Growth-inhibitory effects of somatostatin (analogs) on human breast cancer cells in vitro

Setyono-Han, Buddy; Foekens, John A.; Klijn, Jan G.M.

doi:10.1016/0022-4731(87)91563-9

Cited by 51 publications

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“…. Indeed, we (Setyono-Han et al, 1987) and others (Lamberts of asymptomatic et al, 1991;Weckbecker et al, 1992) have demonstrated direct bination therapy.…”

Section: Anti-tumour Effectssupporting

confidence: 51%

“…British Journal of Cancer (1998) These disappointing results of single somatostatin analogue treatment (or in combination with an anti-prolactin) can be explained by our observation that oestradiol abolished these growth inhibitory effects (Setyono-Han et al, 1987). Therefore, at the start of the present clinical study in 1989 our study design testing these drugs in combination with an anti-oestrogen seems to be more appropriate.…”

Section: Anti-tumour Effectsmentioning

confidence: 90%

“…However, until now a single treatment with these agents showed only minor activity in post-menopausal patients with metastatic breast cancer (European Breast Group, 1972;Minton et al, 1974;Engelsman et al, 1975;Grisoli et al, 1981;Morten et al, 1988;Manni et al, 1989;Vennin et al, 1989;Holtkamp et al, 1990;Klijn et al, 1992). Because unopposed oestrogen action can overrule the growth inhibitory effects of somatostatin analogues (Setyono-Han et al, 1987) and/or anti-prolactions, combination treatment With an anti-oestrogen, a somatostatin analogue and an anti-prolactin might be of value and may increase the efficacy of single treatment with tamoxifen alone. As tamoxifen affects growth factor secretion (Coletti et al, 1989;Pollak et al, 1990;Clarke et al, 1992;Kiang et al, 1992;Lonning et al, 1992;Reed et al, 1992;Winston et al, 1994) Currently, the mean follow-up of all 20 evaluable patients is 3 years (range 3 months-6 years).…”

mentioning

confidence: 99%

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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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“…. Indeed, we (Setyono-Han et al, 1987) and others (Lamberts of asymptomatic et al, 1991;Weckbecker et al, 1992) have demonstrated direct bination therapy.…”

Section: Anti-tumour Effectssupporting

confidence: 51%

Section: Anti-tumour Effectsmentioning

confidence: 90%

mentioning

confidence: 99%

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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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“…This includes modulation of phosphorylated extracellular signal-regulated kinases 1 and 2 (ERK/1/2) and Akt phosphorylation (Moller et al, 2003), the two major signal transduction pathways involved in transformation, and enhanced proliferation and migration of cancer cells (Santen et al, 2002;Liu et al, 2007). The antiproliferative effect of SST in breast cancer cells in vitro has long been known (Setyono-Han et al, 1987), and the particular role of sst2 has been further dissected recently by showing that it mediates an antiproliferative action in MCF-7 cells by inducing apoptosis and G1/S cell cycle arrest, and decreasing expression of epidermal growth factor receptor (He et al, 2009). Similarly, SST inhibits proliferation and migration of other cancer cells through downregulation of Akt and/ or ERK cascades (Pola et al, 2003;Sun et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

The new truncated somatostatin receptor variant sst5TMD4 is associated to poor prognosis in breast cancer and increases malignancy in MCF-7 cells

et al. 2011

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Somatostatin receptors (sst1-5) are present in different types of tumors, where they inhibit key cellular processes such as proliferation and invasion. Although ssts are densely expressed in breast cancer, especially sst2, their role and therapeutic potential remain uncertain. Recently, we identified a new truncated sst5 variant, sst5TMD4, which is related to the abnormal response of certain pituitary tumors to treatment with somatostatin analogs. Here, we investigated the possible role of sst5TMD4 in breast cancer. This study revealed that sst5TMD4 is absent in normal mammary gland, but is abundant in a subset of poorly differentiated human breast tumors, where its expression correlated to that of sst2. Moreover, in the MCF-7 breast cancer model cell, sst5TMD4 expression increased malignancy features such as invasion and proliferation abilities (both in cell cultures and nude mice). This was likely mediated by sst5TMD4-induced increase in phosphorylated extracellular signal-regulated kinases 1 and 2 and p-Akt levels, and cyclin D3 and Arp2/3 complex expression, which also led to mesenchymal-like phenotype. Interestingly, sst5TMD4 interacts physically with sst2 and thereby alters its signaling, enabling disruption of sst2 inhibitory feedback and providing a plausible basis for our findings. These results suggest that sst5TMD4 could be involved in the pathophysiology of certain types of breast tumors.

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“…It was a very important and promising finding that TT-232 proved to be very effective in the D-10 melanoma model (Kéri et al, 1996;Tejeda et al, 1999;Schwab et al, 2001). In addition, TT-232 had practically no growth hormone release inhibitory activity either in superfused rat pituitary cells or in rats in vivo (Kéri et al, 1993a(Kéri et al, , b, 1996, while the application of various other somatostatin analogues (Robbins, 1996;Schally, 1988;Janecka et al, 2001) in tumour therapy is limited because of their endocrine side effects (Setyono-Han et al, 1987). TT-232 was shown to be a potent inducer of apoptosis in a wide array of cancer cell lines in vitro and in animal models in vivo.…”

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confidence: 99%

Effect of a novel somatostatin analogue combined with cytotoxic drugs on human tumour xenografts and metastasis of B16 melanoma

et al. 2003

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A novel somatostatin analogue, TT-232 (which inhibits the proliferation of various cell cultures and transplantable mouse tumours), was examined regarding its effect on human melanoma and lymphoma xenografts as a single treatment or in combination with DTIC (dacarbazine) and etoposide. TT-232 inhibited the growth of HT-18 melanoma xenografts, a dose of 5 mg kg À1 being the most effective. Combination of 1 mg kg À1 TT-232 with 30 or 60 mg kg À1 DTIC (administered daily) resulted in a stronger inhibitory effect compared to TT-232 or DTIC as a single modality. Antimetastatic effect of TT-232 treatment combined with DTIC was studied using the B16 mouse melanoma muscle -lung metastasis model. The number of lung metastases of B16 melanoma could be decreased by the daily administration of 1 mg kg À1 TT-232 or 60 mg kg À1 , but not of 30 mg kg À1 DTIC. TT-232, combined with 30 or 60 mg kg À1 DTIC decreased the lung metastasis number significantly lower than the control. Nearly 50% growth inhibition of HT-58 lymphoma was achieved by daily treatment with 1 mg kg À1 TT-232. 5 mg kg À1 etoposide, administered daily, resulted in a similar effect. The combination of 1 mg kg À1 TT-232 and 5 mg kg À1 etoposide was significantly more effective than TT-232 or etoposide as a single treatment. The very strong tumour growth inhibitory effect of 10 mg kg À1 etoposide could even be increased by combination with TT-232. These experimental data suggest that TT-232 may be an effective new tool in the combination chemotherapy of malignant tumours like melanoma and lymphoma.

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Growth-inhibitory effects of somatostatin (analogs) on human breast cancer cells in vitro

Cited by 51 publications

References 0 publications

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

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

The new truncated somatostatin receptor variant sst5TMD4 is associated to poor prognosis in breast cancer and increases malignancy in MCF-7 cells

Effect of a novel somatostatin analogue combined with cytotoxic drugs on human tumour xenografts and metastasis of B16 melanoma

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