Placebo-Controlled, Double-Blind, Prospective, Randomized Study on the Effect of Octreotide LAR in the Control of Tumor Growth in Patients With Metastatic Neuroendocrine Midgut Tumors: A Report From the PROMID Study Group

Rinke, Anja; Schade‐Brittinger, Carmen; Klose, Klaus–Jochen; Barth, Peter; Wied, M.; Mayer, Christina; Aminossadati, Behnaz; Pape, Ulrich‐Frank; Harder, Jan; Arnold, Christian; Gress, Thomas M.; Arnold, R.

doi:10.1200/jco.2009.22.8510

Cited by 2,194 publications

(1,751 citation statements)

References 38 publications

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“…In striking contrast to the compelling experimental evidence gathered in favor of a potential clinical and therapeutic benefit for SST in breast cancer, and despite the successful application of SST analogs to treat pituitary adenomas and neuroendocrine tumors (Rinke et al, 2009;Ben-Shlomo and Melmed 2010), the early, scarce clinical studies reporting treatment of breast cancer patients with SST analogs only demonstrated, at best, a limited success (Watt et al, 2008). Here, we provide evidence that a new factor in the SST/ssts system, sst5TMD4, is present in breast cancer, where it may counteract normal inhibitory function of SST/sst2 signaling.…”

Section: Introductionmentioning

confidence: 90%

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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Section: Introductionmentioning

confidence: 90%

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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“…SSAs have also been shown to exert a cytostatic effect, which can result in disease stabilization and the lengthening of the median time to tumor progression [92].…”

Section: Somatostatin Analogues and Peptide Receptor Radiotherapymentioning

confidence: 99%

Pancreatic Neuroendocrine Tumors: an Update

2015

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Pancreatic neuroendocrine tumors (pNETs) are rare and comprise only 1-2 % of all pancreatic neoplastic disease. Although the majority of these tumors are sporadic (90 %), pNETs can arise in the setting of several different hereditary genetic syndromes, most commonly multiple endocrine neoplasia type 1 (MEN1). The presentation of pNETs varies widely, with over 60 % having malignant distant disease at the time of initial diagnosis involving the liver or other distant sites. Functioning pNETs represent approximately 10 % of all pNETs, secrete a variety of peptide hormones, and are responsible for several clinical syndromes caused by profound hormonal derangement. Surgery remains the cornerstone of therapy and the only curative approach. It should be pursued for localized disease and for metastatic lesions amenable to resection. Multimodality therapies, including liver-directed therapies and medical therapy, are gaining increasing favor in the treatment of advanced pNETs. Their utility is multifold and spans from ameliorating symptoms of hormonal excess (functional pNETs) to controlling the local and systemic disease burden (non-functional pNETs). The recent introduction of target molecular therapy has promising results especially for the treatment of progressive well-differentiated G1/G2 tumor. In this review, we summarize the current knowledge and give an update on recent advancements made in the therapeutic strategies for pNETs.

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“…Although shown to delay time to tumor progression, there is currently no evidence of improved survival in such patients. 21 Interferon a, like octreotide, has demonstrated antisecretory and antiproliferative effects on metastatic NETs. However, the data is insufficient to recommend its routine use in these patients.…”

Section: Metastatic Diseasementioning

confidence: 99%

Carcinoid and Other Neuroendocrine Tumors of the Colon and Rectum

Eggenberger¹

2011

Clinics in Colon and Rectal Surgery

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Neuroendocrine tumors (NETs) are found throughout the intestinal tract and arise from the Kulchitsky cells located in the crypts of Lieberkühn. They are classified by site of origin and by degree of differentiation, with well-differentiated lesions representing those tumors formerly referred to as carcinoid tumors. The focus of this review is NETs of the appendix, colon, and rectum. The clinical presentation of these tumors is dependent on the primary site and many are discovered incidentally, either during screening or during the investigation of nonspecific abdominal complaints. Treatment is primarily via surgical removal as the response to chemotherapy has been traditionally poor. A noted exception to this has been with treatment of the carcinoid syndrome, which occurs almost exclusively in patients with liver metastases and is due to the release of bioactive peptides and amines directly into the systemic circulation. The use of somatostatin congeners to block the release of these substances has greatly ameliorated the devastating symptoms of this condition. Postresection follow-up is advocated, but specific recommendations are lacking an evidentiary basis. NETS, particularly those of the small bowel, colon, and appendix, are seen in association with other synchronous or metachronous malignancies, often of the gastrointestinal tract. However, the utility of subsequent screening and surveillance is unproven.

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Placebo-Controlled, Double-Blind, Prospective, Randomized Study on the Effect of Octreotide LAR in the Control of Tumor Growth in Patients With Metastatic Neuroendocrine Midgut Tumors: A Report From the PROMID Study Group

Abstract: Octreotide LAR significantly lengthens time to tumor progression compared with placebo in patients with functionally active and inactive metastatic midgut NETs. Because of the low number of observed deaths, survival analysis was not confirmatory.

Cited by 2,194 publications

References 38 publications

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

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

Pancreatic Neuroendocrine Tumors: an Update

Carcinoid and Other Neuroendocrine Tumors of the Colon and Rectum

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