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1. Su Y, Loos M, Giese N, Hines OJ, Diebold I, Görlach A, Metzen E, Pastorekova S, Friess H, Büchler P: PHD3 regulates differentiation, tumour growth and angiogenesis in pancreatic cancer. Br J Cancer; 2010 Nov 9;103(10):1571-9
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

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  • [Title] PHD3 regulates differentiation, tumour growth and angiogenesis in pancreatic cancer.
  • PURPOSE: Tumour hypoxia activates hypoxia-inducible factor-1 (HIF-1) and indluences angiogenesis, cell survival and invasion.
  • The effects of PHD3 in tumour growth are largely unknown.
  • EXPERIMENTAL DESIGN: PHD3 expression was analysed in human pancreatic cancer tissues and cancer cell lines by real-time quantitative PCR and immunohistochemistry.
  • Matrigel invasion assays were performed to examine tumour cell invasion.
  • The effect of PHD3 on tumour growth in vivo was evaluated in an established orthotopic murine model.
  • RESULTS: PHD3 was upregulated in well-differentiated human tumours and cell lines, and regulated hypoxic VEGF secretion.
  • PHD3 overexpression mediated tumour cell growth and invasion by induction of apoptosis in a nerve growth factor-dependent manner by the activation of caspase-3 and phosphorylation of focal adhesion kinase HIF-1 independently.
  • In vivo, PHD3 inhibited tumour growth by abrogation of tumour angiogenesis.
  • CONCLUSION: Our results indicate essential functions of PHD3 in tumour growth, apoptosis and angiogenesis and through HIF-1-dependent and HIF-1-independent pathways.
  • [MeSH-major] Dioxygenases / genetics. Neovascularization, Pathologic / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Animals. Annexin A5 / analysis. Apoptosis. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Pancreatic Ductal / surgery. Caspase 3 / metabolism. Cell Differentiation. Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Hypoxia-Inducible Factor-Proline Dioxygenases. Mice. Neoplasm Invasiveness / genetics. Neoplasm Invasiveness / pathology. Polymerase Chain Reaction. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transplantation, Heterologous. Up-Regulation. Vascular Endothelial Growth Factor A / analysis

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  • (PMID = 20978507.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A5; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Vascular Endothelial Growth Factor A; EC 1.13.11.- / Dioxygenases; EC 1.14.11.29 / EGLN3 protein, human; EC 1.14.11.29 / Hypoxia-Inducible Factor-Proline Dioxygenases; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ PMC2990580
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2. Lee JJ, Natsuizaka M, Ohashi S, Wong GS, Takaoka M, Michaylira CZ, Budo D, Tobias JW, Kanai M, Shirakawa Y, Naomoto Y, Klein-Szanto AJ, Haase VH, Nakagawa H: Hypoxia activates the cyclooxygenase-2-prostaglandin E synthase axis. Carcinogenesis; 2010 Mar;31(3):427-34
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  • Hypoxia-inducible factors (HIFs), in particular HIF-1alpha, have been implicated in tumor biology.
  • However, HIF target genes in the esophageal tumor microenvironment remain elusive.
  • Gene expression profiling was performed upon hypoxia-exposed non-transformed immortalized human esophageal epithelial cells, EPC2-hTERT, and comparing with a gene signature of esophageal squamous cell carcinoma (ESCC).
  • In addition to known HIF-1alpha target genes such as carbonic anhydrase 9, insulin-like growth factor binding protein-3 (IGFBP3) and cyclooxygenase (COX)-2, prostaglandin E synthase (PTGES) was identified as a novel target gene among the commonly upregulated genes in ESCC as well as the cells exposed to hypoxia.
  • Prostaglandin E(2) (PGE(2)) biosynthesis was documented in transformed human esophageal cells by ectopic expression of PTGES as well as RNA interference directed against PTGES.
  • Finally, COX-2 and PTGES were colocalized in primary tumors along with HIF-1alpha and IGFBP3.
  • Activation of the COX-2-PTGES axis in primary tumors was further corroborated by concomitant upregulation of interleukin-1beta and downregulation of hydroxylprostaglandin dehydrogenase.
  • Thus, PTGES is a novel HIF-1alpha target gene, involved in prostaglandin E biosynthesis in the esophageal tumor hypoxic microenvironment, and this has implications in diverse tumors types, especially of squamous origin.

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  • (PMID = 20042640.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K01-DK-06205; United States / NCI NIH HHS / CA / R01 CA100787; United States / NIDDK NIH HHS / DK / R01DK077005; United States / NCI NIH HHS / CA / R01 CA100787-05; United States / NCI NIH HHS / CA / P01-CA-098101
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / IGFBP3 protein, human; 0 / Insulin-Like Growth Factor Binding Protein 3; 0 / Insulin-Like Growth Factor Binding Proteins; 0 / Interleukin-1beta; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / Recombinant Fusion Proteins; 3G0H8C9362 / Cobalt; EC 1.1.1.- / Hydroxyprostaglandin Dehydrogenases; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.99.3 / prostaglandin-E synthase; EVS87XF13W / cobaltous chloride; K7Q1JQR04M / Dinoprostone; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ PMC2832548
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3. Schönleben F, Qiu W, Remotti HE, Hohenberger W, Su GH: PIK3CA, KRAS, and BRAF mutations in intraductal papillary mucinous neoplasm/carcinoma (IPMN/C) of the pancreas. Langenbecks Arch Surg; 2008 May;393(3):289-96
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  • [Title] PIK3CA, KRAS, and BRAF mutations in intraductal papillary mucinous neoplasm/carcinoma (IPMN/C) of the pancreas.
  • BACKGROUND AND AIMS: Recent studies have reported high frequencies of somatic mutations in the phosphoinositide-3-kinase catalytic-alpha (PIK3CA) gene in various human tumors.
  • The BRAF gene is activated by oncogenic RAS, leading to cooperative effects in cells responding to growth factor signals.
  • Here we evaluate the mutational status of PIK3CA, KRAS, and BRAF in intraductal papillary mucinous neoplasm/carcinoma (IPMN/IPMNC) of the pancreas.
  • CONCLUSION: This data is the first report of PIK3CA mutation in pancreatic cancer and it appears to be the first oncogene to be mutated in IPMN/IPMC but not in conventional ductal adenocarcinoma of the pancreas.

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  • (PMID = 18343945.001).
  • [ISSN] 1435-2451
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA095434-05; United States / NCI NIH HHS / CA / R01 CA109525-03; United States / NCI NIH HHS / CA / CA109525-03; United States / NCI NIH HHS / CA / CA109525-04; United States / NCI NIH HHS / CA / R01 CA109525; United States / NCI NIH HHS / CA / R01 CA109525-04; United States / NCI NIH HHS / CA / K01 CA095434; United States / NCI NIH HHS / CA / K01 CA095434-05
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ NIHMS235132; NLM/ PMC3915028
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4. Barth BM, Gustafson SJ, Young MM, Fox TE, Shanmugavelandy SS, Kaiser JM, Cabot MC, Kester M, Kuhn TB: Inhibition of NADPH oxidase by glucosylceramide confers chemoresistance. Cancer Biol Ther; 2010 Dec 1;10(11):1126-36
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  • The bioactive sphingolipid ceramide induces oxidative stress by disrupting mitochondrial function and stimulating NADPH oxidase (NOX) activity, both implicated in cell death mechanisms.
  • Many anticancer chemotherapeutics (anthracyclines, Vinca alkaloids, paclitaxel, and fenretinide), as well as physiological stimuli such as tumor necrosis factor α (TNFα), stimulate ceramide accumulation and increase oxidative stress in malignant cells.
  • Consequently, ceramide metabolism in malignant cells and, in particular the up-regulation of glucosylceramide synthase (GCS), has gained considerable interest in contributing to chemoresistance.
  • We further showed, in both glioblastoma and neuroblastoma cells that glucosylceramide directly interfered with NOX assembly, hence delineating a direct resistance mechanism.

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  • (PMID = 20935456.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM077391; United States / NINDS NIH HHS / NS / U54 NS041069; United States / NIGMS NIH HHS / GM / GM77391; United States / NINDS NIH HHS / NS / U54 NS41069
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; 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 / Glucosylceramides; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; 80168379AG / Doxorubicin; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; EC 1.6.3.1 / NADPH Oxidase; EC 2.4.1.- / Glucosyltransferases; EC 2.4.1.80 / ceramide glucosyltransferase
  • [Other-IDs] NLM/ PMC3047104
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5. Wan X, Shen N, Mendoza A, Khanna C, Helman LJ: CCI-779 inhibits rhabdomyosarcoma xenograft growth by an antiangiogenic mechanism linked to the targeting of mTOR/Hif-1alpha/VEGF signaling. Neoplasia; 2006 May;8(5):394-401
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  • Angiogenesis is one of the critical steps in tumor growth and metastasis.
  • The goal of this study was to evaluate whether the antitumor activity of CCI-779 is related to antiangiogenic effects in vivo in tumors of mice bearing human rhabdomyosarcoma (RMS) xenografts.
  • Based on these data, an intermittent treatment schedule (every 3 days for 30 days) was chosen and displayed a significant suppression of both tumor growth and mTOR signaling.

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  • (PMID = 16790088.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC1592447
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6. Ohashi M, Yoshida K, Kushida M, Miura Y, Ohnami S, Ikarashi Y, Kitade Y, Yoshida T, Aoki K: Adenovirus-mediated interferon alpha gene transfer induces regional direct cytotoxicity and possible systemic immunity against pancreatic cancer. Br J Cancer; 2005 Aug 22;93(4):441-9
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

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  • [Title] Adenovirus-mediated interferon alpha gene transfer induces regional direct cytotoxicity and possible systemic immunity against pancreatic cancer.
  • We previously demonstrated a characteristically high sensitivity of pancreatic cancer cells to interferon alpha (IFN-alpha) gene transfer, which induced a more prominent growth suppression and cell death in pancreatic cancer cells than in other types of cancers and normal cells.
  • The IFN-alpha protein can exhibit both direct cytotoxicity and indirect immunological antitumour activity.
  • Here, we dissected and examined the two mechanisms, taking advantage of the fact that IFN-alpha did not show any cross-species activity in its in vivo effect.
  • When a human IFN-alpha adenovirus was injected into subcutaneous xenografts of human pancreatic cancer cells in nude mice, tumour growth was significantly suppressed due to cell death in an adenoviral dose-dependent manner.
  • The IFN-alpha protein concentration was markedly increased in the injected subcutaneous tumour, but leakage of the potent cytokine into the systemic blood circulation was minimal.
  • When a mouse IFN-alpha adenovirus was injected into the same subcutaneous tumour system, all mice showed significant tumour inhibition, an effect that was dependent on the indirect antitumour activities of IFN-alpha, notably a stimulation of natural killer cells.
  • Moreover, in this case, tumour regression was observed not only for the injected subcutaneous tumours but also for the untreated tumours at distant sites.
  • This study suggested that a local IFN-alpha gene therapy is a promising therapeutic strategy for pancreatic cancer, due to its dual mechanisms of antitumour activities and lack of significant toxicity.
  • [MeSH-major] Genetic Therapy. Interferon-alpha / genetics. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Adenoviridae / genetics. Animals. Cell Line, Tumor. Cell Proliferation. Female. Gene Transfer Techniques. Genetic Vectors. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Metastasis / immunology. Neoplasm Transplantation. Transplantation, Heterologous

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  • (PMID = 16106250.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha
  • [Other-IDs] NLM/ PMC2361577
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7. Choi B, Suh Y, Kim WH, Christa L, Park J, Bae CD: Downregulation of regenerating islet-derived 3 alpha (REG3A) in primary human gastric adenocarcinomas. Exp Mol Med; 2007 Dec 31;39(6):796-804
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  • [Title] Downregulation of regenerating islet-derived 3 alpha (REG3A) in primary human gastric adenocarcinomas.
  • One of the down-regulated genes in gastric cancers was identified as regenerating islet-derived 3 alpha (REG3A), also known as hepatocarcinoma-intestine-pancreas/ pancreatitis-associated protein (HIP/PAP).
  • In addition, REG3A mRNA expression was not detected in stomach cancer cell lines, SNU cells.
  • Treatment with the demethylating agent, 5-aza-2'-deoxycytidine (5-Aza-dC) resulted in the restoration of REG3A mRNA expression in the gastric cancer cell line, indicating that the transcriptional silencing of REG3A in SNU cell lines was caused by DNA methylation.
  • Taken together, these data indicate that REG3A is down-regulated in most primary human gastric cancer cells, and might be useful in the diagnosis of gastric cancer.
  • Further characterization of the differentially expressed gene, REG3A, should lead to a better understanding of the changes occurring at the molecular level during the development and progression of primary human gastric cancer.
  • [MeSH-major] Gastrointestinal Neoplasms / metabolism. Gene Expression Regulation, Neoplastic. Gene Silencing. Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm. Biomarkers, Tumor. Cell Line. Cell Transformation, Neoplastic. Down-Regulation. Gene Expression Profiling. Humans. Lectins, C-Type. Middle Aged. Polymerase Chain Reaction

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  • (PMID = 18160850.001).
  • [ISSN] 1226-3613
  • [Journal-full-title] Experimental & molecular medicine
  • [ISO-abbreviation] Exp. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Proteins; 0 / pancreatitis-associated protein
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8. Kitamura Y, Sato M, Hatamochi A, Yamazaki S: Necrolytic migratory erythema without glucagonoma associated with hepatitis B. Eur J Dermatol; 2005 Jan-Feb;15(1):49-51
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  • Although the most common cause of NME is a glucagon-secreting alpha-islet cell tumor of the pancreas, a dermatitis clinically and histologicaly identical to NME has been described in patients without glucagonoma.
  • We added some discussion on the terminology of this disease.

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  • (PMID = 15701595.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
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9. Li Destri G, Reggio E, Veroux M, Lanzafame S, Puleo S, Minutolo V: A rare cystic non-functioning neuroendocrine pancreatic tumor with an unusual presentation. Tumori; 2006 May-Jun;92(3):260-3
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A rare cystic non-functioning neuroendocrine pancreatic tumor with an unusual presentation.
  • This report describes a patient with a cystic non-functioning neuroendocrine glucagon cell pancreatic tumor presenting with demyelination of the optical nerve that had initially provoked marked monolateral reduced vision and had led to a suspected diagnosis of multiple sclerosis.
  • Cystic degeneration is uncommon in endocrine pancreatic tumors due to their abundant vascular supply.
  • Very few cases of cystic neuroendocrine non-functioning pancreatic tumors have been reported in the international literature.
  • The presence of atypical neurological symptoms, such as sudden visual impairment, should be taken into account in the differential diagnosis for such tumors.
  • The prognosis is poor, because most of these tumors are malignant and diagnosed at an advanced stage.
  • The three-year disease-free survival of our patient, however, encourages the use of aggressive surgical treatment.
  • [MeSH-major] Glucagonoma / complications. Glucagonoma / diagnosis. Pancreatic Cyst / complications. Pancreatic Cyst / diagnosis. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Demyelinating Diseases / etiology. Diagnosis, Differential. Female. Humans. Multiple Sclerosis / diagnosis. Optic Nerve / physiopathology. Vision, Low / etiology

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  • (PMID = 16869249.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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10. Lobo I, Carvalho A, Amaral C, Machado S, Carvalho R: Glucagonoma syndrome and necrolytic migratory erythema. Int J Dermatol; 2010 Jan;49(1):24-9
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  • The glucagonoma syndrome is a rare disorder, characterized by necrolytic migratory erythema, elevated serum glucagon levels, abnormal glucose tolerance, weight loss, and anemia in association with a glucagon-secreting alpha-cell tumor of the pancreas.
  • The clinical investigation revealed a pancreatic glucagonoma with resolution of the cutaneous and systemic features after surgical removal.
  • Early recognition and treatment may prevent metastatic disease and ensure its cure with resolution of the cutaneous and catabolic manifestations.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Skin / pathology
  • [MeSH-minor] Aged. Biopsy. Glucagon / blood. Humans. Male. Necrosis. Pancreatectomy. Tomography, X-Ray Computed

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  • (PMID = 20465606.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-92-5 / Glucagon
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11. Mergler S, Strauss O, Strowski M, Prada J, Drost A, Langrehr J, Neuhaus P, Wiedenmann B, Ploeckinger U: Insulin-like growth factor-1 increases intracellular calcium concentration in human primary neuroendocrine pancreatic tumor cells and a pancreatic neuroendocrine tumor cell line (BON-1) via R-type Ca2+ channels and regulates chromogranin a secretion in BON-1 cells. Neuroendocrinology; 2005;82(2):87-102
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  • [Title] Insulin-like growth factor-1 increases intracellular calcium concentration in human primary neuroendocrine pancreatic tumor cells and a pancreatic neuroendocrine tumor cell line (BON-1) via R-type Ca2+ channels and regulates chromogranin a secretion in BON-1 cells.
  • VOCCs are categorized into L-type channels (Ca(V)1.1-1.4), P/Q-type channels (Ca(V)2.1), N-type channels (Ca(V)2.2), R-type channels (Ca(V)2.3), and T-type channels (Ca(V)3.1-3.3).
  • Aside from regulating membrane excitability, VOCCs influence chromogranin A (CgA) secretion in neuroendocrine tumor (NET) cells.
  • It is not known, whether VOCCs play a role in the IGF-1-dependent regulation of CgA secretion in NET cells.
  • We therefore studied the effects of IGF-1 on individual VOCC subtypes and characterized their role in mediating IGF-1-dependent regulation of CgA secretion in NET cells.
  • Using specific modulators of VOCC subtypes, we identified the functional expression of L-, N-, P/Q- and R-type channels in primary as well as permanent models of NET.
  • The IGF-1-induced intracellular Ca(2+) increase in NET cells was mainly due to the activation of R-type channel activity.
  • The effects on intracellular calcium, observed in whole-cell patch-clamp recordings and fluorescence imaging, were partially blocked by the specific R-type channel blocker SNX-482 and antisense oligonucleotides against the alpha(1) subunit of this channel.
  • The effect of IGF-1 was reduced by both, inhibition of R-type channel activity and a reduction of R-type channel expression using antisense oligonucleotides.
  • Since R-type channels exist in NET cells and couple to both, IGF-1 receptor signaling as well as CgA secretion, pharmacological interference with R-type channels may represent a new therapeutic option by blocking Ca(2+) signaling thereby abrogating IGF-1-dependent hypersecretion in NET disease.
  • [MeSH-major] Calcium / metabolism. Calcium Channels, R-Type / metabolism. Chromogranins / metabolism. Insulin-Like Growth Factor I / pharmacology. Neuroendocrine Tumors / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Line, Tumor. Chromogranin A. Culture Media. Electrophysiology. Fluorescent Antibody Technique. Fluorescent Dyes. Fura-2. Humans. Oligonucleotides, Antisense / pharmacology. Patch-Clamp Techniques. Phenotype

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  • (PMID = 16424676.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CHGA protein, human; 0 / Calcium Channels, R-Type; 0 / Chromogranin A; 0 / Chromogranins; 0 / Culture Media; 0 / Fluorescent Dyes; 0 / Oligonucleotides, Antisense; 67763-96-6 / Insulin-Like Growth Factor I; SY7Q814VUP / Calcium; TSN3DL106G / Fura-2
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12. Yu R, Nissen NN, Dhall D, Heaney AP: Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature. Pancreas; 2008 May;36(4):428-31
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  • [Title] Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature.
  • We report a rare case of nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas.
  • The patient's clinical presentation, diagnosis, treatment, pancreas pathology, and follow-up are reviewed.
  • A 60-year-old patient was incidentally found to harbor a pancreatic mass with markedly elevated glucagon levels but without glucagonoma syndrome.
  • She was initially diagnosed with glucagonoma, and the tumor was resected.
  • Pathological examination demonstrated that the tumor was a nonfunctioning islet cell tumor and revealed nesidioblastosis and hyperplasia of alpha cells and microglucagonoma in the apparently normal surgical margin.
  • No pancreatic tumors recurred 36 months after surgery.
  • This is the third case of alpha-cell nesidioblastosis reported in the English literature.
  • Nesidioblastosis and hyperplasia of alpha cells should be considered in the differential diagnosis of hyperglucagonemia.
  • Somatostatin analog may be used to suppress glucagon secretion in alpha-cell hyperplasia.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / pathology. Glucagonoma / pathology. Islets of Langerhans / pathology. Nesidioblastosis / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18437091.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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13. Hsu MY, Pan KT, Chu SY, Hung CF, Wu RC, Tseng JH: CT and MRI features of acinar cell carcinoma of the pancreas with pathological correlations. Clin Radiol; 2010 Mar;65(3):223-9
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  • [Title] CT and MRI features of acinar cell carcinoma of the pancreas with pathological correlations.
  • AIM: To document the computed tomography (CT) and magnetic resonance imaging (MRI) features of acinar cell carcinoma of the pancreas and to correlate them with pathological findings to determine the unique imaging manifestations of this rare subtype tumour of the pancreas.
  • MATERIALS AND METHODS: From January 1986 to August 2008, six patients (five men and one woman, mean age 61.3 years) with histologically proven acinar cell carcinoma of the pancreas underwent CT (n=6) and MRI (n=4) examinations.
  • The imaging features of each tumour were documented and compared with pathological findings.
  • RESULTS: The tumours were distributed in the head (n=4), body (n=1), and tail (n=1) of the pancreas.
  • Two tumours (33%) exhibited intratumoural haemorrhage, and one tumour (17%) had amorphous intratumoural calcification.
  • In both CT and MRI, the tumours enhanced less than the adjacent normal pancreatic parenchyma.
  • CONCLUSION: Acinar cell carcinoma of the pancreas has distinct imaging features, and both CT and MRI are useful and complementary imaging methods.
  • [MeSH-major] Carcinoma, Acinar Cell. Magnetic Resonance Imaging. Pancreatic Neoplasms. Tomography, X-Ray Computed
  • [MeSH-minor] Adult. Aged. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Pancreas, Exocrine. Retrospective Studies. Sex Distribution. alpha-Fetoproteins / metabolism

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  • [Copyright] Copyright (c) 2010 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 20152279.001).
  • [ISSN] 1365-229X
  • [Journal-full-title] Clinical radiology
  • [ISO-abbreviation] Clin Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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14. Henopp T, Anlauf M, Schmitt A, Schlenger R, Zalatnai A, Couvelard A, Ruszniewski P, Schaps KP, Jonkers YM, Speel EJ, Pellegata NS, Heitz PU, Komminoth P, Perren A, Klöppel G: Glucagon cell adenomatosis: a newly recognized disease of the endocrine pancreas. J Clin Endocrinol Metab; 2009 Jan;94(1):213-7
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  • [Title] Glucagon cell adenomatosis: a newly recognized disease of the endocrine pancreas.
  • BACKGROUND: Glucagon-producing tumors are either solitary neoplasms of the pancreas, occasionally associated with a glucagonoma syndrome, or multiple neoplasms associated with multiple endocrine neoplasia type 1 (MEN1).
  • We observed a previously undescribed multicentric glucagon-producing tumor disease that is not related to MEN1.
  • METHODS: Pancreatic tissue from four patients showing multiple neuroendocrine microadenomas and in two cases also macrotumors were screened for hormones using immunohistochemical and morphometric methods.
  • RESULTS: The pancreatic tissue from the four patients contained more than 870 microadenomas and 10 macrotumors, all of which expressed exclusively glucagon and none of which showed evidence of malignancy.
  • In addition, many islets were unusually large and showed glucagon cell hyperplasia.
  • There was no clinical or molecular evidence of any hereditary tumor disease, and changes in the MEN1 gene were only seen in individual tumors.
  • CONCLUSIONS: The findings are sufficiently distinctive to suggest a new neoplastic disease of the endocrine pancreas that we recommend calling glucagon cell adenomatosis.
  • Clinically, this disease may be an incidental finding, or it may lead to a glucagonoma syndrome.
  • [MeSH-major] Adenoma / pathology. Glucagon / secretion. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Cyclin-Dependent Kinase Inhibitor p27 / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Male. Proto-Oncogene Proteins / genetics. Von Hippel-Lindau Tumor Suppressor Protein / genetics

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  • (PMID = 18957496.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 9007-92-5 / Glucagon; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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15. Hameed O, Xu H, Saddeghi S, Maluf H: Hepatoid carcinoma of the pancreas: a case report and literature review of a heterogeneous group of tumors. Am J Surg Pathol; 2007 Jan;31(1):146-52
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  • [Title] Hepatoid carcinoma of the pancreas: a case report and literature review of a heterogeneous group of tumors.
  • Hepatoid carcinomas are tumors that display, at least focally, cytologic and/or architectural features of hepatocellular carcinoma.
  • We report a case of hepatoid carcinoma of the pancreas that developed in a 41-year-old woman in association with a pancreatic endocrine carcinoma.
  • The fine needle aspiration material was characterized by the presence of monotonous, small-to-medium sized tumor cells with round nuclei and finely granular chromatin, intermixed with more atypical tumor cells displaying larger nuclei with coarse clumped chromatin, prominent nucleoli, and moderate amounts of foamy cytoplasm.
  • The excised specimen displayed a poorly differentiated pancreatic endocrine carcinoma associated with well-defined islands of larger tumor cells growing in a perisinusoidal pattern which, based on their immunohistochemical profile and the demonstration of bile, proved to represent a hepatoid component.
  • This case and prior examples in the literature suggest that hepatoid carcinomas of the pancreas appear to be a heterogeneous group of tumors (pure or associated with another histologic component) that are often associated with early liver metastasis and a short survival, although those arising as a component of endocrine tumors seem to fare slightly better.
  • Hepatoid carcinoma of the pancreas should be included in the differential diagnosis of pancreatic tumors composed of large eosinophilic cells.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Carcinoma, Islet Cell / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Fatal Outcome. Female. Humans. Immunohistochemistry. Neoplasms, Multiple Primary. Tomography, X-Ray Computed. alpha-Fetoproteins / analysis

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  • (PMID = 17197931.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / alpha-Fetoproteins
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16. Pérez-Garay M, Arteta B, Pagès L, de Llorens R, de Bolòs C, Vidal-Vanaclocha F, Peracaula R: alpha2,3-sialyltransferase ST3Gal III modulates pancreatic cancer cell motility and adhesion in vitro and enhances its metastatic potential in vivo. PLoS One; 2010;5(9)
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  • [Title] alpha2,3-sialyltransferase ST3Gal III modulates pancreatic cancer cell motility and adhesion in vitro and enhances its metastatic potential in vivo.
  • BACKGROUND: Cell surface sialylation is emerging as an important feature of cancer cell metastasis.
  • Sialyltransferase expression has been reported to be altered in tumours and may account for the formation of sialylated tumour antigens.
  • We have focused on the influence of alpha-2,3-sialyltransferase ST3Gal III in key steps of the pancreatic tumorigenic process.
  • METHODOLOGY/PRINCIPAL FINDINGS: ST3Gal III overexpressing pancreatic adenocarcinoma cell lines Capan-1 and MDAPanc-28 were generated.
  • They showed an increase of the tumour associated antigen sialyl-Lewis(x).
  • The transfectants' E-selectin binding capacity was proportional to cell surface sialyl-Lewis(x) levels.
  • Moreover, intrasplenic injection of the ST3Gal III transfected cells into athymic nude mice showed a decrease in survival and higher metastasis formation when compared to the mock cells.
  • CONCLUSION: In summary, the overexpression of ST3Gal III in these pancreatic adenocarcinoma cell lines underlines the role of this enzyme and its product in key steps of tumour progression such as adhesion, migration and metastasis formation.
  • [MeSH-major] Neoplasm Metastasis. Pancreatic Neoplasms / enzymology. Pancreatic Neoplasms / physiopathology. Sialyltransferases / metabolism
  • [MeSH-minor] Animals. Cell Adhesion. Cell Line, Tumor. Cell Movement. Female. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Rats. Survival

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  • (PMID = 20824144.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.4.99.- / Sialyltransferases; EC 2.4.99.4 / beta-galactoside alpha-2,3-sialyltransferase
  • [Other-IDs] NLM/ PMC2931708
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17. Kishaba Y, Matsubara D, Niki T: Heterogeneous expression of nestin in myofibroblasts of various human tissues. Pathol Int; 2010 May;60(5):378-85

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  • In this study we explored the distribution of nestin-positive cells in extraneural human tissues with special reference to stromal myofibroblasts.
  • Sections were immunostained for nestin, alpha-smooth muscle actin (alpha-SMA), desmin, vimentin, CD34, and other stromal markers.
  • Nestin was expressed in the myoepithelium of the breast, podocytes of the renal glomerulus, and endothelial cells of most organs.
  • Nestin-positive fibroblast-like cells appeared in the stroma of the kidney, pancreas, lung, and skin in fibrosing conditions.
  • With the notable exception of endometrial stromal cells, most of these nestin-positive stromal cells were alpha-SMA-positive.
  • Further investigation showed that nestin was expressed by stromal fibroblasts in cervical squamous cell carcinoma, but not in lung adenocarcinoma, pointing to heterogeneity of cancer stroma.
  • Nestin-positive myofibroblast may represent a relatively immature subpopulation of cells with multipotentiality.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Female. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Neoplasm Staging. Nestin. Stromal Cells / metabolism. Stromal Cells / pathology. Tissue Array Analysis. Uterine Cervical Neoplasms / metabolism. Uterine Cervical Neoplasms / pathology

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  • (PMID = 20518888.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin
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18. Larsen AE, Crowe TC: Effects of conjugated linoleic acid on myogenic and inflammatory responses in a human primary muscle and tumor coculture model. Nutr Cancer; 2009;61(5):687-95
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  • [Title] Effects of conjugated linoleic acid on myogenic and inflammatory responses in a human primary muscle and tumor coculture model.
  • The antiproliferative and anti-inflammatory properties of conjugated linoleic acid (CLA) make it a potentially novel treatment in chronic inflammatory muscle wasting disease, particularly cancer cachexia.
  • Human primary muscle cells were grown in coculture with MIA PaCa-2 pancreatic tumor cells and exposed to varying concentrations of c9,t11 and t10,c12 CLA.
  • Expression of myogenic (Myf5, MyoD, myogenin, and myostatin) and inflammatory genes (CCL-2, COX-2, IL-8, and TNF-alpha) were measured by real-time PCR.
  • There was a marked decrease in muscle MyoD and myogenin expression (78% and 62%, respectively), but no change in either Myf5 or myostatin, in myotubes grown in coculture with MIA PaCa-2 cells.
  • A similar pattern of myogenic gene expression changes was observed in myotubes treated with TNF-alpha alone.
  • Several-fold significant increases in CCL-2, COX-2, IL-8, and TNF-alpha expression in myotubes were observed with MIA PaCa-2 coculture.
  • The c9,t11 CLA isomer significantly decreased basal expression of TNF-alpha in myotubes and could ameliorate its tumor-induced rise.
  • The study provides insight into the anti-inflammatory and antiproliferative actions of CLA and its application as a therapeutic agent in inflammatory disease states.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Cells, Cultured. Coculture Techniques. Cyclooxygenase 2 / genetics. Cyclooxygenase 2 / metabolism. Cytokines / genetics. Cytokines / metabolism. Gene Expression Regulation. Humans. Isomerism. Male. Mice. Muscle Cells. Muscle Proteins / genetics. Muscle Proteins / metabolism. RNA, Messenger / metabolism. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 19838943.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antineoplastic Agents; 0 / Cytokines; 0 / Linoleic Acids, Conjugated; 0 / Muscle Proteins; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 1.14.99.1 / Cyclooxygenase 2
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19. Kahlert C, Weber H, Mogler C, Bergmann F, Schirmacher P, Kenngott HG, Matterne U, Mollberg N, Rahbari NN, Hinz U, Koch M, Aigner M, Weitz J: Increased expression of ALCAM/CD166 in pancreatic cancer is an independent prognostic marker for poor survival and early tumour relapse. Br J Cancer; 2009 Aug 4;101(3):457-64
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  • [Title] Increased expression of ALCAM/CD166 in pancreatic cancer is an independent prognostic marker for poor survival and early tumour relapse.
  • BACKGROUND: ALCAM (activated leucocyte cell adhesion molecule, synonym CD166) is a cell adhesion molecule, which belongs to the Ig superfamily.
  • Disruption of the ALCAM-mediated adhesiveness by proteolytic sheddases such as ADAM17 has been suggested to have a relevant impact on tumour invasion.
  • Although the expression of ALCAM is a valuable prognostic and predictive marker in several types of epithelial tumours, its role as a prognostic marker in pancreatic cancer has not yet been reported.
  • METHODS: In this study, paraffin-embedded samples of 97 patients with pancreatic cancer undergoing potentially curative resection were immunostained against ALCAM, ADAM17 and CK19.
  • RESULTS: We could show that in normal pancreatic tissue, ALCAM is predominantly expressed at the cellular membrane, whereas in pancreatic tumour cells, it is mainly localised in the cytoplasm.
  • Overexpression of ADAM17 in pancreatic cancer, however, failed to be a significant prognostic marker and was not coexpressed with ALCAM.
  • CONCLUSIONS: Our findings support the hypothesis that the disruption of ALCAM-mediated adhesiveness is a relevant step in pancreatic cancer progression.
  • Moreover, ALCAM overexpression is a relevant independent prognostic marker for poor survival and early tumour relapse in pancreatic cancer.
  • [MeSH-major] Antigens, CD / analysis. Biomarkers, Tumor / analysis. Cell Adhesion Molecules, Neuronal / analysis. Fetal Proteins / analysis. Neoplasm Recurrence, Local / chemistry. Pancreatic Neoplasms / chemistry
  • [MeSH-minor] ADAM Proteins / analysis. Adult. Aged. Aged, 80 and over. Cell Adhesion. Female. Humans. Immunohistochemistry. Male. Middle Aged. Pancreas / chemistry. Prognosis

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  • (PMID = 19603023.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ALCAM protein, human; 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / Cell Adhesion Molecules, Neuronal; 0 / Fetal Proteins; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
  • [Other-IDs] NLM/ PMC2720248
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20. Masamune A, Kikuta K, Watanabe T, Satoh K, Hirota M, Hamada S, Shimosegawa T: Fibrinogen induces cytokine and collagen production in pancreatic stellate cells. Gut; 2009 Apr;58(4):550-9
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  • [Title] Fibrinogen induces cytokine and collagen production in pancreatic stellate cells.
  • OBJECTIVE: Fibroblasts in the area of fibrosis in chronic pancreatitis and of the desmoplastic reaction associated with pancreatic cancer are now recognised as activated pancreatic stellate cells (PSCs).
  • Recent studies have shown strong expression of fibrinogen, the central protein in the haemostasis pathway, in the stromal tissues of pancreatic cancer and chronic pancreatitis, suggesting that PSCs are embedded in and exposed to abundant fibrinogen in these pathological settings.
  • The effects of fibrinogen on cell functions in PSCs were examined here.
  • METHODS: PSCs were isolated from human pancreas tissues of patients undergoing operations for pancreatic cancer, and from rat pancreatic tissues.
  • The effects of fibrinogen on key cell functions and activation of signalling pathways in PSCs were examined.
  • RESULTS: Fibrinogen induced the production of interleukin 6 (IL6), interleukin 8 (IL8), monocyte chemoattractant protein-1, vascular endothelial growth factor, angiopoietin-1 and type I collagen, but not proliferation or intercellular adhesion molecule-1 expression.
  • Fibrinogen increased alpha-smooth muscle actin expression and induced the activation of nuclear factor-kappaB (NF-kappaB), Akt and three classes of mitogen-activated protein kinases (extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase and p38 mitogen-activated protein kinase (MAPK)).
  • Fibrinogen-induced IL6 and IL8 production was inhibited by antibodies against alpha(v)beta(3) and alpha(5)beta(1) integrins, suggesting that these integrins worked as counter receptors for fibrinogen in PSCs.
  • [MeSH-major] Collagen Type I / biosynthesis. Cytokines / biosynthesis. Fibrinogen / pharmacology. Pancreas / drug effects
  • [MeSH-minor] Animals. Cell Movement / physiology. Cells, Cultured. Disease Models, Animal. Dose-Response Relationship, Drug. Humans. Integrin alpha5beta1 / physiology. Integrin alphaVbeta3 / physiology. Interleukin-6 / biosynthesis. Interleukin-8 / biosynthesis. Male. Mice. Mice, Nude. Neoplasm Transplantation. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Pancreatitis, Chronic / metabolism. Pancreatitis, Chronic / pathology. Peptide Fragments / biosynthesis. Procollagen / biosynthesis. Rats. Rats, Wistar. Signal Transduction / drug effects. Signal Transduction / physiology


21. Dubova EA, Shchegolev AI, Mishnev OD, Egorov VI: [Solid pseudopapillary tumor of the pancreas]. Arkh Patol; 2008 Jan-Feb;70(1):49-52
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  • [Title] [Solid pseudopapillary tumor of the pancreas].
  • The paper reviews the data available in the literature and describes the authors' observation of solid pseudopapillary tumor of the pancreas in a 33-year-old woman.
  • Microscopically, the tumor, 2.5 x 2.5 x 2 cm in size, appeared predominantly as solid areas and solitary pseudopapillae comprising monomorphic round and oval cells with a light cytoplasm and round nuclei.
  • Immunohistochemical study revealed diffuse cytoplasmic tumor cell staining in response to vimentin, alpha-antitrypsin, neuronspecific enolase, and cytokeratin 18; focal expression of synaptophysin and CD117; a negative reaction with antibodies to epithelial membrane antigen, S-100 protein, cytokeratins 7, 8, and 19, and CD57.
  • Progesterone receptors were detectable in the nuclei of solitary tumor cells and the reaction with estrogen receptor was negative.
  • [MeSH-major] Carcinoma, Papillary / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18368811.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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22. Kamohara H, Takahashi M, Ishiko T, Ogawa M, Baba H: Induction of interleukin-8 (CXCL-8) by tumor necrosis factor-alpha and leukemia inhibitory factor in pancreatic carcinoma cells: Impact of CXCL-8 as an autocrine growth factor. Int J Oncol; 2007 Sep;31(3):627-32
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  • [Title] Induction of interleukin-8 (CXCL-8) by tumor necrosis factor-alpha and leukemia inhibitory factor in pancreatic carcinoma cells: Impact of CXCL-8 as an autocrine growth factor.
  • Pancreatic carcinoma is one of the most lethal of the gastrointestinal malignant tumors.
  • Chronic inflammation leads to cancer development and progression.
  • We previously reported that CXCL-8 was produced by a variety of human carcinoma cells and tissues, and that CXCL-8 promoted proliferation in pancreatic carcinoma cells (SUIT-2).
  • In the present study, we analyzed whether various cytokines affect cell proliferation by CXCL-8 expression in pancreas carcinoma cells.
  • All examined pancreatic carcinoma cells expressed CXCL-8 and TNFRII mRNA constitutively in RPMI-1640 medium without FBS.
  • TNF-alpha, LIF, IL-1beta, IL-6, IL-8, or IFN-beta enhanced the expression of CXCL-8 mRNA, but IL-10 did not in Hs-700T cells.
  • Actinomycin D suppressed and cycloheximide augmented CXCL-8 mRNA which was induced by TNF-alpha or not.
  • The half-life of CXCL-8 mRNA was 36.5 min by TNF-alpha and 35.2 min by no stimulation.
  • In our previous study, LIF promoted cell growth in Hs-700T cells.
  • Addition of recombinant CXCL-8 did not induce cell growth of Hs-700T.
  • Anti-CXCL-8 IgG significantly suppressed cell growth.
  • CXCL-8 would act as an autocrine growth factor in Hs-700T cells, which expressed CXCL-8 mRNA highly without stimulation.
  • Curcumin (diferuloylmethane), NF-kappaB inhibitor, suppressed cell proliferation in Hs-700T cells.
  • These results suggest that CXCL-8 plays a pivotal role in progression of pancreatic cancer, and its expression is influenced by inflammatory cytokines in pancreatic tumor microenvironment.
  • [MeSH-major] Interleukin-8 / metabolism. Leukemia Inhibitory Factor / metabolism. Pancreatic Neoplasms / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Cycloheximide / pharmacology. Cytokines / metabolism. Dactinomycin / pharmacology. Humans. Immunoglobulin G / chemistry. Inflammation. Intercellular Signaling Peptides and Proteins / metabolism. RNA, Messenger / metabolism. Time Factors

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  • (PMID = 17671691.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cytokines; 0 / Immunoglobulin G; 0 / Intercellular Signaling Peptides and Proteins; 0 / Interleukin-8; 0 / Leukemia Inhibitory Factor; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 1CC1JFE158 / Dactinomycin; 98600C0908 / Cycloheximide
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23. Ikemoto T, Yamaguchi T, Morine Y, Imura S, Soejima Y, Fujii M, Maekawa Y, Yasutomo K, Shimada M: Clinical roles of increased populations of Foxp3+CD4+ T cells in peripheral blood from advanced pancreatic cancer patients. Pancreas; 2006 Nov;33(4):386-90
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  • [Title] Clinical roles of increased populations of Foxp3+CD4+ T cells in peripheral blood from advanced pancreatic cancer patients.
  • OBJECTIVES: Further metastasis should be avoided in pancreatic cancer (PC) patients for effective surgical treatment.
  • Regulatory T cells (Foxp3CD4 T cells including CD4CD25 T cells and CD4CD25 T cells) play important roles in tumor immunity.
  • This study aimed to investigate whether regulatory T cells participate in metastasis.
  • The peripheral blood mononuclear cells (PBMCs) were subjected to FACScan analysis after labeling with anti-CD4, anti-CD25, and anti-Foxp3 antibodies.
  • Tumor markers, including DUPAN2 and CA19-9, surface markers, such as the CD4/CD8 ratio, and the CD57 cell population were assessed.
  • RESULTS: The Foxp3CD4 T-cell population among the PBMCs was significantly increased in PC patients (8.10% +/- 4.65%) compared with healthy donors (2.47 +/- 0.78%) (P < 0.001).
  • No significant relationships existed for the tumor markers, CD4/CD8 ratio, and CD57 cells.
  • However, a significant correlation was found between Foxp3CD4 T cells among the PBMCs and the TNM stage (P < 0.05).
  • CONCLUSIONS: Foxp3CD4 T cells are good markers for metastasis detection in PC patients and more accurate than other conventional tumor markers, especially at advanced stages of the disease.
  • [MeSH-major] Forkhead Transcription Factors / analysis. Pancreatic Neoplasms / immunology. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Aged. Female. Humans. Interleukin-2 Receptor alpha Subunit / analysis. Male. Middle Aged. Neoplasm Staging. T-Lymphocyte Subsets / immunology

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  • (PMID = 17079944.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Interleukin-2 Receptor alpha Subunit
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24. Vervoort L, Burvenich I, Staelens S, Dumolyn C, Waegemans E, Van Steenkiste M, Baird SK, Scott AM, De Vos F: Preclinical evaluation of monoclonal antibody 14C5 for targeting pancreatic cancer. Cancer Biother Radiopharm; 2010 Apr;25(2):193-205
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  • [Title] Preclinical evaluation of monoclonal antibody 14C5 for targeting pancreatic cancer.
  • The use of radiolabeled antibodies that are able to target primary tumors as well as metastatic tumor sites with minimal reactivity to normal tissues is a promising approach for treating pancreatic cancer.
  • In this study, the integrin alpha(v)beta(5) is studied as a target for the diagnosis of and potential therapy for human pancreatic cancer by using the radiolabeled murine monoclonal antibody (mAb) 14C5.
  • Biopsy specimens from human pancreatic tumors were examined for the expression of the integrin alpha(v)beta(5).
  • The pancreatic tumor cell line Capan-1 was used to test the in vitro targeting potency of mAb 14C5 labeled with 125/131-iodine and 111-indium.
  • Biodistribution and tumor-targeting characteristics were studied in Capan-1 xenografts.
  • All tumor sections were positive for the integrin alpha(v)beta(5), with an extensive positive staining of the stroma.
  • In vivo radioisotope tumor uptake was maximum at 48-72 hours, with the uptake of (111)In-p-SCN-Bz-DOTA-14C5 (35.84 +/- 8.64 percentage of injected dose per g [%ID/g]) being 3.9- and 2.2-folds higher than (131)I-14C5 (12.16 +/- 1.03%ID/g) and (111)In-p-SCN-Bz-DTPA-14C5 (14.30 +/- 3.76%ID/g), respectively.
  • Planar gamma imaging with mAb 14C5 indicated clear localization of the pancreatic tumors versus minimal normal tissue uptake. mAb 14C5 is a promising new antibody for targeting the integrin alpha(v)beta(5) for the diagnosis of and potential therapy for pancreatic cancer.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Pancreatic Neoplasms / therapy. Radiopharmaceuticals. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Drug Evaluation, Preclinical. Female. Humans. Iodine Radioisotopes. Mice. Mice, Nude. Pancreas / immunology. Pancreas / metabolism. Pancreas / pathology. Pentetic Acid / analogs & derivatives. Pentetic Acid / pharmacokinetics. Radioimmunoassay. Receptors, Vitronectin / immunology. Receptors, Vitronectin / metabolism. Tissue Distribution. Tumor Cells, Cultured

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  • (PMID = 20423233.001).
  • [ISSN] 1557-8852
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 14C5 monoclonal antibody; 0 / Antibodies, Monoclonal; 0 / Iodine Radioisotopes; 0 / Radiopharmaceuticals; 0 / Receptors, Vitronectin; 0 / integrin alphaVbeta5; 102650-30-6 / 1-(4-isothiocyanatobenzyl)diethylenetriaminepentaacetic acid; 7A314HQM0I / Pentetic Acid
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25. Saadi A, Shannon NB, Lao-Sirieix P, O'Donovan M, Walker E, Clemons NJ, Hardwick JS, Zhang C, Das M, Save V, Novelli M, Balkwill F, Fitzgerald RC: Stromal genes discriminate preinvasive from invasive disease, predict outcome, and highlight inflammatory pathways in digestive cancers. Proc Natl Acad Sci U S A; 2010 Feb 02;107(5):2177-82
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  • [Title] Stromal genes discriminate preinvasive from invasive disease, predict outcome, and highlight inflammatory pathways in digestive cancers.
  • The stromal compartment is increasingly recognized to play a role in cancer.
  • However, its role in the transition from preinvasive to invasive disease is unknown.
  • Most gastrointestinal tumors have clearly defined premalignant stages, and Barrett's esophagus (BE) is an ideal research model.
  • Gene ontology analysis identified a strong inflammatory component in BE disease progression, and key pathways included cytokine-cytokine receptor interactions and TGF-beta.
  • Gene set enrichment analysis of external datasets demonstrated that the stromal signature was also relevant in the preinvasive to invasive transition of the stomach, colon, and pancreas.
  • [MeSH-major] Digestive System Neoplasms / genetics. Digestive System Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / immunology. Adenocarcinoma / pathology. Barrett Esophagus / genetics. Barrett Esophagus / immunology. Barrett Esophagus / pathology. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / genetics. Cytokines / genetics. DNA-Binding Proteins / genetics. Esophageal Neoplasms / genetics. Esophageal Neoplasms / immunology. Esophageal Neoplasms / pathology. Gelatinases / genetics. Humans. Inflammation / genetics. Inflammation / immunology. Inflammation / pathology. Membrane Proteins / genetics. Metaplasia. Neoplasm Invasiveness / genetics. Neoplasm Invasiveness / pathology. Nuclear Proteins / genetics. Oncogenes. Precancerous Conditions / genetics. Precancerous Conditions / immunology. Precancerous Conditions / pathology. Prognosis. Proto-Oncogene Proteins c-bcl-6. Receptors, Cytokine / genetics. Serine Endopeptidases / genetics. Stromal Cells / immunology. Stromal Cells / pathology. Trans-Activators / genetics

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  • (PMID = 20080664.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE19529/ GSE19632
  • [Grant] United Kingdom / Medical Research Council / / G0501974; United Kingdom / Medical Research Council / / MC/ U105365007; United Kingdom / Cancer Research UK / / ; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Cytokines; 0 / DNA-Binding Proteins; 0 / JMY protein, human; 0 / Membrane Proteins; 0 / Nuclear Proteins; 0 / PMEPA1 protein, human; 0 / Proto-Oncogene Proteins c-bcl-6; 0 / Receptors, Cytokine; 0 / SPZ1 protein, human; 0 / Trans-Activators; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
  • [Other-IDs] NLM/ PMC2836667
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26. Quiros RM, Valianou M, Kwon Y, Brown KM, Godwin AK, Cukierman E: Ovarian normal and tumor-associated fibroblasts retain in vivo stromal characteristics in a 3-D matrix-dependent manner. Gynecol Oncol; 2008 Jul;110(1):99-109
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  • [Title] Ovarian normal and tumor-associated fibroblasts retain in vivo stromal characteristics in a 3-D matrix-dependent manner.
  • Here, we introduce an in vivo-like 3-D system of mesenchymal stromal progression during ovarian tumorigenesis to support the study of stroma permissiveness in human ovarian neoplasias.
  • METHODS: To sort 3-D cultures into 'normal,' 'primed' and 'activated' stromagenic stages, 29 fibroblastic cell lines from 5 ovarian tumor samples (tumor ovarian fibroblasts, TOFs) and 14 cell lines from normal prophylactic oophorectomy samples (normal ovarian fibroblasts, NOFs) were harvested and characterized for their morphological, biochemical and 3-D culture features.
  • RESULTS: Under 2-D conditions, cells displayed three distinct morphologies: spread, spindle, and intermediate.
  • We found that spread and spindle cells have similar levels of alpha-SMA, a desmoplastic marker, and consistent ratios of pFAKY(397)/totalFAK.
  • In 3-D intermediate cultures, alpha-SMA levels were virtually undetectable while pFAKY(397)/totalFAK ratios were low.
  • In addition, we used confocal microscopy to assess in vivo-like extracellular matrix topography, nuclei morphology and alpha-SMA features in the 3-D cultures.

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  • (PMID = 18448156.001).
  • [ISSN] 1095-6859
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA109442; United States / NCI NIH HHS / CA / CA113451-03; United States / NCI NIH HHS / CA / R01 CA113451-03; United States / NCI NIH HHS / CA / R01-CA113451; United States / NCI NIH HHS / CA / R01 CA113451; United States / NCI NIH HHS / CA / CA109442-02; United States / NCI NIH HHS / CA / R21 CA109442-02; United States / NCI NIH HHS / CA / R01 CA113451-02; United States / NCI NIH HHS / CA / R01 CA113451-01A2; United States / NCI NIH HHS / CA / P50 CA083638; United States / NCI NIH HHS / CA / CA113451-02; United States / NCI NIH HHS / CA / P30 CA006927; United States / NCI NIH HHS / CA / R21 CA109442-01; United States / NCI NIH HHS / CA / CA109442-01; United States / NCI NIH HHS / CA / CA113451-01A2; United States / NCI NIH HHS / CA / CA-06927
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS59278; NLM/ PMC2612536
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27. Wei H, Wang C, Chen L: Proliferating cell nuclear antigen, survivin, and CD34 expressions in pancreatic cancer and their correlation with hypoxia-inducible factor 1alpha. Pancreas; 2006 Mar;32(2):159-63
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  • [Title] Proliferating cell nuclear antigen, survivin, and CD34 expressions in pancreatic cancer and their correlation with hypoxia-inducible factor 1alpha.
  • OBJECTIVE: Hypoxia-inducible factor 1alpha (HIF-1alpha) has been universally detected in many types of cells and plays a key role in modulation of tumor-related genes.
  • The purpose of this study was to explore the relationship between HIF-1alpha messenger RNA (mRNA) expression and biologic characteristics in pancreatic cancer, such as tumor angiogenesis, tumor cell proliferation, differentiation, apoptosis, and metastasis.
  • The expressions of survivin, proliferating cell nuclear antigen (PCNA), and CD34 proteins were measured immunohistochemically.
  • RESULTS: There was very significant difference in the expression of HIF-1alpha between the pancreatic cancer tissue and adjacent normal tissue (P < 0.01), but no significant difference was found among tumor histopathologic grades (P > 0.05).
  • There was significant difference in the expression of HIF-1alpha mRNA between Japanese Pancreatic Society stages I to II and stages III to IV (P < 0.05).
  • CONCLUSION: The expression level of HIF-1alpha mRNA is surmised to have a significant correlation with tumor angiogenesis, cell proliferation, apoptosis, and metastasis.
  • Inhibition of HIF-1alpha may be an important and approachable therapeutic target for pancreatic cancer.
  • [MeSH-major] Antigens, CD34 / genetics. Microtubule-Associated Proteins / genetics. Neoplasm Proteins / genetics. Pancreatic Neoplasms / genetics. Proliferating Cell Nuclear Antigen / genetics
  • [MeSH-minor] DNA Primers. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Inhibitor of Apoptosis Proteins. Neoplasm Staging. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis

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  • (PMID = 16552335.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / BIRC5 protein, human; 0 / DNA Primers; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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28. Wei HY, Chen LB, Wang CY: [Correlation of mRNA expression of hypoxia inducible factor-1alpha to biological features of pancreatic cancer]. Ai Zheng; 2005 Feb;24(2):184-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Correlation of mRNA expression of hypoxia inducible factor-1alpha to biological features of pancreatic cancer].
  • BACKGROUND & OBJECTIVE: Hypoxia inducible factor-1alpha(HIF-1alpha) is universally expressed in many types of cells, and plays a key role in modulation of tumor related genes under hypoxia.
  • Our research was to detect mRNA expression of HIF-1alpha,and explore its relationship with biological characteristics of pancreatic cancer, such as tumor angiogenesis, tumor cell proliferation, differentiation, and metastasis.
  • METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect mRNA expression of HIF-1alpha in 50 specimens of pancreatic cancer tissues and relevant adjacent tissues.
  • Expressions of Survivin, proliferating cell nuclear antigen (PCNA), and CD34 were measured by SP immunohistochemistry.
  • RESULTS: mRNA level of HIF-1alpha in pancreatic cancer tissues was significantly higher than that in adjacent tissues (0.77+/-0.04 vs. 0.56+/-0.01, P < 0.01).
  • No significant difference in mRNA expression of HIF-1alpha was observed among tumor tissues of different pathologic grades (P > 0.05).
  • mRNA level of HIF-1alpha in pancreatic cancer tissues of stages I-II was significantly higher than that in cancer tissues of stages III-IV (0.79+/-0.05 vs. 0.76+/-0.04, P < 0.05).
  • CONCLUSION: mRNA expression of HIF-1alpha has significant correlations with tumor angiogenesis, cell proliferation, apoptosis, and metastasis of pancreatic cancer.
  • [MeSH-major] Antigens, CD34 / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Pancreatic Neoplasms / metabolism. Proliferating Cell Nuclear Antigen / metabolism
  • [MeSH-minor] Adult. Aged. Apoptosis. Cell Proliferation. Female. Humans. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Neoplasm Staging. Neovascularization, Pathologic. Pancreas / metabolism. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 15694030.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / BIRC5 protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proliferating Cell Nuclear Antigen; 0 / RNA, Messenger
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29. Tomimaru Y, Eguchi H, Nagano H, Wada H, Tomokuni A, Kobayashi S, Marubashi S, Takeda Y, Tanemura M, Umeshita K, Doki Y, Mori M: MicroRNA-21 induces resistance to the anti-tumour effect of interferon-α/5-fluorouracil in hepatocellular carcinoma cells. Br J Cancer; 2010 Nov 9;103(10):1617-26
Hazardous Substances Data Bank. FLUOROURACIL .

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  • [Title] MicroRNA-21 induces resistance to the anti-tumour effect of interferon-α/5-fluorouracil in hepatocellular carcinoma cells.
  • The aim of this study was to investigate the anti-tumour effects of microRNA (miR)-21 on the sensitivity of HCC cells to IFN-α/5-FU and whether miR-21 can be used as a predictor of the response to such therapy in HCC.
  • METHODS: Changes in the sensitivity of HCC cells (PLC/PRF/5 and HepG2) to IFN-α/5-FU were examined after transfection with pre-miR-21 or anti-miR-21.
  • RESULTS: Hepatocellular carcinoma cells transfected with pre-miR-21 were significantly resistant to IFN-α/5-FU.
  • Annexin V assay showed that the percentage of apoptotic cells was significantly lower in cells transfected with pre-miR-21 than control cells.
  • Transfection of anti-miR-21 rendered HCC cells sensitive to IFN-α/5-FU, and such sensitivity was weakened by transfection of siRNAs of target molecules, PETN and PDCD4. miR-21 expression in clinical HCC specimens was significantly associated with the clinical response to the IFN-α/5-FU combination therapy and survival rate.
  • CONCLUSIONS: The miR-21 in HCC cell lines and clinical HCC samples is a significant modulator of the anti-tumour effect of IFN-α and 5-FU.
  • [MeSH-major] Carcinoma, Hepatocellular / drug therapy. Liver Neoplasms / drug therapy. MicroRNAs / genetics
  • [MeSH-minor] Antineoplastic Agents / antagonists & inhibitors. Antineoplastic Agents / therapeutic use. Cell Division / drug effects. DNA Primers. Drug Evaluation, Preclinical. Drug Resistance. Drug Resistance, Neoplasm. Fluorouracil / antagonists & inhibitors. Fluorouracil / therapeutic use. Humans. Immunohistochemistry. Interferon-alpha / antagonists & inhibitors. Interferon-alpha / therapeutic use. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Transfection

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  • (PMID = 20978511.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA Primers; 0 / Interferon-alpha; 0 / MicroRNAs; 0 / RNA, Messenger; 0 / RNA, Neoplasm; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2990590
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30. Lindzen M, Lavi S, Leitner O, Yarden Y: Tailored cancer immunotherapy using combinations of chemotherapy and a mixture of antibodies against EGF-receptor ligands. Proc Natl Acad Sci U S A; 2010 Jul 13;107(28):12559-63
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  • [Title] Tailored cancer immunotherapy using combinations of chemotherapy and a mixture of antibodies against EGF-receptor ligands.
  • Growth factors are implicated in several processes essential for cancer progression.
  • Specifically, growth factors that bind to ErbB family receptors have been implicated in cell proliferation and in resistance of solid tumors to chemotherapy.
  • We quantified ligand secretion by several human cancer cell lines, and generated mAbs against two ligands, namely TGF-alpha and heparin-binding EGF-like growth factor.
  • These growth factors are frequently secreted by pancreatic tumor cell lines, including BxPC3 cells.
  • The monoclonal antibodies were tested for their antigen specificity and ability to inhibit growth of BxPC3 cells in vitro.
  • Combining the two antibodies resulted in enhanced inhibition of BxPC3 cell growth, both in vitro and in tumor-bearing animals.
  • Hence, we combined the two antibodies with gemcitabine, an effective chemotherapeutic drug commonly used to treat pancreatic cancer patients.
  • Because treatment with a combination of two monoclonal antibodies enhanced the ability of chemotherapy to inhibit BxPC3 tumors in mice, we propose a general cancer therapeutic strategy that entails profiling the repertoire of growth factors secreted by a tumor, and combining with chemotherapy several antibodies capable of blocking autocrine ligands.

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  • (PMID = 20616021.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA072981; United States / NCI NIH HHS / CA / R37 CA072981; United States / NCI NIH HHS / CA / CA072981
  • [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 / Antibodies; 0 / Antibodies, Monoclonal; 0 / HBEGF protein, human; 0 / Hbegf protein, mouse; 0 / Heparin-binding EGF-like Growth Factor; 0 / Intercellular Signaling Peptides and Proteins; 0 / Transforming Growth Factor alpha; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2906586
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31. Farrow B, Rowley D, Dang T, Berger DH: Characterization of tumor-derived pancreatic stellate cells. J Surg Res; 2009 Nov;157(1):96-102
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  • [Title] Characterization of tumor-derived pancreatic stellate cells.
  • BACKGROUND: Pancreatic stellate cells (PSCs) are key mediators of the desmoplastic reaction that characterizes pancreatic adenocarcinoma.
  • We sought to isolate and characterize tumor-derived pancreatic stellate (TDPS) cells to further understand how these stromal cells influence pancreatic cancer behavior.
  • METHODS: We established a stable line of non-immortalized PSCs from a patient with pancreatic adenocarcinoma using a modified prolonged outgrowth method.
  • Cell staining for cytokeratin, vimentin, and alpha smooth muscle actin (alphaSMA) was performed.
  • Total RNA was harvested from TDPS and panc-1 cells and gene expression determined by microarray analysis.
  • RESULTS: TDPS cells contain lipid droplets in the cytoplasm, and later stain positive for both vimentin and alphaSMA, indicative of activated myofibroblasts.
  • Microarray analysis revealed a distinct gene expression profile compared with pancreatic cancer cells, including expression of proteases that facilitate cancer cell invasion and growth factors known to activate pancreatic cancer cells.
  • Additionally, TDPS cells expressed many of the key components of the pancreatic tumor stroma, including collagen, fibronectin, and S100A4, confirming their importance in the tumor microenvironment.
  • CONCLUSIONS: Characterization of tumor-derived PSCs will facilitate further studies to determine how the tumor microenvironment promotes the aggressive behavior of pancreatic cancer.
  • [MeSH-major] Adenocarcinoma / pathology. Cell Culture Techniques / methods. Pancreatic Neoplasms / pathology. Stromal Cells / cytology. Stromal Cells / physiology
  • [MeSH-minor] Actins / metabolism. Cell Communication. Fibroblasts / cytology. Fibroblasts / physiology. Gene Expression Regulation, Neoplastic. Humans. Keratins / metabolism. Oligonucleotide Array Sequence Analysis. Phenotype. Tumor Cells, Cultured. Vimentin / metabolism

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  • (PMID = 19726060.001).
  • [ISSN] 1095-8673
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Vimentin; 68238-35-7 / Keratins
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32. Issa Y, Nummer D, Seibel T, Müerköster SS, Koch M, Schmitz-Winnenthal FH, Galindo L, Weitz J, Beckhove P, Altevogt P: Enhanced L1CAM expression on pancreatic tumor endothelium mediates selective tumor cell transmigration. J Mol Med (Berl); 2009 Jan;87(1):99-112
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  • [Title] Enhanced L1CAM expression on pancreatic tumor endothelium mediates selective tumor cell transmigration.
  • L1 cell adhesion molecule (L1CAM) is a transmembrane cell adhesion molecule initially defined as a promigratory molecule in the developing nervous system that appears to be also expressed in some endothelial cells.
  • However, little is known about the functional role of L1CAM on endothelial cells.
  • We observed that L1CAM expression was selectively enhanced on endothelium associated with pancreatic adenocarcinoma in situ and on cultured pancreatic tumor-derived endothelial cells in vitro.
  • L1CAM expression of endothelial cells could be augmented by incubation with immunomodulatory cytokines such as tumor necrosis factor alpha, interferon gamma, or transforming growth factor beta 1.
  • Antibodies to L1CAM and the respective ligand neuropilin-1 blocked tube formation and stromal cell-derived factor 1beta induced transmigration of tumor endothelial cells in vitro.
  • L1CAM expression on tumor-derived-endothelial cells enhanced Panc1 carcinoma cell adhesion to endothelial cell monolayers and transendothelial migration.
  • Our data demonstrate a functional role of L1CAM expression on tumor endothelium that could favor metastasis and angiogenesis during tumor progression.
  • [MeSH-major] Adenocarcinoma / metabolism. Cell Movement. Endothelium / metabolism. Gene Expression Regulation, Neoplastic. Neoplasm Proteins / biosynthesis. Neural Cell Adhesion Molecule L1 / biosynthesis. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Antibodies, Neoplasm / pharmacology. Cytokines / pharmacology. Humans. Neoplasm Metastasis. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / pathology. Neuropilin-1 / antagonists & inhibitors. Neuropilin-1 / metabolism. Tumor Cells, Cultured

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  • (PMID = 18931829.001).
  • [ISSN] 0946-2716
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Cytokines; 0 / Neoplasm Proteins; 0 / Neural Cell Adhesion Molecule L1; 144713-63-3 / Neuropilin-1
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33. Reiser-Erkan C, Erkan M, Pan Z, Bekasi S, Giese NA, Streit S, Michalski CW, Friess H, Kleeff J: Hypoxia-inducible proto-oncogene Pim-1 is a prognostic marker in pancreatic ductal adenocarcinoma. Cancer Biol Ther; 2008 Sep;7(9):1352-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypoxia-inducible proto-oncogene Pim-1 is a prognostic marker in pancreatic ductal adenocarcinoma.
  • BACKGROUND: Pim-1 is a proto-oncogene involved in cell survival, differentiation and proliferation in several hematologic and epithelial malignancies.
  • Clinically, absence of Pim-1 expression correlates with poor prognosis in prostate cancer.
  • In the present study, the expression of Pim-1 is analyzed in pancreatic cancer and correlated to clinicopathological parameters.
  • RESULTS: Compared to benign, inflammatory and pre-malignant conditions (i.e., the normal pancreas, chronic pancreatitis and benign intraductal papillary mucinous neoplasm), expression of Pim-1 mRNA and protein increased significantly in pancreatic malignancies.
  • Absence of Pim-1 immunopositivity in cancer cells strongly correlated with a poor prognosis (median survival 13.8 vs. 23.4 months, p = 0.0016).
  • In vitro, rapidly dividing (high versus low serum concentrations) and hypoxic cells displayed higher Pim-1 mRNA and protein levels.
  • Ex vivo expression analysis using semi-quantitative immunohistochemistry was performed using human pancreatic tissues of the normal pancreas (n = 10), chronic pancreatitis (n = 30), pancreatic ductal adenocarcinoma (n = 59) and other pancreatic tumors (n = 42).
  • In consecutive sections HIF1-alpha was used as a marker of hypoxia.
  • In vitro analyses were performed using cultured pancreatic cancer cell lines (n = 8) and primary human pancreatic stellate cells.
  • Compared to non-malignant tissues Pim-1 significantly increases in pancreatic cancer.
  • However, the presence of Pim-1 in cancer cells has a positive prognostic impact.
  • [MeSH-major] Anoxia / metabolism. Biomarkers, Tumor / analysis. Carcinoma, Pancreatic Ductal / genetics. Pancreatic Neoplasms / genetics. Proto-Oncogene Proteins c-pim-1 / analysis

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  • [CommentIn] Cancer Biol Ther. 2008 Sep;7(9):1360-1 [18836287.001]
  • (PMID = 18708761.001).
  • [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 / Biomarkers, Tumor; EC 2.7.11.1 / PIM1 protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-pim-1
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34. Libé R, Chanson P: [Endocrine tumors of the pancreas (EPTs) in multiple endocrine neoplasia (MEN1): up-date on prognostic factors, diagnostic procedures and treatment]. Ann Endocrinol (Paris); 2007 Jun;68 Suppl 1:1-8
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  • [Title] [Endocrine tumors of the pancreas (EPTs) in multiple endocrine neoplasia (MEN1): up-date on prognostic factors, diagnostic procedures and treatment].
  • [Transliterated title] Les tumeurs endocrines du pancréas lors de la néoplasie endocrinienne multiple type 1 (NEM1): actualités sur les facteurs pronostiques, l'imagerie et le traitement.
  • Endocrine pancreatic tumors (EPTs) are uncommon tumors, representing 1-2% of all pancreatic neoplasms.
  • They are categorized on the basis of their clinical features into functioning and non-functioning tumors.
  • EPTs may be part of the multiple endocrine neoplasia type 1 (MEN 1), an autosomal dominant syndrome due to inactivating germline mutation of the menin gene.
  • Somatic mutations of menin are present in about 20% of sporadic neoplasms, particularly gastrinomas and insulinomas.
  • Among the different imaging techniques, echoendoscopy, computed tomography (CT) and magnetic resonance imaging (MRI) are indicated for the detection of the primary tumor, but (III)In-octreotide scintigraphy has the highest sensitivity for detecting metastases.
  • The choice of treatment is still debated and is different when the tumor occurs as a part of the MEN syndrome.
  • The medical treatment includes somatostatin analogues (SA), chemotherapy and interferon-alpha (IFN-alpha).
  • Chemotherapy, which is generally proposed as a combination of streptozotocin (STZ) and 5-fluorouracil (5-FU) or doxorubicin, is indicated when the tumors tend to grow.
  • Interferon-alpha (IFN-alpha) stimulates the immune system, blocks the tumor cells in the G1/S-phase of the cell cycle, inhibits protein and hormone synthesis and inhibits angionenesis.
  • Treatment with IFN has been shown to produce symptomatic response in 40-60% of patients, a biochemical response in 30-60% and tumor shrinkage in 10-15%.
  • [MeSH-major] Carcinoma, Islet Cell. Multiple Endocrine Neoplasia Type 1

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  • [ErratumIn] Ann Endocrinol (Paris). 2008 Nov;69(5):459-60
  • (PMID = 17961653.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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35. Uchida H, Sasaki A, Iwaki K, Tominaga M, Yada K, Iwashita Y, Shibata K, Matsumoto T, Ohta M, Kitano S: An extramural gastrointestinal stromal tumor of the duodenum mimicking a pancreatic head tumor. J Hepatobiliary Pancreat Surg; 2005;12(4):324-7
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  • [Title] An extramural gastrointestinal stromal tumor of the duodenum mimicking a pancreatic head tumor.
  • We report the case of a 53-year-old woman with a gastrointestinal stromal tumor (GIST) of the duodenum that showed only extramural growth, mimicking a pancreatic tumor.
  • Preoperatively, computed tomography (CT) and angiography revealed a hypervascular mass, 3.0 cm in diameter, in the pancreatic head.
  • Hypotonic duodenography showed compression of the second and third portions of the duodenum by the pancreatic lesion.
  • The pancreatic head tumor was diagnosed preoperatively as a nonfunctioning islet cell tumor of the pancreas, and the patient underwent pylorus-preserving pancreaticoduodenectomy.
  • A hard mass was palpated intraoperatively in the pancreatic head region, and neither peritoneal dissemination nor metastasis was detected.
  • Histologically, the tumor was composed of spindle-shaped cells with a fascicular growth pattern, and only a few mitotic features were seen.
  • Immunohistochemically, most of the tumor cells were positive for c-kit oncoprotein and CD34, but negative for alpha-smooth muscle actin and S-100 protein.
  • Therefore, this neoplasm was finally diagnosed as a duodenal GIST of the uncommitted type.
  • This is a rare case of a duodenal GIST with exclusively extramural growth mimicking a pancreatic head tumor.
  • [MeSH-major] Duodenal Neoplasms / pathology. Gastrointestinal Stromal Tumors / pathology. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Middle Aged

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  • (PMID = 16133702.001).
  • [ISSN] 0944-1166
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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36. Cao D, Maitra A, Saavedra JA, Klimstra DS, Adsay NV, Hruban RH: Expression of novel markers of pancreatic ductal adenocarcinoma in pancreatic nonductal neoplasms: additional evidence of different genetic pathways. Mod Pathol; 2005 Jun;18(6):752-61
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  • [Title] Expression of novel markers of pancreatic ductal adenocarcinoma in pancreatic nonductal neoplasms: additional evidence of different genetic pathways.
  • Solid pseudopapillary tumor, pancreatoblastoma, undifferentiated carcinoma with osteoclastic-like giant cells, and acinar cell carcinomas are rare pancreatic nonductal neoplasms.
  • Compared to the significant advances in our understanding of the pathogenesis of pancreatic ductal adenocarcinomas in the last decades, the molecular mechanisms underlying pancreatic nonductal neoplasms are poorly understood.
  • In order to elucidate their molecular pathogenesis, we constructed tissue microarrays to study the expression of some novel pancreatic ductal adenocarcinoma-associated tumor markers in these nonductal pancreatic neoplasms.
  • We analyzed nine markers including tumor suppressor gene (14-3-3 sigma), proliferation marker (topoisomerase II alpha), epithelial markers (prostate stem cell antigen, mesothelin and cytokeratin 19), stromal markers (fascin, hsp47 and fibronectin), and gamma-synuclein whose function is not delineated.
  • In addition, we included tumor suppressor gene DPC4 and oncogene Beta-catenin to further confirm their expression in pancreatic nonductal tumors.
  • Our results showed that in contrast to pancreatic ductal adenocarcinomas that show loss of Dpc4 protein in 55% of cases, loss of Dpc4 expression is absent in pancreatic nonductal neoplasms.
  • Expression of 14-3-3 sigma is frequently seen in both pancreatic nonductal neoplasms (25-100%) and ductal adenocarcinomas (89%).
  • Aberrant nuclear expression of beta-catenin is common in pancreatic nonductal neoplasms, specifically in solid pseudopapillary tumors (88%) and pancreatoblastomas (100%) but is rarely seen in pancreatic ductal adenocarcinomas (<5%).
  • Expression of topoisomerase II alpha is not seen in solid pseudopapillary tumors and undifferentiated carcinomas with osteoclastic-like giant cells but is focally seen in pancreatoblastomas (50%) and acinar cell carcinomas (85%).
  • Expression of PSCA and mesothelin was observed in pancreatic nonductal neoplasms but their expression was seen less frequently (0-50%) and weaker than that in pancreatic ductal adenocarcinomas (60-100%).
  • CK19, a marker of pancreatic ductal adenocarcinomas, is not expressed in pancreatic nonductal neoplasms.
  • Our findings indicate pancreatic nonductal neoplasms have distinctive patterns of protein expression relative to pancreatic ductal adenocarcinomas and suggest that pancreatic nonductal neoplasms have different genetic pathways from the more common pancreatic ductal adenocarcinomas.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] 14-3-3 Proteins. Antigens, Neoplasm. Carcinoma, Acinar Cell / metabolism. Carcinoma, Acinar Cell / pathology. Carrier Proteins / analysis. Cytoskeletal Proteins / analysis. DNA-Binding Proteins / analysis. Exonucleases / analysis. Exoribonucleases. Fibronectins / analysis. GPI-Linked Proteins. HSP47 Heat-Shock Proteins. Heat-Shock Proteins / analysis. Humans. Immunohistochemistry. Keratins / analysis. Membrane Glycoproteins / analysis. Microfilament Proteins / analysis. Neoplasm Proteins / analysis. Nerve Tissue Proteins / analysis. Serpins / analysis. Smad4 Protein. Synucleins. Trans-Activators / analysis. beta Catenin. gamma-Synuclein

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  • (PMID = 15696124.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA62924
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 14-3-3 Proteins; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / Carrier Proteins; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Fibronectins; 0 / GPI-Linked Proteins; 0 / HSP47 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / Membrane Glycoproteins; 0 / Microfilament Proteins; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / PSCA protein, human; 0 / SERPINH1 protein, human; 0 / SMAD4 protein, human; 0 / Serpins; 0 / Smad4 Protein; 0 / Synucleins; 0 / Trans-Activators; 0 / beta Catenin; 0 / gamma-Synuclein; 0 / mesothelin; 146808-54-0 / fascin; 68238-35-7 / Keratins; EC 3.1.- / Exonucleases; EC 3.1.- / Exoribonucleases; EC 3.1.- / SFN protein, human
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37. Pejcić I, Vrbić S, Filipović S, Sćekić M, Petković I, Pejcić L, Djenić N: [Significance of serum tumor markers monitoring metastases in carcinomas of unknown primary site]. Vojnosanit Pregl; 2010 Sep;67(9):723-31
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  • [Title] [Significance of serum tumor markers monitoring metastases in carcinomas of unknown primary site].
  • BACKGROUND/AIM: Unknown primary tumors represent a heterogeneous group of malignancies that are indicative of ominous prognosis.
  • Cancer of unknown primary site (CUP) is defined as the lack of any detectable primary site after full evaluation, and accounts for approximately 3-5% of all newly diagnosed patients with malignancies.
  • The aim of this report was to present the prognostic and predictive value of 8 serum tumor markers in this group of patients.
  • On histological examination, all the patients were presented with metastatic tumors whose primary site (origin) could not be detected with noninvasive diagnostic techniques.
  • In all the cases we evaluated 8 serum tumor markers: alpha-fetoproteins (AFP), chronic gonadotrophin beta submit, human (beta-HCG), neuron specific enolase (NSE), marker of malignant ovarian tumors (CA 125), prostate-specific antigene (PSA), marker of malignant brest tumor (CA 15-3), marker of malignant pancreas tumor and gastrointestinal tumor (Ca 19-9), carcinoembryonic antigen (CEA) at the time of diagnosis.
  • The patients responding to chemotherapy with complete response (CR), partial response (PR) or stable disease (SD) had the markers determined after three-month periods until the time of relapse or progression.
  • Average tumor marker values before and after the chemotherapy were significantly lower for NSE and CA 125.
  • CONCLUSION: Increased values of serum tumor markers are very often in CUP.
  • The tumors show nonspecific overexpression of tumor markers.
  • However, a routine evaluation of commonly used serum tumor markers has not been proven of any prognostic and predictive assistance.
  • [MeSH-major] Adenocarcinoma / secondary. Biomarkers, Tumor / blood. Carcinoma / secondary. Carcinoma, Squamous Cell / secondary. Neoplasms, Unknown Primary / pathology


38. Harikumar KB, Sung B, Tharakan ST, Pandey MK, Joy B, Guha S, Krishnan S, Aggarwal BB: Sesamin manifests chemopreventive effects through the suppression of NF-kappa B-regulated cell survival, proliferation, invasion, and angiogenic gene products. Mol Cancer Res; 2010 May;8(5):751-61
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  • [Title] Sesamin manifests chemopreventive effects through the suppression of NF-kappa B-regulated cell survival, proliferation, invasion, and angiogenic gene products.
  • Agents that are safe, affordable, and efficacious are urgently needed for the prevention of chronic diseases such as cancer.
  • Because the transcription factor NF-kappaB has been associated with inflammation, carcinogenesis, tumor cell survival, proliferation, invasion, and angiogenesis of cancer, we postulated that sesamin might mediate its effect through the modulation of the NF-kappaB pathway.
  • We found that sesamin inhibited the proliferation of a wide variety of tumor cells including leukemia, multiple myeloma, and cancers of the colon, prostate, breast, pancreas, and lung.
  • Sesamin also potentiated tumor necrosis factor-alpha-induced apoptosis and this correlated with the suppression of gene products linked to cell survival (e.g., Bcl-2 and survivin), proliferation (e.g., cyclin D1), inflammation (e.g., cyclooxygenase-2), invasion (e.g., matrix metalloproteinase-9, intercellular adhesion molecule 1), and angiogenesis (e.g., vascular endothelial growth factor).
  • Overall, our results showed that sesamin may have potential against cancer and other chronic diseases through the suppression of a pathway linked to the NF-kappaB signaling.

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  • (PMID = 20460401.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-124787-01A2; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P01 CA124787; United States / NCI NIH HHS / CA / P01 CA091844-020004; United States / NCI NIH HHS / CA / P01 CA091844; United States / NCI NIH HHS / CA / CA-16 672; United States / NCI NIH HHS / CA / CA124787-020002; United States / NCI NIH HHS / CA / CA091844-010004; United States / NCI NIH HHS / CA / P01 CA124787-01A20002; United States / NCI NIH HHS / CA / P01 CA091844-010004; United States / NCI NIH HHS / CA / CA091844-020004; United States / NCI NIH HHS / CA / CA124787-01A20002; United States / NCI NIH HHS / CA / P01 CA124787-020002
  • [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 / Angiogenic Proteins; 0 / Antineoplastic Agents; 0 / Antioxidants; 0 / Dioxoles; 0 / Growth Inhibitors; 0 / Lignans; 0 / NF-kappa B; 8008-74-0 / Sesame Oil; S7946O4P76 / sesamin
  • [Other-IDs] NLM/ NIHMS196068; NLM/ PMC2895997
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39. Santos AM, Jung J, Aziz N, Kissil JL, Puré E: Targeting fibroblast activation protein inhibits tumor stromagenesis and growth in mice. J Clin Invest; 2009 Dec;119(12):3613-25
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting fibroblast activation protein inhibits tumor stromagenesis and growth in mice.
  • As the cell surface serine protease fibroblast activation protein (FAP) is selectively expressed on tumor-associated fibroblasts and pericytes in epithelial tumors, we set out to investigate the role of FAP in mouse models of epithelial-derived solid tumors.
  • In this study, we demonstrate that genetic deletion and pharmacologic inhibition of FAP inhibited tumor growth in both an endogenous mouse model of lung cancer driven by the K-rasG12D mutant and a mouse model of colon cancer, in which CT26 mouse colon cancer cells were transplanted into immune competent syngeneic mice.
  • Interestingly, growth of only the K-rasG12D-driven lung tumors was also attenuated by inhibition of the closely related protease dipeptidyl peptidase IV (DPPIV).
  • Our results indicate that FAP depletion inhibits tumor cell proliferation indirectly, increases accumulation of collagen, decreases myofibroblast content, and decreases blood vessel density in tumors.
  • These data provide proof of principle that targeting stromal cell-mediated modifications of the tumor microenvironment may be an effective approach to treating epithelial-derived solid tumors.

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  • (PMID = 19920354.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA124495; United States / NCI NIH HHS / CA / T32 CA009171; United States / NCI NIH HHS / CA / T32 CA09171
  • [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 / 1-(((3-hydroxy-1-adamantyl)amino)acetyl)-2-cyanopyrrolidine; 0 / Membrane Proteins; 0 / Protease Inhibitors; 0 / Pyrrolidines; 9007-34-5 / Collagen; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases; PJY633525U / Adamantane
  • [Other-IDs] NLM/ PMC2786791
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40. Guan Y, Reddy KR, Zhu Q, Li Y, Lee K, Weerasinghe P, Prchal J, Semenza GL, Jing N: G-rich oligonucleotides inhibit HIF-1alpha and HIF-2alpha and block tumor growth. Mol Ther; 2010 Jan;18(1):188-97
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  • [Title] G-rich oligonucleotides inhibit HIF-1alpha and HIF-2alpha and block tumor growth.
  • Hypoxia-inducible factor-1 (HIF-1) plays crucial roles in tumor promotion by upregulating its target genes, which are involved in energy metabolism, angiogenesis, cell survival, invasion, metastasis, and drug resistance.
  • The HIF-1alpha subunit, which is regulated by O2-dependent hydroxylation, ubiquitination, and degradation, has been identified as an important molecular target for cancer therapy.
  • We have rationally designed G-rich oligodeoxynucleotides (ODNs) as inhibitors of HIF-1alpha for human cancer therapy.
  • The lead compounds, JG243 and JG244, which form an intramolecular parallel G-quartet structure, selectively target HIF-1alpha and decreased levels of both HIF-1alpha and HIF-2alpha (IC50 < 2 micromol/l) and also inhibited the expression of HIF-1-regulated proteins [vascular endothelial growth factor (VEGF), Bcl-2, and Bcl-XL], but did not disrupt the expression of p300, Stat3, or p53.
  • JG243 and JG244 dramatically suppressed the growth of prostate, breast, and pancreatic tumor xenografts.
  • Western blots from tumor tissues showed that JG-ODNs significantly decreased HIF-1alpha and HIF-2alpha levels and blocked the expression of VEGF.
  • The JG-ODNs are novel anticancer agents that suppress tumor growth by inhibiting HIF-1.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / antagonists & inhibitors. Hypoxia-Inducible Factor 1, alpha Subunit / antagonists & inhibitors. Neoplasms / drug therapy. Oligonucleotides / therapeutic use
  • [MeSH-minor] Animals. Blotting, Western. Breast Neoplasms / drug therapy. Cell Line, Tumor. Female. Humans. Magnetic Resonance Spectroscopy. Male. Mice. Mice, Nude. Prostatic Neoplasms / drug therapy. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19755960.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA104035; United States / NIDDK NIH HHS / DK / T32 DK060445; United States / NCI NIH HHS / CA / CA104035; United States / NIDDK NIH HHS / DK / T32 DK60445
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / ODN JG244; 0 / Oligonucleotides; 0 / endothelial PAS domain-containing protein 1
  • [Other-IDs] NLM/ PMC2839212
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41. Tapia B, Ahrens W, Kenney B, Touloukian R, Reyes-Múgica M: Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature. Pediatr Dev Pathol; 2008 Sep-Oct;11(5):384-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature.
  • Primary epithelial tumors of the pancreas are extremely uncommon in children, and among these, acinar cell carcinoma (ACC) is the most rare.
  • The histologic diagnosis of ACC was supported by both immunohistochemistry and electron microscopy.
  • Despite its rarity, ACC should be kept in the differential diagnosis of pediatric pancreatic exocrine tumors.
  • We also provide a comparison with an example of solid pseudopapillary tumor, another relatively infrequent epithelial tumor of the pancreas in the young.
  • We review the relevant literature addressing the clinical and pathologic features of ACC and its distinction from other pancreatic neoplasms.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / pathology. Pancreatic Cyst / pathology. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Child. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Pancreatectomy. Treatment Outcome. alpha 1-Antitrypsin / metabolism

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  • (PMID = 19006424.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SERPINA1 protein, human; 0 / alpha 1-Antitrypsin
  • [Number-of-references] 37
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42. Fétaud V, Frossard JL, Farina A, Pastor CM, Bühler L, Dumonceau JM, Hadengue A, Hochstrasser DF, Lescuyer P: Proteomic profiling in an animal model of acute pancreatitis. Proteomics; 2008 Sep;8(17):3621-31
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  • Acute pancreatitis (AP) is an inflammatory disease of the pancreas, which evolves in approximately 20% of the patients to a severe illness associated with a high mortality rate.
  • In this study, we performed a comparative proteomic analysis of pancreatic tissue extracts from rats with AP and healthy rodent controls in order to identify changes in protein expression related to the pathobiological processes of this disease.
  • Pancreatic extracts from diseased and controls rats were analyzed by 2-DE and MS/MS.
  • Comparative analysis allowed the detection of 42 proteins or protein fragments differentially expressed between diseased and control pancreas, some of them being newly described in AP.
  • Interestingly, these changes were representative of the main pathobiological pathways involved in this disease.
  • We observed activation of digestive proteases and increased expression of various inflammatory markers, including several members of the alpha-macroglobulin family.
  • We also detected changes related to oxidative and cell stress responses.
  • These results showed the interest of proteomic analysis to identify changes characterizing pancreatic tissue damage and, therefore, to highlight new potential biomarkers of AP.
  • [MeSH-minor] 14-3-3 Proteins / metabolism. Acute Disease. Animals. Antigens, Neoplasm / metabolism. Biomarkers / analysis. Biomarkers, Tumor / metabolism. Ceruletide. Disease Models, Animal. Electrophoresis, Gel, Two-Dimensional. Lectins, C-Type / metabolism. Lithostathine / metabolism. Male. Oxidative Stress / physiology. Pancreas / chemistry. Rats. Rats, Sprague-Dawley. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Tandem Mass Spectrometry

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  • (PMID = 18686302.001).
  • [ISSN] 1615-9861
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 14-3-3 Proteins; 0 / Antigens, Neoplasm; 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Lithostathine; 0 / pancreatitis-associated protein; 888Y08971B / Ceruletide
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43. Saif MW: Pancreatoblastoma. JOP; 2007;8(1):55-63
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

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  • Pancreatoblastoma (PB), or infantile pancreatic carcinoma, is an extremely rare pancreatic tumor in childhood, comprising 0.5% of pancreatic non-endocrine tumors.
  • Mechanical obstruction of the upper duodenum and gastric outlet by tumor in the head of the pancreas may be associated with vomiting, jaundice and gastrointestinal bleeding.
  • Histologically, PB is characterized with distinct acinar and squamoid cell differentiation.
  • The majority of these tumors arise in the head of the pancreas.
  • Alpha-fetoprotein may be elevated in up to 68% of patients with PB.
  • Ultrasound and CT scan may be useful but preoperative diagnosis is often quite difficult.
  • Prognosis of this rare tumor is good, when resected completely.
  • On the whole, PB is regarded to be a curable tumor; hence the clinical diagnosis should be made early.
  • Awareness of this rare tumor of pancreas is essential for early detection and proper management.
  • The author review the clinical presentation, etiology, diagnosis, treatment and prognosis of PB in this presentation.
  • [MeSH-major] Carcinoma / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Infant. Male. Middle Aged. Pancreas / pathology

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  • (PMID = 17228135.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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44. Ferrand A, Vatinel S, Kowalski-Chauvel A, Bertrand C, Escrieut C, Fourmy D, Dufresne M, Seva C: Mechanism for Src activation by the CCK2 receptor: Patho-physiological functions of this receptor in pancreas. World J Gastroenterol; 2006 Jul 28;12(28):4498-503
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  • [Title] Mechanism for Src activation by the CCK2 receptor: Patho-physiological functions of this receptor in pancreas.
  • AIM: To investigate in vivo, whether CCK2 receptors (CCK2R) regulate proteins known to play a crucial role in cell proliferation and cancer development and analyse in vitro the molecular mechanisms that lead to Src activation; in particular, to identify the domains within the CCK2R sequence that are implicated in this activation.
  • We used pancreatic tissues derived from wild type or Elas-CCK2 mice that expressed the CCK2R in pancreatic acini, displayed an increased pancreatic growth and developed preneoplastic lesions.
  • The pancreatic tumor cell line AR4-2J expressing the endogenous CCK2R or COS-7 cells transiently transfected with wild type or mutant CCK2R were used as in vitro models to study the mechanism of Src activation.
  • Src activation was measured by in vitro kinase assays, ERK activation by western blot using anti-phospho-ERK antibodies and the involvement of Src in gastrin-induced cell proliferation by MTT test.
  • RESULTS: We showed in vivo that the targeted CCK2R expression in the pancreas of Elas-CCK2 mice, led to the activation of Src and the ERK pathway.
  • Src was activated upstream of the ERK pathway by the CCK2R in pancreatic tumoral cells and contributed to the proliferative effects mediated by this receptor.
  • CONCLUSION: Deregulation of the Src/ERK pathway by the CCK2R might represent an early step that contributes to cell proliferation, formation of preneoplastic lesions and pancreatic tumor development.
  • [MeSH-major] Pancreas / metabolism. Pancreatic Neoplasms / physiopathology. Precancerous Conditions / physiopathology. Receptor, Cholecystokinin B / physiology. src-Family Kinases / metabolism
  • [MeSH-minor] Amino Acid Motifs / physiology. Animals. Cell Line. Cell Proliferation. Cell Transformation, Neoplastic. Enzyme Activation / physiology. Extracellular Signal-Regulated MAP Kinases / metabolism. GTP-Binding Protein alpha Subunits, Gq-G11 / physiology. Gene Expression Regulation. Gene Expression Regulation, Neoplastic. Mice. Mice, Transgenic. Protein Structure, Tertiary / physiology. Signal Transduction / physiology

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  • (PMID = 16874861.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Receptor, Cholecystokinin B; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gq-G11
  • [Other-IDs] NLM/ PMC4125636
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45. Liao DJ, Wang Y, Wu J, Adsay NV, Grignon D, Khanani F, Sarkar FH: Characterization of pancreatic lesions from MT-tgf alpha, Ela-myc and MT-tgf alpha/Ela-myc single and double transgenic mice. J Carcinog; 2006 Jul 05;5:19
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  • [Title] Characterization of pancreatic lesions from MT-tgf alpha, Ela-myc and MT-tgf alpha/Ela-myc single and double transgenic mice.
  • In order to identify good animal models for investigating therapeutic and preventive strategies for pancreatic cancer, we analyzed pancreatic lesions from several transgenic models and made a series of novel findings.
  • Female MT-tgf alpha mice of the MT100 line developed pancreatic proliferation, acinar-ductal metaplasia, multilocular cystic neoplasms, ductal adenocarcinomas and prominent fibrosis, while the lesions in males were less severe.
  • MT-tgf alpha-ES transgenic lines of both sexes developed slowly progressing lesions that were similar to what was seen in MT100 males.
  • In both MT100 and MT-tgf alpha-ES lines, TGF alpha transgene was expressed mainly in proliferating ductal cells.
  • Ela-myc transgenic mice with a mixed C57BL/6, SJL and FVB genetic background developed pancreatic tumors at 2-7 months of age, and half of the tumors were ductal adenocarcinomas, similar to what was reported originally by Sandgren et al 1.
  • However, in 20% of the mice, the tumors metastasized to the liver.
  • MT100/Ela-myc and MT-tgf alpha-ES/Ela-myc double transgenic mice developed not only acinar carcinomas and mixed carcinomas as previously reported but also various ductal-originated lesions, including multilocular cystic neoplasms and ductal adenocarcinomas.
  • The double transgenic tumors were more malignant and metastasized to the liver at a higher frequency (33%) compared with the Ela-myc tumors.
  • Sequencing of the coding region of p16ink4, k-ras and Rb cDNA in small numbers of pancreatic tumors did not identify mutations.
  • The short latency for tumor development, the variety of tumor morphology and the liver metastases seen in Ela-myc and MT-tgf alpha/Ela-myc mice make these animals good models for investigating new therapeutic and preventive strategies for pancreatic cancer.

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  • (PMID = 16822304.001).
  • [ISSN] 1477-3163
  • [Journal-full-title] Journal of carcinogenesis
  • [ISO-abbreviation] J Carcinog
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100864
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC1559682
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46. Rajpal S, Warren RS, Alexander M, Yeh BM, Grenert JP, Hintzen S, Ljung BM, Bergsland EK: Pancreatoblastoma in an adult: case report and review of the literature. J Gastrointest Surg; 2006 Jun;10(6):829-36
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  • An abdominal computed tomography scan demonstrated a 12 x 12-cm pancreatic mass involving the greater curvature of the stomach and multiple hypervascular hepatic metastases.
  • An initial fine needle aspiration of the pancreatic mass was nondiagnostic, and a subsequent fine needle aspiration of a liver mass was read as metastatic acinar cell carcinoma.
  • The patient underwent a palliative resection for tumor-associated pain and gastrointestinal hemorrhage that revealed a large pancreatic tumor invading through the full thickness of the colon at the splenic flexure and adherent to the posterior gastric wall.
  • The pathology from the distal pancreatectomy, splenectomy, partial gastrectomy, partial colectomy, and cholecystectomy unexpectedly supported a diagnosis of pancreatoblastoma with evidence for squamoid corpuscles as well as areas of acinar formation.
  • Despite multiple chemotherapy regimens, the patient's disease continued to progress in the liver and the lungs.
  • During the course of his therapy, the patient's serum alpha-fetoprotein levels and serum lipase levels rose concurrently, suggesting tumor-associated production of both of these factors.
  • Seventeen months after the diagnosis of metastatic pancreatoblastoma, the patient died from his disease.
  • Our case illustrates the fact that pancreatoblastomas are extremely difficult to diagnosis preoperatively.
  • In addition, our case demonstrates that pancreatoblastomas can be alpha-fetoprotein producing, hormone producing, and enzyme producing when it occurs in adults.
  • [MeSH-major] Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Abdominal Pain / etiology. Biopsy, Fine-Needle. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / secondary. Disease Progression. Humans. Immunohistochemistry. Liver Neoplasms / secondary. Male. Middle Aged. Nausea / etiology. Neoplasm Invasiveness. Satiety Response. Splenic Vein / diagnostic imaging. Splenic Vein / pathology. Stomach / pathology. Tomography, X-Ray Computed. Vomiting / etiology

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  • (PMID = 16769539.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 21
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47. Ikeda K, Iyama K, Ishikawa N, Egami H, Nakao M, Sado Y, Ninomiya Y, Baba H: Loss of expression of type IV collagen alpha5 and alpha6 chains in colorectal cancer associated with the hypermethylation of their promoter region. Am J Pathol; 2006 Mar;168(3):856-65
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  • [Title] Loss of expression of type IV collagen alpha5 and alpha6 chains in colorectal cancer associated with the hypermethylation of their promoter region.
  • Type IV collagen, a major component of the basement membrane (BM), is composed of six genetically distinct alpha(IV) chains, alpha1(IV) to alpha6(IV).
  • Loss of the alpha5(IV)/alpha6(IV) chains in epithelial BM occur in the early stage of cancer invasion.
  • However, the regulatory mechanism of the specific loss of the alpha5(IV)/alpha6(IV) chains during cancer cell invasion is still undetermined.
  • In the present study, we examined the expression of the alpha5(IV)/alpha6(IV) chains and the methylation profiles of the bidirectional promoter region of COL4A5/COL4A6 in colon cancer cell lines and colorectal tumor tissues.
  • The expression of the alpha5(IV)/alpha6(IV) chains was down-regulated in colorectal cancer, and the loss of expression of the alpha5(IV)/alpha6(IV) chains was associated with the hypermethylation of their promoter region.
  • In conclusion, the hypermethylation of the bidirectional promoter region of COL4A5/COL4A6 is one of the events that is responsible for the loss of expression of the alpha5(IV)/alpha6(IV) chains and the remodeling of the epithelial BM during cancer cell invasion.
  • [MeSH-major] Collagen Type IV / genetics. Colorectal Neoplasms / genetics. DNA Methylation. Gene Expression Regulation, Neoplastic. Promoter Regions, Genetic
  • [MeSH-minor] Aged. Aged, 80 and over. Azacitidine / pharmacology. Basement Membrane / metabolism. Cell Line, Tumor. Collagen / metabolism. DNA, Neoplasm / metabolism. Down-Regulation. Drug Combinations. Female. Genes, Neoplasm. Genes, Reporter. Humans. Laminin / metabolism. Male. Middle Aged. Neoplasm Invasiveness. Proteoglycans / metabolism. RNA, Messenger / analysis. RNA, Messenger / metabolism

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  • [CommentIn] Am J Pathol. 2006 Mar;168(3):715-7 [16507886.001]
  • (PMID = 16507901.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / COL4A5 protein, human; 0 / Collagen Type IV; 0 / DNA, Neoplasm; 0 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 0 / RNA, Messenger; 119978-18-6 / matrigel; 9007-34-5 / Collagen; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC1606532
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48. Yadav VR, Sung B, Prasad S, Kannappan R, Cho SG, Liu M, Chaturvedi MM, Aggarwal BB: Celastrol suppresses invasion of colon and pancreatic cancer cells through the downregulation of expression of CXCR4 chemokine receptor. J Mol Med (Berl); 2010 Dec;88(12):1243-53
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Celastrol suppresses invasion of colon and pancreatic cancer cells through the downregulation of expression of CXCR4 chemokine receptor.
  • Although metastasis accounts for >90% of cancer-related deaths, no therapeutic that targets this process has yet been approved.
  • Because the chemokine receptor CXCR4 is one of the targets closely linked with tumor metastasis, inhibitors of this receptor have the potential to abrogate metastasis.
  • In the current report, we demonstrate that celastrol can downregulate the CXCR4 expression on breast cancer MCF-7 cells stably transfected with HER2, an oncogene known to induce the chemokine receptor.
  • Downregulation of CXCR4 by the triterpenoid was not cell type-specific as downregulation occurred in colon cancer, squamous cell carcinoma, and pancreatic cancer cells.
  • Abrogation of the chemokine receptor by celastrol or by gene-silencing was accompanied by suppression of invasiveness of colon cancer cells induced by CXCL12, the ligand for CXCR4.
  • This effect was not cell type-specific as celastrol also abolished invasiveness of pancreatic tumor cells, and this effect again correlated with the disappearance of both the CXCR4 mRNA and CXCR4 protein.
  • Overall, these results show that celastrol has potential in suppressing invasion and metastasis of cancer cells by down-modulation of CXCR4 expression.

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  • [ErratumIn] J Mol Med (Berl). 2013 Mar;91(3):407-8
  • (PMID = 20798912.001).
  • [ISSN] 1432-1440
  • [Journal-full-title] Journal of molecular medicine (Berlin, Germany)
  • [ISO-abbreviation] J. Mol. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA124787; United States / NCI NIH HHS / CA / P01 CA124787-01A2; United States / NCI NIH HHS / CA / CA-124787-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / HSP90 Heat-Shock Proteins; 0 / NF-kappa B; 0 / Receptors, CXCR4; 0 / Triterpenes; 0 / Tumor Necrosis Factor-alpha; 34157-83-0 / tripterine
  • [Other-IDs] NLM/ NIHMS307553; NLM/ PMC3142743
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49. Zhang JJ, Wu HS, Wang L, Tian Y, Zhang JH, Wu HL: Expression and significance of TLR4 and HIF-1alpha in pancreatic ductal adenocarcinoma. World J Gastroenterol; 2010 Jun 21;16(23):2881-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and significance of TLR4 and HIF-1alpha in pancreatic ductal adenocarcinoma.
  • AIM: To investigate the expression of toll-like receptor (TLR) 4, nuclear factor-kappaB (NF-kappaB) p65 and hypoxia-inducible transcription factor 1alpha (HIF-1alpha) in pancreatic ductal adenocarcinoma and their clinical significance.
  • METHODS: The mRNA of TLR4 and HIF-1alpha were investigated by real-time polymerase chain reaction in 30 cases of pancreatic ductal adenocarcinoma and its adjacent tissues, and expression of TLR4, NF-kappaB p65 and HIF-1alpha protein were detected by immunohistochemistry in 65 cases of pancreatic ductal adenocarcinoma tissues and 38 cases of corresponding adjacent tissues.
  • Kaplan-Meier method was used to assess the impact of expression of TLR4 and HIF-1alpha on survival of patients with pancreatic cancer.
  • RESULTS: The relative quantification of TLR4 and HIF-1alpha mRNA in tumor tissues was 0.81 +/- 0.10 and 0.87 +/- 0.11, respectively, significantly higher than that in adjacent tissues (0.81 +/- 0.10 vs 0.70 +/- 0.16, P = 0.002; 0.87 +/- 0.11 vs 0.68 +/- 0.13, P = 0.000).
  • The protein expression of TLR4, NF-kappaB p65 and HIF-1alpha in tumor tissues was 69.20%, 66.15% and 70.80%, respectively, being significantly higher than that in adjacent normal tissues (69.20% vs 39.50%, P = 0.003; 66.15% vs 31.58%, P = 0.001; 70.80% vs 36.80%, P = 0.001).
  • There was no significant correlation between TLR4 or HIF-1alpha expression and the age, gender, tumor location, the degree of tumor differentiation in the patients (P > 0.05).
  • However, there was significant correlation between the expression of TLR4 or HIF-1alpha and tumor size, lymph node metastasis, venous invasion and clinical staging (P < 0.05).
  • The expression of TLR4 and HIF-1alpha had a significant impact on survival of patients with pancreatic adenocarcinoma.
  • CONCLUSION: TLR4, NF-kappaB p65 and HIF-1alpha are overexpressed in pancreatic adenocarcinoma, TLR4 may be partly involved in up-regulating HIF-1alpha, and both synergestically promote development of pancreatic adenocarcinoma.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Pancreatic Ductal / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / metabolism. Toll-Like Receptor 4 / genetics. Toll-Like Receptor 4 / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Base Sequence. Female. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Transcription Factor RelA / metabolism

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  • (PMID = 20556833.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RELA protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / TLR4 protein, human; 0 / Toll-Like Receptor 4; 0 / Transcription Factor RelA
  • [Other-IDs] NLM/ PMC2887583
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50. Yanai H, Nakamura K, Hijioka S, Kamei A, Ikari T, Ishikawa Y, Shinozaki E, Mizunuma N, Hatake K, Miyajima A: Dlk-1, a cell surface antigen on foetal hepatic stem/progenitor cells, is expressed in hepatocellular, colon, pancreas and breast carcinomas at a high frequency. J Biochem; 2010 Jul;148(1):85-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dlk-1, a cell surface antigen on foetal hepatic stem/progenitor cells, is expressed in hepatocellular, colon, pancreas and breast carcinomas at a high frequency.
  • Dlk-1 is also expressed in a subpopulation of hepatic oval cells, which are considered as stem/progenitor cells in rat adult liver.
  • In HCC, hDlk-1 was positive for 20.5% of the cases examined and was localized in both cytoplasm and cell membrane, whereas hDlk-1 was undetected in viral hepatitis, nodular cirrhosis.
  • Interestingly, hDlk-1 positive HCC was found more frequently in younger patients and its expression was correlated with alpha-fetoprotein expression.
  • Furthermore, hDlk-1 was also detected frequently in colon adenocarcinomas (58%), pancreatic islet carcinoma (50%), and small cell lung carcinoma (50%).
  • Thus, hDlk-1 is a cell surface protein expressed in many carcinomas including HCC and may be a potential target for monoclonal antibody therapy for carcinomas.
  • [MeSH-major] Antigens, Neoplasm / analysis. Antigens, Surface / metabolism. Fetus / cytology. Hepatocytes / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Membrane Proteins / metabolism. Neoplasms / metabolism. Stem Cells / metabolism
  • [MeSH-minor] Adult. Animals. Antibodies, Monoclonal / immunology. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Cell Line. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Female. Flow Cytometry. Humans. Immunohistochemistry. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Mice. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Rats

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  • [CommentIn] J Biochem. 2012 Aug;152(2):121-3 [22692292.001]
  • (PMID = 20356822.001).
  • [ISSN] 1756-2651
  • [Journal-full-title] Journal of biochemistry
  • [ISO-abbreviation] J. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Antigens, Surface; 0 / DLK1 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins
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51. Xu L, Kwon YJ, Frolova N, Steg AD, Yuan K, Johnson MR, Grizzle WE, Desmond RA, Frost AR: Gli1 promotes cell survival and is predictive of a poor outcome in ERalpha-negative breast cancer. Breast Cancer Res Treat; 2010 Aug;123(1):59-71
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gli1 promotes cell survival and is predictive of a poor outcome in ERalpha-negative breast cancer.
  • Gli1 is a transcription factor and oncogene with documented roles in the progression of several cancer types, including cancers of the skin and pancreas.
  • The contribution of Gli1 to the progression of breast cancer is less established.
  • In order to investigate the functional impact of Gli1 in breast cancer, expression of Gli1 and its contribution to cell growth was assessed in breast cancer cell lines.
  • In these cancers, the association of Gli1 with expression of estrogen receptor alpha (ERalpha) and progesterone receptor (PR), ErbB2, p53, the rate of proliferation, and clinicopathologic parameters and outcome was assessed.
  • Expression of Gli1 and ERalpha mRNA was strongly correlated in ERalpha-positive cell lines (r = 0.999).
  • Treatment with estrogen increased expression of Gli1 in 2 of 3 ERalpha-positive cell lines; this increase was prevented by treatment with the ERalpha-specific antagonist MPP.
  • Silencing of Gli1 by shRNA markedly reduced the survival of two ERalpha-negative cell lines, but caused only a modest reduction in ERalpha-positive cell lines.
  • In breast cancer tissues, cancers with nuclear localization of Gli1 had a higher ERalpha (P=0.027) and lower p53 expression (P=0.017) than those without nuclear localization of Gli1.
  • However, nuclear localization of Gli1 was predictive of a poorer cancer-specific survival in ERalpha-negative, including triple negative, cancers (P = 0.005), but not ERalpha-positive cancers.

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  • (PMID = 19902354.001).
  • [ISSN] 1573-7217
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA130057-02; United States / NCI NIH HHS / CA / R03 CA130057; United States / NCI NIH HHS / CA / R03 CA130057-02
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Gli protein; 0 / Oncogene Proteins; 0 / Trans-Activators; 4TI98Z838E / Estradiol
  • [Other-IDs] NLM/ NIHMS172145; NLM/ PMC2888711
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52. Abe Y, Ito T, Baba E, Nagafuji K, Kawabe K, Choi I, Arita Y, Miyamoto T, Teshima T, Nakano S, Harada M: Nonmyeloablative allogeneic hematopoietic stem cell transplantation as immunotherapy for pancreatic cancer. Pancreas; 2009 Oct;38(7):815-9
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  • [Title] Nonmyeloablative allogeneic hematopoietic stem cell transplantation as immunotherapy for pancreatic cancer.
  • OBJECTIVE: Advanced unresectable pancreatic cancer has an extremely poor prognosis despite intensive chemotherapy.
  • As a new therapeutic modality, we investigated nonmyeloablative allogeneic hematopoietic stem cell transplantation from a related donor.
  • METHODS: Five patients with chemotherapy-resistant pancreatic cancer received allogeneic peripheral blood stem cell transplantation after a conditioning regimen consisting of low-dose total body irradiation and fludarabine.
  • The prophylaxis for graft-versus-host disease consisted of mycophenolate mofetil and cyclosporine.
  • RESULTS: The median age of the 5 patients was 54 years, and the median duration from diagnosis to nonmyeloablative allogeneic hematopoietic stem cell transplantation was 10 months.
  • Three of the 5 patients achieved complete donor chimerism of peripheral T cells, at a median time of day 42.
  • Acute graft-versus-host disease developed in 3 patients: grade 2 in 2 patients and grade 1 in 1.
  • Tumor reduction was observed in 2 patients: 1 patient showed disappearance of the pancreatic tumor, and the other patient showed approximately 20% reduction of the tumor.
  • Marked elevation of tumor necrosis factor alpha was observed as the tumor regressed.
  • CONCLUSIONS: Although advanced pancreatic cancer progresses rapidly, some graft-versus-tumor effects and pivotal role of tumor necrosis factor alpha were suggested.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Immunotherapy / methods. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Adult. Antineoplastic Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclosporine / administration & dosage. Female. Graft vs Host Disease / metabolism. Graft vs Host Disease / prevention & control. Humans. Male. Middle Aged. Mycophenolic Acid / administration & dosage. Mycophenolic Acid / analogs & derivatives. Time Factors. Transplantation Conditioning. Transplantation, Homologous. Tumor Necrosis Factor-alpha / metabolism. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Whole-Body Irradiation

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  • (PMID = 19696692.001).
  • [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 / Antineoplastic Agents; 0 / Tumor Necrosis Factor-alpha; 83HN0GTJ6D / Cyclosporine; 9242ECW6R0 / mycophenolate mofetil; FA2DM6879K / Vidarabine; HU9DX48N0T / Mycophenolic Acid; P2K93U8740 / fludarabine
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53. Murtaza I, Adhami VM, Hafeez BB, Saleem M, Mukhtar H: Fisetin, a natural flavonoid, targets chemoresistant human pancreatic cancer AsPC-1 cells through DR3-mediated inhibition of NF-kappaB. Int J Cancer; 2009 Nov 15;125(10):2465-73
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  • [Title] Fisetin, a natural flavonoid, targets chemoresistant human pancreatic cancer AsPC-1 cells through DR3-mediated inhibition of NF-kappaB.
  • Death receptors of the tumor necrosis factor (TNF) receptor super family have been implicated in constitutive activation of nuclear factor-kappa B (NF-kappaB) in pancreatic cancer (PaC) cells.
  • In this study, we demonstrate that fisetin, a natural flavonoid, induces apoptosis and inhibits invasion of chemoresistant PaC AsPC-1 cells through suppression of DR3-mediated NF-kappaB activation.
  • Fisetin treatment resulted in dose-dependent inhibition of PaC cell growth and cell proliferation with concomitant induction of apoptosis.
  • Down-regulation of DR3 in PaC cells was found to down regulate activated pNF-kappaB/p65, pIkBalpha/beta kinases (pIKK's), MMP9 and XIAP that mostly impart chemoresistance in PaC.
  • Importantly, consistent with these findings, we further found that transient down-regulation of DR3 by RNA interference significantly augmented fisetin induced changes in cell proliferation, cell invasion and apoptosis paralleled with decrease in pNF-kappaB, pIKKalpha/beta, MMP9, XIAP and NF-kappaB DNA binding activity.
  • These data provide evidence that fisetin could provide a biological rationale for treatment of pancreatic cancer or as an adjuvant with conventional therapeutic regimens.

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  • (PMID = 19670328.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA101039; United States / NCI NIH HHS / CA / R01CA78809; United States / NCI NIH HHS / CA / R01 CA078809; United States / NCI NIH HHS / CA / R01 CA078809-10; United States / NCI NIH HHS / CA / R01 CA120451-05; United States / NCI NIH HHS / CA / CA078809-10; United States / NCI NIH HHS / CA / R01 CA101039; United States / NCI NIH HHS / CA / R01CA120451; United States / NCI NIH HHS / CA / R01 CA120451; United States / NCI NIH HHS / CA / R01 CA101039-05
  • [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 / Flavonoids; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / RNA, Small Interfering; 0 / Receptors, Tumor Necrosis Factor, Member 25; 0 / TNFRSF25 protein, human; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human; 139874-52-5 / NF-kappaB inhibitor alpha; EC 3.4.24.35 / Matrix Metalloproteinase 9; OO2ABO9578 / fisetin
  • [Other-IDs] NLM/ NIHMS137972; NLM/ PMC2944651
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54. Conti JA, Kendall TJ, Bateman A, Armstrong TA, Papa-Adams A, Xu Q, Packham G, Primrose JN, Benyon RC, Iredale JP: The desmoplastic reaction surrounding hepatic colorectal adenocarcinoma metastases aids tumor growth and survival via alphav integrin ligation. Clin Cancer Res; 2008 Oct 15;14(20):6405-13
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  • [Title] The desmoplastic reaction surrounding hepatic colorectal adenocarcinoma metastases aids tumor growth and survival via alphav integrin ligation.
  • Human colorectal adenocarcinoma cell lines HT-29, KM12SM, and KM12c were grown on wild-type collagen I or IV, or cleavage-resistant r/r collagen I, and assessed for their growth, survival, and resistance to 5-fluorouracil.
  • The effect of alpha(v)beta(3) and alpha(v)beta(5) integrin blockade by neutralizing antibodies was examined.
  • RESULTS: Collagen I, in contrast to collagen IV, significantly enhanced the growth, survival, and chemoresistance of colorectal carcinoma cells.
  • Blockade of the alpha(v)beta(3) and alpha(v)beta(5) integrins significantly reduced colorectal carcinoma cell proliferation on collagen, especially in the cell line with the most metastatic potential.
  • Using matrix metalloproteinase-resistant r/r collagen I as a dominant negative ligand for alpha(v) integrins, we showed a key role for this integrin-ligand interaction in mediating the survival and proliferation of colorectal carcinoma cells.
  • The interaction between integrin and collagen I is identified as a potential therapeutic target.
  • [MeSH-major] Collagen Type I / metabolism. Collagen Type IV / metabolism. Integrin alphaV / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adenocarcinoma / secondary. Antimetabolites, Antineoplastic / pharmacology. Apoptosis / drug effects. Apoptosis / physiology. Cell Adhesion / drug effects. Cell Adhesion / physiology. Cell Proliferation / drug effects. Colorectal Neoplasms / metabolism. Colorectal Neoplasms / pathology. Colorectal Neoplasms / surgery. Drug Resistance, Neoplasm. Flow Cytometry. Fluorouracil / pharmacology. Hepatectomy. Humans. Immunoblotting. Immunoenzyme Techniques. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Liver Neoplasms / secondary. Tumor Cells, Cultured

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  • (PMID = 18927279.001).
  • [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
  • [Grant] United Kingdom / Wellcome Trust / / 072662; United Kingdom / Medical Research Council / / G0600033; United Kingdom / Medical Research Council / / G116\97; United Kingdom / Medical Research Council / / G9900297
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Collagen Type I; 0 / Collagen Type IV; 0 / Integrin alphaV; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2590496; NLM/ UKMS2734
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55. Egberts JH, Cloosters V, Noack A, Schniewind B, Thon L, Klose S, Kettler B, von Forstner C, Kneitz C, Tepel J, Adam D, Wajant H, Kalthoff H, Trauzold A: Anti-tumor necrosis factor therapy inhibits pancreatic tumor growth and metastasis. Cancer Res; 2008 Mar 1;68(5):1443-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-tumor necrosis factor therapy inhibits pancreatic tumor growth and metastasis.
  • Chronic inflammation has been implicated in the pathogenesis of many severe autoimmune disorders, as well as in diabetes, pulmonary diseases, and cancer.
  • Inflammation accompanies most solid cancers including pancreatic ductal adenocarcinoma (PDAC), one of the most fatal cancers with surgery being the only curative therapeutic approach currently available.
  • In the present work, we investigated the role of the major proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) in the malignancy of PDAC cells in vitro and in vivo.
  • In vitro, TNFalpha strongly increased invasiveness of Colo357, BxPc3, and PancTuI cells and showed only moderate antiproliferative effect.
  • TNFalpha treatment of mice bearing orthotopically growing PDAC tumors led to dramatically enhanced tumor growth and metastasis.
  • Notably, we found that PDAC cells themselves secrete TNFalpha.
  • Although inhibition of TNFalpha with infliximab or etanercept only marginally affected proliferation and invasiveness of PDAC cells in vitro, both reagents exerted strong antitumoral effects in vivo.
  • In severe combined immunodeficient mice with orthotopically growing Colo357, BxPc3, or PancTuI tumors, human-specific anti-TNF antibody infliximab reduced tumor growth and metastasis by about 30% and 50%, respectively.
  • Importantly, in a PDAC resection model performed with PancTuI cells, we found an even stronger therapeutic effect for both anti-TNF compounds.
  • Infliximab and etanercept reduced the number of liver metastases by 69% and 42%, respectively, as well as volumes of recurrent tumors by 73% and 51%.
  • Thus, tumor cell-derived TNFalpha plays a profound role in malignancy of PDAC, and inhibition of TNFalpha represents a promising therapeutic option particularly in adjuvant therapy after subtotal pancreatectomy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Pancreatic Ductal / pathology. Gene Expression Regulation, Neoplastic. Pancreatic Neoplasms / pathology. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Female. Humans. Interleukin-8 / metabolism. Mice. Mice, SCID. Neoplasm Invasiveness. Neoplasm Metastasis

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  • (PMID = 18316608.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interleukin-8; 0 / Tumor Necrosis Factor-alpha
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56. Uysal M, Temiz S, Gul N, Yarman S, Tanakol R, Kapran Y: Hypoglycemia due to ectopic release of insulin from a paraganglioma. Horm Res; 2007;67(6):292-5
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  • Insulin-secreting pancreatic tumors and insulin-like growth hormone-secreting non-islet cell tumors can cause hypoglycemia.
  • Abdominal MRI revealed a retroperitoneal mass measuring 4.5 cm in the pancreatic region.
  • She was treated with an alpha-blocking agent to control blood pressure preceding the removal of the mass.
  • Histopathological diagnosis was paraganglioma, and immunohistochemically insulin staining in the neoplastic cells was demonstrated.
  • Paraganglioma is a rare tumor of the neural crest, and co-secretion of insulin and catecholamines has been reported only by a single case report in the literature.
  • [MeSH-major] Hormones, Ectopic / secretion. Hypoglycemia / etiology. Insulin / secretion. Paraganglioma / complications. Retroperitoneal Neoplasms / complications

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  • [Copyright] Copyright 2007 S. Karger AG, Basel.
  • (PMID = 17284922.001).
  • [ISSN] 0301-0163
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Hormones, Ectopic; 0 / Insulin
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57. Ringel J, Jesnowski R, Moniaux N, Lüttges J, Ringel J, Choudhury A, Batra SK, Klöppel G, Löhr M: Aberrant expression of a disintegrin and metalloproteinase 17/tumor necrosis factor-alpha converting enzyme increases the malignant potential in human pancreatic ductal adenocarcinoma. Cancer Res; 2006 Sep 15;66(18):9045-53
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  • [Title] Aberrant expression of a disintegrin and metalloproteinase 17/tumor necrosis factor-alpha converting enzyme increases the malignant potential in human pancreatic ductal adenocarcinoma.
  • To understand the role of ADAM17/tumor necrosis factor-alpha (TNF-alpha) converting enzyme (TACE) in pancreatic ductal adenocarcinoma (PDAC), we investigated its expression, function, and in vitro regulation.
  • ADAM17/TACE mRNA was expressed in 3 of 10 normal pancreatic tissues, 6 of 8 samples from patients with chronic pancreatitis, 10 of 10 PDAC tissues, and 9 of 9 pancreatic cancer cell lines, but it was absent in primary duct epithelial cells.
  • Immunohistochemical staining revealed positive cancer cells in 8 of 10 PDACs but no staining of ducts in normal pancreas.
  • ADAM17/TACE was found in 0 of 16 pancreatic intraepithelial neoplasia (PanIN)-1A lesions, 1 of 30 PanIN-1B lesions, 2 of 13 PanIN-2 lesions but, in 13 of 15 PanIN-3 lesions, associated with PDAC.
  • Western blot, flow cytometry, and confocal microscopy analyses showed the aberrant expression of ADAM17/TACE protein in pancreatic cancer cell lines.
  • The proteolytic activity of ADAM17/TACE, assessed by the release of TNF-alpha, was inhibited by TNF-alpha protease inhibitor.
  • Furthermore, ADAM17/TACE mRNA expression was down-regulated in pancreatic cancer cells arrested in G2-M phase as well as in a time-dependent manner after TNF-alpha and interleukin-6 incubation.
  • [MeSH-major] ADAM Proteins / biosynthesis. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / enzymology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Cycle / genetics. Cell Growth Processes / genetics. Cell Line, Tumor. Disease Progression. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. Immunohistochemistry. Neoplasm Invasiveness. Pancreatitis, Chronic / enzymology. Pancreatitis, Chronic / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 16982746.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA772712
  • [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 / RNA, Messenger; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
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58. Ma RY, Tam TS, Suen AP, Yeung PM, Tsang SW, Chung SK, Thomas MK, Leung PS, Yao KM: Secreted PDZD2 exerts concentration-dependent effects on the proliferation of INS-1E cells. Int J Biochem Cell Biol; 2006;38(5-6):1015-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secreted PDZD2 exerts concentration-dependent effects on the proliferation of INS-1E cells.
  • PDZD2 (PDZ domain containing 2) is a multi-PDZ protein expressed in pancreas and many other tissues.
  • To understand the possible functional role of PDZD2 in pancreas, we investigated the cellular distribution of PDZD2 in adult pancreas using an antiserum that recognizes both the full-length and secreted forms of PDZD2.
  • Immunohistochemical analysis revealed a strong expression of PDZD2 in pancreatic islet beta cells but not alpha cells.
  • Consistent with the beta-cell-enriched expression of PDZD2, immunoblot analysis indicated expression of both full-length PDZD2 and sPDZD2 in the insulinoma cell line INS-1E.
  • A recombinant sPDZD2 protein was synthesized for study of its functional effect on INS-1E cells.
  • In culture media with limiting serum, co-incubation with sPDZD2 stimulated the proliferation of INS-1E cells.
  • As a potential mitogen of beta-like cells, sPDZD2 may be useful for the optimization of beta-cell growth and differentiation in vitro.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adult. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Insulin-Secreting Cells / metabolism. Mitogens / pharmacology. Neoplasm Proteins. Pancreas / metabolism

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  • (PMID = 16413998.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Intracellular Signaling Peptides and Proteins; 0 / Mitogens; 0 / Neoplasm Proteins; 0 / PDZD2 protein, human
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59. Muehlemann M, Miller KD, Dauphinee M, Mizejewski GJ: Review of Growth Inhibitory Peptide as a biotherapeutic agent for tumor growth, adhesion, and metastasis. Cancer Metastasis Rev; 2005 Sep;24(3):441-67
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Review of Growth Inhibitory Peptide as a biotherapeutic agent for tumor growth, adhesion, and metastasis.
  • This review surveys the biological activities of an alpha-fetoprotein (AFP) derived peptide termed the Growth Inhibitory Peptide (GIP), which is a synthetic 34 amino acid segment produced from the full length 590 amino acid AFP molecule.
  • The GIP has been shown to be growth-suppressive in both fetal and tumor cells but not in adult terminally-differentiated cells.
  • The mechanism of action of this peptide has not been fully elucidated; however, GIP is highly interactive at the plasma membrane surface in cellular events such as endocytosis, cell contact inhibition and cytoskeleton-induced cell shape changes.
  • The GIP was shown to be growth-suppressive in nine human tumor types and to suppress the spread of tumor infiltrates and metastases in human and mouse mammary cancers.
  • The AFP-derived peptide and its subfragments were also shown to inhibit tumor cell adhesion to extracellular matrix (ECM) proteins and to block platelet aggregation; thus it was expected that the GIP would inhibit cell spreading/migration and metastatic infiltration into host tissues such as lung and pancreas.
  • It was further found that the cyclic versus linear configuration of GIP determined its biological and anti-cancer efficacy.
  • Genbank amino acid sequence identities with a variety of integrin alpha/beta chain proteins supported the GIP's linkage to inhibition of tumor cell adhesion and platelet aggregation.
  • The combined properties of tumor growth suppression, prevention of tumor cell-to-ECM adhesion, and inhibition of platelet aggregation indicate that tumor-to-platelet interactions present promising targets for GIP as an anti-metastatic agent.
  • Finally, based on cholinergic studies, it was proposed that GIP could influence the enzymatic activity of membrane acetylcholinesterases during tumor growth and metastasis.
  • It was concluded that the GIP derived from full-length AFP represents a growth inhibitory motif possessing instrinsic properties that allow it to interfere in cell surface events such as adhesion, migration, metastasis, and aggregation of tumor cells.
  • [MeSH-major] Biological Products / therapeutic use. Growth Inhibitors / therapeutic use. Neoplasms / drug therapy. Neoplasms / pathology. Neoplasms / therapy. Peptides / therapeutic use. alpha-Fetoproteins / therapeutic use
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Adhesion. Cell Line, Tumor. Cell Membrane / metabolism. Cell Movement. Cytoskeleton / metabolism. Disease Progression. Endocytosis. Humans. Mice. Models, Biological. Molecular Sequence Data. Neoplasm Metastasis. Neoplasm Transplantation. Neoplasms, Experimental / drug therapy. Platelet Aggregation. Protein Conformation. Protein Structure, Tertiary. Time Factors

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  • (PMID = 16258731.001).
  • [ISSN] 0167-7659
  • [Journal-full-title] Cancer metastasis reviews
  • [ISO-abbreviation] Cancer Metastasis Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biological Products; 0 / Growth Inhibitors; 0 / Peptides; 0 / alpha-Fetoproteins
  • [Number-of-references] 81
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60. Yip-Schneider MT, Nakshatri H, Sweeney CJ, Marshall MS, Wiebke EA, Schmidt CM: Parthenolide and sulindac cooperate to mediate growth suppression and inhibit the nuclear factor-kappa B pathway in pancreatic carcinoma cells. Mol Cancer Ther; 2005 Apr;4(4):587-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Parthenolide and sulindac cooperate to mediate growth suppression and inhibit the nuclear factor-kappa B pathway in pancreatic carcinoma cells.
  • Activation of the transcription factor nuclear factor-kappa B (NF-kappa B) has been implicated in pancreatic tumorigenesis.
  • We evaluated the effect of a novel NF-kappa B inhibitor, parthenolide, a sesquiterpene lactone isolated from the herb feverfew, in three human pancreatic tumor cell lines (BxPC-3, PANC-1, and MIA PaCa-2).
  • Parthenolide inhibited pancreatic cancer cell growth in a dose-dependent manner with substantial growth inhibition observed between 5 and 10 micromol/L parthenolide in all three cell lines.
  • Parthenolide treatment also dose-dependently increased the amount of the NF-kappa B inhibitory protein, I kappa B-alpha, and decreased NF-kappa B DNA binding activity.
  • We have previously shown that nonsteroidal anti-inflammatory drugs (NSAID) suppress the growth of pancreatic cancer cells.
  • To determine whether inhibition of the NF-kappa B pathway by parthenolide could sensitize pancreatic cancer cells to NSAID inhibition, BxPC-3, PANC-1, and MIA PaCa-2 cells were treated with parthenolide and the NSAID sulindac, either alone or in combination.
  • Treatment with the combination of parthenolide and sulindac inhibited cell growth synergistically in MIA PaCa-2 and BxPC-3 cells and additively in PANC-1 cells.
  • Increased levels of I kappa B-alpha protein were detected, especially in MIA PaCa-2 cells, after treatment with parthenolide and sulindac compared with each agent alone.
  • Similarly, decreased NF-kappa B DNA binding and transcriptional activities were detected in cells treated with the combination compared with the single agents, demonstrating cooperative targeting of the NF-kappa B pathway.
  • These data provide preclinical support for a combined chemotherapeutic approach with NF-kappa B inhibitors and NSAIDs for the treatment of pancreatic adenocarcinoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma / drug therapy. Drug Synergism. NF-kappa B / metabolism. Pancreatic Neoplasms / drug therapy. Sesquiterpenes / administration & dosage. Sulindac / administration & dosage
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Apoptosis. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Humans. Models, Biological. Phosphorylation. Protein Binding. Transcription, Genetic. Transfection

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  • (PMID = 15827332.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / NF-kappa B; 0 / Sesquiterpenes; 184SNS8VUH / Sulindac; 2RDB26I5ZB / parthenolide
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61. Souzaki R, Tajiri T, Kinoshita Y, Tanaka S, Koga Y, Suminoe A, Hara T, Kohashi K, Oda Y, Taguchi T: Successful treatment of advanced pancreatoblastoma by a pylorus-preserving pancreatoduodenectomy after radiation and high-dose chemotherapy. Pediatr Surg Int; 2010 Oct;26(10):1045-8
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  • BACKGROUND: Pancreatoblastoma (PB) is a rare malignant pancreatic tumor in children and approximately 200 cases have been reported in the literature.
  • This report presents the case of a 6-year-old female with advanced PB treated successfully by a pylorus-preserving pancreatoduodenectomy (PPPD) after induction chemotherapy, radiation and stem cell transplantation (SCT).
  • Abdominal computed tomography (CT) scan showed a 9-cm heterogeneous mass located at the pancreatic head and body, and the duodenum was completely compressed.
  • The inferior vena cava, superior mesenteric artery, and vein were encased by the tumor.
  • The tumor had well-defined margins and calcification.
  • She showed severe anemia and her hemoglobin level was 4.0 g/dl, and the serum alpha-fetoprotein (AFP) level was elevated (884.8 ng/ml).
  • Initially, a resection of the tumor was impossible.
  • An open biopsy was performed and the histopathological diagnosis was PB.
  • She underwent five cycles of the induction chemotherapy regimen for advanced neuroblastoma (cyclophosphamide, etoposide, vincristine, pirarubicin and cisplatin), and the tumor size was decreased to a diameter of 7.5 cm.
  • The serum AFP level decreased to 41.1 ng/ml, and the tumor size was decreased to a diameter of 6.5 cm.
  • Then she underwent a PPPD and the tumor was completely resected.
  • The child was administered mild postoperative chemotherapy using irinotecan and has been disease-free for 4 months and, and her serum AFP levels remain within normal values.
  • [MeSH-minor] Child. Female. Follow-Up Studies. Humans. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / radiotherapy. Pancreatic Neoplasms / surgery. Radiotherapy, Adjuvant

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  • [Cites] Pediatr Blood Cancer. 2010 May;54(5):675-80 [19998473.001]
  • [Cites] J Pediatr Hematol Oncol. 2005 Nov;27(11):604-6 [16282892.001]
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  • (PMID = 20632017.001).
  • [ISSN] 1437-9813
  • [Journal-full-title] Pediatric surgery international
  • [ISO-abbreviation] Pediatr. Surg. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; Pancreatoblastoma
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62. Weiss FU, Marques IJ, Woltering JM, Vlecken DH, Aghdassi A, Partecke LI, Heidecke CD, Lerch MM, Bagowski CP: Retinoic acid receptor antagonists inhibit miR-10a expression and block metastatic behavior of pancreatic cancer. Gastroenterology; 2009 Dec;137(6):2136-45.e1-7
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  • [Title] Retinoic acid receptor antagonists inhibit miR-10a expression and block metastatic behavior of pancreatic cancer.
  • BACKGROUND & AIMS: The infiltrating ductal adenocarcinoma of the pancreas is among the most lethal of all solid malignancies, largely owing to a high frequency of early metastasis.
  • We identified microRNA-10a (miR-10a) as an important mediator of metastasis formation in pancreatic tumor cells and investigated the upstream and downstream regulatory mechanisms of miR-10a.
  • METHODS: Northern blot analysis revealed increased expression levels of miR-10a in metastatic pancreatic adenocarcinoma.
  • The role of miR-10a was analyzed by Morpholino and short interfering RNA transfection of pancreatic carcinoma cell lines and resected specimens of human pancreatic carcinoma.
  • Metastatic behavior of primary pancreatic tumors and cancer cell lines was tested in xenotransplantation experiments in zebrafish embryos.
  • RESULTS: We show that miR-10a expression promotes metastatic behavior of pancreatic tumor cells and that repression of miR-10a is sufficient to inhibit invasion and metastasis formation.
  • Interestingly, suppression of HOXB1 and HOXB3 in pancreatic cancer cells is sufficient to promote metastasis formation.
  • CONCLUSIONS: These findings suggest that miR-10a is a key mediator of metastatic behavior in pancreatic cancer, which regulates metastasis via suppression of HOXB1 and HOXB3.
  • [MeSH-major] Adenocarcinoma / therapy. Benzoates / pharmacology. Chromans / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Genetic Therapy. MicroRNAs / metabolism. Pancreatic Neoplasms / therapy. Receptors, Retinoic Acid / antagonists & inhibitors
  • [MeSH-minor] Animals. Blotting, Northern. Cadherins / metabolism. Cell Line, Tumor. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Morpholines / metabolism. Neoplasm Invasiveness. Oligonucleotides, Antisense / metabolism. RNA Interference. RNA, Small Interfering / metabolism. Retinoids / pharmacology. Transfection. Up-Regulation. Xenograft Model Antitumor Assays. Zebrafish / embryology. alpha Catenin / metabolism. beta Catenin / metabolism

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  • (PMID = 19747919.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzoates; 0 / CDH1 protein, human; 0 / CTNNB1 protein, human; 0 / Cadherins; 0 / Chromans; 0 / HOXB1 homeodomain protein; 0 / Homeodomain Proteins; 0 / HoxB3 protein, human; 0 / MicroRNAs; 0 / Morpholines; 0 / Oligonucleotides, Antisense; 0 / RNA, Small Interfering; 0 / Receptors, Retinoic Acid; 0 / Retinoids; 0 / alpha Catenin; 0 / beta Catenin; 144092-31-9 / Ro 41-5253
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63. Li Z, Fallon J, Mandeli J, Wetmur J, Woo SL: A genetically enhanced anaerobic bacterium for oncopathic therapy of pancreatic cancer. J Natl Cancer Inst; 2008 Oct 1;100(19):1389-400
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A genetically enhanced anaerobic bacterium for oncopathic therapy of pancreatic cancer.
  • BACKGROUND: A major obstacle in treatment of solid tumors is the inefficient delivery of therapeutic agents to the hypoxic cores.
  • Hypoxia offers the potential for anaerobic bacteria colonization and tumor destruction by the bacteria, and dormant spores of wild-type Clostridium perfringens (Cp) germinate and proliferate within the hypoxic cores of pancreatic tumors in mice.
  • METHODS: Recombinant Cp strains in which superoxide dismutase, a major oxygen tolerance gene, was deleted (Cp/sod(-)) were constructed to enhance its selective growth in tumors.
  • The ability of the recombinant Cp strains to kill tumors was investigated in C57/BL6 mice bearing murine PANC02 tumors.
  • RESULTS: Cp/sod(-) showed reduced toxic effects compared with wild-type Cp when spores were administered intravenously into PANC02 tumor-bearing mice.
  • Mice treated with Cp/sod(-)/PVL spores demonstrated a reduction in neutrophils and macrophages in tumors, logarithmically elevated growth of intratumoral bacteria, enhanced tumor necrosis, and substantially prolonged survival without apparent systemic and organ toxic effects, compared with mice treated with both wild-type Cp and Cp/sod(-) spores.
  • Accordingly, 47% of Cp/sod(-)/PVL-treated mice (n = 15) achieved tumor-free survival for over 120 days, whereas all mice treated with Cp/sod(-) or phosphate-buffered saline (n = 10 per group) died within 50 days.
  • CONCLUSIONS: Cp/sod(-)/PVL provides a prototype for a novel class of oncopathic microbes that may have potential for the safe and effective treatment of pancreatic cancer and other poorly vascularized tumors.

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  • [CommentIn] NIH Guide Grants Contracts. 2016 Jul 29;:NOT-OD-16-124 [27483554.001]
  • [RetractionIn] Li Z, Fallon J, Mandeli J, Wetmur J, Woo SL. J Natl Cancer Inst. 2010 Feb 24;102(4):283 [20176752.001]
  • [CommentIn] Fed Regist. 2016 Jul 25;81(142):48426-48427 [27737274.001]
  • (PMID = 18812551.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-120017
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / Biomarkers, Tumor; 0 / Exotoxins; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Leukocidins; 0 / Panton-Valentine leukocidin; EC 1.15.1.1 / Superoxide Dismutase
  • [Other-IDs] NLM/ PMC2720732
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64. Vakiani E, Young RH, Carcangiu ML, Klimstra DS: Acinar cell carcinoma of the pancreas metastatic to the ovary: a report of 4 cases. Am J Surg Pathol; 2008 Oct;32(10):1540-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cell carcinoma of the pancreas metastatic to the ovary: a report of 4 cases.
  • We report 4 cases of acinar cell carcinoma of the pancreas, 3 presenting as metastases in the ovary, the first report of this circumstance, which may pose a broad differential diagnosis and caused significant diagnostic difficulty in all the cases.
  • In 3 cases, the ovarian tumors were detected before the pancreatic tumor; in 1 case, a large abdominal mass and ovarian tumors were discovered synchronously.
  • The ovarian tumors were large, solid, white-tan on gross examination, and bilateral in 3 cases; the single case involving only 1 ovary had 2 discrete masses of tumor.
  • Microscopic examination showed highly cellular neoplasms with a small amount of fibrous stroma.
  • Two cases had a predominant acinar growth pattern of cells with brightly eosinophilic, granular cytoplasm.
  • In 2 cases, the pattern was predominantly solid-cribriform with areas of comedolike necrosis, and the cells had pale eosinophilic, finely granular cytoplasm.
  • The main differential diagnostic consideration was well-differentiated neuroendocrine neoplasm (carcinoid tumor); positive immunostaining with antibodies against chymotrypsin and trypsin and negative immunostaining with antibodies against synaptophysin and chromogranin helped exclude this diagnosis.
  • We observed focal alpha-inhibin immunostaining in 2 cases, which may represent a potential diagnostic pitfall, as a Sertoli cell tumor or unusual granulosa cell tumor may also enter the differential diagnosis.
  • Inclusion of antibodies against the pancreatic enzymes chymotrypsin and trypsin in the immunohistochemical panel is critical in establishing the correct diagnosis and should be considered when evaluating ovarian tumors with architectural (mainly acinar) and cytologic (granular eosinophilic cytoplasm) characteristics that should bring a metastatic acinar cell carcinoma into consideration.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Ovarian Neoplasms / secondary. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Middle Aged

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  • (PMID = 18724247.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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65. Neesse A, Wagner M, Ellenrieder V, Bachem M, Gress TM, Buchholz M: Pancreatic stellate cells potentiate proinvasive effects of SERPINE2 expression in pancreatic cancer xenograft tumors. Pancreatology; 2007;7(4):380-5
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  • [Title] Pancreatic stellate cells potentiate proinvasive effects of SERPINE2 expression in pancreatic cancer xenograft tumors.
  • We have previously reported that inducible overexpression of the serine protease inhibitor nexin 2 (SERPINE2) significantly increases local invasiveness of subclones of the pancreatic cancer cell-line SUIT-2 in nude mouse xenografts.
  • This was associated with a striking increase of extracellular matrix deposition in the invasive tumors.
  • Pancreatic stellate cells (PSCs) have recently been identified as the major source of fibrosis in pancreatic adenocarcinomas.
  • Here we report that co-injection of PSCs and tumor cells dramatically enhances the invasive potential of serine protease inhibitor Nexin 2 (SERPINE2)-expressing SUIT-2 cells.
  • 100% (24 of 24) of the SERPINE2-expressing tumors with PSCs grew aggressively invasive, as compared to 39% of SERPINE2-negative tumors with PSCs and 27% of SERPINE2-expressing tumors without PSCs.
  • In contrast to pure cancer cell preparations, SERPINE2 overexpression in the presence of PSCs also resulted in increased tumor growth.
  • Histological evaluation demonstrated the presence of large amounts of ECM deposits co-localizing with cells staining positive for the PSC marker alpha-SMA.
  • We conclude that PSCs actively proliferate in pancreatic cancer xenograft tumors and significantly contribute to the local invasive potential of the tumors.
  • Presence of PSCs enhances the pro-invasive effects of SERPINE2 expression, and SERPINE2 influences tumor growth (as opposed to invasiveness) only in the presence of PSCs.
  • Our data thus suggest that SERPINE2 is an important modulator of tumor cell/host interactions in pancreatic cancer.
  • [MeSH-major] Amyloid beta-Protein Precursor / metabolism. Pancreas / cytology. Receptors, Cell Surface / metabolism
  • [MeSH-minor] Animals. Gene Expression Regulation, Neoplastic. Mice. Mice, Nude. Neoplasm Invasiveness. Neoplasms, Experimental. Pancreatic Neoplasms. Protease Nexins. Transplantation, Heterologous

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  • [Copyright] 2007 S. Karger AG, Basel and IAP
  • (PMID = 17703087.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Protease Nexins; 0 / Receptors, Cell Surface
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66. Fahrig R, Quietzsch D, Heinrich JC, Heinemann V, Boeck S, Schmid RM, Praha C, Liebert A, Sonntag D, Krupitza G, Hänel M: RP101 improves the efficacy of chemotherapy in pancreas carcinoma cell lines and pancreatic cancer patients. Anticancer Drugs; 2006 Oct;17(9):1045-56
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  • [Title] RP101 improves the efficacy of chemotherapy in pancreas carcinoma cell lines and pancreatic cancer patients.
  • RP101 [(E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU)], which supports apoptosis and prevents the acquisition of chemoresistance, was tested in cultured human pancreatic tumor cells.
  • Furthermore, RP101 activated antitumor immunity as demonstrated by enhanced cytolytic activity of NK-92 natural killer cells.
  • This was concomitant with an enhanced expression of lymphotoxins alpha and beta, natural killer cell transcript 4, tumor necrosis factor LIGHT/TNFSF-14, and intercellular adhesion molecule-1 in pancreas carcinoma cells.
  • These results encouraged us to investigate the effect of RP101 in pancreas cancer patients.
  • In a first pilot study, 13 patients in stage III and VI of the disease were treated with gemcitabine +cisplatin+RP101.
  • A second study with 21 patients in similar stages of disease, treated with RP101+gemcitabine alone, confirmed the results of the pilot study.
  • Considering both studies, the tumor control was 94%.
  • [MeSH-major] Bromodeoxyuridine / analogs & derivatives. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Cell Line, Tumor. Cisplatin / pharmacology. DNA-(Apurinic or Apyrimidinic Site) Lyase / genetics. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacokinetics. Deoxycytidine / pharmacology. Humans. Killer Cells, Natural / immunology. Middle Aged


67. Vaidyanathan G, Affleck DJ, Schottelius M, Wester H, Friedman HS, Zalutsky MR: Synthesis and evaluation of glycosylated octreotate analogues labeled with radioiodine and 211At via a tin precursor. Bioconjug Chem; 2006 Jan-Feb;17(1):195-203
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  • Carbohydration of N-terminus and substitution of a threonine for the threoninol residue at the C-terminus of Tyr3-octreotide (TOC) has resulted in improved pharmacokinetics and tumor targeting of its radioiodinated derivatives.
  • Solid-phase synthesis and subsequent modifications delivered an iodo standard of the target peptide N(alpha)-(1-deoxy-D-fructosyl)-N(epsilon)-(3-iodobenzoyl)-Lys0-octreotate (GIBLO) and the corresponding tin precursor N(alpha)-(1-deoxy-D-fructosyl)-N(epsilon)-[(3-tri-n-butylstannyl)benzoyl]-Lys0-octreotate (GTBLO).
  • GIBLO displaced [125I]TOC from somatostatin receptor subtype 2 (SSTR2)-positive AR42J rat pancreatic tumor cell membranes with an IC50 of 0.46 +/- 0.05 nM suggesting that GIBLO retained affinity to SSTR2.
  • GTBLO was radiohalogenated to [131I]GIBLO and N(alpha)-(1-deoxy-D-fructosyl)-N(epsilon)-(3-[211At]astatobenzoyl)-Lys0-octreotate ([211At]GABLO) in 21.2 +/- 4.9% and 46.8 +/- 9.5% radiochemical yields, respectively.
  • From a paired-label internalization assay using D341 Med medulloblastoma cells, the maximum specific internalized radioactivity from [131I]GIBLO was 1.78 +/- 0.8% of input dose compared to 9.67 +/- 0.43% for N(alpha)-(1-deoxy-D-fructosyl)-[125I]iodo-Tyr3-octreotate ([125I]I-Gluc-TOCA).
  • Over a 4 h period, the extent of internalization of [131I]GIBLO and [211At]GABLO was similar in this cell line.
  • Taken together, although GIBLO maintained affinity to SSTR2, its tumor uptake both in vitro and in vivo was substantially lower than that of I-Gluc-TOCA suggesting other factors such as net charge and overall geometry of the peptide may be important.
  • [MeSH-minor] Animals. Astatine. Cell Line, Tumor. Glycosylation. Humans. Iodine Radioisotopes. Medulloblastoma / metabolism. Mice. Mice, Nude. Neoplasm Transplantation. Rats. Receptors, Somatostatin / metabolism. Tissue Distribution

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  • (PMID = 16417269.001).
  • [ISSN] 1043-1802
  • [Journal-full-title] Bioconjugate chemistry
  • [ISO-abbreviation] Bioconjug. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA42324; United States / NCI NIH HHS / CA / CA78417; United States / NCI NIH HHS / CA / CA91927; United States / NCI NIH HHS / CA / CA93371
  • [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 / Iodine Radioisotopes; 0 / Peptides; 0 / Peptides, Cyclic; 0 / Receptors, Somatostatin; 0 / octreotate, Tyr(3)-; 0 / somatostatin receptor 2; 7440-31-5 / Tin; XI595HAL7H / Astatine
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68. Sawai H, Okada Y, Funahashi H, Matsuo Y, Takeyama H, Manabe T: Anaplastic carcinoma of the pancreas with squamous features: report of a case and immunohistochemical study. Med Sci Monit; 2005 Nov;11(11):CS65-8
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  • [Title] Anaplastic carcinoma of the pancreas with squamous features: report of a case and immunohistochemical study.
  • BACKGROUND: Anaplastic carcinomas of the pancreas are rare aggressive tumors with survival measurable in weeks.
  • Many terms have been applied used to describe these tumors, and anaplastic foci are identified in ductal adenocarcinomas and in ectopic pancreata, but are not the dominant pattern of growth.
  • We herein present our experience with a case of anaplastic carcinoma of the pancreas with squamous features in order that allowed us to delineate the clinicopathologic and immunohistochemical features of this rare entity.
  • CASE REPORT: According to imaging findings, the 77-year-old Japanese man was diagnosed as the malignant pancreatic tumor, and underwent a surgical resection.
  • Histopathologically, anaplastic tumor cells showed focal ductal and squamous features infiltrated into pancreatic parenchyma, extrapancreatic fatty tissue, and stomach.
  • The tumor cells showed strong reactivity for cytokeratin, alpha-SMA, vimentin, NSE, and S-100 protein.
  • Although immunoreactivity against p53 was negative, strong positive immunostaining for proliferating cell nuclear antigen and interleukin-1 receptor type I (IL-1RI) was observed in a the majority of tumor cells, while the alpha6 integrin subunit was predominantly strong expressed in the adenocarcinomatous lesion.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma / diagnosis. Integrins / analysis. Pancreatic Neoplasms / diagnosis. Receptors, Interleukin-1 / analysis
  • [MeSH-minor] Aged. Carcinoma, Squamous Cell / diagnosis. Fatal Outcome. Humans. Immunohistochemistry. Male. Peritoneal Neoplasms / diagnosis. Peritoneal Neoplasms / secondary. Prognosis

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  • (PMID = 16258403.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Integrins; 0 / Receptors, Interleukin-1
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69. Maher JC, Savaraj N, Priebe W, Liu H, Lampidis TJ: Differential sensitivity to 2-deoxy-D-glucose between two pancreatic cell lines correlates with GLUT-1 expression. Pancreas; 2005 Mar;30(2):e34-9
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  • [Title] Differential sensitivity to 2-deoxy-D-glucose between two pancreatic cell lines correlates with GLUT-1 expression.
  • OBJECTIVES: To determine whether the differential growth inhibition of pancreatic tumor cells to the glycolytic inhibitor 2-deoxy-D-glucose (2-DG) correlates with uptake, expression of GLUT-1 transporter, and levels of hypoxic-inducible factor-1alpha.
  • METHODS: Growth inhibition assays with 2-DG, lactic acid analysis, Western blots of GLUT-1, and hypoxic-inducible factor-1alpha were correlated with each other and with uptake and accumulation of radio-labeled 2-DG in 2 pancreatic cell lines.
  • RESULTS: Under normal oxygen tension, we find that the pancreatic cell line MIA PaCa2 (1420) is 7 times more sensitive to 2-DG and equally sensitive to oxamate, as compared with Panc-1 (1469).
  • Lactate levels in both cell types are similarly low, indicating that mitochondria are functioning normally in these cells and that they are not solely dependent on glycolysis for survival under an aerobic microenvironment.
  • Since oxamate does not use glucose transporters for entry into the cell, the equal sensitivity to this drug suggests that the selective growth inhibition of 2-DG in these 2 cell types might be reflective of differential expression of glucose transporters.
  • Indeed, we find that GLUT-1 is more highly expressed in 1420 and that this cell line accumulates 2-DG twice as much as 1469.
  • Additionally, hypoxic-inducible factor, which is known to upregulate the expression of GLUT-1, is found at equally low levels in both cell types.
  • CONCLUSION: Overall, our results suggest that certain pancreatic tumors may be inherently sensitive to 2-DG, even under normal oxygen tension, due to greater intracellular accumulation of this inhibitor.
  • Moreover, if 2-DG shows clinical efficacy, it may be possible to predict which pancreatic tumors would be sensitive to this agent based on their GLUT-1 expression profile and their increased uptake of 2-fluoro-deoxy-D-glucose currently used to image tumors via PET scanning.
  • [MeSH-major] Antimetabolites / pharmacokinetics. Deoxyglucose / pharmacokinetics. Excitatory Amino Acid Transporter 2 / metabolism. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Line, Tumor. Drug Resistance, Neoplasm. Glycolysis / drug effects. Glycolysis / physiology. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Lactic Acid / metabolism. Mitochondria / metabolism

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  • (PMID = 15714127.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA37109
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites; 0 / Biomarkers, Tumor; 0 / Excitatory Amino Acid Transporter 2; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 33X04XA5AT / Lactic Acid; 9G2MP84A8W / Deoxyglucose
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70. El-Rayes BF, Ali S, Philip PA, Sarkar FH: Protein kinase C: a target for therapy in pancreatic cancer. Pancreas; 2008 May;36(4):346-52
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  • [Title] Protein kinase C: a target for therapy in pancreatic cancer.
  • OBJECTIVES: Protein kinase C (PKC) is involved in tumor growth and apoptosis and hence represents a potential target for cancer therapy.
  • This study investigated the expression of PKC in pancreatic tumor tissue in comparison to adjacent normal tissue and determined the modulation of PKC by bryostatin-1 (BRYO) on pancreatic cancer cell lines.
  • METHODS: Pancreatic tissue was obtained from 18 patients who had a resection (14 with ductal adenocarcinoma and 4 with adenoma and high-grade dysplasia).
  • HPAC cells were treated with gemcitabine and BRYO and in sequential and concomitant combination.
  • To evaluate cell viability, apoptosis, and electrophoretic mobility shift assay, 3-(4,5-dimetylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, enzyme-linked immunosorbent assay, and nuclear factor kappaB (NF-kappaB) assays were used.
  • RESULTS: As compared with the adjacent normal tissue, PKC-alpha, PKC-beta1, and PKC-delta were higher in the tumor; PKC-epsilon was higher in the normal tissue.
  • Pretreatment with gemcitabine followed by BRYO resulted in decreased cell viability, increased apoptosis, and inhibited NF-kappaB than either agent alone or BRYO followed by gemcitabine.
  • CONCLUSION: Protein kinase C is overexpressed and activated in pancreatic cancer as compared with normal tissue.
  • Inhibition of PKC could sensitize pancreatic cancer cell lines to the effects of gemcitabine.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Isoenzymes / antagonists & inhibitors. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / enzymology. Protein Kinase C / antagonists & inhibitors
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / enzymology. Adenocarcinoma / pathology. Adenoma / drug therapy. Adenoma / enzymology. Adenoma / pathology. Bryostatins / administration & dosage. Cell Survival / drug effects. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Humans. Protein Kinase Inhibitors / therapeutic use. Reference Values

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  • (PMID = 18437080.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bryostatins; 0 / Isoenzymes; 0 / Protein Kinase Inhibitors; 0W860991D6 / Deoxycytidine; 37O2X55Y9E / bryostatin 1; B76N6SBZ8R / gemcitabine; EC 2.7.11.13 / Protein Kinase C
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71. Ralhan R, Desouza LV, Matta A, Tripathi SC, Ghanny S, Datta Gupta S, Bahadur S, Siu KW: Discovery and verification of head-and-neck cancer biomarkers by differential protein expression analysis using iTRAQ labeling, multidimensional liquid chromatography, and tandem mass spectrometry. Mol Cell Proteomics; 2008 06;7(6):1162-73
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  • [Title] Discovery and verification of head-and-neck cancer biomarkers by differential protein expression analysis using iTRAQ labeling, multidimensional liquid chromatography, and tandem mass spectrometry.
  • Multidimensional LC-MS/MS has been used for the analysis of biological samples labeled with isobaric mass tags for relative and absolute quantitation (iTRAQ) to identify proteins that are differentially expressed in human head-and-neck squamous cell carcinomas (HNSCCs) in relation to non-cancerous head-and-neck tissues (controls) for cancer biomarker discovery.
  • Fifteen individual samples (cancer and non-cancerous tissues) were compared against a pooled non-cancerous control (prepared by pooling equal amounts of proteins from six non-cancerous tissues) in five sets by on-line and off-line separation.
  • Some of the proteins include stratifin (14-3-3sigma); YWHAZ (14-3-3zeta); three calcium-binding proteins of the S100 family, S100-A2, S100-A7 (psoriasin), and S100-A11 (calgizarrin); prothymosin alpha (PTHA); L-lactate dehydrogenase A chain; glutathione S-transferase Pi; APC-binding protein EB1; and fascin.
  • Verification of differential expression of YWHAZ, stratifin, and S100-A7 proteins in clinical samples of HNSCCs and paired and non-paired non-cancerous tissues by immunohistochemistry, immunoblotting, and RT-PCR confirmed their overexpression in head-and-neck cancer.
  • Verification of YWHAZ, stratifin, and S100-A7 in an independent set of HNSCCs achieved a sensitivity of 0.92 and a specificity of 0.87 in discriminating cancerous from non-cancerous head-and-neck tissues, thereby confirming their overexpressions and utility as credible cancer biomarkers.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Chromatography, Liquid / methods. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Head and Neck Neoplasms / metabolism. Proteomics / methods. Tandem Mass Spectrometry / methods
  • [MeSH-minor] 14-3-3 Proteins / chemistry. Calcium-Binding Proteins / chemistry. Epithelium / metabolism. Exonucleases / chemistry. Exoribonucleases. Humans. Immunohistochemistry / methods. Models, Molecular. Neoplasm Proteins / chemistry. S100 Proteins. Sensitivity and Specificity


72. Schwartz GG, Eads D, Naczki C, Northrup S, Chen T, Koumenis C: 19-nor-1 alpha,25-dihydroxyvitamin D2 (paricalcitol) inhibits the proliferation of human pancreatic cancer cells in vitro and in vivo. Cancer Biol Ther; 2008 Mar;7(3):430-6
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  • [Title] 19-nor-1 alpha,25-dihydroxyvitamin D2 (paricalcitol) inhibits the proliferation of human pancreatic cancer cells in vitro and in vivo.
  • 1,25-dihydroxyvitamin D(3), (1,25(OH)(2)D(3); calcitriol), the hormonal form of vitamin D, exerts growth-inhibitory, pro-apoptotic and anti-metastatic effects on tumor cells in vitro and in vivo but its clinical use is limited by its calcemic effects.
  • Previous studies have shown that the antiproliferative effects of the less calcemic calcitriol analog 19-nor-1,25-(OH)(2)D(2) (paricalcitol) on prostate tumor cell lines are indistinguishable from those of 1,25(OH)(2)D(3).
  • We therefore investigated the anti-proliferative effects of paricalcitol on the growth of pancreatic tumor cell lines in vitro and in vivo.
  • This antiproliferative activity correlated with upregulation of the cell cycle inhibitors p21 (Waf1/CIP1) and p27(Kip1).
  • A fourth pancreatic cell line, Hs766T was unresponsive to both paricalcitol and calcitriol.
  • Hs766T cells also failed to upregulate p21/Waf-1/Cip1 or p27/KiP in response to treatments with these agents.
  • Paricalcitol, given three times per week inhibited the growth of AsPC-1 pancreatic tumor cell xenografts in nude mice at a dose that did not cause hypercalcaemia.
  • Tumor inhibition was accompanied by in vivo upregulation of p21 and p27 expression.
  • Given the few therapeutic options for patients with pancreatic cancer, further exploration of paricalcitol, an FDA-approved medication, is warranted.
  • [MeSH-major] Bone Density Conservation Agents / pharmacology. Cell Division / drug effects. Ergocalciferols / pharmacology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Line, Tumor. Humans. Models, Molecular

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  • [CommentIn] Cancer Biol Ther. 2008 Mar;7(3):437-9 [18421252.001]
  • (PMID = 18094617.001).
  • [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 / Bone Density Conservation Agents; 0 / Ergocalciferols; 6702D36OG5 / paricalcitol
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73. Chang Q, Qin R, Huang T, Gao J, Feng Y: Effect of antisense hypoxia-inducible factor 1alpha on progression, metastasis, and chemosensitivity of pancreatic cancer. Pancreas; 2006 Apr;32(3):297-305
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  • [Title] Effect of antisense hypoxia-inducible factor 1alpha on progression, metastasis, and chemosensitivity of pancreatic cancer.
  • OBJECTIVES: The aim of the study was to observe the effect of antisense hypoxia-inducible factor 1alpha (HIF-1alpha) on progression, metastasis, and chemosensitivity of pancreatic cancer.
  • METHODS: BxPc-3 cells transfected with antisense HIF-1alpha plasmid were exposed to 0.5% O2 for 4 hours.
  • Growth inhibition rates and apoptosis rates of BxPc-3 cells under different dosages of chemotherapy agents (5-fluorouracil, doxorubicin, and gemcitabine) were measured by MTT colorimetric assay and flow cytometry.
  • The migration of BxPc-3 cells was assayed using transwell cell culture chambers.
  • Subcutaneous transplantation of BxPc-3 cells in nude mice for 8 weeks was to assess progression and metastasis of pancreatic cancer.
  • The number of migrated BxPc-3 cells in the experimental group was far less than in control (P < 0.05).
  • In vivo, the tumor size and weight in the experimental group were significantly lower than those in control (P < 0.05).
  • CONCLUSION: Our data demonstrate that antisense HIF-1alpha inhibits expressions of survivin and beta1 integrin, enhancing apoptosis in human pancreatic cancer cells and restraining the progression and metastasis of pancreatic cancer.
  • Therefore, HIF-1alpha may play a very important role in progression, metastasis, and chemosensitivity of human pancreatic cancer.
  • Blocking HIF-1alpha in pancreatic cancer cells may offer an avenue for gene therapy.
  • [MeSH-major] Antisense Elements (Genetics) / pharmacology. Hypoxia-Inducible Factor 1, alpha Subunit / antagonists & inhibitors. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antigens, CD29 / analysis. Antigens, CD29 / genetics. Apoptosis. Cell Line, Tumor. Cell Movement. Colorimetry. Disease Progression. Flow Cytometry. Genetic Therapy. Humans. Inhibitor of Apoptosis Proteins. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / genetics. Neoplasm Metastasis. Neoplasm Proteins / analysis. Neoplasm Proteins / genetics. Neoplasm Transplantation. Transplantation, Heterologous

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  • (PMID = 16628086.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD29; 0 / Antisense Elements (Genetics); 0 / BIRC5 protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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74. Ji Y, Wang XN, Lou WH, Sujie A, Tan YS, Jin DY: Serous cystic neoplasms of the pancreas: a clinicopathologic and immunohistochemical analysis. Chin J Dig Dis; 2006;7(1):39-44
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  • [Title] Serous cystic neoplasms of the pancreas: a clinicopathologic and immunohistochemical analysis.
  • OBJECTIVE: To clarify whether the various subtypes of serous cystic neoplasms (SCNs) of the pancreas can be distinguished from each other by marker profiles.
  • In addition, we examined the expression of calrentinin and alpha-inhibin.
  • RESULTS: SCN included 7 cases of serous microcystic adenomas (SMA), 3 cases of serous oligocystic ill-defined adenomas (SOIA), 1 case of solid serous adenoma (SSA), 1 case of von Hippel-Lindau-associated cystic neoplasm (VHL-CN), and 1 case of serous cystadenocarcinoma (SCC).
  • These neoplasms are histologically similar, but differ in their localization, gross appearance, gender distribution, and biological behavior.
  • Other markers that were commonly expressed in the SCNs were alpha-inhibin (85%), MUC1 (69%) and MUC6 (77%).
  • CONCLUSION: The results suggest that, despite their biologic differences, the various types of SCNs have the same (or a very similar) cell type and may therefore have a common direction of differentiation.
  • A centroacinar origin is supported by the finding that a number of SCNs share MUC1 and MUC6 expression with pancreatic centroacinar cells.
  • Alpha-inhibin, and MUC6 may be regarded as new markers for this type of pancreatic tumor.
  • [MeSH-major] Cystadenoma, Serous / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Biomarkers, Tumor. Female. Humans. Immunohistochemistry. Male. Middle Aged. Tomography, X-Ray Computed


75. Holloway SE, Beck AW, Girard L, Jaber MR, Barnett CC Jr, Brekken RA, Fleming JB: Increased expression of Cyr61 (CCN1) identified in peritoneal metastases from human pancreatic cancer. J Am Coll Surg; 2005 Mar;200(3):371-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased expression of Cyr61 (CCN1) identified in peritoneal metastases from human pancreatic cancer.
  • BACKGROUND: Identification of extracellular matrix proteins (ECM) associated with tumor cell metastasis may generate targets for future therapy against pancreatic cancer metastases.
  • We hypothesized that comparison of ECM-associated gene expression in primary and metastatic pancreatic tumors would identify ECM proteins associated with pancreatic metastasis.
  • STUDY DESIGN: A clinically relevant model of pancreatic cancer was used to generate RNA from primary and metastatic tumors; it was evaluated by microarray analysis with subsequent cluster analysis.
  • Target genes (Cyr61 and integrins alpha(v) and beta(3)) identified by microarray analysis were confirmed by reverse transcription polymerase chain reaction and immunohistochemistry analysis.
  • RESULTS: Peritoneal metastases at sites distant from the primary tumor were present in all animals bearing orthotopic tumors.
  • High-density microarray comparison of gene expression in metastases versus primary pancreatic tumors identified a greater than twofold increase in the expression of Cyr61, a secreted matricellular protein that binds to integrins.
  • Reverse transcription polymerase chain reaction confirmed the microarray results, and immunohistochemistry analysis demonstrated increased Cyr61 protein and persistent alpha(v)beta(3) expression in peritioneal metastases.
  • Additionally, immunohistochemistry demonstrated increased collocalization of Cyr61 and alpha(v) in metastases relative to primary tumor.
  • CONCLUSIONS: The ECM protein Cyr61 shows increased expression in metastatic lesions in a clinically relevant model of pancreatic adenocarcinoma.
  • Protein analysis confirms the microarray results and collocalization of Cyr61, and alpha(v) suggests that interaction between Cyr61 and alpha(v)beta(3) promotes formation of peritoneal metastases.
  • [MeSH-major] Adenocarcinoma / secondary. Gene Expression Regulation, Neoplastic / genetics. Immediate-Early Proteins / genetics. Intercellular Signaling Peptides and Proteins / genetics. Pancreatic Neoplasms / pathology. Peritoneal Neoplasms / secondary
  • [MeSH-minor] Animals. Antibodies, Neoplasm / immunology. Cluster Analysis. Cysteine-Rich Protein 61. Extracellular Matrix Proteins / genetics. Extracellular Matrix Proteins / metabolism. Female. Humans. Immunohistochemistry. Mice. Mice, Nude. Neoplasm Transplantation. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 15737847.001).
  • [ISSN] 1072-7515
  • [Journal-full-title] Journal of the American College of Surgeons
  • [ISO-abbreviation] J. Am. Coll. Surg.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / CYR61 protein, human; 0 / Cyr61 protein, mouse; 0 / Cysteine-Rich Protein 61; 0 / Extracellular Matrix Proteins; 0 / Immediate-Early Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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76. Seo DW: EUS-Guided Antitumor Therapy for Pancreatic Tumors. Gut Liver; 2010 Sep;4 Suppl 1:S76-81

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  • [Title] EUS-Guided Antitumor Therapy for Pancreatic Tumors.
  • Endoscopic ultrasound (EUS) is a very useful modality for the diagnosis and staging of pancreatic masses.
  • With the advent of EUS-guided fine-needle aspiration technology, this modality has made a tremendous leap from imaging modality to histologic diagnosis and therapeutic intervention.
  • EUS offers high-resolution images of and unparalleled access to the pancreas.
  • After locating the tip of the echoendoscope in the duodenum or stomach, several drugs or local treatment modalities can be delivered directly into the pancreas.
  • EUS-guided ethanol lavage with/without paclitaxel injection has been tested for the treatment of cystic tumors of the pancreas, with complete resolution of cystic tumor being observed in up to 70-80% of patients.
  • Ethanol injection is also performed for the management of solid neuroendocrine tumors of the pancreas.
  • Various type of EUS-guided injection have also been investigated for the treatment of pancreatic cancer.
  • An activated allogenic mixed lymphocyte culture (Cytoimplant) was injected in patients with advanced pancreatic cancer.
  • A replication-deficient adenovirus vector carrying the tumor necrosis factor-alpha gene was also delivered intratumorally by EUS.
  • ONYX-015 is an oncolytic attenuated adenovirus that exhibits replication preferentially in malignant cells, causing cell death, and this has also been injected into pancreatic cancers under EUS guidance.
  • This article reviews the various applications of EUS for the treatment of pancreatic tumors.

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  • (PMID = 21103299.001).
  • [ISSN] 2005-1212
  • [Journal-full-title] Gut and liver
  • [ISO-abbreviation] Gut Liver
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2989554
  • [Keywords] NOTNLM ; Brachytherapy / Cystic tumor / Cytoimplant / Endoscopic ultrasonography / Immunotherapy / Pancreas cancer / Photodynamic therapy / Radiofrequency ablation
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77. Korkolis DP, Aggeli C, Plataniotis GD, Gontikakis E, Zerbinis H, Papantoniou N, Xinopoulos D, Apostolikas N, Vassilopoulos PP: Successful en bloc resection of primary hepatocellular carcinoma directly invading the stomach and pancreas. World J Gastroenterol; 2009 Mar 7;15(9):1134-7
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  • [Title] Successful en bloc resection of primary hepatocellular carcinoma directly invading the stomach and pancreas.
  • Multivisceral surgical resection for cure was successfully performed in a 70-year-old man suffering from a primary hepatocellular carcinoma (HCC) associated with direct invasion to the stomach and pancreas.
  • The patient presented with gastric outlet obstruction, upper abdominal pain and a history of chronic liver disease due to hepatitis B virus (HBV) infection.
  • Upper gastrointestinal (GI) endoscopy revealed an infiltrating tumor protruding through the gastric wall and obliterating the lumen.
  • Computer tomograghy (CT) and magnetic resonance imaging (MRI) scan demonstrated a 15-cm tumor in the left lateral segment of the liver with invasion to the stomach and pancreas.
  • Alpha-foetoprotein (AFP) levels and liver function tests were normal.
  • Pathology revealed a poorly differentiated, giant cell HCC involving the stomach and pancreas.
  • Disease-free margins of resection were achieved.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Liver Neoplasms / pathology. Liver Neoplasms / surgery. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery. Stomach Neoplasms / surgery
  • [MeSH-minor] Aged. Endoscopy. Gastrectomy. Hepatectomy. Humans. Middle Aged. Neoplasm Invasiveness / pathology. Pancreatectomy. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 19266609.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2655177
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78. Li Q, Feng FY, Chen Q, Jiao SC, Li F, Wang HQ, Huang WX, Ling CQ, Li MZ, Ren J, Zhang Y, Qin FZ, Zhou MZ, Zhu RZ: [Multicenter phase II clinical trial of uroacitides injection in the treatment for advanced malignant tumors]. Zhonghua Zhong Liu Za Zhi; 2008 Jul;30(7):534-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Multicenter phase II clinical trial of uroacitides injection in the treatment for advanced malignant tumors].
  • OBJECTIVE: To investigate the efficacy, safety and the life quality improvement of uroacitides injection in the treatment for patients with advanced malignant tumors.
  • METHODS: A total of 160 patients with advanced stage cancers were enrolled into this multicenter, open and non-randomized phase II clinical trial, including cancers of the lung (33 cases), liver (45 cases), breast (17 cases), esophagus (11 cases), stomach (18 cases), colon (19 cases), pancreas (3 cases) and kidney (4 cases), and glioma (10 cases).
  • The total objective response rate (ORR, CR + PR)) and tumor control rate (CR + PR + MR + SD) of the 138 evaluable patients were 5.8% and 65.2%, respectively.
  • [MeSH-major] Liver Neoplasms / drug therapy. Lung Neoplasms / drug therapy. Methyltransferases / therapeutic use. Peptides / therapeutic use. Phenylacetates / therapeutic use
  • [MeSH-minor] Breast Neoplasms / blood. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. CA-19-9 Antigen / blood. Carcinoembryonic Antigen / blood. Carcinoma, Non-Small-Cell Lung / blood. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / pathology. Catheterization, Central Venous. Colorectal Neoplasms / blood. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / pathology. Humans. Nausea / chemically induced. Neoplasm Staging. Quality of Life. Remission Induction. Salvage Therapy. Treatment Outcome. Vomiting / chemically induced. alpha-Fetoproteins / metabolism

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  • (PMID = 19062723.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] Clinical Trial, Phase II; English Abstract; Journal Article; Multicenter Study
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CA-19-9 Antigen; 0 / Carcinoembryonic Antigen; 0 / Peptides; 0 / Phenylacetates; 0 / alpha-Fetoproteins; 0 / cell differentiation agent II; EC 2.1.1.- / Methyltransferases
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79. Zou GM, Maitra A: Small-molecule inhibitor of the AP endonuclease 1/REF-1 E3330 inhibits pancreatic cancer cell growth and migration. Mol Cancer Ther; 2008 Jul;7(7):2012-21
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  • [Title] Small-molecule inhibitor of the AP endonuclease 1/REF-1 E3330 inhibits pancreatic cancer cell growth and migration.
  • APE1 is overexpressed in several human cancers, and disruption of APE1 function has detrimental effects on cancer cell viability.
  • However, the selective contribution of the redox and the DNA repair domains to maintenance of cellular homeostasis in cancer has not been elucidated.
  • In the present study, we used E3330, a small-molecule inhibitor of APE1 redox domain function, to interrogate the functional relevance of sustained redox function in pancreatic cancer.
  • We show that E3330 significantly reduces the growth of human pancreatic cancer cells in vitro.
  • This phenomenon was further confirmed by a small interfering RNA experiment to knockdown APE1 expression in pancreatic cancer cells.
  • E3330 exposure promotes endogenous reactive oxygen species formation in pancreatic cancer cells, and the resulting oxidative stress is associated with higher levels of oxidized, and hence inactive, SHP-2, an essential protein tyrosine phosphatase that promotes cancer cell proliferation in its active state.
  • Finally, E3330 treatment inhibits pancreatic cancer cell migration as assessed by in vitro chemokine assays.
  • E3330 shows anticancer properties at multiple functional levels in pancreatic cancer, such as inhibition of cancer cell growth and migration.
  • Inhibition of the APE1 redox function through pharmacologic means has the potential to become a promising therapeutic strategy in this disease.
  • [MeSH-major] Benzoquinones / pharmacology. Cell Movement / drug effects. DNA-(Apurinic or Apyrimidinic Site) Lyase / antagonists & inhibitors. Enzyme Inhibitors / pharmacology. Pancreatic Neoplasms / enzymology. Pancreatic Neoplasms / pathology. Propionates / pharmacology
  • [MeSH-minor] Antigens, CD44 / metabolism. Cell Hypoxia / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Chemokine CXCL12 / metabolism. DNA, Neoplasm / metabolism. Enzyme Activation / drug effects. Epithelial Cells / drug effects. Epithelial Cells / pathology. G1 Phase / drug effects. G2 Phase / drug effects. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Models, Biological