IGF1 receptors (IGF1-R) in 72 primary human breast cancer. Relation with estradiol and progesterone receptors (ER, PgR)

Jp, Peyrat; Bonneterre, Jacques; Djiane, Jean; Barenton, Bruno; Beuscart, R.; Leroy‐Martin, B.; Demaille, A

doi:10.1016/0277-5379(87)90682-1

European Journal of Cancer and Clinical Oncology

1987

DOI: 10.1016/0277-5379(87)90682-1

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IGF1 receptors (IGF1-R) in 72 primary human breast cancer. Relation with estradiol and progesterone receptors (ER, PgR)

Peyrat Jp¹,

Jacques Bonneterre²,

Jean Djiane³

et al.

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1992

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Cited by 10 publications

(18 citation statements)

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“…Chemical cross-linking experiments revealed that the apparent molecular weight of the binding site was 130,000 daltons (Peyrat et al, 1988a). Therefore, the IGF1 specific binding sites share a close structural homology with insulin receptor and correspond to the previously described type I IGF receptors (IGF1-R) in normal tissues.…”

supporting

confidence: 52%

“…The first step in IGFI action is its binding to membrane receptors (Rosenfeld & Hintz, 1988 (Furnaletto & Di Carlo, 1984;Myal et al, 1984;De Leon et al, 1988;Pollak et al, 1988;Peyrat et al, 1989) as well as in breast cancers (Peyrat et al, 1988a) or in benign breast diseases (Peyrat et al, 1988b). We demonstrated that IGF2 was a good competitor of the binding of "251-IGF1 to IGFI-R whereas insulin competed with a potency lower than 1/100th of IGFI's potency.…”

mentioning

confidence: 67%

“…Several authors have demonstrated that most breast cancers contain IGF1-R (Peyrat et al, 1988a;Pollack et al, 1987;Pekonen, 1988;Foekens et al, 1989). In our study, the presence of IGF1-R is associated to a better prognosis (Bonneterre et al, 1990).…”

mentioning

confidence: 99%

“…We have used this technique to specify the localisation and to quantify high affinity IGFI-R in (Peyrat et al, 1988a).…”

mentioning

confidence: 99%

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Insulin-like growth factor 1 receptors in human breast tumour: Localisation and quantification by histo-autoradiographic analysis

Jammes¹,

Jp²,

Ban³

et al. 1992

Br J Cancer

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To assess the precise role of IGF1 in benign and malignant breast diseases, we analysed the tissular localisation, characterised, and quantified specific insulin-like growth factor 1 (IGF1) binding sites in these heterogenous tissues, using histo-autoradiographic analysis (HAA). The 125I-IGF1 binding was performed on frozen tissue sections and analysed using 3H Ultrofilm autoradiography coupled to computerised image analysis. Competitive binding experiments using unlabelled IGF1, IGF2 and insulin showed that the tissues exhibited typical type I IGF binding sites. This specificity was confirmed by the use of alpha IR-3 monoclonal antibody, as inhibitor of 125I-IGF1 binding. IGF1 binding sites were detected in 18 human primary breast cancers, 12 benign breast tumours and two normal breast tissues. Using HAA we found that the human breast carcinomas studied exhibit a specific and high binding capacity for 125I-IGF1 exclusively localised on the proliferative epithelial component. The 125I-IGF1 binding activity of benign breast tumours or normal breast tissue was significantly lower than in cancerous tissues. There was a significant correlation between IGF1-R concentrations detected with HAA and those detected with a classical biochemical method. Moreover, HAA could be useful in further detailing whether a tumour is IGF1-R positive or negative HAA appears to be a useful method for the detection of growth factor receptors, specially in small biopsy specimens. Images Figure 2 Figure 3

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supporting

confidence: 52%

mentioning

confidence: 67%

mentioning

confidence: 99%

“…We have used this technique to specify the localisation and to quantify high affinity IGFI-R in (Peyrat et al, 1988a).…”

mentioning

confidence: 99%

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Insulin-like growth factor 1 receptors in human breast tumour: Localisation and quantification by histo-autoradiographic analysis

Jammes¹,

Jp²,

Ban³

et al. 1992

Br J Cancer

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“…The growth effects of both are mediated predominantly via IGF-1 receptors, which have been demonstrated in 67-93% of primary human breast cancers (Pekonen et al, 1988;Peyrat et al, 1988a;Foekens et al, 1989a;Klijn et al, 1993) at higher density than in normal or benign breast tissue (Peyrat et al, 1988b). In vivo, pituitary-derived growth hormone (GH) regulates endocrinologically the secretion of IGF-1 (Kelly et al, 1991;Lamberts et al, 1991), but possibly also has regulatory effects on local IGF-1 secretion within (tumour) tissues (Davoren et al, 1986;Schally et al, 1987;Kelly et al, 1991).…”

mentioning

confidence: 99%

Feasibility, endocrine and anti-tumour effects of a triple endocrine therapy with tamoxifen, a somatostatin analogue and an antiprolactin in post-menopausal metastatic breast cancer: a randomized study with long-term follow-up

Bontenbal

Foekens²,

Lamberts³

et al. 1998

Br J Cancer

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Summary Suppression of the secretion of prolactin, growth hormone and insulin-like growth factor 1 (IGF-1) might be important in the growth regulation and treatment of breast cancer. Because oestrogens may counteract the anti-tumour effects of such treatment, the combination of an anti-oestrogen (tamoxifen), a somatostatin analogue (octreotide) and a potent anti-prolactin (CV 205-502) might be attractive. In this respect, we performed a first exploratory long-term study on the feasibility of combined treatment and possible clear differences in endocrine and anti-tumour effects during such combined treatment vs standard treatment with tamoxifen alone. Twenty-two post-menopausal patients with metastatic breast cancer (ER and/or PR positive or unknown) were randomized to receive either 40 mg of tamoxifen per day or the combination of 40 mg of tamoxifen plus 75 ig of CV 205-502 orally plus 3 x 0.2 mg of octreotide s.c. as first-line endocrine therapy. An objective response was found in 36% of the patients treated with tamoxifen alone and in 55% of the patients treated with combination therapy. Median time to progression was 33 weeks for patients treated with tamoxifen and 84 weeks for patients treated with combination therapy, but the numbers are too small for hard conclusions. There was no difference in overall post-relapse survival between the two treatment arms. With respect to the endocrine parameters, there was a significant decrease of plasma IGF-1 levels in both treatment arms, whereas during combined treatment plasma growth hormone tended to decrease and plasma prolactin levels were strongly suppressed; in some patients insulin and transforming growth factor a (TGF-a) decreased during the triple therapy. Although there was no significant difference in mean decrease of plasma IGF-1 levels between the two treatment arms, combined treatment resulted in a more uniform suppression of IGF-1. Therefore, the addition of a somatostatin analogue and an anti-prolactin may potentially enhance the efficacy of anti-oestrogens in the treatment of breast cancer owing to favourable endocrine and possible direct anti-tumour effects. Large phase IlIl trials using depot formulations (to increase the feasibility) of somatostatin analogues are warranted to demonstrate the potential extra beneficial anti-tumour effects of such combination therapy.

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Type 1 IGF receptor in human breast diseases

Bonneterre

1992

Breast Cancer Res Tr

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The first step of the action of IGF1 and IGF2 (IGFs) is their binding to membrane receptors. IGF binding sites have been characterized by competitive binding and cross-linking techniques in human breast cancer cell lines as well as in human breast cancers and in human benign breast diseases. IGF2 is a good competitor of 125I-IGF1 binding to IGF1-R; insulin competes but with a potency 1/100 lower than the IGF1 potency. Chemical cross-linking experiments revealed that the apparent molecular weight of the IGF1-binding sites is 130,000. Alpha IR-3, a murine monoclonal antibody against the IGF1-R, blocks IGF1-binding to this receptor. This antibody inhibits the IGF1-stimulated growth of breast cancer cells. Therefore, the IGF1 specific binding sites correspond to the previously described type 1 IGF receptors (IGF1-R) in normal tissues. Cross-linking experiments with labeled IGF2 resulted in a major band of apparent Mr 260,000-270,000 that was inhibited by unlabeled IGF2 but not by insulin, and corresponds to the type 2 IGF receptor; a second band of apparent Mr 130,000 was inhibited by excess IGFs and insulin (Type I receptor). The alpha-IR3 inhibition of the IGF2 mitogenic activity suggest that IGF1-R partially mediates the growth effect of IGF2 in these cells. We and others have demonstrated that most breast cancer cell lines contain IGF1-R.(ABSTRACT TRUNCATED AT 250 WORDS)

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IGF1 receptors (IGF1-R) in 72 primary human breast cancer. Relation with estradiol and progesterone receptors (ER, PgR)

Cited by 10 publications

References 0 publications

Insulin-like growth factor 1 receptors in human breast tumour: Localisation and quantification by histo-autoradiographic analysis

Insulin-like growth factor 1 receptors in human breast tumour: Localisation and quantification by histo-autoradiographic analysis

Feasibility, endocrine and anti-tumour effects of a triple endocrine therapy with tamoxifen, a somatostatin analogue and an antiprolactin in post-menopausal metastatic breast cancer: a randomized study with long-term follow-up

Type 1 IGF receptor in human breast diseases

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