1995
DOI: 10.1016/0002-9378(95)91420-x
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Insulin-like growth factor I promotes leiomyoma cell growth in vitro

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Cited by 68 publications
(42 citation statements)
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“…These factors are structurally related to proinsulin and promote cellular proliferation, differentiation, and cell survival Yu and Berkel 1999). Evidence exists for dissimilar roles of the two IGFs, in that IGF-II appears to be primarily responsible for the terminal differentiation of skeletal muscle cells and the down-regulation of IGF-I receptor gene expression, whereas IGF-I is responsible for myogenesis (Rosenthal et al 1994;Strawn et al 1995). In most situations the IGF binding proteins inhibit the actions of IGFs by blocking their binding to the receptor; in certain circumstances, however, these binding proteins may be able to enhance the action of IGF-I by binding to it and preventing its degradation, thereby increasing its bioavailability in target tissues (Yu and Berkel 1999).…”
Section: Growth Factors Identified In Fibroidsmentioning
confidence: 99%
“…These factors are structurally related to proinsulin and promote cellular proliferation, differentiation, and cell survival Yu and Berkel 1999). Evidence exists for dissimilar roles of the two IGFs, in that IGF-II appears to be primarily responsible for the terminal differentiation of skeletal muscle cells and the down-regulation of IGF-I receptor gene expression, whereas IGF-I is responsible for myogenesis (Rosenthal et al 1994;Strawn et al 1995). In most situations the IGF binding proteins inhibit the actions of IGFs by blocking their binding to the receptor; in certain circumstances, however, these binding proteins may be able to enhance the action of IGF-I by binding to it and preventing its degradation, thereby increasing its bioavailability in target tissues (Yu and Berkel 1999).…”
Section: Growth Factors Identified In Fibroidsmentioning
confidence: 99%
“…IGF-1 stimulates mitogenesis of the normal epithelium and proliferation of both endometrial cancers and leiomyoma cells (Strawn et al, 1995;Klotz et al, 2000). In the mouse uterine model, the in vivo proliferative response of IGF-1 requires ERa, even in the presence of a functional IGF-1 signaling response, as IGF-1 signaling to MAPK or Akt is unaffected by the loss of ER (Klotz et al, 2002).…”
Section: Igf1-r Crosstalk With Er and Prmentioning
confidence: 99%
“…Although the exact etiology of UL is unknown, there are several factors influencing the growth of UL [5]. They www.…”
Section: Introductionmentioning
confidence: 99%