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Insulin‐like growth factor II mRNA, peptides, and receptors in a thoracopulmonary malignant small round cell tumor
Insulin‐like growth factor‐(IGF) II and the IGF‐I and IGF‐II/mannose 6‐phosphate receptors were expressed in a thoracopulmonary malignant small round cell tumor (MSRCT) from a 14‐year‐old boy. Northern analysis showed that the MSRCT expresses multiple IGF‐II mRNA of 6.0, 4.8, 4.2, and 2.2 kilobase f...
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Published in: | Cancer 1994-02, Vol.73 (4), p.1312-1319 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | Insulin‐like growth factor‐(IGF) II and the IGF‐I and IGF‐II/mannose 6‐phosphate receptors were expressed in a thoracopulmonary malignant small round cell tumor (MSRCT) from a 14‐year‐old boy. Northern analysis showed that the MSRCT expresses multiple IGF‐II mRNA of 6.0, 4.8, 4.2, and 2.2 kilobase from promoters P3 and P4 of the human IGF‐II gene. Chromatography and radioimmunoassay revealed two forms of IGF‐II with molecular masses of 7.5 kilodalton (kDa) and 10 kDa, corresponding to mature IGF‐II and IGF‐II with a C‐terminal extension, in concentrations of 61 and 41 ng/g/tumor tissue, respectively. By a combined reverse transcriptionpolymerase chain reaction analysis, the authors also show that the MSRCT expresses IGF‐I and IGF‐II/mannose 6‐phosphate receptor mRNA. The plasma concentration of IGF‐II was 600 ng/ml and within the normal range of serum IGF‐II. IGF binding proteins (IGFBP) of 41.5, 38.5, 34, 30, and 24 kDa were present in serum. Compared with normal plasma from healthy subjects and an age‐matched group of boys, the level of the 41.5, 38.5, and 30 kDa IGFBP were approximately 3‐fold elevated. The authors conclude that transcription of the IGF‐II gene leads to the production of significant amounts of 10 kDa IGF‐II and 7.5 kDa IGF‐II. IGF‐II may stimulate the proliferation of MSRCT by interaction with IGF‐I receptors on the cells. Cancer 1994; 73:1312–9. |
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ISSN: | 0008-543X 1097-0142 |
DOI: | 10.1002/1097-0142(19940215)73:4<1312::AID-CNCR2820730429>3.0.CO;2-D |