Expression of insulin‐like growth factor‐I and ‐II genes in rat medullary thyroid carcinoma

Höppener, Jo W.M.; Steenbergh, P. H.; Slebos, Robert J. C.; Pagter-Holthuizen, P. de; Roos, Bernard A.; Jansen, M.; Brande, J. L. Van den; Sussenbach, J.S.; Jansz, H.S.; Lips, Cornelis J.M.

doi:10.1016/0014-5793(87)80125-4

Cited by 24 publications

(11 citation statements)

References 24 publications

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“…These include Wilms' tumor, rhabdomyosarcoma, adrenal pheochromocytoma, medullary thyroid carcinoma, leiomyosarcoma, hepatoma, liposarcoma, and breast carcinoma (Reeve et al, 1985;Scott et al, 1985;Haselbacher et al, 1987;Hoppener et al, 1987;Daughaday et al, 1988;Su et al, 1989;Tricoli et al, 1986;Yee et al, 1988). Several of these hu- man tumors synthesize both IGF-I and IGF-I1 mRNA (Daughaday et al, 1988;Su et al, 1989;Hoppener et al, 1987) as in the case of colorectal tumors taken from patients at surgery (Tricoli et al, 1986). However, recent studies have shown that the levels of IGF-I1 mRNA and protein are not necessarily correlated (Haselbacher et al, 1987;Graham et al, 1986).…”

Section: Discussionmentioning

confidence: 92%

“…A number of tumors appear to express elevated levels of IGF-I1 mRNA. These include Wilms' tumor, rhabdomyosarcoma, adrenal pheochromocytoma, medullary thyroid carcinoma, leiomyosarcoma, hepatoma, liposarcoma, and breast carcinoma (Reeve et al, 1985;Scott et al, 1985;Haselbacher et al, 1987;Hoppener et al, 1987;Daughaday et al, 1988;Su et al, 1989;Tricoli et al, 1986;Yee et al, 1988). Several of these hu- IGF-II(o), insulin (m), and 7.5 K-peak (0) on specific binding of '"51-IGF-11 to HT-29 cells.…”

Section: Discussionmentioning

confidence: 99%

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Production of insulin‐like growth factor II (IGF‐II) and different forms of IGF‐binding proteins by HT‐29 human colon carcinoma cell line

Culouscou¹,

Remacle‐Bonnet

Garrouste³

et al. 1990

Journal Cellular Physiology

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The serum-free medium conditioned by the human colon cancer cell line HT-29 contains insulin-like growth factors (IGF) that are entirely complexed to binding proteins (IGF-BP). Gel filtration in acid conditions of the cell-conditioned medium permits separation of IGF-BP from two molecular forms of IGF of 15,000 and 7,500 Mr. As determined by ligand blotting, IGF-BP are heterogeneous and constituted of three molecular forms of 31,000, 28,000, and 26,000 Mr. Using IGF-I and IGF-II radioreceptor assays, IGF-I radioimmunoassay (RIA), and competitive protein-binding assay specific for IGF-II, it is shown that the IGF-type eluting in 15 K and 7.5 K position from gel filtration is restricted to IGF-II. Its concentration is approximately 6 ng/10(6) HT-29 cells with 60% present as a high-molecular-weight form of IGF-II. This large 15 K IGF molecule is devoided of any IGF-binding activity and might represent incomplete processing of pro-IGF-II peptide. By contrast, the level of IGF-I detected by RIA is barely measurable and considered negligible (0.57 pg/10(6) HT-29 cells). Although these IGF-II-like peptides exhibit a growth-promoting activity on FR3T3 fibroblasts, they cannot stimulate, as recombinant IGF-I or IGF-II, 3H-thymidine incorporation into DNA of HT-29 cells, whatever the experimental conditions used. Finally, we have shown that IGF binding is restricted predominantly to the basolateral domain of the cell membrane by using HT-29-D4 clonal cells, derived from the parental HT-29 cell line, maintained in a differentiated state by culture in a medium in which glucose is replaced by galactose.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Production of insulin‐like growth factor II (IGF‐II) and different forms of IGF‐binding proteins by HT‐29 human colon carcinoma cell line

Culouscou¹,

Remacle‐Bonnet

Garrouste³

et al. 1990

Journal Cellular Physiology

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“…Whereas several molecular species of IGF-I have been reported for rat thyroid medullary carcinoma tissue, ranging in size from 1 to 7 Kb approximately [73], in our experimental conditions, hybridisation of the IGF-I specific probe to a thyroid RNA species of approximately 1000 nucleotides was documented.…”

Section: Igf-i/igf-ir Expression In Thyroid Neo-plasmsmentioning

confidence: 95%

The IGF-I Axis in Thyroid Carcinoma

Ciampolillo

Tullio²,

Perlino³

et al. 2007

CPD

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Insulin like-growth factor I (IGF-I) has been involved in the pathogenesis of a variety of human neoplasia due to the mitogenic and anti-apoptotic properties of its cognate receptor. In human thyroid carcinomas, we have previously documented an increased immunoreactivity of both IGF-I and the IGF-I receptor (IGF-I R) associated with up regulation of IGF-I mRNA . Immunoreactivity of IGF-I and cognate receptor positively correlated with tumor diameter and wide intrathyroidal extension but not with patient's gender and age or with the stage of the tumors and the occurrence of limph node metastases. Most experimental studies indicate that the effects of IGF-I on target cells are regulated in a complex fashion and depend on the simultaneous occurrence of IGF-IR and the binding proteins.

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“…Thesubunit of IGF-1R binds IGF-I, IGF-II, and insulin at supraphysiological doses; the -subunits contain the TK domain [122]. IGF-II and IGF-1R are overexpressed in many cancer types, including MTC [123]. IGF-1R up-regulation was found to mediate resistance to TKIs in different types of cancer cells.…”

Section: Insulin-like Growth Factor Receptor Pathwaymentioning

confidence: 99%

“…IGF-I and IGF-1R are over-expressed in thyroid cancer, particularly in the most aggressive variants [124]. Importantly, IGF-I and insulin are essential for the mitogenic action of TSH and EGF in thyroid follicular cells [123]. ADW742 is a specific inhibitor of IGF-1R phosphorylation and of its signaling pathway.…”

Section: Insulin-like Growth Factor Receptor Pathwaymentioning

confidence: 99%

Medullary Thyroid Cancer: A Promising Model for Targeted Therapy

Torino¹,

Paragliola

Barnabei³

et al. 2010

CMM

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Abstract:In recent years, the clinical validation of molecular targeted therapies inhibiting the action of pathogenic tyrosine kinase (TK) has been one of the most exciting developments in cancer research. In this context, medullary thyroid carcinoma (MTC) represents a promising model. It is well known that in MTC, the RET receptor TK and its signal transduction pathways, lead to subsequent neoplastic transformation. Several strategies aimed at blocking the activation and signaling of RET have been preclinically tested. The most advanced results have been obtained by competitive inhibition of RET-TK activity by tyrosine kinases inhibitors (TKI). However, although the inhibition of the RET pathway is actually one of the most studied for therapeutic purposes, other signal transduction pathways have been recognized to contribute to the growth and functional activity of MTC and are considered attractive therapeutic targets.To date, surgery represents the only curative treatment of MTC. Despite promising initial results, studies on targeted agents are in early stages and several issues regarding preclinical evaluations and clinical trials of new targeted agents in MTC are still unresolved. Now, available mouse models bearing mutations of RET or other genes, which spontaneously develop MTC, promise to improve preclinical evaluation of activity of targeted compounds. Furthermore, the rarity of the disease and the number of patients available for enrolment may lessen the relevance of clinical trials. A major effort needs to be made by endocrinologists and oncologists to refer their patients for multi-institutional trials in order to optimize them, perform translational studies and expedite the availability of novel beneficial selective therapies.

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Expression of insulin‐like growth factor‐I and ‐II genes in rat medullary thyroid carcinoma

Cited by 24 publications

References 24 publications

Production of insulin‐like growth factor II (IGF‐II) and different forms of IGF‐binding proteins by HT‐29 human colon carcinoma cell line

Production of insulin‐like growth factor II (IGF‐II) and different forms of IGF‐binding proteins by HT‐29 human colon carcinoma cell line

The IGF-I Axis in Thyroid Carcinoma

Medullary Thyroid Cancer: A Promising Model for Targeted Therapy

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