Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A tumor-associated epidermal growth factor (EGF)-like activity was detected in the urine of breast cancer patients by means of an EGF radioreceptor assay and an anchorage-independent growth assay. The clonogenic growth factor activity of pooled void volume eluate fractions from a Bio-Gel P-30 column was completely neutralized by an anti-human epidermal growth factor antiserum but not by an anti-transforming growth factor alpha antiserum. This activity was determined in the urine of 71 breast cancer patients. A statistically significant correlation was found between EGF-like clonogenic activity and axillary lymph node status, tumor size, stage of disease, and grade of differentiation of the primary tumor. The Bio-Gel P-30 void volume fraction was used to purify the EGF-related polypeptide to apparent homogeneity by subsequent binding to and elution from A431 cells followed by isoelectric focusing. A polypeptide of a pI of approximately 3.4 was identified to be related to EGF by neutralization and immunoprecipitation experiments with anti-human epidermal growth factor antisera. This polypeptide migrated as a single band of Mr 43,000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis.
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PMID:A Mr 43,000 epidermal growth factor-related protein purified from the urine of breast cancer patients. 229 5

A high molecular weight form of epidermal growth factor (EGF) was detected by means of an EGF radio-receptor assay and an anchorage-independent growth assay in the urine of breast cancer patients. Preliminary data indicate that the activity of this growth factor is associated with lymph node status and tumor size and that the activity becomes reduced after removal of the primary tumor. The EGF-related polypeptide was purified to homogeneity by a combination of Sephadex G-25 and Bio Gel P-30 chromatography followed by binding to, and elution from, EGF receptor rich A431 cells. Final purification was achieved after isoelectric focusing by following the biological activity of eluted polypeptides. A polypeptide of a pI of 3.4 was identified to carry EGF-like activity. This polypeptide migrated as a single band of 43 kDa in SDS-PAGE. Its biological activity was neutralized by a specific anti-hEGF-antibody indicating an immunological relationship with hEGF.
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PMID:Purification of a high molecular weight form of epidermal growth factor from urine of breast cancer patients. 278 43

A case of hyperamylasemia with lung cancer is described. Macroamylasemia was excluded by a normal amylase/creatinine clearance ratio and by a sedimentation constant obtained by sucrose density gradient centrifugation. Positive immunofluorescent staining of tumor cells with a specific antibody against human salivary amylase and significant amylase activity in the primary tumor and metastases support the hypothesis of independent production of amylase by the lung tumor. Cellulose--acetate membrane electrophoresis demonstrated three bands of amylase activity. The major component corresponded to normal salivary amylase in electrophoretic mobility, isoelectric point and molecular size. The minor bands, one of which occupied about 10% of the total amylase activity in serum, urine and tissue homogenates, demonstrated a lower electrophoretic mobility and a more acidic isoelectric point. Gel filtration and electrophoresis disclosed that these minor bands were derived from an amylase isozyme with a larger molecular size than that of normal salivary amylase. The results suggest ectopic tumor production of heterogenous amylase isozymes, with the larger form being secreted into the circulation.
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PMID:Amylase-producing lung cancer: case report and review of the literature. 617 Apr 23

Cellular retinol binding protein is present in the cytosol of Lewis lung primary tumor, as detected by DEAE-filter disk method. Gel filtration, followed by non-denaturing polyacrylamide gel electrophoresis, reveals the presence of two binding components. One of them binds retinol specifically as the [3H]retinol can be replaced by unlabeled retinol, but not by unlabeled retinoic acid. In contrast, [3H]retinol radioactivity of the second binding component can be abolished by both unlabeled retinol and unlabeled retinoic acid. SDS polyacrylamide gel electrophoresis shows that the two components have similar migration distances which correspond to an apparent molecular weight of 15,000.
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PMID:Two retinol binding proteins in Lewis lung tumor cytosol. 689 Jul 57

Tumor progression is frequently associated with changes in responsiveness of tumor cells to paracrine growth factors. A potential major source of such paracrine factors in solid tumors are endothelial cells since this type of cell can constitute a sizeable fraction of the cellular composition of solid tumors. As an initial step to examining the possible effects of endothelial cell-associated growth factors on tumor cell growth, a panel of human melanoma cell lines representative of different stages of tumor progression was employed for studies utilizing endothelial cell-derived growth modulators. Macrovascular or microvascular human endothelial cells from umbilical vein or from skin, respectively, inhibited melanoma cell growth in direct coculture experiments. The potency of this inhibitory effect diminished as a function of melanoma progression. Conditioned media from endothelial cell cultures mimicked the effect of the cell coculture experiments, suggesting the involvement of soluble growth factor(s). Approximately 50-75% of the conditioned media inhibitory effect was abrogated by addition of the neutralizing antibody to interleukin-6 (IL-6). Gel filtration chromatography revealed the presence of additional inhibitors in endothelial cell conditioned medium. Two peaks of activity were detected with apparent molecular weights of approximately 100-150 Kd and 20-30 Kd, the latter containing IL-6 activity. Whereas early-stage radial growth phase (RGP) primary tumor-derived melanoma cells were sensitive to at least three different endothelial products of high or low molecular weight (including IL-6), melanoma cells from more advanced metastatic lesions were resistant to the latter activities, and retained only partial sensitivity to the high molecular weight inhibitor. More advanced vertical growth phase (VGP) primary melanoma cell lines expressed intermediate inhibition-sensitive phenotypes. Thus human melanoma development appears to be associated with progressive loss of sensitivity to the growth inhibitory effects of IL-6 and other factors produced by endothelial cells. This is likely to be a result of a selection process when tumor cells are confronted with adjacent vasculature during the progress of tumor angiogenesis.
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PMID:Progressive loss of sensitivity to endothelium-derived growth inhibitors expressed by human melanoma cells during disease progression. 816 65

The clonal development of colorectal carcinoma resulting from specific mutations in certain oncogenes and/or tumor suppressor genes is a well-accepted model. It is increasingly recognized that a majority of colorectal cancers are polyclonal on the basis of molecular analysis that demonstrates cells with different mutations within a given oncogene or tumor suppressor gene in the same tumor. This polyclonal pattern may occur as a result of either clonal convergence or divergence during the many steps of oncogenesis. Further complicating this picture is the fact that metastatic lesions may arise from only one of the clonal populations within a tumor and thereby present only a partial molecular make-up of the whole tumor. There are few data available that define clonal selection or specificity of circulating tumor cells in patients undergoing curative resection of colorectal carcinoma. The purpose of this paper is to describe the clonal distribution of circulating tumor cells in four patients with multiple K-ras mutations present in the primary lesion. Patients were selected who were known to have polyclonal primary colorectal cancers resected for cure. All patients had multiple mutations present in exon one, codon 12 and/or 13, of the K-ras gene. Blood samples were drawn immediately before surgery and at 2-week to 6-month intervals postoperatively. Epithelial cells were isolated from peripheral blood mononuclear cells using Dynal Immunobeads coated with antiepithelial antibodies. DNA was extracted from these cells and analyzed for all K-ras mutations present in codons 12 and 13 of the patient's primary tumor using allele-specific polymerase chain reaction followed by Microwell Array Diagonal Gel Electrophoresis. Circulating tumor cells were identified in all four patients. However, in each case of positive circulating cells the only mutation identified was an aspartic acid mutation at codon 13. Once positive the circulating tumor cells persisted in subsequent multiple blood samples. These results provide further strength for the theory of polyclonal progression in primary colorectal cancers, although there may be specific mutational patterns that confer the ability to metastasize. The significance of this persistence of the glycine-to-aspartic acid mutation at codon 13 remains to be defined given that none of these patients has clinical evidence of recurrent cancer at the time of this report.
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PMID:K-ras mutational analysis of polyclonal colorectal cancers identifies uniclonal circulating tumor cells. 1151 May 88