Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the case of a patient with Verner-Morrison syndrome due to a malignant MEN I-associated vipoma. Marked tumor-associated hypercalcemia could be treated successfully with somatostatin analogues prior to surgical therapy of the pancreatic tumor. Sixteen months after extirpation of the primary tumor recurrent tumor growth was diagnosed; at this time the patient was clinically asymptomatic and had no abnormal laboratory test results. Liver metastases and local metastases were identified using somatostatin receptor scintigraphy. We report and discuss the use of somatostatin in the treatment of tumor-associated symptoms in endocrine tumors and the possibility of identifying endocrine tumors by means of somatostatin receptor scintigraphy.
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PMID:[Somatostatin in preoperative therapy and postoperative diagnosis of a patient with Verner Morrison syndrome]. 128 41

Endocrine-paracrine (APUD, neuroendocrine) cells are located in the prostatic ductal and acinar epithelium. These cells are of the open and closed type and have dendritic processes. There is a wide range of secretory granule morphology presumably indicating a variety of different cell "types." Secretory immunoreactive peptides include serotonin, calcitonin (and related peptides), somatostatin, bombesin-like, thyroid-stimulating hormone-like (beta chain), and alpha-glycoprotein chain-like. These cells may function by endocrine, paracrine, neurocrine, and lumencrine mechanisms and play an important regulatory role both during growth and differentiation of the prostate as well as in the secretory process of the mature gland. Neuroendocrine differentiation in prostatic carcinoma is a frequent occurrence and manifests itself in several forms, including (1) small cell carcinoma, (2) carcinoid and carcinoid-like tumors, and (3) conventional adenocarcinoma with focal neuroendocrine differentiation. This latter pattern is the most common, and there is evidence that all or nearly all prostatic adenocarcinomas show at least some focal neuroendocrine differentiation. A review of the world's literature on this topic is included. Neuroendocrine differentiation generally portends a poorer prognosis but may also correlate directly with the grade. There is some evidence to suggest that neoplastic cells with neuroendocrine differentiation are resistant to hormonal therapy. Eutopic and ectopic hormone production may allow screening for prostatic carcinoma and/or monitoring for recurrence of prostatic carcinomas. Finally, the more basic implications of endocrine-paracrine cells and neuroendocrine differentiation are speculated on in reference to prostatic carcinogenesis and autocrine/paracrine tumor growth factor activity.
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PMID:Neuroendocrine differentiation in human prostatic carcinoma. 131 90

Nude mice bearing xenografts of MIA PaCa-2 human pancreatic cancer cell line were treated for 4 weeks with AN-51, a somatostatin octapeptide analog D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Thr-NH2 (RC-121) containing methotrexate attached to the alpha-amino group of D-Phe in position 1. Control groups of mice received saline, RC-121 or methotrexate. Drugs were given in equimolar doses by daily s.c. injections. After 7 days of treatment with 25 micrograms/day of AN-51, tumor growth was completely inhibited although the treatment had to be suspended because of toxic side effects, especially on the gastrointestinal tract, accompanied by major weight loss of the animals. Mice were allowed to recover for 1 week and treatment was continued with 12.5 micrograms/day AN-51. After 2 weeks of additional therapy, tumor volume, percentage change in tumor volume, and tumor weights were significantly decreased, compared with controls, only in the group treated with AN-51. Methotrexate and RC-121 also inhibited tumor growth, but their effects were not statistically significant. AN-51 retained its hormonal activity and decreased serum growth hormone levels in mice. Binding affinity of AN-51 for somatostatin receptors on MIA PaCa-2 cells was found to be 2.5-times lower than that of parent compound RC-121. This is the first report on inhibition of human pancreatic cancer growth in vivo by somatostatin analogs carrying cytotoxic radicals.
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PMID:Cytotoxic analog of somatostatin containing methotrexate inhibits growth of MIA PaCa-2 human pancreatic cancer xenografts in nude mice. 131 46

Female BDF1 mice inoculated with MXT (3.2) estrogen independent mouse mammary carcinoma were treated for three weeks with microcapsules of the luteinizing hormone-releasing hormone (LH-RH) agonist [D-Trp6]LH-RH, the antagonist SB-75, the somatostatin analog RC-160, or combinations. The lack of estrogen dependence of the tumor was proved by bilateral surgical ovariectomy, which had no effect. In two experiments, treatment with 25 micrograms/day doses of each analog alone resulted in a significant inhibition of tumor growth as shown by a 40-53% inhibition of tumor volumes, 38-43% decrease in tumor weights, and histological signs of tumor regression. However, the combination of SB-75 or [D-Trp6]LH-RH with somatostatin analog RC-160 caused greater reduction of tumor volume (68 and 61%) or tumor weights (59 and 56%), than single analogs, and histologically the occurrence of apoptosis and decrease in AgNOR numbers was more pronounced in the groups receiving combination therapy. Specific binding sites for [D-Trp6]LH-RH, EGF, and IGF-I were demonstrated in the tumor membranes. The binding capacity of LH-RH receptors was decreased by treatment with the analogs, the greatest down-regulation being caused by combination therapy. A significant decrease in EGF binding capacity was observed after treatment with the LH-RH analogs, alone or especially in combination with somatostatin analog RC-160. The combination of these analogs also caused a reduction in IGF-I receptors. The finding that LH-RH agonists and antagonists and somatostatin analogs inhibit the growth of estrogen independent mammary tumors, and that combinations are more effective than single analogs, might be of practical importance in human breast cancer therapy.
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PMID:Growth inhibition of estrogen independent MXT mouse mammary carcinomas in mice treated with an agonist or antagonist of LH-RH, an analog of somatostatin, or a combination. 135 75

Somatostatin analogs are used in the control of hormonal hypersecretion and tumor growth of patients with acromegaly, islet cell carcinomas and carcinoids. Recently we showed that somatostatin receptor positive tumors can be visualized in vivo after the administration of radioactive isotope-labelled somatostatin analogs. Receptor imaging was positive in 18/21 islet cell tumors, 30/31 carcinoids, 26/28 paragangliomas, 9/14 medullary thyroid carcinomas, 5/7 small cell lung cancers, 6/7 neuroblastomas, 38/49 primary breast cancers, and 0/18 pancreatic adenocarcinomas. Also 11/11 meningiomas, 4/4 astrocytomas and 0/3 glioblastomas could be visualized. Somatostatin receptor imaging is an easy, harmless and painless diagnostic method. It is an in vivo method for the recognition of neuroendocrine cancers. It localizes multiple and/or metastatic tumors, predicts the successful control of hormonal hypersecretion by octreotide and seems of prognostic value in certain types of cancer. This scintigraphic method might help in patient selection for clinical trials with somatostatin analogs in the treatment of neuroendocrine cancers.
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PMID:Somatostatin receptor imaging in the diagnosis and treatment of neuroendocrine tumors. 135 13

The effect of somatostatin analogue RC-160 on the growth of hepatic metastases of colon cancer was investigated in rats using magnetic resonance imaging. Experimental liver metastatic tumors were established in syngeneic BDIX rats after intrasplenic injection of DHD/K12 colon adenocarcinoma cells. Each rat with implanted liver tumors received s.c. injections of somatostatin analogue RC-160 (50 micrograms/kg) or the vehicle (control) twice a day for 4 weeks, starting 3 weeks after tumor inoculation. During the treatment with RC-160, the growth of liver tumors was studied quantitatively by measuring liver tumor volumes in vivo with magnetic resonance imaging at intervals of 7 days. Chronic administration of RC-160 inhibited the growth of hepatic metastases of colon cancer in rats. Significant inhibition of liver tumor growth in RC-160-treated rats was observed throughout the treatment. The final liver tumor volume in the treated rats was decreased by 56.1% as compared to the controls. The treatment with RC-160 reduced the percentage increase in liver tumor volume from 1575 +/- 674% (mean +/- SEM) for the control to 1034 +/- 727% in the treated group. The tumor volume doubling time in treated rats was 3.7 days longer than the controls. The liver tumor growth delay time was 15.1 days. At the end of the treatment, the incidence of ascites and the weights of tumorous livers were also decreased by RC-160 treatment. Administration of RC-160 prolonged the median survival time by 13 days in treated rats. In cell cultures, significant inhibitory effects of somatostatin-14 and RC-160 on the growth of DHD/K12 colon cancer cells were determined by MTT assay and [3H]-thymidine incorporation assay, indicating direct effects of these peptides on the growth of colon cancer cells in vitro. These data suggest that administration of RC-160 could inhibit the growth of colon cancer and their hepatic metastases in rats. Somatostatin analogue RC-160 might be considered as a potential new agent for the treatment of patients with hepatic metastases of colorectal cancers.
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PMID:Inhibitory effect of somatostatin analogue RC-160 on the growth of hepatic metastases of colon cancer in rats: a study with magnetic resonance imaging. 135 23

The effects of treatment with a bombesin receptor antagonist [D-Tpi6, Leu13 psi (CH2NH) Leu14]BN(6-14)(RC-3095) and the combination of an agonist of luteinizing hormone-releasing hormone [D-Trp6]-LH-RH and somatostatin analog D-Phe-Cys-Tyr-D-Trp-Lys-Val- Cys-Trp-NH2 (RC-160) were studied in nude mice bearing xenografts of the hormone-dependent human prostate tumor PC-82. During the 5 weeks of treatment, tumor growth was decreased in all treated groups compared with controls. Bombesin antagonist RC-3095 and the combination of [D-Trp6]-LH-RH and RC-160 caused a greater inhibition of tumor growth than [D-Trp6]-LH-RH or RC-160 alone as based on measurement of tumor volume and percentage change in tumor volume. The largest decrease in tumor weight was also seen in the groups treated with the bombesin antagonist and with the combination of RC-160 and [D-Trp6]-LH-RH. Serum prostatic-specific antigen levels were greatly decreased, and insulin-like growth factor I (IGF-I) as well as growth hormone levels were reduced in all treated groups. Specific binding sites for [D-Trp6]-LH-RH, epidermal growth factor (EGF), IGF-I, and somatostatin (SS-14) were found in the tumor membranes. Receptors for EGF were significantly down-regulated by treatment with the bombesin antagonist or RC-160. Combination of LH-RH agonists with somatostatin analog RC-160 might be considered for improvement of hormonal therapy for prostate cancer. The finding that bombesin antagonist RC-3095 inhibits the growth of PC-82 prostate cancer suggests the merit of further studies to evaluate the possible usefulness of antagonists of bombesin in the management of prostatic carcinoma.
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PMID:Inhibition of growth of PC-82 human prostate cancer line xenografts in nude mice by bombesin antagonist RC-3095 or combination of agonist [D-Trp6]-luteinizing hormone-releasing hormone and somatostatin analog RC-160. 137 10

Hormonally active neuroendocrine tumors may easily be diagnosed by elevated serum levels of their specific peptides and hormonal products, but there are no reliable markers for neuroendocrine tumors without hormonal activity. Chromogranin A (CgA), a secretory protein of neuroendocrine cells, has recently been characterized as a valuable tissue marker in hormonally active and non-functioning neuroendocrine tumors. This study analyzes the role of CgA as a serum marker for different neuroendocrine tumors. Thirty-three patients with neuroendocrine tumors of the stomach (n = 7), the ileum (n = 18), and the pancreas (n = 8) were investigated. Serum CgA levels were analyzed by radioimmunoassay at the time of diagnosis and during follow-up under different therapeutic regimens. Serum CgA was elevated in 30 (91%) patients. Mean CgA serum levels varied with tumor location (pancreas: 7068 +/- 3008 ng/ml, ileum: 5381 +/- 1740 ng/ml, stomach: 529 +/- 179 ng/ml, x +/- SEM ng/ml) but did not differ between functioning and non-functioning tumors. Eight of 10 patients treated with either somatostatin or interferon-alpha showed changes of CgA concentrations corresponding to tumor growth. We conclude that CgA is a useful broad-spectrum tumor marker in gastroenteropancreatic neuroendocrine tumors. Its determination is especially recommended in tumors without hormonal activity.
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PMID:Serum chromogranin A in the diagnosis and follow-up of neuroendocrine tumors of the gastroenteropancreatic tract. 141 39

The effect of somatostatin analogue RC-160 on the growth of DHD/K12 rat colon cancer has been investigated in vivo as well as in vitro. Twenty syngeneic BDIX rats with s.c. implanted tumors were divided randomly into 2 groups. The rats from each group received a daily s.c. injection of either RC-160 (100 micrograms/kg/day) or injection vehicle as control for 37 days starting from the day of tumor inoculation. Tumor volumes were measured every 3-4 days. At the end of the treatment, the mean tumor volume was 504.5 +/- 97.0 mm3 in the control group and 177.8 +/- 60.5 mm3 in the RC-160 treated group (p less than 0.01). The tumor volume doubling time was calculated to be 11 days in the control group and 13.5 days in the RC-160 group, respectively. The tumor growth delay time was 18 days. Using bromodeoxyuridine labelling in vivo, the mean labelling index in the tumors was decreased by 35% (p less than 0.01) after RC-160 treatment. Total protein and total DNA contents in the tumors were decreased by 70.1% (p less than 0.05) and 68.7% (p less than 0.05), respectively. The data indicate that somatostatin analogue RC-160 inhibits the growth of DHD/K12 colon cancer in vivo. In 2 studies in vitro, DHD/K12 cells were cultured for 72 hr with RC-160 and natural somatostatin-14 (S-S-14) at concentrations ranging from 62.5 ng/ml to 2,000 ng/ml. Tumor-cell growth was measured spectrophotometrically by the crystal violet staining assay. No direct effect on tumor cell growth in vitro was observed with either RC-160 or S-S-14, possibly because of the loss of somatostatin receptors in previous passages of the DHD/K12 cell line.
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PMID:Somatostatin analogue RC-160 inhibits the growth of transplanted colon cancer in rats. 167 6

The effects of insulin and somatostatin on the growth and the colony formation of two human pancreatic cancer cell lines, BxPC-3 and SOJ-6, were studied. The BxPC-3 cell line (American Type Culture Collection no. CRL 1687) was derived from a moderately differentiated pancreatic adenocarcinoma. The SOJ-6 cell line is a subclone of SOJ that was initiated from ascites of a well-differentiated pancreatic adenocarcinoma. Both cell lines express fetoacinar pancreatic antigen, an antigen that might be associated with early transformation stages. However, these lines have different proliferation and tumoral powers. SOJ-6 cells showed an almost twofold higher division rate over BxPC-3 cells when cultured in RPMI-1640 medium containing 10% fetal bovine serum. The tumorigenic degree of SOJ-6 cells, as assessed by tumor growth in nude mice, was about three times greater than that of BxPC-3. The in vitro growth of BxPC-3 cells was significantly promoted by insulin, and was slightly inhibited by somatostatin, whereas the growth of SOJ-6 cells was not influenced by these hormones. Using a clonogenic assay in soft agar, the average ratio of colony numbers formed by SOJ-6 and BxPC-3 was about 10/1, indicating a good correlation between the colony formation and tumorigenic degree in vivo. In this test, the number of colonies formed by BxPC-3 cells was increased about twofold in insulin-supplemented medium. On the other hand, somatostatin inhibited the colony formation by a factor of four to six. However, no hormonal modulation of the colony formation of SOJ-6 cells was observed. Our data show that pancreatic cancer cell lines respond differently to pancreatic hormones, and suggest that this may be correlated to a tumour stage or a tumour type.
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PMID:Effects of insulin and somatostatin on the growth and the colony formation of two human pancreatic cancer cell lines. 167 59


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