Abstract
The role of insulin-like growth factors (IGF) and their specific binding proteins (IGFBP) has been shown to be an integral part of the growth promotion in a number of neoplasms. IGFBPs are a family of homologues proteins that regulate the biological activities of the IGFs, and may also be capable of IGF-independent actions [1,2]. Proceeding from our previous reports on expression of IGFs and IGFBPs in human leucemic lymphoblasts, we studied the gene expression of IGFBP-rP2/CTGF (connective tissue growth factor) in acute lymphoblastic leucemia [3,4]. CTGF has been identified as a major chemotactic and mitogenic factor for connective tissue cells. It has platelet-derived growth factor (PDGF)-related biological and immunological activities [5]. The amino acid sequence shares an overall 28-38% identity to IGFBPs and contains critical conserved sequences including the common IGFBP motif. It could be demonstrated that human CTGF binds specifically IGFs with a low affinity [6]. IGFBP-rP2/CTGF is considered to be a new member of the IGFBP superfamily that regulates cell growth through both IGF-dependent and IGF-independent actions [6]. The CTGF gene encodes a 38-kDa prepeptide containing 349 amino acids [5]. Northern blot analysis of various normal human tissues showed expression of CTGF mRNA at high levels in spleen, ovary, gastrointestinal tract, prostate, heart, and testis. No expression was found in peripheral blood leukocytes, liver and brain
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© 2001 Springer-Verlag Berlin Heidelberg
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Vorwerk, P., Elsner, J., Mohnike, K., Oh, Y., Rosenfeld, R.G., Mittler, U. (2001). Expression of IGFBP-rP2 / CTGF is Specific for Malignant Lymphoblasts of Children with Acute Lymphoblastic Leucemia (ALL). In: Büchner, T., Hiddemann, W., Wörmann, B., Schellong, G., Ritter, J., Creutzig, U. (eds) Acute Leukemias VIII. Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, vol 40. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-18156-6_15
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DOI: https://doi.org/10.1007/978-3-642-18156-6_15
Publisher Name: Springer, Berlin, Heidelberg
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