producing soluble CD44. Although studies have proposed the use of serum HA and soluble CD44, specifically soluble CD44v6 (sCD44v6) levels, as a tumor markers, its diagnostic utility in body fluid samples has not been clearly established. The purpose of this study was to correlate HA and sCD44v6 levels in effusions with the cytology diagnosis and to assess their usefulness in differentiating between malignant and nonmalignant effusions. In this retrospective study we evaluated HA and sCD44v6 contents in 20 effusions from cytologically positive samples and 10 effusions from cytologically negative samples. Corresponding cytopathology slides were reviewed to confirm the diagnoses. Malignant effusions included 18 cases of metastatic adenocarcinomas (9 ovarian, 3 breast, 3 pulmonary, 3 adenocarcinoma of unknown primary) and 2 cases of lymphomas. The level of HA and sCD44v6 were measured using a sandwich enzyme-linked immunoadsorbent assay. For HA, we used hyaluronic acid quantitative test kit (Corgenix, Denver, CO) and for sCD44v6 we used Human sCD44v6 Instant ELISA (Bender MedSystems, Vienna, Austria). HA concentrations (microg/mL) and sCD44v6 concentrations (ng/mL) were calculated and correlated with clinical data as well as cytodiagnosis. The mean concentration of HA (22.42 +/- 5 microg/mL) and sCD44v6 (70 +/- 42 ng/mL) in the cytologically positive samples was significantly higher than those in the cytologically negative samples for HA (5.5 +/- 5 microg/mL, P < 0.01) and sCD44V6 (17 +/- 10 ng/mL, P < 0.01). Using benign effusions as control and the upper limits of its mean levels for HA (10.5 microg/mL) as the positive boundary value, HA levels exceeded the boundary line in 17 out of 20 malignant effusions and 2 out of 10 benign effusions. Meanwhile, sCD44v6 exceeded the boundary line (27 ng/mL) in 18 out of 20 malignant effusions and 3 out of 10 benign effusions. The calculated sensitivity and specificity of this assay to the diagnosis of malignant effusions were 85 and 80% for HA and 90 and 70% for CD44v6, respectively. We conclude that the HA and sCD44v6 levels in body fluids correlate with the cytology diagnosis and could be used as an ancillary study in cytology to differentiate nonmalignant from malignant effusions.
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PMID:Correlation of cytologic examination with ELISA assays for hyaluronan and soluble CD44v6 levels in evaluation of effusions. 1723 May 76

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