Therapeutic response to somatostatin analogue, BIM 23014, in metastatic prostatic cancer

Parmar, H.; Charlton, Christopher; Phillips, Robert; Edwards, Laura; Bejot, J; Thomas, François; Lightman, Stafford L.

doi:10.1007/bf00163570

Cited by 24 publications

(6 citation statements)

References 14 publications

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“…Thus, they tried to delay or prevent the relapse, and to improve the therapy of PC. Parmar et al [96] treated 16 of 25 poor-risk patients with hormone refractory metastatic PC (failing to respond to total androgen blockade) with an SST analog BIM-23014. 2 of these 16 patients showed partial response and 3 no change of the disease, with only a few side effects, such as mild diarrhea and abdominal cramps.…”

Section: Controlled Clinical Trialsmentioning

confidence: 99%

Octreotide in the Management of Hormone-Refractory Prostate Cancer

Vainas

2001

Chemotherapy

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Patients with advanced or metastatic prostate cancer (PC), a partially hormone-resistant disease, will require some form of hormonal manipulations or some new therapeutic modalities. Octreotide, as somatostatin (SST) analogs, has been found to inhibit the growth of experimental PCs via several mechanisms, as indirect antihormonal and direct antimitogenic actions, mainly due to inhibition of SST receptor subtypes (SSTR-1–5). Sporadic clinical trials with octreotide (alone or with a complete antiandrogen blockade) treatment of patients with advanced stage D2 PC demonstrated promising results. Unfortunately, at present these clinical trials have some disadvantages and leave some uncertainty with regard to the trial design, the SSTR subtype determination and tumor localization with SSTR scintigraphy before the start of a selective SST analog, and finally the randomization in groups according to hormone resistance, dosage regimen and route of administration.

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Section: Controlled Clinical Trialsmentioning

confidence: 99%

Octreotide in the Management of Hormone-Refractory Prostate Cancer

Vainas

2001

Chemotherapy

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“…It has been suggested that these effects may result from a direct action at glandular level, or from an indirect action on local growth factors or on GH and PRL circulating levels (4). Moreover, our data may explain the lack of results in the treatment of prostate cancer with some SRIH analogues (1,24,25) with high affinity for SSTR2 subtype, and suggest the need to look for new analogues with high affinity for SSTR1. Exact functions mediated by different SSTR subtypes is not yet clearly established, but several findings suggest that SSTR1 and SSTR2 subtypes may be responsible for the antiproliferative effects of SRIH (13,14).…”

Section: Discussionmentioning

confidence: 87%

Different Expression Patterns of Somatostatin Receptor Subtypes in Cultured Epithelial Cells from Human Normal Prostate and Prostate Cancer1

Sinisi

Bellastella

Prezioso³

et al. 1997

The Journal of Clinical Endocrinology &Amp; Metabolism

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The transcripts of five SRIH receptor subtypes (SSTR1, SSTR2, SSTR3, SSTR4, and SSTR5) were investigated by RT-PCR in epithelial cells (EC) and stromal cells (SC) from primary cultures of five normal human prostates and six prostate cancers. Primary cultures of prostate EC were established in serum-free keratynocyte medium with 5% FCS, epidermal growth factor, and bovine pituitary extract; SC were cultured in MEM with 10% FCS. Total RNA was extracted from EC and SC using a modified guanidine thiocyanate method. RT-PCR was performed after deoxyribonuclease treatment, using SSTR1-, SSTR2-, SSTR3-, SSTR4-, and SSTR5-specific-primers and adding glyceraldehyde-3-phosphate dehydrogenase-specific primers as internal control. A PCR product of the expected size of 334 bp, corresponding to SSTR1, was expressed only in EC from prostate cancer, whereas the expected 461-bp product of SSTR2 was found only in EC from normal prostate. SSTR3 messenger RNA was undetectable in normal and cancer EC, whereas SSTR4 and SSTR5 were present in both cell types. SSTR1, SSTR2, SSTR3, SSTR4, and SSTR5 messenger RNAs were not expressed in SC from both normal and cancer prostates. The RT-PCR method clearly demonstrated SSTRs' expression in the human prostate EC in vitro with differences between normal and tumoral samples. Our results may explain the ineffectiveness of some SSTR2 selective SRIH analogues in the treatment of prostate cancer and suggest that the absence of SSTR2 could represent a growth advantage in prostate cancer.

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“…In a study including stage D2 prostate cancer patients who relapsed after castration and flutamide, somatostatin analogs alone or in combination with bromocriptine were tested 7. In another study including 16 hormone-refractory metastatic prostate cancer patients, a partial response was observed in two patients treated with lanreotide 33. Only progressive disease was observed in another study testing the efficacy of octreotide.…”

Section: Somatostatin Analogs In Prostate Cancermentioning

confidence: 99%

A review of the use of somatostatin analogs in oncology

Keskin¹,

Yalçın²

2013

OTT

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Somatostatin is a neuropeptide produced by paracrine cells that are located throughout the gastrointestinal tract, lung, and pancreas, and is also found in various locations of the nervous system. It exerts neural control over many physiological functions including inhibition of gastrointestinal endocrine secretion through its receptors. Potent and biologically stable analogs of somatostatin have been developed. These somatostatin analogs show different efficacy on different receptors, and receptors are varyingly concentrated in specific tissues. Antitumor and antisecretory effects of somatostatin analogs in cancer have been shown in several in vivo and in vitro studies. However, these activities have not always yielded into clinically relevant patient outcome benefit. Somatostatin analogs are of clinical benefit in treating symptoms of ectopic hormone secretion (adrenocorticotropic hormone, growth hormone-releasing hormone) in lung cancer, without inducing a significant tumor response. They have also been shown to induce a statistically significant decrease in bone pain and increase in Karnofsky performance status in patients with metastatic prostate cancer. Somatostatin analogs alone or in combination with other agents have only limited antitumoral effect in breast cancer. In gastrointestinal cancers, studies have not shown an objective tumor response to somatostatin analogs except in endocrine tumors of the liver with symptomatic and biochemical improvement. In neuroendocrine tumors of the gastrointestinal system and pancreas, very high symptomatic and biochemical response rates have been achieved with somatostatin analogs. Antiproliferative activity has been clearly shown in metastatic midgut neuroendocrine tumors.

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Therapeutic response to somatostatin analogue, BIM 23014, in metastatic prostatic cancer

Cited by 24 publications

References 14 publications

Octreotide in the Management of Hormone-Refractory Prostate Cancer

Octreotide in the Management of Hormone-Refractory Prostate Cancer

Different Expression Patterns of Somatostatin Receptor Subtypes in Cultured Epithelial Cells from Human Normal Prostate and Prostate Cancer1

A review of the use of somatostatin analogs in oncology

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