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1. Schwarz RE, Awasthi N, Konduri S, Caldwell L, Cafasso D, Schwarz MA: Antitumor effects of EMAP II against pancreatic cancer through inhibition of fibronectin-dependent proliferation. Cancer Biol Ther; 2010 Apr 15;9(8):632-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor effects of EMAP II against pancreatic cancer through inhibition of fibronectin-dependent proliferation.
  • Pancreatic ductal adenocarcinoma (PDAC) is highly resistant to conventional chemotherapy.
  • We tested the efficacy of endothelial monocyte-activating polypeptide II (EMAP II) to inhibit PDAC progression and its ability to interfere with FN-integrin angiogenesis signaling.
  • In heterotopic PDAC tumors EMAP II caused a significant reduction (>65%) in tumor growth, accompanied by a >50 and 44% decrease in microvessel density and proliferative activity, respectively.
  • EMAP II therapy caused a 62 and 56% reduction in host and tumor cell FN expression.
  • 3D FN matrices increased ASPC-1 cell proliferation by >50%, and this induction was significantly blocked by alpha3, alpha5, alpha6 and alphaV integrin funtional blocking antibodies, while alpha1, alpha2 and alpha4 antibodies had no effect.
  • These findings suggest that EMAP II demonstrates significant antitumor activity against PDAC cells, and that this effect may be in part mediated through targeted interference with stromal FN-integrin dependent PDAC cell proliferation.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / drug therapy. Cytokines / pharmacology. Neoplasm Proteins / pharmacology. Pancreatic Neoplasms / drug therapy. RNA-Binding Proteins / pharmacology
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Animals. Antineoplastic Agents / pharmacology. Cell Growth Processes / drug effects. Cell Growth Processes / physiology. Fibronectins / antagonists & inhibitors. Fibronectins / biosynthesis. Fibronectins / metabolism. Humans. Immunohistochemistry. Integrins / biosynthesis. Integrins / metabolism. Mice. Mice, Nude. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / pathology. Xenograft Model Antitumor Assays

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  • (PMID = 20212356.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Cytokines; 0 / Fibronectins; 0 / Integrins; 0 / Neoplasm Proteins; 0 / RNA-Binding Proteins; 0 / small inducible cytokine subfamily E, member 1
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2. Szepeshazi K, Schally AV, Halmos G, Sun B, Hebert F, Csernus B, Nagy A: Targeting of cytotoxic somatostatin analog AN-238 to somatostatin receptor subtypes 5 and/or 3 in experimental pancreatic cancers. Clin Cancer Res; 2001 Sep;7(9):2854-61
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  • [Title] Targeting of cytotoxic somatostatin analog AN-238 to somatostatin receptor subtypes 5 and/or 3 in experimental pancreatic cancers.
  • PURPOSE: The expression of somatostatin receptors (SSTRs) allows the localization and treatment of some tumors with radiolabeled SST analogues.
  • We investigated whether SSTRs on human pancreatic cancer lines xenografted into nude mice can be used for targeting of cytotoxic somatostatin analogue AN-238, consisting of 2-pyrrolinodoxorubicin (AN-201) linked to octapeptide carrier RC-121.
  • EXPERIMENTAL DESIGN: AN-238 and AN-201 were administered i.v. to nude mice bearing SW-1990 pancreatic cancers.
  • Tumor growth reduction and survival were analyzed, and cell proliferation and apoptosis were determined with histological methods.
  • The effects of repeated administration of AN-238 and AN-201 were also evaluated on xenografted Panc-1, MiaPaCa-2, CFPAC-1, Capan-1, and Capan-2 pancreatic cancers.
  • SW-1990 expressed mRNA for SSTR subtypes 3 and 5, whereas various patterns of subtypes 2A, 3, and 5 were found in other pancreatic cancers.
  • CONCLUSIONS: Growth of experimental human pancreatic cancers that express SSTRs can be inhibited by cytotoxic somatostatin analogue AN-238.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Doxorubicin / therapeutic use. Pancreatic Neoplasms / drug therapy. Pyrroles / therapeutic use. Receptors, Somatostatin / metabolism
  • [MeSH-minor] Animals. Binding, Competitive. Cell Division / drug effects. Gene Expression Regulation, Neoplastic. Humans. Male. Mice. Mice, Nude. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / genetics. Neoplasms, Experimental / metabolism. RNA, Messenger / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Survival Analysis. Time Factors. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 11555603.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AN 238; 0 / Antibiotics, Antineoplastic; 0 / Pyrroles; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 3; 0 / somatostatin receptor 5; 80168379AG / Doxorubicin
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3. Nasir A, Gardner NM, Strosberg J, Ahmad N, Choi J, Malafa MP, Coppola D, Kwekkeboom DJ, Teunissen JJ, Kvols LK: Multimodality management of a polyfunctional pancreatic endocrine carcinoma with markedly elevated serum vasoactive intestinal polypeptide and calcitonin levels. Pancreas; 2008 Apr;36(3):309-13
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  • [Title] Multimodality management of a polyfunctional pancreatic endocrine carcinoma with markedly elevated serum vasoactive intestinal polypeptide and calcitonin levels.
  • We present an unusual case of a 52-year-old woman with severe, uncontrollable, refractory diarrhea attributable to pancreatic endocrine carcinoma (ECA) with markedly elevated serum vasoactive intestinal polypeptide (VIP) and calcitonin levels.
  • The pancreatosplenectomy specimen showed a poorly differentiated ECA of the distal pancreas, immunoreactive for synaptophysin, CD56, and S100 protein, with morphologically similar hepatic and lymph node metastases.
  • Systemic chemotherapy with etoposide and cisplatin did not result in any radiographic and biochemical improvement.
  • In summary, this is a unique case of metastatic VIP- and calcitonin-secreting pancreatic ECA with dramatic sustained clinical, biochemical, and objective tumor response to peptide receptor radionuclide therapy.
  • [MeSH-major] Calcitonin / blood. Pancreatic Neoplasms / blood. Pancreatic Neoplasms / therapy. Paraneoplastic Endocrine Syndromes / blood. Paraneoplastic Endocrine Syndromes / therapy. Vasoactive Intestinal Peptide / blood
  • [MeSH-minor] Combined Modality Therapy. Diarrhea / etiology. Diarrhea / therapy. Female. Heterocyclic Compounds, 1-Ring / therapeutic use. Humans. Lutetium / therapeutic use. Middle Aged. Peptides, Cyclic / therapeutic use. Radiopharmaceuticals / therapeutic use

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  • (PMID = 18362846.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 177Lu-DOTA-lanreotide; 0 / Heterocyclic Compounds, 1-Ring; 0 / Peptides, Cyclic; 0 / Radiopharmaceuticals; 37221-79-7 / Vasoactive Intestinal Peptide; 5H0DOZ21UJ / Lutetium; 9007-12-9 / Calcitonin
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4. Pahlavan PS, Kanthan R: Goblet cell carcinoid of the appendix. World J Surg Oncol; 2005 Jun 20;3:36
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  • [Title] Goblet cell carcinoid of the appendix.
  • BACKGROUND: Goblet cell carcinoid (GCC) of the appendix is a rare neoplasm that share histological features of both adenocarcinoma and carcinoid tumor.
  • The clinical presentations of this neoplasm are also varied.
  • METHODS: Published studies in the English language between 1966 to 2004 were identified through Medline keyword search utilizing terms "goblet cell carcinoid," "adenocarcinoid", "mucinous carcinoid" and "crypt cell carcinoma" of the appendix.
  • Accurate diagnosis of this neoplasm requires astute observations within an acutely inflamed appendix as this neoplasm has a prominent pattern of submucosal growth and usually lacks the formation of a well-defined tumor mass.
  • The most common surgical treatment of choice was appendectomy with right hemicolectomy in 34.70% followed by simple appendectomy in 24.57%.
  • Local lymph node involvement was seen in 8.76% of patients at the time of diagnosis.
  • GCC's of the appendix remains a neoplasm of unpredictable biological behavior and thus warrants lifelong surveillance for recurrence of the disease upon diagnosis and successful surgical extirpation.
  • CONCLUSION: GCC of the appendix is a rare neoplasm.
  • Due to its wide range of presentation, this tumor should be considered as a possible diagnosis in many varied situations leading to abdominal surgery.
  • Histopathological features such as increased number of Paneth cells, increased amount of mucin secretion and presence of pancreatic polypeptide may predict a more aggressive behavior.
  • In cases with obvious spread of the disease chemotherapy, mostly with 5-FU and leucovorin is advised.
  • Cytoreductive surgery with adjuvant intraperitoneal chemotherapy can offer improved survival in cases with advanced peritoneal dissemination.

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  • (PMID = 15967038.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1182398
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5. Mizuno N, Naruse S, Kitagawa M, Ishiguro H, Ito O, Ko SB, Yoshikawa T, Tanahashi C, Ito M, Hayakawa T: Insulinoma with subsequent association of Zollinger-Ellison syndrome. Intern Med; 2001 May;40(5):386-90
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  • [Title] Insulinoma with subsequent association of Zollinger-Ellison syndrome.
  • We report a patient with insulinoma associated with Zollinger-Ellison syndrome.
  • Abdominal computed tomography (CT) revealed a large pancreatic tumor, which was then diagnosed as an unresectable pancreatic adenocarcinoma.
  • Plasma gastrin, glucagon, vasoactive intestinal polypeptide and somatostatin levels were all normal.
  • Abdominal CT scan showed multiple liver metastases.
  • Chemotherapy with 5-fluorouracil and doxorubicin was performed.
  • Plasma gastrin level was 1,960 pg/ml at that time.
  • [MeSH-major] Insulinoma / complications. Pancreatic Neoplasms / complications. Zollinger-Ellison Syndrome / complications
  • [MeSH-minor] Aged. Cholangiopancreatography, Endoscopic Retrograde. Fatal Outcome. Female. Humans. Tomography, X-Ray Computed

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  • [ErratumIn] Intern Med 2001 Jun;40(6):553
  • (PMID = 11393407.001).
  • [ISSN] 0918-2918
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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6. Nikou GC, Toubanakis C, Nikolaou P, Giannatou E, Safioleas M, Mallas E, Polyzos A: VIPomas: an update in diagnosis and management in a series of 11 patients. Hepatogastroenterology; 2005 Jul-Aug;52(64):1259-65
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  • BACKGROUND/AIMS: VIPoma is a rare pancreatic endocrine tumor (PET) which secretes excessive amounts of VIP (Vasoactive Intestinal Peptide) that causes a special clinical syndrome characterized by secretory diarrhea, hypokalemia and achlorhydria.
  • Among a total number of 76 patients (pts) with PETs, we present in this study 11 pts with VIPoma syndrome focusing on our diagnostic and therapeutic approach, in parallel with a brief review of the literature.
  • The diagnosis was based upon compatible clinical features and serum VIP values and was supported by the estimation of other peptides and neuroendocrine markers such as gastrin, pancreatic polypeptide and chromogranin-A (CgA).
  • VIP levels at the time of diagnosis were more than 3 or 10 times the upper normal limit in 7/11 (63.6%) or 4/11 (36.4%) pts, respectively.
  • A surgical resection was possible in 7/11 (63.6%) pts, while pts with metastatic disease already or poorly differentiated tumors also received additional treatment with somatostatin analogues and chemotherapy.
  • Also, surgical treatment, as extensive as possible, in combination with somatostatin analogues or chemotherapy when necessary, may also result in prolonged survival, also in patients with advanced disease.
  • [MeSH-major] Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy. Vipoma / diagnosis. Vipoma / therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Child, Preschool. Disease-Free Survival. Female. Follow-Up Studies. Humans. Male. Middle Aged. Octreotide / therapeutic use. Pancreatectomy. Survival Rate

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  • (PMID = 16001675.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
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7. Lambertini D, Bottini E, Talassi E, Tarchini R, Gaetti L, Bellomi A: [Acute renal failure caused by VIP-secreting tumor]. G Ital Nefrol; 2003 Jul-Aug;20(4):419-22
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  • [Title] [Acute renal failure caused by VIP-secreting tumor].
  • A 74-year-old woman had secretory diarrhea, severe metabolic acidosis, hypokalemia, hypovolemia, and acute renal failure caused by a pancreatic vasoactive intestinal polypeptide (VIP)-secreting tumor.
  • Vipoma is a rare neuroendocrine tumor.
  • Diagnosis requires the documentation of large volumes of secretory diarrhea, elevated VIP plasma levels, and the localization of the VIP-secreting tumor.
  • Metastases are present in 50% of patients at the time of diagnosis.
  • Treatment includes correction of volume, electrolyte, and metabolic abnormalities; CVVH during ARF; pharmacotherapy to decrease gastrointestinal secretion; and surgical resection of the vipoma.
  • [MeSH-major] Acute Kidney Injury / etiology. Pancreatic Neoplasms / complications. Vipoma / complications

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  • (PMID = 14523904.001).
  • [ISSN] 0393-5590
  • [Journal-full-title] Giornale italiano di nefrologia : organo ufficiale della Società italiana di nefrologia
  • [ISO-abbreviation] G Ital Nefrol
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Italy
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8. Schwarz RE, Awasthi N, Konduri S, Cafasso D, Schwarz MA: EMAP II-based antiangiogenic-antiendothelial in vivo combination therapy of pancreatic cancer. Ann Surg Oncol; 2010 May;17(5):1442-52
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  • [Title] EMAP II-based antiangiogenic-antiendothelial in vivo combination therapy of pancreatic cancer.
  • BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) frequently resists conventional cytotoxic therapy.
  • The antitumor effects of endothelial monocyte-activating polypeptide II (EMAP) have been attributed to its antiendothelial and antiangiogenic activities.
  • We tested the hypothesis that a combination of EMAP with bevacizumab (Bev) and gemcitabine (Gem) targets different pathways of PDAC progression and represents more effective treatment.
  • METHODS: Proliferation of PDAC and endothelial cell lines was evaluated in vitro.
  • In vivo tumor growth and survival PDAC xenograft experiments were performed with EMAP, Bev, and Gem, either alone or in combination.
  • Intratumoral microvessel density and proliferative activity were analyzed by immunostaining with PECAM-1 and proliferating cell nuclear antigen antibodies, and apoptotic activity was measured by the TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling) procedure.
  • RESULTS: Compared with controls, net reduction in tumor growth in EMAP, Bev, Gem, EMAP + Bev, EMAP + Gem, Bev + Gem, and EMAP + Bev + Gem groups was 58, 40, 40, 67, 68, 69, and 96%, respectively.
  • Addition of EMAP to the Bev + Gem group statistically significantly improved survival at a median of >8 days while inducing long-term survival in some animals after maintenance therapy.
  • Combination treatment of EMAP with Bev and Gem reduced proliferation of endothelial but not of PDAC cells.
  • This multitargeting strategy to prevent PDAC progression shows therapeutic promise and may overcome limitations by combinations of Gem with anti-vascular endothelial growth factor agents alone.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Pancreatic Ductal / blood supply. Endothelium, Vascular / drug effects. Neovascularization, Pathologic / drug therapy. Pancreatic Neoplasms / blood supply
  • [MeSH-minor] Animals. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antigens, CD31 / metabolism. Apoptosis / drug effects. Bevacizumab. Blotting, Western. Cell Proliferation / drug effects. Cytokines / administration & dosage. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Female. Immunoenzyme Techniques. Mice. Mice, Nude. Neoplasm Proteins / administration & dosage. RNA-Binding Proteins / administration & dosage. Survival Rate. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 20041350.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD31; 0 / Cytokines; 0 / Neoplasm Proteins; 0 / RNA-Binding Proteins; 0 / small inducible cytokine subfamily E, member 1; 0W860991D6 / Deoxycytidine; 2S9ZZM9Q9V / Bevacizumab; B76N6SBZ8R / gemcitabine
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9. Mishra G, Liu TF, Frankel AE: Recombinant toxin DAB389EGF is cytotoxic to human pancreatic cancer cells. Expert Opin Biol Ther; 2003 Oct;3(7):1173-80
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  • [Title] Recombinant toxin DAB389EGF is cytotoxic to human pancreatic cancer cells.
  • Few malignancies have frustrated the persistent efforts of the oncologist like pancreatic cancer.
  • Pancreatic cancer is usually unresectable at the time of diagnosis because of metastasis or local extension.
  • Despite the aggressive nature of this deadly disease, systemic treatment options are limited.
  • Clearly, alternative, more effective regimens are needed for treating pancreatic carcinoma.
  • In pancreatic cancer, there is overexpression of growth factors and growth factor receptors, including epidermal growth factor receptor (EGFR).
  • Targeted toxins consist of a targeting polypeptide covalently linked to a peptide toxin.
  • The authors have previously shown that DAB(389)EGF is selectively toxic to EGFR-overexpressing cells, including human brain tumour and lung carcinoma cell lines.
  • Pancreatic adenocarcinoma should be responsive to this fusion protein based on its EGFR overexpression.
  • However, the cytotoxic effect of DAB(389)EGF on human pancreatic carcinoma cell lines has yet to be explored.
  • The authors describe preliminary data showing the potent cytotoxicity of DAB(389)EGF to human pancreatic carcinoma cell lines.
  • Because of the nonspecific toxicity to liver and kidney (which possess EGFR) of systemic administration, they also propose a potential novel drug delivery system for direct toxin implantation into pancreatic tumours using endoscopic ultrasound guided fine-needle injection (EUS-FNI).
  • Hopefully, the use of these targeted therapeutic approaches in combination with other modalities may further extend survival and quality of life in patients with pancreatic adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / pharmacology. Pancreatic Neoplasms / drug therapy. Recombinant Fusion Proteins / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Diphtheria Toxin / genetics. Genes, erbB-1 / genetics. Humans. Injections. Pancreas


10. Wlcek K, Svoboda M, Thalhammer T, Sellner F, Krupitza G, Jaeger W: Altered expression of organic anion transporter polypeptide (OATP) genes in human breast carcinoma. Cancer Biol Ther; 2008 Sep;7(9):1450-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Altered expression of organic anion transporter polypeptide (OATP) genes in human breast carcinoma.
  • Organic anion transporter polypeptides (OATPs) mediate the transmembrane uptake of endogenous compounds and clinically important drugs in various tissues thereby effecting drug disposition and tissue penetration.
  • OATPs have also been identified in gastric, pancreatic and colon carcinomas but little is known about their expression in breast carcinoma.
  • We therefore analyzed the expression pattern of all 11 known OATPs in three breast cancer cell lines (MCF-7, ZR-75-1, MDA-MB-231) and one immortalized breast epithelial cell line (MCF-10A) using quantitative real-time RT-PCR.
  • Transcripts of 7/11 OATP genes with heterogeneity in their expression profile were detected in control and/or cancer cell lines.
  • Of these seven OATPs, five were also expressed in breast tumor and adjacent non-tumorous specimens from 13 patients.
  • OATP2B1, not found in the analyzed cell lines, was verified in the tissue samples.
  • Interestingly, mRNA expression of OATP2B1, OPATP3A1 and OATP4A1 was significantly higher (p < 0.022) in non-malignant specimens as compared to tumor tissue samples.
  • [MeSH-minor] Carcinoma / genetics. Carcinoma / metabolism. Carcinoma / pathology. Case-Control Studies. Cell Line, Transformed. Cell Line, Tumor. Female. Gene Expression Profiling. Humans. RNA, Messenger / analysis. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [CommentIn] Cancer Biol Ther. 2008 Sep;7(9):1456-9 [18836293.001]
  • (PMID = 18948755.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Organic Anion Transporters; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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11. Kianmanesh R, O'toole D, Sauvanet A, Ruszniewski P, Belghiti J: [Surgical treatment of gastric, enteric, and pancreatic endocrine tumors Part 1. Treatment of primary endocrine tumors]. J Chir (Paris); 2005 May-Jun;142(3):132-49
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Surgical treatment of gastric, enteric, and pancreatic endocrine tumors Part 1. Treatment of primary endocrine tumors].
  • [Transliterated title] Traitement chirurgical des tumeurs endocrines gastro-entéro-pancréatiques.
  • They are classified into two principal types: gastrointestinal ET's (formerly called carcinoid tumors) which are the most common, and pancreaticoduodenal ET's.
  • Functioning ET's secrete polypeptide hormones which cause characteristic hormonal syndromes.
  • Poorly-differentiated ET's have a poor prognosis and are treated by chemotherapy.
  • Surgical excision is the only curative treatment of well-differentiated ET's.
  • The surgical goals are to: 1. prolong survival by resecting the primary tumor and any nodal or hepatic metastases, 2. control the symptoms related to hormonal secretion, 3. prevent or treat local complications.
  • The most common sites of gastrointestinal ET's ( carcinoids) are the appendix and the rectum; these are often small (<1 cm), benign, and discovered fortuitously at the time of appendectomy or colonoscopic removal.
  • Ileal ET's, even if small, are malignant, frequently multiple, and complicated in 30-50% of cases by bowel obstruction, mesenteric invasion, or bleeding.
  • The carcinoid syndrome (consisting of abdominal pain, flushing, diarrhea, hypertension, bronchospasm, and right sided cardiac vegetations) is caused by the hypersecretion of serotonin into the systemic circulation; it occurs in 10% of cases and is usually associated with hepatic metastases.
  • More than half of the cases of pancreatic ET are non-functional.
  • Insulinoma and gastrinoma (cause of the Zollinger-Ellison syndrome) are the most common functional ET's. 80% are sporadic; in these cases, tumor size, location, and malignant potential determine the type of resection which may vary from a simple enucleation to a formal pancreatectomy.
  • In 10-20% of cases, pancreaticoduodenal ET presents in the setting of multiple endocrine neoplasia (NEM type I), an autosomal-dominant genetic disease with multifocal endocrine involvement of the pituitary, parathyroid, pancreas, and adrenal glands.
  • For insulinoma with NEM-I, enucleation of lesions in the pancreatic head plus a caudal pancreatectomy is the most appropriate procedure.
  • The lesions are frequently small, multiple, and widespread and recurrence is frequent after excision.
  • [MeSH-major] Carcinoid Tumor / surgery. Carcinoma, Islet Cell / surgery. Carcinoma, Neuroendocrine / surgery. Insulinoma / surgery. Intestinal Neoplasms / surgery. Multiple Endocrine Neoplasia Type 1 / surgery. Pancreatic Neoplasms / surgery. Stomach Neoplasms / surgery. Zollinger-Ellison Syndrome / surgery
  • [MeSH-minor] Adult. Gastrinoma / diagnosis. Gastrinoma / surgery. Glucagonoma / diagnosis. Glucagonoma / surgery. Humans. Liver Neoplasms / secondary. Lymphatic Metastasis. Malignant Carcinoid Syndrome / diagnosis. Malignant Carcinoid Syndrome / surgery. Multicenter Studies as Topic. Pancreatectomy. Postoperative Care. Postoperative Complications. Prognosis. Somatostatinoma / diagnosis. Somatostatinoma / surgery. Vipoma / diagnosis. Vipoma / surgery

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  • (PMID = 16142076.001).
  • [ISSN] 0021-7697
  • [Journal-full-title] Journal de chirurgie
  • [ISO-abbreviation] J Chir (Paris)
  • [Language] fre
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 236
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12. Nilsson UW, Abrahamsson A, Dabrosin C: Angiogenin regulation by estradiol in breast tissue: tamoxifen inhibits angiogenin nuclear translocation and antiangiogenin therapy reduces breast cancer growth in vivo. Clin Cancer Res; 2010 Jul 15;16(14):3659-69
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  • [Title] Angiogenin regulation by estradiol in breast tissue: tamoxifen inhibits angiogenin nuclear translocation and antiangiogenin therapy reduces breast cancer growth in vivo.
  • PURPOSE: Angiogenin, a 14.2-kDa polypeptide member of the RNase A superfamily, has potent angiogenic effects.
  • Increased angiogenin expression has been associated with the transition of normal breast tissue into invasive breast carcinoma.
  • In this article, we investigated whether estradiol (E(2)) affected angiogenin in breast tissue.
  • In vitro cultures of whole normal breast tissue, breast cancer cells, and endothelial cells were used.
  • RESULTS: We show that extracellular angiogenin correlated significantly with E(2) in normal human breast tissue in vivo and that exposure of normal breast tissue biopsies to E(2) stimulated angiogenin secretion.
  • In breast cancer patients, the in vivo angiogenin levels were significantly higher in tumors compared with the adjacent normal breast tissue.
  • Moreover, E(2)-induced angiogenin derived from cancer cells significantly increased endothelial cell proliferation.
  • Additionally, treating tumor-bearing mice with an antiangiogenin antibody resulted in tumor stasis, suggesting a role for angiogenin in estrogen-dependent breast cancer growth.
  • CONCLUSION: Our results suggest previously unknown mechanisms by which estrogen and antiestrogen regulate angiogenesis in normal human breast tissue and breast cancer.
  • This may be important for estrogen-driven breast cancer progression and a molecular target for therapeutic interventions.
  • [MeSH-major] Breast Neoplasms / drug therapy. Cell Nucleus / drug effects. Estradiol / pharmacology. Ribonuclease, Pancreatic / metabolism. Tamoxifen / pharmacology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Cell Proliferation / drug effects. Disease Models, Animal. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Microdialysis. Middle Aged. Neoplasm Transplantation. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / metabolism. Tumor Cells, Cultured. Xenograft Model Antitumor Assays. Young Adult

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  • [Copyright] Copyright 2010 AACR.
  • (PMID = 20501617.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 094ZI81Y45 / Tamoxifen; 4TI98Z838E / Estradiol; EC 3.1.27.- / angiogenin; EC 3.1.27.5 / Ribonuclease, Pancreatic
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13. Reubi JC: In vitro evaluation of VIP/PACAP receptors in healthy and diseased human tissues. Clinical implications. Ann N Y Acad Sci; 2000;921:1-25
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  • [Title] In vitro evaluation of VIP/PACAP receptors in healthy and diseased human tissues. Clinical implications.
  • The evaluation of peptide receptors in man is relevant to identifying the physiological target tissues of a given peptide and to selecting diseases with a sufficient receptor overexpression for diagnostic or therapeutic intervention.
  • VIP/PACAP receptors have been evaluated in normal and diseased human non-neuronal tissues by using in vitro receptor autoradiography with 125I-VIP or 125I-PACAP in tissue sections.
  • As assessed by subtype-selective VIP analogs, VIP receptors of the VPAC1 subtype are found in a wide variety of tissues including liver, breast, kidney, prostate, ureter, bladder, pancreatic ducts, gastrointestinal mucosa, lung, thyroid, adipose, and lymphoid tissues.
  • VIP/PACAP receptors are expressed in the majority of the most frequently occurring human tumors, including breast, prostate, pancreas, lung, colon, stomach, liver, and bladder carcinomas, as well as lymphomas and meningiomas, predominantly as VPAC1 receptors, as do their tissues of origin.
  • Moreover, the receptor expression in tumors is the molecular basis for clinical applications of VIP/PACAP such as in vivo scintigraphy and radiotherapy of tumors as well as VIP/PACAP analog treatment for tumor growth inhibition.
  • [MeSH-minor] Autoradiography. Epithelium / metabolism. Female. Humans. In Vitro Techniques. Male. Neoplasm Metastasis. Neoplasms / drug therapy. Neoplasms / metabolism. Neoplasms / radiotherapy. Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide. Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I. Receptors, Vasoactive Intestinal Peptide, Type II. Receptors, Vasoactive Intestinal Polypeptide, Type I. Tissue Distribution


14. Wice BM, Wang S, Crimmins DL, Diggs-Andrews KA, Althage MC, Ford EL, Tran H, Ohlendorf M, Griest TA, Wang Q, Fisher SJ, Ladenson JH, Polonsky KS: Xenin-25 potentiates glucose-dependent insulinotropic polypeptide action via a novel cholinergic relay mechanism. J Biol Chem; 2010 Jun 25;285(26):19842-53
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  • [Title] Xenin-25 potentiates glucose-dependent insulinotropic polypeptide action via a novel cholinergic relay mechanism.
  • Agents that increase GLP-1 action are effective therapies in type 2 diabetes mellitus (T2DM).
  • However, GIP action is blunted in T2DM, and GIP-based therapies have not been developed.
  • We developed mice lacking GIP-producing K cells.
  • Like humans with T2DM, "GIP/DT" animals exhibited a normal insulin secretory response to exogenous GLP-1 but a blunted response to GIP.
  • Pharmacologic doses of xenin-25, another peptide produced by K cells, restored the GIP-mediated insulin secretory response and reduced hyperglycemia in GIP/DT mice.
  • Studies with islets, insulin-producing cell lines, and perfused pancreata indicated xenin-25 does not enhance GIP-mediated insulin release by acting directly on the beta-cell.
  • Consistent with this, carbachol potentiated GIP-mediated insulin release from in situ perfused pancreata of GIP/DT mice.
  • These data suggest that xenin-25 potentiates GIP-mediated insulin release by activating non-ganglionic cholinergic neurons that innervate the islets, presumably part of an enteric-neuronal-pancreatic pathway.
  • [MeSH-major] Gastric Inhibitory Polypeptide / metabolism. Glucagon-Like Peptide 1 / pharmacology. Glucose / pharmacology. Neurotensin / pharmacology
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Blotting, Western. Carbachol / pharmacology. Cell Line, Tumor. Cholinergic Agonists / pharmacology. Drug Synergism. Enzyme-Linked Immunosorbent Assay. Fasting / blood. Female. Humans. Insulin / blood. Insulin / secretion. Insulin-Secreting Cells / cytology. Insulin-Secreting Cells / drug effects. Insulin-Secreting Cells / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Pancreas / drug effects. Pancreas / metabolism

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  • (PMID = 20421298.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R37 DK031842; United States / NIDDK NIH HHS / DK / P30 DK056341; United States / NCRR NIH HHS / RR / UL1 RR024992; United States / NIDDK NIH HHS / DK / RC1DK086163; United States / NIDDK NIH HHS / DK / 5P30 DK052574; United States / NIDDK NIH HHS / DK / DK31842; United States / NCATS NIH HHS / TR / UL1 TR000448; United States / NIDDK NIH HHS / DK / P60 DK020579; United States / NIDDK NIH HHS / DK / R01 DK088126; United States / NIDDK NIH HHS / DK / R01 DK031842; United States / NIDDK NIH HHS / DK / P30 DK052574; United States / NIDDK NIH HHS / DK / RC1 DK086163
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Cholinergic Agonists; 0 / Insulin; 144092-28-4 / xenin 25; 39379-15-2 / Neurotensin; 59392-49-3 / Gastric Inhibitory Polypeptide; 89750-14-1 / Glucagon-Like Peptide 1; 8Y164V895Y / Carbachol; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2888395
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15. Tanaka C, O'Reilly T, Kovarik JM, Shand N, Hazell K, Judson I, Raymond E, Zumstein-Mecker S, Stephan C, Boulay A, Hattenberger M, Thomas G, Lane HA: Identifying optimal biologic doses of everolimus (RAD001) in patients with cancer based on the modeling of preclinical and clinical pharmacokinetic and pharmacodynamic data. J Clin Oncol; 2008 Apr 1;26(10):1596-602
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  • PURPOSE: To use preclinical and clinical pharmacokinetic (PK)/pharmacodynamic (PD) modeling to predict optimal clinical regimens of everolimus, a novel oral mammalian target of rapamycin (mTOR) inhibitor, to carry forward to expanded phase I with tumor biopsy studies in cancer patients.
  • A PK/PD model was used to describe the relationship between everolimus concentrations and S6K1 inhibition in PBMCs of cancer patients and in PBMCs and tumors of everolimus-treated CA20948 pancreatic tumor-bearing rats.
  • RESULTS: Time- and dose-dependent S6K1 inhibition was demonstrated in human PBMCs.
  • This allowed development of a direct-link PK/PD model that predicted PBMC S6K1 inhibition-time profiles in patients.
  • Comparison of rat and human profiles simulated by the model suggested that a weekly 20- to 30-mg dose of everolimus would be associated with an antitumor effect in an everolimus-sensitive tumor and that daily administration would exert a greater effect than weekly administration at higher doses.
  • CONCLUSION: A direct-link PK/PD model predicting the time course of S6K1 inhibition during weekly and daily everolimus administration allowed extrapolation from preclinical studies and first clinical results to select optimal doses and regimens of everolimus to explore in future clinical trials.
  • [MeSH-major] Immunosuppressive Agents / administration & dosage. Neoplasms / drug therapy. Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors. Sirolimus / analogs & derivatives
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Drug Administration Schedule. Everolimus. Humans. Models, Biological. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / metabolism. Rats

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  • (PMID = 18332467.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK73802; United States / NCI NIH HHS / CA / U01 CA84292-06
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 9HW64Q8G6G / Everolimus; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; EC 2.7.11.1 / ribosomal protein S6 kinase, 70kD, polypeptide 1; W36ZG6FT64 / Sirolimus
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16. Langer M, Kratz F, Rothen-Rutishauser B, Wunderli-Allenspach H, Beck-Sickinger AG: Novel peptide conjugates for tumor-specific chemotherapy. J Med Chem; 2001 Apr 26;44(9):1341-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel peptide conjugates for tumor-specific chemotherapy.
  • One of the major problems in cancer chemotherapy are the severe side effects that limit the dose of the anticancer drugs because of their unselectivity for tumor versus normal cells.
  • The peptide-drug conjugate was designed to bind to specific receptors expressed on the tumor cells with subsequent internalization of the ligand-receptor complex.
  • Neuropeptide Y (NPY), a 36-amino acid peptide of the pancreatic polypeptide family, was chosen as model peptide because NPY receptors are overexpressed in a number of neuroblastoma tumors and the thereof derived cell lines.
  • Daunorubicin and doxorubicin, two widely used antineoplastic agents in tumor therapy, were covalently linked to NPY via two spacers that differ in stability: an acid-sensitive hydrazone bond at the 13-keto position of daunorubicin and a stable amide bond at the 3'-amino position of daunorubicin and doxorubicin.
  • Receptor binding of these three conjugates ([C(15)]-NPY-Dauno-HYD, [C(15)]-NPY-Dauno-MBS, and [C(15)]-NPY-Doxo-MBS) was determined at the human neuroblastoma cell line SK-N-MC, which selectively expresses the NPY Y(1) receptor subtype, and cytotoxic activity was evaluated using a XTT-based colorimetric cellular cytotoxicity assay.
  • This cytotoxicity is Y(1) receptor-mediated as shown in blocking studies with BIBP 3226, because tumor cells that do not express NPY receptors were sensitive to free daunorubicin, but not to the peptide-drug conjugate.
  • We found evidence that the active conjugate [C(15)]-NPY-Dauno-HYD releases daunorubicin, which is localized close to the nucleus, whereas the inactive conjugate [C(15)]-NPY-Dauno-MBS is distributed distantly from the nucleus and does not seem to release the drug within the cell.
  • [MeSH-minor] Colorimetry. Drug Screening Assays, Antitumor. Humans. Image Processing, Computer-Assisted. Microscopy, Confocal. Structure-Activity Relationship. Tumor Cells, Cultured

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  • (PMID = 11311056.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Neuropeptide Y; 80168379AG / Doxorubicin; ZS7284E0ZP / Daunorubicin
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17. Szepeshazi K, Schally AV, Nagy A, Halmos G: Inhibition of growth of experimental human and hamster pancreatic cancers in vivo by a targeted cytotoxic bombesin analog. Pancreas; 2005 Oct;31(3):275-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of growth of experimental human and hamster pancreatic cancers in vivo by a targeted cytotoxic bombesin analog.
  • OBJECTIVES: Targeting anticancer agents to receptors for peptide hormones such as bombesin/gastrin-releasing peptide (GRP) on tumor cells increases the efficacy and lowers the toxicity of cancer therapy.
  • We studied the expression of bombesin/GRP receptors in 6 experimental pancreatic cancers and evaluated tumor inhibition in vivo produced by targeted chemotherapy with the cytotoxic bombesin analog AN-215.
  • METHODS: Nude mice with xenografts of Panc-1, CFPAC-1, Capan-1, Capan-2, MiaPaCa-2, and SW-1990 human ductal pancreatic cancers, as well as hamsters with nitrosamine-induced pancreatic cancers, were treated with AN-215 or its cytotoxic radical 2-pyrrolinodoxorubicin (AN-201) for 7 to 12 weeks.
  • Tumor growth reduction and survival were analyzed, and cell proliferation rate and apoptosis were examined by histologic methods.
  • AN-215 powerfully inhibited the growth of all pancreatic cancers that expressed functional receptors for bombesin/GRP.
  • CONCLUSIONS: Bombesin/GRP receptors are expressed on most ductal pancreatic carcinoma cell lines and can be used for targeted chemotherapy with the cytotoxic bombesin analog AN-215.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Bombesin / analogs & derivatives. Carcinoma, Pancreatic Ductal / drug therapy. Doxorubicin / analogs & derivatives. Pancreatic Neoplasms / drug therapy

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  • (PMID = 16163060.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AN 215; 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / Receptors, Bombesin; 80168379AG / Doxorubicin; PX9AZU7QPK / Bombesin
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18. Liu SH, Davis A, Li Z, Ballian N, Davis E, Wang XP, Fisher W, Brunicardi FC: Effective ablation of pancreatic cancer cells in SCID mice using systemic adenoviral RIP-TK/GCV gene therapy. J Surg Res; 2007 Jul;141(1):45-52
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  • [Title] Effective ablation of pancreatic cancer cells in SCID mice using systemic adenoviral RIP-TK/GCV gene therapy.
  • BACKGROUND: Studies have demonstrated that adenovirus subtype 5 mediated rat insulin promoter directed thymidine kinase (A-5-RIP-TK)/ganciclovir (GCV) gene therapy resulted in significant enhanced cytotoxicity to both PANC-1 and MIA PaCa2 pancreatic cancer cells in vitro.
  • In this study we examine the in vivo safety and efficacy of intravenous A-5-RIP-TK/GCV gene therapy.
  • MATERIALS AND METHODS: 1 x 10(6) Mia PaCa2 cells were injected intraperitoneally (i.p.) into SCID mice to create a mouse model of human pancreatic cancer.
  • Intravenous injection of A-5-RIP-lacZ reporter gene constructs was used for evaluation of Ad-RIP-gene expression in tumors and other tissues.
  • Optimal adenoviral and GCV doses and treatment duration were determined.
  • Tumor volume, serum insulin, and glucose levels were measured.
  • RESULTS: All A-5-RIP-TK/GCV-treated mice had reduced tumor volume compared with controls, but maximal tumor volume reduction was observed with 10(8) vp followed by GCV treatment for 4 wk.
  • A-5-RIP-TK/GCV gene therapy contributed to significant survival advantage in MIA PaCa2 bearing mice, and the greatest survival benefit was observed with 10(8) vp and was not affected by length of treatment of GCV.
  • A-5-RIP-TK/GCV therapy increased PDX-1 expression and tumor cells apoptosis, and altered islet morphology.
  • However, A-5-RIP-TK/GCV gene therapy caused diabetes associated with islet cell apoptosis, increased delta-cells and reduced pancreatic polypeptide (PP)-cell numbers.
  • CONCLUSIONS: Systemically administered A-5-RIP-TK/GCV is an effective treatment of pancreatic cancer.
  • A-5-RIP-TK/GCV cytotoxicity to malignant cells varies with adenoviral dose and length of GCV treatment.
  • However, A-5-RIP-TK/GCV is associated with islet cell toxicity and diabetogenesis.
  • The type of diabetes observed is distinct from Types 1 and 2 and is associated with islet cell apoptosis and reduced delta- and PP-cells.
  • [MeSH-major] Adenoviridae / genetics. Antiviral Agents / therapeutic use. Ganciclovir / therapeutic use. Genetic Therapy / methods. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / therapy. Thymidine Kinase / genetics
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Diabetes Mellitus / etiology. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Injections, Intraperitoneal. Islets of Langerhans / pathology. Male. Mice. Mice, SCID. Trans-Activators / genetics. Trans-Activators / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 17512546.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA95731
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Homeodomain Proteins; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
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19. Awasthi N, Schwarz MA, Schwarz RE: Combination effects of bortezomib with gemcitabine and EMAP II in experimental pancreatic cancer. Cancer Biol Ther; 2010 Jul 1;10(1):99-107
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination effects of bortezomib with gemcitabine and EMAP II in experimental pancreatic cancer.
  • The proteasome inhibitor bortezomib (B) has been shown to enhance gemcitabine (G) effects against pancreatic ductal adenocarcinoma (PDAC).
  • Endothelial monocyte activating polypeptide II (EMAP, E) is an antiendothelial and antiangiogenic cytokine.
  • The relative local tumor growth compared to controls after bortezomib, EMAP, gemcitabine, B + G, E + G or B + E + G was 92, 52, 48, 36, 18 and 35%, respectively.
  • The potential value of proteasome inhibition in experimental therapy approaches for PDAC appears to relate primarily to the combination with the cytotoxic drug rather than with the antiendothelial agent.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Pancreatic Ductal / drug therapy. Endothelium, Vascular / drug effects. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Bevacizumab. Blotting, Western. Cell Proliferation. Cells, Cultured. Cytokines / administration & dosage. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Female. Humans. Mice. Mice, Inbred NOD. Mice, Nude. Mice, SCID. Neoplasm Proteins / administration & dosage. RNA-Binding Proteins / administration & dosage. Survival Rate. Xenograft Model Antitumor Assays

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  • [CommentIn] Cancer Biol Ther. 2010 Jul 1;10(1):108-9 [20581450.001]
  • (PMID = 20495354.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Cytokines; 0 / Neoplasm Proteins; 0 / RNA-Binding Proteins; 0 / small inducible cytokine subfamily E, member 1; 0W860991D6 / Deoxycytidine; 2S9ZZM9Q9V / Bevacizumab; B76N6SBZ8R / gemcitabine
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20. Kapurniotu A, Schmauder A, Tenidis K: Structure-based design and study of non-amyloidogenic, double N-methylated IAPP amyloid core sequences as inhibitors of IAPP amyloid formation and cytotoxicity. J Mol Biol; 2002 Jan 18;315(3):339-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pancreatic amyloid is formed by the aggregation of the 37-residue islet amyloid polypeptide (IAPP) in type II diabetes patients and is cytotoxic.
  • Pancreatic amyloid deposits are found in more than 95 % of type II diabetes patients and their formation is strongly associated with disease progression.
  • Double N-methylated derivatives of amyloidogenic and cytotoxic partial IAPP sequences generated included F(N-Me)GA(N-Me)IL, NF(N-Me)GA(N-Me)IL, SNNF(N-Me)GA(N-Me)IL, and SNNF(N-Me)GA(N-Me)ILSS and were found to be devoid of beta-sheet structure, amyloidogenicity and cytotoxicity according to Fourier transform-infrared spectroscopy (FT-IR), Congo red (CR) staining, electron microscopy (EM), and cell viability tests.
  • [MeSH-major] Amyloid / antagonists & inhibitors. Amyloid / chemistry. Amyloidosis. Drug Design. Protein Engineering
  • [MeSH-minor] Amino Acid Sequence. Binding Sites. Cell Survival / drug effects. Circular Dichroism. Congo Red. Humans. Hydrogen Bonding. Islet Amyloid Polypeptide. Methylation. Microscopy, Electron. Models, Molecular. Molecular Sequence Data. Pancreatic Diseases / drug therapy. Protein Structure, Quaternary / drug effects. Protein Structure, Secondary / drug effects. Reproducibility of Results. Spectroscopy, Fourier Transform Infrared. Structure-Activity Relationship. Tumor Cells, Cultured

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  • [Copyright] Copyright 2002 Academic Press.
  • (PMID = 11786016.001).
  • [ISSN] 0022-2836
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid; 0 / Islet Amyloid Polypeptide; 3U05FHG59S / Congo Red
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21. Pathak RD, Tran TH, Burshell AL: A case of dopamine agonists inhibiting pancreatic polypeptide secretion from an islet cell tumor. J Clin Endocrinol Metab; 2004 Feb;89(2):581-4
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  • [Title] A case of dopamine agonists inhibiting pancreatic polypeptide secretion from an islet cell tumor.
  • A patient with a large prolactinoma developed a metastatic islet cell tumor secreting pancreatic polypeptide.
  • Dopamine agonist drugs reduced the prolactin levels to normal, caused a 7-fold decrease in the pancreatic polypeptide levels, and inhibited the liver metastases.
  • Dopamine receptors are found in many endocrine tissues, and the expression of dopamine-2 receptor on endocrine tumors establishes the potential for response to dopamine agonist treatment.
  • The relatively benign risk profile of dopaminergic agents makes further testing of these drugs to treat neuroendocrine tumors a worthwhile endeavor.
  • [MeSH-major] Adenoma, Islet Cell / drug therapy. Adenoma, Islet Cell / metabolism. Bromocriptine / therapeutic use. Dopamine Agonists / therapeutic use. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / metabolism. Pancreatic Polypeptide / antagonists & inhibitors
  • [MeSH-minor] Chromogranin A. Chromogranins / blood. Dose-Response Relationship, Drug. Female. Humans. Liver Neoplasms / diagnosis. Liver Neoplasms / secondary. Neoplasms, Multiple Primary / metabolism. Prolactinoma / diagnosis. Prolactinoma / drug therapy

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  • (PMID = 14764765.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Dopamine Agonists; 3A64E3G5ZO / Bromocriptine; 59763-91-6 / Pancreatic Polypeptide
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22. Schwarz RE, Konduri S, Awasthi N, Cafasso D, Schwarz MA: An antiendothelial combination therapy strategy to increase survival in experimental pancreatic cancer. Surgery; 2009 Aug;146(2):241-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An antiendothelial combination therapy strategy to increase survival in experimental pancreatic cancer.
  • BACKGROUND: Combination treatments in addition to gemcitabine have failed to improve outcomes in pancreatic cancer.
  • We tested gemcitabine in combination with the antiendothelial agent endothelial monocyte-activating polypeptide II (EMAP II).
  • METHODS: Human pancreatic cancer cell line murine xenografts were treated with recombinant EMAP II (80 mug/kg), gemcitabine (100 mg/kg), or a combination, and survival and local tumor outcomes were studied.
  • RESULTS: Both EMAP II and gemcitabine inhibited tumor growth, but the combination of both was always more effective.
  • There was a significant extension of survival after EMAP II and gemcitabine combination therapy compared with controls in 2 different pancreatic cancer cell line models at P = .0001 and P = .006, respectively.
  • EMAP II had no impact on gemcitabine-induced antiproliferative effects against pancreatic cancer cells in vitro.
  • CONCLUSION: The antiendothelial agent EMAP II enhanced gemcitabine-mediated tumor inhibition, pointing toward a promising strategy for improved combination treatment of pancreatic cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Angiogenesis Inhibitors / administration & dosage. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cytokines / administration & dosage. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Female. Humans. Mice. Mice, Nude. Neoplasm Proteins / administration & dosage. Neoplasm Transplantation. RNA-Binding Proteins / administration & dosage. Xenograft Model Antitumor Assays

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  • (PMID = 19628080.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cytokines; 0 / Neoplasm Proteins; 0 / RNA-Binding Proteins; 0 / small inducible cytokine subfamily E, member 1; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
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23. Ehehalt F, Saeger HD, Schmidt CM, Grützmann R: Neuroendocrine tumors of the pancreas. Oncologist; 2009 May;14(5):456-67
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This literature review briefly summarizes the epidemiology, pathophysiology, clinical management, and outcomes of patients with pancreatic neuroendocrine tumors (PNETs) and highlights recent advances in PNET research.
  • PNETs are rare neoplasms, compared with carcinomas arising from pancreatic exocrine tissue.
  • They, like other neuroendocrine tumor types, display variable malignant potential, hormone-related syndromes (functionality), localization, and genetic background.
  • Although tumor origin and molecular pathogenesis remain poorly understood, recently established grading and staging systems facilitate patient risk stratification, and thereby directly impact clinical decision making.
  • Although the optimal clinical management of PNETs involves a multidisciplinary approach, surgery remains the only curative treatment for early-stage disease.
  • Alternative therapeutic approaches applied to PNETs, including chemotherapy, radiofrequency ablation, transarterial chemoembolization, biotherapy, polypeptide radionuclide receptor therapy, antiangiogenic therapy, and selective internal radiotherapy, have failed to demonstrate a long-term survival benefit.
  • Surgery remains the primary therapeutic option for patients with PNETs.
  • Research on PNETs is desperately needed to improve the therapeutic options for patients with this disease.
  • [MeSH-major] Neuroendocrine Tumors. Pancreatic Neoplasms
  • [MeSH-minor] Gastrinoma / diagnosis. Gastrinoma / therapy. Humans. Incidence. Insulinoma / diagnosis. Insulinoma / therapy. Neoplasm Staging. Prognosis

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  • (PMID = 19411317.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 130
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