Octreotide Acetate Long-Acting Formulation Versus Open-Label Subcutaneous Octreotide Acetate in Malignant Carcinoid Syndrome

Rubin, Joseph; Ajani, Jaffer A.; Schirmer, William J.; Venook, Alan P.; Bukowski, Ronald M.; Pommier, Rodney F.; Saltz, Leonard; Dandona, Paresh; Anthony, Lowell

doi:10.1200/jco.1999.17.2.600

Cited by 351 publications

(234 citation statements)

References 16 publications

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“…It can be used as an effective treatment for various endocrine tumors, e.g., malignant carcinoid syndrome, acromegaly, and thyrotropin-stimulating hormone-secreting pituitary adenoma. [16][17][18] Long-acting octreotide preparation has also been used in short bowel syndrome, resulting in satisfactory prolongation of small bowel transit time. 19 A recent preliminary study shows promising clinical improvement in patients with rheumatoid arthritis treated with long-acting octreotide.…”

Section: H Epatocellular Carcinoma (Hcc) Is Responsiblementioning

confidence: 99%

A randomized placebo-controlled study of long-acting octreotide for the treatment of advanced hepatocellular carcinoma

et al. 2002

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Although various types of treatment of hepatocellular carcinoma (HCC) have been tried, the prognosis remains dismal, especially in patients with advanced stage of the disease. Somatostatin analogues exert antitumor effects. HCC have been shown to exhibit somatostatin receptors. The present randomized placebo-controlled study aimed at examining the efficacy of long-acting octreotide (Sandostatin LAR) for the treatment of advanced HCC. Seventy patients were randomized to receive a 2-week course of 250 g short-acting octreotide twice daily followed by Sandostatin LAR 30 mg injection once every 4 weeks for 6 doses (n ‫؍‬ 35) or placebo (control group) (n ‫؍‬ 35). The clinical and laboratory parameters were monitored. There was no difference in the cumulative survival between the Sandostatin LAR-treated group compared with the control group [median survival 1.93 months vs. 1.97 months, respectively, P ‫؍‬ NS (log-rank test)]. There was no tumor regression and no reduction of ␣-fetoprotein (AFP) levels in patients receiving Sandostatin LAR treatment. There was no improvement of quality of life assessed by Karnofsky performance score. In conclusion, Sandostatin LAR monotherapy did not have survival benefit in our selected group of patients with advanced HCC. Further studies should be performed in patients with less advanced disease and/or different etiology to evaluate its benefit. (HEPATOLOGY 2002;36:687-691.) H epatocellular carcinoma (HCC) is responsible for nearly a quarter of a million deaths per year in the world. 1 It is of particular importance in endemic areas such as Asia where there is a high prevalence of chronic hepatitis B virus (HBV) infection. Although a screening program increases the chance of receiving more curative treatment, 2,3 many patients still present at a relatively late stage with advanced disease.Surgical resection is the first choice of treatment in patients without portal vein involvement and distant metastasis. However, it requires a relatively good liver function reserve. 4 Only less than 30% of patients are eligible for resection because of the high prevalence of underlying cirrhosis secondary to HBV infection. 2 For patients with unresectable HCC, there are few options. Transcatheter arterial chemoembolization (TACE) requires a reasonable liver reserve because of the risk of hepatic decompensation after TACE. 5,6 Liver transplantation, another option for small HCC with poor liver reserve, is limited by the scarcity of organ donation. Other modalities of treatment include percutaneous alcohol injection, which is only applicable for tumors less than 3 cm. 7 Thermal ablation for small tumors using heating effect by radiofrequency or microwave has also been tried. 8 These local ablative therapies are not suitable for patients with large HCC or advanced HCC with portal vein thrombosis with or without distant metastasis. Despite the extensive efforts in exploring the treatment of HCC, the prognosis remains dismal. The prognosis is even worse in patients with advanced unresectable HCC and...

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Section: H Epatocellular Carcinoma (Hcc) Is Responsiblementioning

confidence: 99%

A randomized placebo-controlled study of long-acting octreotide for the treatment of advanced hepatocellular carcinoma

et al. 2002

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“…Long-term octreotide treatment (greater than 1 month) is associated with 20±30% of cholesterol gallstone, and is symptomatic in 1% of the patients with cholelithiasis per year [2]. A recent randomized controlled trial evaluating the ef®cacy of octreotide long acting formulation, LAR, compared to octreotide demonstrated that both formulations are effective in controlling biochemical and clinical symptoms of carcinoid syndrome [29]. Octreotide in either formulation is, therefore, part of the on going treatment for patients with carcinoid syndrome.…”

Section: Discussionmentioning

confidence: 99%

Regression of metastatic carcinoid tumors with octreotide therapy: Two case reports and a review of the literature

Leong

Pasieka

2002

Journal of Surgical Oncology

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Background: The antiproliferative effect of the somatostatin analogue, octreotide, on metastatic carcinoid tumors is poorly understood. Partial tumor regression seen radiogaphically has been reported with the use of octreotide therapy for neuroendocrine tumors. Complete regression of carcinoid tumors is rarely reported. Results: Two patients with metastatic midgut carcinoid tumors were treated with subcutaneous octreotide 300 mg/day for symptomatic control of their carcinoid syndrome before debulking palliative surgery. During the laporatomies, both patients were found to have complete macroscopic regression of the metastastatic lesions that had been identi®ed radiologically before surgery, including liver metastases in one patient and periportal and retrocaval lymph nodes in the other. After surgery, the patients were evaluated every 3 months, and had no detectable disease at 30 and 43 months, respectively. Thirty cases of partial tumor regression with octreotide administered with or without other treatment modalities have been reported in the literature. Most of the patients involved received other treatment modalities. Only one other case reported in the literature showed complete regression with octreotide monotherapy. Conclusions: We report two cases of metastatic midgut carcinoid tumors that demonstrated a signi®cant anti-proliferative response to octreotide monotherapy. Review of the literature failed to identify any speci®c prognostic factors with which the response to octreotide can be predicted. Possible mechanisms for this antiproliferative effect of octreotide on carcinoid tumors are discussed.

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“…In a local setting, surgery is the treatment of choice for metastatic disease and clinical management is aimed at reducing hormone-associated symptoms. The mainstay of treatment for patients with metastatic disease consists of long-acting somatostatin analogues which improve quality of life by controlling symptoms related to hormonal hypersecretion [1]. Of the somatostatin analogues, octreotide has been shown to stabilise tumour progression in some welldifferentiated NETs [2] and SOM230 (which displays broader receptor affinity) possesses anti-angiogenic activity [3].…”

Section: Introductionmentioning

confidence: 99%

Adenosine A2A and A2B receptor expression in neuroendocrine tumours: potential targets for therapy

Kalhan

Gharibi

Vazquez

et al. 2011

Purinergic Signalling

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The clinical management of neuroendocrine tumours is complex. Such tumours are highly vascular suggesting tumour-related angiogenesis. Adenosine, released during cellular stress, damage and hypoxia, is a major regulator of angiogenesis. Herein, we describe the expression and function of adenosine receptors (A 1 , A 2A , A 2B and A 3 ) in neuroendocrine tumours. Expression of adenosine receptors was investigated in archival human neuroendocrine tumour sections and in two human tumour cell lines, BON-1 (pancreatic) and KRJ-I (intestinal). Their function, with respect to growth and chromogranin A secretion was carried out in vitro. Immunocytochemical data showed that A 2A and A 2B receptors were strongly expressed in 15/15 and 13/18 archival tumour sections. Staining for A 1 (4/18) and A 3 (6/18) receptors was either very weak or absent. In vitro data showed that adenosine stimulated a three-to fourfold increase in cAMP levels in BON-1 and KRJ-1 cells. The non-selective adenosine receptor agonist (adenosine-5′N-ethylcarboxamide, NECA) and the A 2A R agonist (CGS21680) stimulated cell proliferation by up to 20-40% which was attenuated by A 2B (PSB603 and MRS1754) and A 2A (SCH442416) receptor selective antagonists but not by the A 1 receptor antagonist (PSB36). Adenosine and NECA stimulated a twofold increase in chromogranin A secretion in BON-1 cells. Our data suggest that neuroendocrine tumours predominantly express A 2A and A 2B adenosine receptors; their activation leads to increased proliferation and secretion of chromogranin A. Targeting adenosine signal pathways, specifically inhibition of A 2 receptors, may thus be a useful addition to the therapeutic management of neuroendocrine tumours.

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Octreotide Acetate Long-Acting Formulation Versus Open-Label Subcutaneous Octreotide Acetate in Malignant Carcinoid Syndrome

Cited by 351 publications

References 16 publications

A randomized placebo-controlled study of long-acting octreotide for the treatment of advanced hepatocellular carcinoma

A randomized placebo-controlled study of long-acting octreotide for the treatment of advanced hepatocellular carcinoma

Regression of metastatic carcinoid tumors with octreotide therapy: Two case reports and a review of the literature

Adenosine A2A and A2B receptor expression in neuroendocrine tumours: potential targets for therapy

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