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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in vivo localization of a monoclonal antibody A7 against a human colorectal cancer was studied in nude mice bearing human solid carcinomas, to evaluate potential applications of this antibody for radioimmunodetection of cancer. The tissue distribution of 125I-labeled A7 MoAb at 3 days after i.v. injection into mice bearing five different kinds of human solid tumors revealed a high uptake ratio by colon cancer, mammary cancer, and glioblastoma. In contrast, the uptake ratio by murine colorectal cancer (Colon-38) was extremely low. In immunoscintigraphic studies, HCT-15, one of the human colon cancer, was clearly visualized with 111In-DTPA-A7 MoAb. Glioblastoma was also imaged with the same extent. These results suggest that A7 MoAb would be applicable to the in vivo radioimmunodetection of colon- and mammary-cancer, and of glioblastoma.
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PMID:Radioimmunodetection of human colon cancer in nude mice by a new monoclonal antibody A7 against human colorectal cancer. 180 Apr 60

As part of an ongoing research program in the biology of human colon cancer cells, a database is being generated on the radiation responses of established lines in vitro. In this report, data are summarized on the graded single dose clonogenic survival responses to graded single doses of 250 kVp X rays of 16 exponentially growing lines. These data were analyzed using the linear quadratic (LQ) formalism for X ray inactivation; the 95% confidence limits on the colony forming efficiencies (CFEs), the alpha and beta parameters from the LQ equation, the surviving percentage at 2 Gy, and the mean inactivation dose (D, Gy) are listed herein. The average D from these 16 colon tumor lines was 2.35 Gy (95% confidence limits 2.10-2.60 Gy), which indicates that these tumor cells are of equal radioresistance to melanoma or head and neck cells, with only glioblastoma cells being of greater radioresistance.
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PMID:In vitro radiation survival parameters of human colon tumor cells. 199 79

An autopsy case of glioblastoma multiforms of the pons with a colon cancer, a rectal carcinoid, a renal adenoma and three gastric leiomyomas in a 81-year-old-woman is reported with a statistical analysis on multiple primary cancers associated with primary brain tumors as reported in the Japan autopsy annuals. Out of 329, 705 autopsy cases from 1975 to 1984 in the Japan autopsy registry, double cancers and triple cancers that included a primary brain tumor amounted to 123 cases (0.037%) and 12 cases (0.0036%), respectively. Other sites for primary cancers were the thyroid (23%), the stomach (15%), the lungs (12%), and the colon (10%) in that order of frequency.
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PMID:[An autopsy case of triple primary cancers consisting of glioblastoma multiforme of the pons, colon cancer and rectal carcinoid--a statistical analysis of cases of brain tumor combined with other primary cancers in Japan autopsy annuals]. 282 42

The influence of parity on the risk of cancers of the female breast and reproductive organs is well established. However, non-reproductive sites have received less attention. Mail questionnaire data gathered from incident female cases (169 brain; 332 colon; 260 rectal; 145 kidney; and 169 pancreas cancers), and 821 population-based controls in Iowa (United States) were used to measure the effect of parity and age at first birth on risk of these malignancies. Relative to nulliparous women, ever-parous women were at significantly decreased risk of brain cancer (odds ratio [OR] = 0.44, 95 percent confidence interval [CI] = 0.3-0.7) and of colon cancer (OR = 0.67, CI = 0.5-0.97), after adjustment for age and other risk factors. The OR for the other sites did not differ significantly from 1.0. The lower risk of brain cancer among parous women was similar in younger and older age groups, in patients diagnosed with glioblastoma and astrocytoma, and among ever- and never-smokers. The findings for colon cancer are consistent with observations from other studies. In the context of limited laboratory and clinical evidence implicating hormones in brain neoplasia, these findings may suggest a role for hormonal factors in brain cancer etiology. Hormonal factors deserve more detailed future consideration as risk factors in brain cancer.
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PMID:Reproductive factors and risk of brain, colon, and other malignancies in Iowa (United States). 828 Aug 27

The specificity of A7 monoclonal antibody (A7 MoAb), raised against a human colon cancer, was investigated in detail and compared with that of anti-CEA MoAb. Firstly, the biodistributions of radiolabeled A7 MoAb and anti-CEA MoAb were examined in human colon cancer (LS-174T)-, glioblastoma- and lung cancer (Lu-65)-bearing nude mice. 125I-A7 MoAb was highly concentrated into LS-174T and also, to a lesser extent, in glioblastoma, whereas 125I-anti-CEA MoAb was significantly taken up only by LS-174T. Both of these antibodies were taken up at only very low concentrations into Lu-65. Secondly, in vitro binding studies of 125I-A7 MoAb and 125I-anti-CEA MoAb with LS-174T cells and glioblastoma cells revealed high binding activity of these MoAbs to LS-174T cells, though A7 MoAb had a much higher affinity than that of anti-CEA MoAb. Neither of them showed high affinity for glioblastoma cells. Thirdly, competitive binding assay using A7 MoAb and anti-CEA MoAb to LS-174T cells showed that the binding of each 125I-MoAb was not inhibited by the other MoAb. Finally, in radioimmuno-imaging studies of LS-174T- and glioblastoma-bearing mice with 131I-A7 MoAb and -anti-CEA MoAb, both tumors were clearly visualized with the former, while the latter visualized only LS-174T. The A7 MoAb is clearly different from anti-CEA MoAb and may be useful for the in vivo radioimmunodetection and treatment of colon cancer.
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PMID:Differences between A7 antibody and anti-CEA antibody. 838 59

An IgM human monoclonal antibody (HuMAb) SK1 was generated from mesenteric nodal lymphocytes of a colon cancer patient that were fused with a human B-lymphoblastoid cell line SHFP-1. The reactivities of HuMAb SK1 to various human cell lines were screened by cell enzyme linked immunosorbent assay and immunocytochemical staining. The HuMAb SK1 reacted strongly with all 11 human carcinoma cell lines that were tested and had no detectable binding with noncarcinoma cell lines of the following origins: fibroblast; fetal lung; melanoma; soft tissue sarcoma; neuroblastoma; and glioblastoma. Carcinoma preferred reactivity of HuMAb SK1 was further confirmed by immunoperoxidase staining of a large number of frozen tissues, both malignant and benign. The antigen SK1 (AgSK1) in human carcinoma detected by immunoperoxidase staining was also identified biochemically as a sialoglycoprotein that migrated at M(r) 42,000 with an isoelectric point (pI) of approximately 5.9. A preferential staining by HuMAb SK1 was seen among colorectal, gastric, pancreatic, and lung cancers. Competitive inhibition study in solid-phase immunoassay suggested that the HuMAb SK1 did not cross-react with other antibodies specific for CEA, CA 19-9, and TAG 72. The AgSK1 appears to be a novel carcinoma associated antigen which may be a useful tumor marker in cancer diagnosis and treatment.
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PMID:AgSK1, a novel carcinoma associated antigen. 843 57

Eukaryotic chromosomes contain specialized structures at the termini called telomeres. This region of DNA is required for replication and stability of the chromosome. Telomere reduction can contribute to genetic instability and has been described in certain malignancies (e.g., colon, leukemia, giant cell tumor of bone). To determine whether telomere reduction is a generalized phenomenon in malignancies, the telomere integrity of genomic DNA isolated from tumor cells was determined from 39 individuals with 15 different malignancies categorized as musculoskeletal, epithelial, cranial, or other, and peripheral blood leukocytes from the same patient, when possible, or age-matched controls. Significant telomere reduction occurred randomly across histopathologic groups including giant cell tumor of bone, glioblastoma, colon cancer, and Wilms' tumor while telomere elongation occurred in chordoma. The other remaining 10 malignancies do not show significant differences in telomere lengths compared with controls.
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PMID:Chromosome telomere integrity of human solid neoplasms. 861 86

Folinic acid (leucovorin) is frequently used to augment and modulate the clinical activity of 5-fluorouracil (5-FU) in patients with advanced gastrointestinal (Gl) cancer. However, there are conflicting opinions concerning the optimal doses for these patients, and whether folinic acid modulates the clinical activity of 5-FU in patients with non-Gl cancer. To elucidate these questions, model experiments have been performed on human tumor cell lines in vitro to determine the modulatory activity of various concentrations of folinic acid on 5-FU mediated cytotoxicity using a clonogenic assay. Three cell lines of colon cancer and 3 of glioblastoma origin were exposed to 5-FU alone or with folinic acid for 24 hours. It was observed that relatively low concentrations of folinic acid enhanced the cytotoxicity of 5-FU against the colon cancer lines whereas higher concentrations were less effective. Folinic acid did not enhance the 5-FU mediated killing of the glioma cell lines at any concentration (0.01-100 micrograms/ml). On the contrary, folinic acid seemed to counteract the cytotoxic effect of 5-FU in a reasonably dose-dependent fashion. These results may suggest that the value of folinic acid in the treatment of non-Gl cancer with 5-FU should be evaluated within the framework of controlled clinical trials, and that high doses of folinic acid may not necessarily be more effective than low.
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PMID:Dual effects of folinic acid in 5-fluorouracil induced killing of human tumor cell lines in vitro. 891 76

CD44 belongs to a family of adhesion molecules displayed by a wide range of normal and malignant cells. Several studies implicated its presence as a marker for poor prognosis or metastases, especially in breast and colon cancer. CD44 has been proposed as an invasion marker for glioblastoma. We studied 75 astrocytic tumors with different degrees of anaplasia including juvenile pilocytic astrocytoma (JPA), low-grade astrocytoma (LGA), anaplastic astrocytoma (AA), and glioblastoma multiforme (GBM) to determine whether standard CD44 (CD44s) can be used as a clinically useful marker distinguishing between low- and high-grade gliomas. Archival paraffin-embedded tissues from 19 JPAs, 20 LGAs, 17 AAs, and 19 GBMs were immunostained with standard CD44 monoclonal antibody and compared with glial fibrillary acidic protein, using the streptavidin-complex peroxidase technique. Immunostaining was rated on a three-tiered scale by two observers. The expression of variant-splice forms of CD44 (CD44v) have been variably reported in brain tumors; a subset of these gliomas were tested with anti-CD44v monoclonal antibodies. In the tumors studied, 89% of JPAs, 90% of LGAs, 76% of AAs, and 84% of GBMs have 2+ or 3+ intensity for CD44s. Low- and high-grade gliomas showed no significant difference in staining (P > .05). Therefore, CD44s does not seem to correlate with the grading range of astrocytomas. The overall intensity of CD44s immunostaining usually, but not always, showed concordance with glial fibrillary acidic protein immunostaining, but the distinctive membrane staining of CD44s surface staining revealed fine cytologic detail in tumor cell processes in diagnostic sections. Some very anaplastic tumors were negative for CD44s, and gliomas were immunonegative for CD44v6. If variant chains (CD44v) are not found in gliomas and if this large series of low- and high-grade gliomas show no difference in CD44 expression, other factors must be explored to understand the differential behavior of low- and high-grade astrocytomas.
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PMID:CD44 expression in astrocytic tumors. 943 70

From January 1984 to December 1997, a total of six patients with malignant gliomas accompanied with visceral malignancies were treated in our department. We reviewed their radiological findings and clinical course. They consisted of four patients with glioblastoma and two patients with anaplastic astrocytoma. Classified according to visceral malignancies, three cases had colon cancer and the rest consisted of thyroid, uterus and prostate cancers. In radiological examinations of the brain (CT scans and MR images), these gliomas were relatively well-circumscribed, as if they were metastatic brain tumors. Of all these six cases, two cases survived more than five years and there were two cases in which there was recurrence within a year. Particularly, in four cases, whose gliomas developed after the treatment for visceral malignancies, two cases survived long-term (more than five years) and there was recurrence in only one case. We speculated that visceral malignancies could affect the nature of glioma progression. Thinking about its mechanisms, we hypothesized as follows; (1) visceral malignancies may activate non-specific, or common antitumor, immunity. (2) visceral malignancies may produce some factors which could affect the biological nature of gliomas. (3) glioma accompanied with visceral malignancy may have genetic uniqueness. Although the cases were limited in number, the present study may be helpful in designing the treatment for such cases and in elucidating the invasive nature of gliomas.
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PMID:[A survey of malignant gliomas accompanied with visceral malignancies]. 978 96


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