| 11. |
- Nilsson, Ola, 1957, et al.
(författare)
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Presence of IGF-I in human midgut carcinoid tumours--an autocrine regulator of carcinoid tumour growth?
- 1992
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Ingår i: International journal of cancer. Journal international du cancer. - 0020-7136. ; 51:2, s. 195-203
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Tidskriftsartikel (refereegranskat)abstract
- The presence of IGF-I and IGF-I receptors in human midgut carcinoid tumours has been investigated. Using immunocytochemistry, IGF-I-positive tumour cells were demonstrated in 11/11 tumour cases studied. Labelling of consecutive sections with antibodies against IGF-I and proliferating cell nuclear antigen (PCNA)/cyclin demonstrated a co-distribution of the 2 antigens in carcinoid tumours. Extracts of tumour tissues were subjected to radioimmunoassay and shown to contain significant amounts of IGF-I. Reverse-phase HPLC of tumour extracts demonstrated a major IGF-I-immunoreactive component eluting in the position of rhIGF-I, but also 2 other more hydrophobic forms. Conditioned serum-free media from primary cultures of carcinoid tumors contained detectable amounts of IGF-I, indicating a spontaneous release of IGF-I from tumour cells into the culture medium. Levels of IGF-I in media were reduced (19%) after incubation of cultures with a somatostatin analogue for 4 days. IGF-I receptors were observed on tumour cells in 4/10 tumours by immunocytochemistry. Tumour cells with immunoreactive IGF-I receptors could be stimulated to enhanced growth, measured as an increase in DNA contents, by exogenous administration of IGF-I every 3-4 days for 2 weeks. The results show that cultured human midgut carcinoid tumours secrete IGF-I and that some of the tumours also have IGF-I receptors. We therefore suggest that IGF-I may act as an autocrine or paracrine regulator of carcinoid tumour-cell growth.
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| 12. |
- Syvänen, Ann-Christine, et al.
(författare)
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N-ras gene mutations in acute myeloid leukemia : accurate detection by solid-phase minisequencing
- 1992
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Ingår i: International Journal of Cancer. - 0020-7136 .- 1097-0215. ; 50:5, s. 713-718
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Tidskriftsartikel (refereegranskat)abstract
- Mutations in the N-ras gene are found in one-third of patients with acute myeloid leukemia. The N-ras mutations could serve as markers for residual cells, if a highly sensitive method for detecting the mutations was available. We applied a new method, solid-phase minisequencing, to analyze bone-marrow cells from 16 patients with acute myeloid leukemia for mutations in codon 12, 13 and 61 of the N-ras gene. In the solid-phase minisequencing technique the mutations are identified by a primer extension reaction, in which a single labelled nucleoside triphosphate is incorporated into an immobilized DNA fragment previously amplified by the polymerase chain reaction. We identified N-ras mutations in 5 of the patients (30%). In one patient, we observed 2 mutations that were shown to be located in different alleles. With the solid-phase minisequencing method, we were able to determine the proportion of mutated cells in the samples. We found that in 4 of the samples only a fraction (7-64%) of the blasts carried an N-ras mutation, and in one sample practically all blast cells were mutated. The method was highly sensitive, allowing us to identify N-ras mutations even when the sample consisted of 99.7% normal cells and only 0.3% mutated blasts.
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| 13. |
- Zhang, K, et al.
(författare)
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A secreted mucin carrying sialyl-Lewis a from colon carcinoma cells binds to E-selectin and inhibits HL-60 cell adhesion.
- 1994
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Ingår i: International journal of cancer. Journal international du cancer. - 0020-7136. ; 59:6, s. 823-9
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Tidskriftsartikel (refereegranskat)abstract
- Sialyl-Lewis x and a are known as ligands for E-selectin (ELAM-I) involved in leukocyte-endothelial adhesion. L-CanAg (light cancer antigen), secreted by a colon carcinoma cell line COLO 205, is a soluble mucin-type glycoprotein expressing sialyl-Lewis a antigens. L-CanAg was purified from spent culture medium by trichloracetic acid precipitation and Superose 6 gel filtration. With a monoclonal antibody against E-selectin (BBAI) as a positive control, the purified L-CanAg was shown to bind to E-selectin-Fc coated into plastic microtiter wells and to the surface of transiently E-selectin-transfected COS-I cells in a Ca(2+)-dependent way. Immunofluorescent double labelling showed that both BBAI and L-CanAg stained the same cells and morphological co-localization on E-selectin-transfected COS-I cells. Like BBAI, L-CanAg can inhibit leukocyte HL-60 cell adhesion to E-selectin-transfected COS-I cells, and this inhibition can be blocked by a F(ab')2 fragment directed against the sialyl-Lewis a epitope.
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