Octreotide for Cancer of the Liver and Biliary Tree

Kouroumalis, Elias

doi:10.1159/000049167

Cited by 26 publications

(19 citation statements)

References 76 publications

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“…9 Different mechanisms of action including stimulation of Kupffer cells and antimitotic effect through inhibition of insulin-like growth factor I and engagement of receptors expressed by tumor cells have been postulated. 10,11 Forty-one percent of HCC express somatostatin receptors according to one study. 12 HCC predominantly expresses somatostatin-receptor subtype 2.…”

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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“…9 These results suggest that octreotide may indirectly affect tumor growth through inhibition of release of some peptides or growth factors such as insulin, EGF and IGF-1, which promote tumor proliferation. 26 Although octreotide could inhibit the growth of gastric adenocarcinoma, the inhibition rate (60.6%) for gastric xenografts treated by octreotide alone 8 was also much lower than the result of rofecoxib plus octreotide in vivo with the same animal model, drug doses and schedules. Furthermore, the combination therapy potentially promoted the fibrosis of gastric adenocarcinoma in nude mice when compared with the rofecoxib group or control.…”

Section: Discussionmentioning

confidence: 98%

Enhanced inhibitive effects of combination of rofecoxib and octreotide on the growth of human gastric cancer

Tang¹,

Liu²,

Zhou³

et al. 2004

Intl Journal of Cancer

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Our previous studies indicated that cyclooxygenase-2 inhibitor or octreotide could suppress the proliferation of gastric adenocarcinoma in vitro or in vivo. The present study was aimed to find whether rofecoxib combined with octreotide could enhance the inhibitive effects on the growth of gastric cancer. The effect of rofecoxib or octreotide on proliferation of gastric cancer cell line was determined by 3 H-thymidine ribotide incorporation. The TdT-mediated dUTP nick endlabeling assay was used to detect the apopotosis. To determine their synergic antineoplastic effects, the interaction between rofecoxib and octreotide on SGC-7901 cell was evaluated by the median effect plot. After orthotopical implantion of xenografts of human gastric cancer in stomach, nude mice were given rofecoxib plus octreotide for 8 weeks. Cyclooxygenase-2 in gastric cancer tissues was measured by immunohistochemistry. Combination of rofecoxib and octreotide presented synergistic effect (combination index < 1) in the majority of responses. The inhibitory rate for xenografts in nude mice was 89.7% in rofecoxib group. Combination of rofecoxib and octreotide enhanced inhibitory rate to 98.8%. The combination greatly increased the apoptotic index (78.20% ؎ 6.45%) of the xenografts as compared with that of using rofecoxib alone (46.60% ؎ 3.42%); the difference was very significant (p < 0.001). Rofecoxib could inhibit the activity of cyclooxygenase-2 in the tissue of gastric adenocarcinomas of nude mice. Our results indicate that combination of rofecoxib and octreotide significantly enhances the antiproliferative effect in gastric adenocarcinoma, which might have potential therapeutic value. © 2004 Wiley-Liss, Inc. Key words: rofecoxib; octreotide; gastric adenocarcinoma; cyclooxygenase-2The poor prognosis of unresectable gastric adenocarcinoma and the various disappointing therapeutic modalities make further investigation of new therapeutic approach for advanced gastric cancer of primary importance. Accumulative evidence has shown that overexpression of cyclooxygenase-2 (COX-2) in gastric adenocarcinoma might play a crucial role in invasive tumor growth and offer a new strategy against cancer by the use of COX-2 inhibitors. [1][2][3][4] The inhibitive effect of aspirin or rofecoxib, a higher selective COX-2 inhibitor 5 on the proliferation of gastric cancer, has been observed in our previous studies. 6,7 Various studies have demonstrated that the growth of normal cells and malignant tumor may be regulated by gut peptides. 8,9 In the stomach, besides the known inhibitory function of somatostatin (SST) on acid secretion, it has been suggested that the analogues of SST could be candidates for arresting the growth of gastric adenocarcinoma. Previous data from the literature have shown that the mean tumor volume in nude mice treated with octreotide, an analogue of SST, was significantly lower than that of control group with an inhibitory rate of 60.6%. 6,10 The antineoplastic action of octreotide is thought to be mediated through the receptors for S...

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“…OCT is a cyclic octapeptide containing two D-configuration amino acids, with high binding affinity for somatostatin receptor (SSTR) 2 and 5, reduced affinity for SSTR3, and no affinity for SSTR1 and SSTR4 (1). The therapeutic potential of OCT has recently been extended to nonendocrine tumors, particularly primary hepatocelluar carcinoma (HCC) (2). Substantial evidence from experimental studies and clinical trials showed that OCT improved the survival benefits of patients with HCC (3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

“…Substantial evidence from experimental studies and clinical trials showed that OCT improved the survival benefits of patients with HCC (3)(4)(5). The antineoplastic effects have been attributed to indirect inhibition of insulinlike growth factor-1 (IGF-1) through downregulation of growth hormone (GH) release, direct inhibition of tumor angiogenesis, antiproliferation of tumor cells, and stimulation of the reticuloendothelial system (RES) by unknown mechanisms (2,6,7).…”

Section: Introductionmentioning

confidence: 99%

Reversible Lipidization Prolongs the Pharmacological Effect, Plasma Duration, and Liver Retention of Octreotide

2005

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Octreotide for Cancer of the Liver and Biliary Tree

Cited by 26 publications

References 76 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

Enhanced inhibitive effects of combination of rofecoxib and octreotide on the growth of human gastric cancer

Reversible Lipidization Prolongs the Pharmacological Effect, Plasma Duration, and Liver Retention of Octreotide

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