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6. Altadill A, Rodríguez M, González LO, Junquera S, Corte MD, González-Dieguez ML, Linares A, Barbón E, Fresno-Forcelledo M, Rodrigo L, Vizoso FJ: Liver expression of matrix metalloproteases and their inhibitors in hepatocellular carcinoma. Dig Liver Dis; 2009 Oct;41(10):740-8
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  • [Title] Liver expression of matrix metalloproteases and their inhibitors in hepatocellular carcinoma.
  • BACKGROUND: Several studies have suggested the significance of some metalloproteases in the malignant behaviour of hepatocellular carcinoma.
  • Increased TIMP-2 expression was associated with higher preoperative serum levels of alpha-fetoprotein (p<0.01).
  • Unsupervised hierarchical clustering for total score values designated two groups, one of them characterised by high MMPs and TIMPs expressions, including 21 cases (70%) for tumour cell clustering, 5 cases for fibroblasts (16.6%) and 6 cases for inflammatory cells (20%).
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Liver Neoplasms / metabolism. Matrix Metalloproteinase 1 / metabolism. Matrix Metalloproteinase 13 / metabolism. Tissue Inhibitor of Metalloproteinase-1 / metabolism. Tissue Inhibitor of Metalloproteinase-2 / metabolism

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  • [CommentIn] Dig Liver Dis. 2009 Oct;41(10):707-8 [19699696.001]
  • (PMID = 19372066.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Tissue Inhibitor of Metalloproteinase-1; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; EC 3.4.24.- / Matrix Metalloproteinase 13; EC 3.4.24.7 / Matrix Metalloproteinase 1
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7. Nishioka C, Ikezoe T, Jing Y, Umezawa K, Yokoyama A: DHMEQ, a novel nuclear factor-kappaB inhibitor, induces selective depletion of alloreactive or phytohaemagglutinin-stimulated peripheral blood mononuclear cells, decreases production of T helper type 1 cytokines, and blocks maturation of dendritic cells. Immunology; 2008 Jun;124(2):198-205
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  • Dehydroxymethylepoxyquinomicin (DHMEQ), a novel nuclear factor kappaB (NF-kappaB) inhibitor, has been shown to be active against variety types of solid tumours as well as haematological malignant cells.
  • In addition, real-time polymerase chain reaction showed that DHMEQ decreased PHA-stimulated expression of T helper type 1 (Th1) cytokines, including interleukin-2, interferon-gamma, and tumour necrosis factor alpha, in PBMC as well as Jurkat T-lymphoblastic leukaemia cells, and also decreased levels of p65 isoforms of NF-kappaB in the nucleus.
  • Furthermore, we found that DHMEQ inhibited the endocytic capacity of dendritic cells (DCs) and down-regulated the expression of cell surface antigen CD40, suggesting that DHMEQ blocked the maturation as well as the function of DCs.
  • Taken together, the results suggest that DHMEQ may be useful for treatment of inflammatory diseases, including graft-versus-host disease after allogenic haematopoietic stem cell transplantation.
  • [MeSH-minor] Apoptosis / drug effects. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. Endocytosis / drug effects. Humans. Jurkat Cells. Lymphocyte Culture Test, Mixed. Phytohemagglutinins / immunology. Th1 Cells / drug effects. Th1 Cells / immunology

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  • (PMID = 18217958.001).
  • [ISSN] 1365-2567
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Benzamides; 0 / Cyclohexanones; 0 / Cytokines; 0 / Phytohemagglutinins; 0 / dehydroxymethylepoxyquinomicin
  • [Other-IDs] NLM/ PMC2566624
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8. Colović R, Matić S, Micev M, Grubor N, Latincić S: [Glucagonoma without glucagonoma syndrome]. Srp Arh Celok Lek; 2010 Mar-Apr;138(3-4):244-7
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  • [Title] [Glucagonoma without glucagonoma syndrome].
  • INTRODUCTION: Glucagonomas are rare, frequently malignant tumours, arising from the Langerhans' islets of the pancreas.
  • They usually secrete large amounts of glucagon that can cause a characteristic "glucagonoma syndrome", which includes necrolytic migratory erythema, glucose intolerance or diabetes, weight loss and sometimes, normochromic normocytic anaemia, stomatitis or cheilitis, diarrhoea or other digestive symptoms, thoromboembolism, hepatosplenomegaly, depression or other psychiatric and paraneoplastic symptoms.
  • In certain cases, some or all glucagonoma symptoms may appear late, or even may be completely absent.
  • CASE OUTLINE: The authors present a 43-year-old woman in whom an investigation for abdominal pain revealed a tumour of the body of the pancreas.
  • During operation, the tumour of the body of the pancreas extending to the mesentery measuring 85 x 55 x 55 mm was excised.
  • Histology and immunohistochemistry showed malignant glucagonoma, with co-expression of somatostatin in about 5% and pancreatic polypeptide in a few tumour cells.
  • CONCLUSION: Glucagonoma syndrome may be absent in glucagonoma tumour patients so that in unclear pancreatic tumours the clinician should frequently request the serum hormone level (including glucagon) measurement by radioimmunoassay and the pathologist should perform immunohistochemistry investigation.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20499510.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Serbia
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9. Catassi A, Paleari L, Servent D, Sessa F, Dominioni L, Ognio E, Cilli M, Vacca P, Mingari M, Gaudino G, Bertino P, Paolucci M, Calcaterra A, Cesario A, Granone P, Costa R, Ciarlo M, Alama A, Russo P: Targeting alpha7-nicotinic receptor for the treatment of pleural mesothelioma. Eur J Cancer; 2008 Oct;44(15):2296-311
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  • Human malignant pleural mesothelioma (MPM) is a dreadful disease and there is still no standard therapy available for a consistent therapeutic approach.
  • This research is aimed at the evaluation of the potential therapeutic effect of a specific nicotinic receptor (nAChR) antagonist, namely alpha-Cobratoxin (alpha-CbT).
  • Its effectiveness was tested in mesothelioma cell lines and in primary mesothelioma cells in vitro, as well as in vivo, in orthotopically xenotransplanted NOD/SCID mice.
  • Cells showed alpha7-nAChR expression and their growth was significantly inhibited by alpha-CbT.
  • Severe induction of apoptosis was observed after exposure to alpha-CbT [IC(80-90)].
  • In vivo, the alpha-CbT acute LD(50) was 0.15 mg/kg.
  • Phase II experiments with 0.12 ng/kg alpha-CbT (1/1000 of LD(10)) were done in 53 xenotransplanted mice, inhibiting tumour development as confirmed by chest X-ray examinations, autopsy and microscopical findings.
  • The growth of human proliferating T lymphocytes and of mesothelial cells in primary culture was not affected by alpha-CbT.
  • Non-immunogenic derivatives of the alpha-CbT molecule need to be developed for possible human use.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical / methods. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Proteins / metabolism. Neoplasm Transplantation. Reverse Transcriptase Polymerase Chain Reaction / methods. Transplantation, Heterologous. Tumor Cells, Cultured. alpha7 Nicotinic Acetylcholine Receptor

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  • (PMID = 18722110.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chrna7 protein, human; 0 / Chrna7 protein, mouse; 0 / Cobra Neurotoxin Proteins; 0 / Neoplasm Proteins; 0 / Nicotinic Antagonists; 0 / Receptors, Nicotinic; 0 / alpha7 Nicotinic Acetylcholine Receptor; 69344-74-7 / alpha-cobratoxin
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10. Yamamoto E, Ino K, Miyoshi E, Shibata K, Takahashi N, Kajiyama H, Nawa A, Nomura S, Nagasaka T, Kikkawa F: Expression of N-acetylglucosaminyltransferase V in endometrial cancer correlates with poor prognosis. Br J Cancer; 2007 Dec 3;97(11):1538-44
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  • N-acetylglucosaminyltransferase V (GnT-V) is an enzyme that catalyses beta1-6 branching of N-acetylglucosamine on asparagine-linked oligosaccharides of cell proteins.
  • High GnT-V expression in tumour cells was found in 43 (58.1%) of the 74 cases, and was positively correlated with advanced patient age, histological grade, and lymph vascular space involvement.
  • These results suggested that high GnT-V expression was correlated with an unfavourable clinical outcome, and that GnT-V is involved in the malignant potential of endometrial cancer by increasing the synthesis of beta1-6 branching of asparagine-linked oligosaccharides.

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  • (PMID = 17971775.001).
  • [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
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  • [Other-IDs] NLM/ PMC2360248
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11. Mendoza-Guil F, Hernández-Jurado I, Burkhardt P, Linares J, Naranjo R: [Necrolytic migratory erythema associated with glucagonoma]. Actas Dermosifiliogr; 2005 Apr;96(3):175-8
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  • [Title] [Necrolytic migratory erythema associated with glucagonoma].
  • [Transliterated title] Eritema necrolítico migratorio asociado a glucagonoma.
  • Glucagonoma is a rare pancreatic tumor that is usually associated with a syndrome that includes diabetes, anemia, weight loss and skin lesions in the form of necrolytic migratory erythema.
  • We present the case of a patient with malignant glucagonoma treated with surgery and octreotide, which manifested with skin lesions.
  • The discussion will review the physiopathology, other causes of necrolytic erythema, diagnosis and differential diagnosis and treatment.
  • [MeSH-major] Erythema / complications. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications

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  • (PMID = 16476361.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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12. Sánchez Carazo JL, Mahiques Santos L, Oliver Martinez V: Safety of etanercept in psoriasis: a critical review. Drug Saf; 2006;29(8):675-85
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  • The drug is a competitive inhibitor of tumour necrosis factor-alpha (TNFalpha) that prevents interaction between this cytokine and its cell surface receptors.
  • Etanercept also modulates the activity of other inflammatory cytokines and does not induce complement-mediated cell lysis in vitro.
  • The most common adverse effect during drug administration is mild injection site reactions.
  • There are no data showing that treatment with etanercept results in an increase in the occurrence of malignant neoplasms.
  • Etanercept must be used with extreme caution in patients with heart failure because of several reports indicating a worsening or de novo occurrence of congestive heart failure while receiving the drug.
  • In patients with hepatitis C viral infection, etanercept does not increase transaminase levels or viral load and in some instances has allowed the concomitant use of interferon which had previously been discontinued because of a worsening of psoriasis.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / adverse effects. Immunoglobulin G / adverse effects. Psoriasis / drug therapy. Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • [MeSH-minor] Child. Etanercept. Female. Humans. Practice Guidelines as Topic. Pregnancy. Randomized Controlled Trials as Topic. Receptors, Tumor Necrosis Factor

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  • (PMID = 16872241.001).
  • [ISSN] 0114-5916
  • [Journal-full-title] Drug safety
  • [ISO-abbreviation] Drug Saf
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept
  • [Number-of-references] 86
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13. Nakashima C, Tanioka M, Takahashi K, Miyachi Y: Diffuse large B-cell lymphoma in a patient with rheumatoid arthritis treated with infliximab and methotrexate. Clin Exp Dermatol; 2008 Jul;33(4):437-9
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  • [Title] Diffuse large B-cell lymphoma in a patient with rheumatoid arthritis treated with infliximab and methotrexate.
  • Infliximab is a tumour necrosis factor (TNF)-alpha blocking drug classified as a biological response modifier.
  • It has been suggested that the risk of malignancies, especially lymphomas, is increased in patients with rheumatoid arthritis (RA) treated with anti-TNF-alpha antibody therapy.
  • We present a case of malignant lymphoma during the treatment of RA with infliximab and methotrexate.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antirheumatic Agents / adverse effects. Arthritis, Rheumatoid / drug therapy. Lymphoma, Large B-Cell, Diffuse / chemically induced. Methotrexate / adverse effects. Skin Neoplasms / chemically induced


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4. Kenny PA: Three-dimensional extracellular matrix culture models of EGFR signalling and drug response. Biochem Soc Trans; 2007 Aug;35(Pt 4):665-8
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  • Three-dimensional extracellular matrix culture, on substrata such as Matrigel, restores many aspects of the differentiated state to non-malignant cells from a variety of tissues.
  • We have adapted these techniques to study EGFR (epidermal growth factor receptor) signalling and drug response in breast cancer cell lines.
  • EGFR-dependent breast cancer cell lines undergo a striking reversion of the malignant phenotype upon treatment with inhibitors targeting the receptor, or downstream signalling intermediates such as mitogen-activated protein kinase and PI3K (phosphoinositide 3-kinase).
  • Using this approach, we have recently reported that EGFR signalling in breast cancer can be effectively inhibited by blocking the activity of a key protease, TACE [TNFalpha (tumour necrosis factor alpha)-converting enzyme], which regulates the bioavailability of EGFR ligands.
  • [MeSH-minor] Humans. Tumor Cells, Cultured

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  • (PMID = 17635116.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 38
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15. de Mestier L, Hammel P, Hentic O, Dove P, Lévy P, Ruszniewski P: [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency]. Gastroenterol Clin Biol; 2010 Jan;34(1):106-10
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  • [Title] [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency].
  • [Transliterated title] Efficacité spectaculaire d'une chimiothérapie par 5-fluoro-uracile et dacarbazine chez un malade atteint de glucagonome métastatique avec insuffisance cardiaque.
  • Malignant glucagonoma is an exceptional pancreatic endocrine tumour, with frequent dermatologic symptoms, diabetes and degradation of the general health status.
  • We report here an observation of a patient who was treated for a glucagonoma with multiple liver metastases, migratory necrolytic erythema, dilated cardiomypathy and diabetes that dramatically improved after a dacarbazin-based chemotherapy, allowing subsequent surgical resection of the primary.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cardiomyopathy, Dilated / complications. Glucagonoma / drug therapy. Liver Neoplasms / drug therapy
  • [MeSH-minor] Adult. Dacarbazine / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery

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  • [Copyright] Copyright 2009. Published by Elsevier Masson SAS.
  • (PMID = 19875259.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 7GR28W0FJI / Dacarbazine; U3P01618RT / Fluorouracil
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16. Sheldrake HM, Patterson LH: Function and antagonism of beta3 integrins in the development of cancer therapy. Curr Cancer Drug Targets; 2009 Jun;9(4):519-40
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  • The integrin family of cell surface receptors integrates cell-extracellular matrix interactions with the cell cytoskeleton and signalling across the cell membrane, resulting in an important role in cell adhesion, mobility and migration, proliferation, and survival.
  • Changes in the number and identity of integrin receptors are common in cancer cells resulting in alteration of the ability of malignant cells to interact with the extracellular matrix, and promoting migration as well as facilitating survival outside the tumour normal environment. beta(3) integrins are potentially involved in every step of the metastatic process and expression of both alpha(IIb)beta(3) and alpha(n)beta(3) is correlated with metastatic ability of tumour cells.
  • In this review, we summarize the role of the beta(3)-subfamily of integrins when expressed in normal and tumour tissue, the development of small-molecule antagonists of beta(3) integrins and their potential anti-cancer applications.

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  • (PMID = 19519320.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Disintegrins; 0 / Integrin beta3; 0 / Integrins; 0 / Peptides; 0 / Peptides, Cyclic
  • [Number-of-references] 265
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17. Miao R, Wei J, Zhang Q, Sajja V, Yang J, Wang Q: Redifferentiation of human hepatoma cells (SMMC-7721) induced by two new highly oxygenated bisabolane-type sesquiterpenes. J Biosci; 2008 Dec;33(5):723-30
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  • Bisabolane-type sesquiterpenes are a class of biologically active compounds that has antitumour,antifungal, antibacterial,antioxidant and antivenom properties.We investigated the effect of two new highly oxygenated bisabolane-type sesquiterpenes (HOBS)isolated from Cremanthodium discoideum (C.discoideum) on tumour cells.
  • Our results showed that HOBS induced morphological differentiation and reduced microvilli formation on the cell surface in SMMC-7721 cells.Flow cytometry analysis demonstrated that HOBS could induce cell-cycle arrest in the G1 phase.
  • Moreover,HOBS was able to increase tyrosine-alpha ketoglutarate transaminase activity,decrease alpha- foetoprotein level and gamma-glutamyl transferase activity.
  • In addition,we found that HOBS inhibited the anchorage- independent growth of SMMC-7721 cells in a dose-dependent manner.Taken together,all the above observations indicate that HOBS might be able to normalize malignant SMMC-7721 cells by inhibiting cell proliferation and inducing redifferentiation.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Carcinoma, Hepatocellular / metabolism. Sesquiterpenes / pharmacology
  • [MeSH-minor] Asteraceae / chemistry. Cell Cycle / drug effects. Cell Differentiation / drug effects. Hepatocytes / drug effects. Humans. Molecular Structure. Structure-Activity Relationship. alpha-Fetoproteins / metabolism. gamma-Glutamyltransferase / metabolism

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  • (PMID = 19179760.001).
  • [ISSN] 0250-5991
  • [Journal-full-title] Journal of biosciences
  • [ISO-abbreviation] J. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] India
  • [Chemical-registry-number] 0 / 1beta,8-diangeloyloxy-2beta-acetoxy-4alpha-chloro-11-methoxy-3beta, 10-dihydroxybisabola-7(14)-ene; 0 / 1beta,8-diangeloyloxy-2beta-acetoxy-4alpha-chloro-3beta-hydroxy-10, 11-o,o-isopropylidenebis-aboia-7(14)-ene; 0 / Antineoplastic Agents, Phytogenic; 0 / Sesquiterpenes; 0 / alpha-Fetoproteins; EC 2.3.2.2 / gamma-Glutamyltransferase
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18. Ringdén O, Karlsson H, Olsson R, Omazic B, Uhlin M: The allogeneic graft-versus-cancer effect. Br J Haematol; 2009 Dec;147(5):614-33
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  • Allogeneic haematological stem cell transplantation (HSCT) has developed into immunotherapy.
  • Donor CD4+, CD8+ and natural killer (NK) cells have been reported to mediate graft-versus-leukaemia (GVL) effects, using Fas-dependent killing and perforin degranulation to eradicate malignant cells.
  • Cytokines, such as interleukin-2, interferon-gamma and tumour necrosis factor-alpha potentiate the GVL effect.
  • Post-transplant adoptive therapy of cytotoxic T-cells (CTL) against leukaemia-specific antigens, minor histocompatibility antigens, or T-cell receptor genes may constitute successful approaches to induce anti-tumour effects.
  • An anti-tumour effect has also been reported for myeloma, lymphoma and solid tumours.
  • Reduced intensity conditioning enables HSCT in older and disabled patients and relies on the graft-versus-tumour effect.
  • A high CD34+ cell dose of peripheral blood stem cells increases GVL.
  • For instance, T-cell depletion of the graft increases the risk of relapse.
  • [MeSH-major] Graft vs Tumor Effect / immunology. Hematopoietic Stem Cell Transplantation / methods. Neoplasms / therapy

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  • (PMID = 19735262.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 243
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19. Stremenova J, Krepela E, Mares V, Trim J, Dbaly V, Marek J, Vanickova Z, Lisa V, Yea C, Sedo A: Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade. Int J Oncol; 2007 Oct;31(4):785-92
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  • [Title] Expression and enzymatic activity of dipeptidyl peptidase-IV in human astrocytic tumours are associated with tumour grade.
  • Alterations in dipeptidyl peptidase-IV (DPP-IV) enzymatic activity are characteristic of malignant transformation.
  • Through its well-characterized functionality in regulating the activity of bioactive peptides by removal of the N-terminal dipeptide, DPP-IV activity may have profound effects upon metastatic potential and cell growth.
  • Although DPP-IV/CD26 (EC 3.4.14.5) is the canonical representative of the group, a number of other proteins including DPP-7, 8, 9, and seprase/fibroblast activation protein-alpha (FAP-alpha) have been shown to have similar enzymatic activity.
  • This study was set up to address the relative representation and enzymatic activity of plasma membrane localized DPP-IV/CD26 and FAP-alpha in human brain and astrocytic tumours.
  • In parallel, expression of CXCR4, receptor for glioma cell growth stimulator chemokine SDF-1alpha known to be a DPP-IV substrate, was investigated.
  • This is the first report showing that non-malignant brain tissue contains a DPP-IV-like enzymatic activity attributable mostly to DPP-8/9, while the substantial part of the activity in glioma is due to increased DPP-IV/CD26, localized in both the vascular and parenchymal compartments.
  • DPP-IV enzymatic activity increased dramatically with tumour grade severity.
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / genetics. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Brain Neoplasms / enzymology. Brain Neoplasms / genetics. Brain Neoplasms / pathology. Cell Membrane / metabolism. Female. Gelatinases. Humans. Immunoenzyme Techniques. Male. Membrane Proteins. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Receptors, CXCR4 / genetics. Receptors, CXCR4 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Serine Endopeptidases / genetics. Serine Endopeptidases / metabolism. Tumor Cells, Cultured

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  • (PMID = 17786309.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, CXCR4; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
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20. Zisakis A, Piperi C, Themistocleous MS, Korkolopoulou P, Boviatsis EI, Sakas DE, Patsouris E, Lea RW, Kalofoutis A: Comparative analysis of peripheral and localised cytokine secretion in glioblastoma patients. Cytokine; 2007 Aug;39(2):99-105
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  • BACKGROUND: Malignant gliomas are the most common primary brain tumours of both children and adults.
  • The unique aspects of their biology and anatomic site render them refractory to conventional therapeutic strategies such as surgery and chemotherapy.
  • METHODS: To further understand the immunobiology of glioblastomas in clinical settings, we examined the secretion of four main cytokines in the peripheral blood and in primary cell cultures of 33 human glioblastoma patients.
  • An ELISPOT methodology was used for the first time to examine Th1, and Th2 cytokine secretion from both peripheral lymphocytes and glioma tumour cells.
  • RESULTS: Th1 cytokines (tumour necrosis factor (TNF-alpha), interferon (IFN-gamma) were markedly reduced compared to control levels (P=0.01 and P<0.001, respectively), whereas in contrast, Th2 (interleukin (IL)-4 and IL-10) were strongly expressed in both peripheral lymphocytes and glioma cell cultures (P=0.05 and P<0.001, respectively).
  • Furthermore, ELISPOT methodology can be used for monitoring of cytokine secretion from tumour cells, in addition to the well-established peripheral cytokine secretion.
  • [MeSH-minor] Adult. Aged. Cells, Cultured. Female. Humans. Interferon-gamma / metabolism. Interferon-gamma / secretion. Interleukin-10 / metabolism. Interleukin-10 / secretion. Interleukin-1beta / metabolism. Interleukin-1beta / secretion. Interleukin-4 / metabolism. Interleukin-4 / secretion. Male. Middle Aged. Tumor Necrosis Factor-alpha / metabolism. Tumor Necrosis Factor-alpha / secretion

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  • (PMID = 17697783.001).
  • [ISSN] 1043-4666
  • [Journal-full-title] Cytokine
  • [ISO-abbreviation] Cytokine
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 82115-62-6 / Interferon-gamma
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21. Sulkowska M, Wincewicz A, Sulkowski S, Koda M, Kanczuga-Koda L: Relations of TGF-beta1 with HIF-1 alpha, GLUT-1 and longer survival of colorectal cancer patients. Pathology; 2009;41(3):254-60
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  • [Title] Relations of TGF-beta1 with HIF-1 alpha, GLUT-1 and longer survival of colorectal cancer patients.
  • AIMS AND METHODS: During colorectal carcinogenesis, transforming growth factor beta 1 (TGF-beta1) undergoes a functional change from suppression of cancer cell proliferation to inhibition of T cell mediated anti-cancer immunity.
  • We aimed to evaluate relations among TGF-beta1 and cancer cell survival factors hypoxia inducible factor-1 alpha (HIF-1 alpha) and glucose transporter 1 (GLUT-1) by immunohistochemistry in 108 colorectal cancers.
  • RESULTS: TGF-beta1 was detected in 87% (94/108), HIF-1 alpha in 85% (92/108), and GLUT-1 in 65% (70/108) of colorectal cancers.
  • GLUT-1 was visualised in a membranous fashion while HIF-1 was expressed in a paranuclear pattern and occasionally in nuclei of malignant cells.
  • Cancer immunoreactivities to TGF-beta1 correlated with HIF-1 alpha (p < 0.001, r = 0.516) and GLUT-1 (p < [corrected] 0.001, r = 0.355) in general and subgroups of different clinicopathological traits.
  • TGF-beta1 expressions of inflammatory infiltrates correlated with longer patient survival (p = 0.05, r = 0.449) and immunoreactivities to HIF-1 alpha of cancer cells (p = 0.008, r = 0.254) particularly in node positive and deeply invading cancers but failed to associate significantly with GLUT-1.
  • CONCLUSIONS: HIF-1 alpha and GLUT-1 could cooperate with TGF-beta1, and TGF-beta1 might mediate cross-talk between the inflammatory environment and tumour with a favourable impact on patient survival.
  • [MeSH-major] Colorectal Neoplasms / metabolism. Colorectal Neoplasms / mortality. Glucose Transporter Type 1 / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Transforming Growth Factor beta1 / metabolism
  • [MeSH-minor] Biomarkers, Tumor / analysis. Humans. Immunohistochemistry. Receptor Cross-Talk / physiology

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  • [ErratumIn] Pathology. 2009;41(6):612
  • (PMID = 19142800.001).
  • [ISSN] 1465-3931
  • [Journal-full-title] Pathology
  • [ISO-abbreviation] Pathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glucose Transporter Type 1; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transforming Growth Factor beta1
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22. Hadar T, Shvero J, Yaniv E, Shvili I, Leabu M, Koren R: Human topoisomerase II-alpha is highly expressed in sinonasal-inverted papilloma, but not in inflammatory polyp. J Cell Mol Med; 2008 Sep-Oct;12(5A):1551-8
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  • [Title] Human topoisomerase II-alpha is highly expressed in sinonasal-inverted papilloma, but not in inflammatory polyp.
  • Sinonasal-inverted papilloma is a benign tumour with a high rate of recurrence, but possible malignant transformation.
  • Therefore, investigation of predisposition to malignant transformation of sinonasal-inverted papilloma gives clinicians the opportunity for adequate treatment.
  • Topoisomerase II-alpha (topoII-alpha) and Ki67 are markers of cell proliferation in both normal and neoplastic tissues and its level o expression could be used as a predictive parameter.
  • TopoI alpha nuclear immunostaining showed a differential positivity in the investigated cases.
  • The topoII-alpha index was 30.6 +/- 12.8 in inverte papilloma, 10.7 +/- 6.6 in the adjacent epithelium of inverted papilloma, but only 2.3 +/- 2.0 in the normal sinonasal epithelium.
  • The differences in topoII-alpha expression between inverted papilloma and normal sinonasal epithelia were statistically significant.
  • In inflammatory nasal polyp group, topoII-alpha index was 2.4 +/- 2.1, and the difference in the topoII-alpha index between inverted papilloma and inflammatory polyp group was also statistically significant.
  • Significant correlation coefficients were found between topoII-alpha and epithelial thickness (r = 0.70, P > 0.0001), and between Ki67 index and epithelial thickness (r = 0.71, P> 0.0001).
  • Significant correlation coefficient was found between topoII-alpha index and Ki67 index in inverted papilloma (r = 0.42, P > 0.05).
  • These results suggest that the inverte papilloma contains a significantly higher cell population with proliferative activity by comparison with normal sinonasal and inflammatory polyp epithelia, showing a significant correlation between topoII-alpha and Ki67 expression, and indicating that topoII-alpha could be a independent prognostic factor for a putative malignant transformation.

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  • (PMID = 18544048.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  • [Other-IDs] NLM/ PMC3918071
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23. Buritica C, Serrano M, Zuluaga A, Arrabal M, Regauer S, Nogales FF: Mixed epithelial and stromal tumour of the kidney with luteinised ovarian stroma. J Clin Pathol; 2007 Jan;60(1):98-100
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  • [Title] Mixed epithelial and stromal tumour of the kidney with luteinised ovarian stroma.
  • We report a case of a 9-cm mixed epithelial and stromal tumour of the kidney in an obese 70-year-old woman with diabetes.
  • The ovarian-type stroma had a spindle cell component that was positive for progesterone receptors and had the hitherto unreported presence of abundant foci of luteinised stromal cells with characteristic immunohistochemical positivity to alpha-inhibin, calretinin, aromatase and gonadotropin-releasing hormone (GnRH) receptors.
  • [MeSH-major] Kidney Neoplasms / pathology. Mixed Tumor, Malignant / pathology. Neoplasms, Glandular and Epithelial / pathology

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  • [Cites] Am J Surg Pathol. 2000 Jul;24(7):958-70 [10895818.001]
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  • (PMID = 17213356.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1860583
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24. Daniels RA, Turley H, Kimberley FC, Liu XS, Mongkolsapaya J, Ch'En P, Xu XN, Jin BQ, Pezzella F, Screaton GR: Expression of TRAIL and TRAIL receptors in normal and malignant tissues. Cell Res; 2005 Jun;15(6):430-8
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  • [Title] Expression of TRAIL and TRAIL receptors in normal and malignant tissues.
  • TRAIL, tumor necrosis factor-related apoptosis-inducing ligand, is a member of the TNF family of proteins.
  • Tumour cells were initially found to have increased sensitivity to TRAIL compared with normal cells, raising hopes that TRAIL would prove useful as an anti-tumor agent.
  • The production of reliable monoclonal antibodies against TRAIL and its receptors that can stain fixed specimens will allow a thorough analysis of their expression on normal and malignant tissues.
  • Here we report the generation of monoclonal antibodies against TRAIL and its four membrane-bound receptors (TR1-4), which have been used to stain a range of normal and malignant cells, as routinely fixed specimens.
  • TR1 and TR2 expression increases significantly in a number of malignant tissues, but in some common malignancies their expression was low, or patchy, which may limit the therapeutic role of TRAIL.
  • [MeSH-major] Membrane Glycoproteins / biosynthesis. Neoplasms / physiopathology. Receptors, Tumor Necrosis Factor / biosynthesis. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Antibodies, Monoclonal / biosynthesis. Apoptosis / drug effects. Apoptosis Regulatory Proteins. Female. GPI-Linked Proteins. Humans. Immunohistochemistry / methods. Jurkat Cells. Male. Receptors, TNF-Related Apoptosis-Inducing Ligand. Receptors, Tumor Necrosis Factor, Member 10c. Staining and Labeling / methods. TNF-Related Apoptosis-Inducing Ligand. Tissue Distribution. Tumor Necrosis Factor Decoy Receptors

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  • (PMID = 15987601.001).
  • [ISSN] 1001-0602
  • [Journal-full-title] Cell research
  • [ISO-abbreviation] Cell Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0400720
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Apoptosis Regulatory Proteins; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Member 10c; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFRSF10C protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor Decoy Receptors; 0 / Tumor Necrosis Factor-alpha
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25. Nakabayashi H, Yawata T, Shimizu K: Anti-invasive and antiangiogenic effects of MMI-166 on malignant glioma cells. BMC Cancer; 2010;10:339
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  • [Title] Anti-invasive and antiangiogenic effects of MMI-166 on malignant glioma cells.
  • BACKGROUND: The constitutive overexpression of matrix metalloproteinases (MMPs) is frequently observed in malignant tumours.
  • In particular, MMP-2 and MMP-9 have been reported to be closely associated with invasion and angiogenesis in malignant gliomas.
  • Our study aimed to evaluate the antitumour effects of MMI-166 (Nalpha-[4-(2-Phenyl-2H- tetrazole-5-yl) phenyl sulfonyl]-D-tryptophan), a third generation MMP inhibitor, on three human glioma cell lines (T98G, U87MG, and ONS12) in vitro and in vivo.
  • The angiogenesis assay showed that MMI-166 had a suppressive effect on glioma cell-induced angiogenesis.
  • However, MMI-166 did not suppress glioma cell proliferation in the MTT assay.
  • In vivo, MMI-166 suppressed tumour growth in athymic mice implanted orthotropically with T98G cells and showed an inhibitory effect on tumour-induced angiogenesis and tumour growth.
  • This is the first report of the effect of a third generation MMP inhibitor on malignant glioma cells.
  • CONCLUSIONS: These results suggest that MMI-166 may have potentially suppressive effects on the invasion and angiogenesis of malignant gliomas.
  • [MeSH-minor] Animals. Brain Neoplasms / blood supply. Brain Neoplasms / drug therapy. Brain Neoplasms / pathology. Female. Humans. Matrix Metalloproteinase Inhibitors. Mice. Mice, Inbred BALB C. Mice, Nude. Middle Aged. Neoplasm Invasiveness. Tumor Cells, Cultured


26. Balkwill F: Tumour necrosis factor and cancer. Nat Rev Cancer; 2009 May;9(5):361-71
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  • [Title] Tumour necrosis factor and cancer.
  • Tumour necrosis factor (TNF) is a major inflammatory cytokine that was first identified for its ability to induce rapid haemorrhagic necrosis of experimental cancers.
  • When efforts to harness this anti-tumour activity in cancer treatments were underway, a paradoxical tumour-promoting role of TNF became apparent.
  • Now that links between inflammation and cancer are appreciated, is TNF a target or a therapeutic in malignant disease -- or both?
  • [MeSH-major] Neoplasms / etiology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Animals. Clinical Trials as Topic. Cytotoxicity, Immunologic. DNA Damage. Endotoxins / toxicity. Humans. Inflammation / etiology. Receptors, Tumor Necrosis Factor / physiology. Recombinant Proteins / therapeutic use

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  • (PMID = 19343034.001).
  • [ISSN] 1474-1768
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501974
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Endotoxins; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha
  • [Number-of-references] 171
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27. Buckstein R, Meyer RM, Seymour L, Biagi J, Mackay H, Laurie S, Eisenhauer E: Phase II testing of sunitinib: the National Cancer Institute of Canada Clinical Trials Group IND Program Trials IND.182-185. Curr Oncol; 2007 Aug;14(4):154-61
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  • Sunitinib (SU11248) is an orally bioavailable inhibitor that affects the receptor tyrosine kinases involved in tumour proliferation and angiogenesis, including vascular endothelial growth factor (VEGF) receptors 1, 2, 3, and platelet-derived growth factor receptors alpha (PDGFRA) and beta (PDGFRB).
  • In the present article, we discuss the biologic and clinical rationales that have recently led the Investigational New Drug Program of the National Cancer Institute of Canada Clinical Trials Group to initiate four phase ii trials testing this agent in the following four different tumour types: relapsed diffuse large cell lymphoma, malignant pleural mesothelioma, locally advanced or metastatic cervical cancer and recurrent epithelial ovarian, fallopian tube, or primary peritoneal carcinoma.

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  • (PMID = 17710208.001).
  • [ISSN] 1198-0052
  • [Journal-full-title] Current oncology (Toronto, Ont.)
  • [ISO-abbreviation] Curr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC1948864
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28. Siddiqui EJ, Shabbir M, Thompson CS, Mumtaz FH, Mikhailidis DP: Growth inhibitory effect of doxazosin on prostate and bladder cancer cells. Is the serotonin receptor pathway involved? Anticancer Res; 2005 Nov-Dec;25(6B):4281-6
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  • Alpha-adrenoceptor antagonists also inhibit growth and induce apoptosis in malignant prostatic cells.
  • The apoptotic activity is independent of their capacity to antagonize alpha-adrenoceptors.
  • The effect of doxazosin on the growth of prostate and bladder cancer cell lines was assessed and whether the growth inhibitory effect of doxazosin on prostate cancer cells is serotonin (5-hydroxtryptamine; 5HT)-dependent was investigated.
  • MATERIALS AND METHODS: PC3 (androgen-independent prostate cancer) and HT1376 (grade III transitional cell carcinoma) cells were plated.
  • After 72 h, cell viability was assessed (crystal violet assay).
  • Cell viability was assessed at 72 h.
  • RESULTS: Doxazosin caused a dose-dependent inhibition of PC3 and HT1376 cell growth with a maximum inhibition of 80% (n=12, p < 0.0001) and 91% (n=12, p < 0.0001), respectively, at a concentration of 10(-4)M, at 72 h.
  • CONCLUSION: Doxazosin significantly inhibited prostate (PC3) and bladder cancer (HT1376) cell growth.
  • Furthermore, prior incubation of PC3 cells with 5HT or 5HT(1B) agonist increased cell viability as compared to treatment with doxazosin alone.
  • The effect of alpha1-adrenoceptor antagonists on tumour cell growth merits further investigation.
  • [MeSH-major] Adrenergic alpha-Antagonists / pharmacology. Carcinoma, Transitional Cell / drug therapy. Doxazosin / pharmacology. Prostatic Neoplasms / drug therapy. Receptor, Serotonin, 5-HT1B / metabolism. Serotonin / pharmacology. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Adrenergic alpha-1 Receptor Antagonists. Humans. Male. Pyridines / pharmacology. Pyrroles / pharmacology. Serotonin 5-HT1 Receptor Agonists

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  • (PMID = 16309229.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / Pyridines; 0 / Pyrroles; 0 / Receptor, Serotonin, 5-HT1B; 0 / Serotonin 5-HT1 Receptor Agonists; 127792-75-0 / 3-(1,2,5,6-tetrahydropyrid-4-yl)pyrrolo(3,2-b)pyrid-5-one; 333DO1RDJY / Serotonin; NW1291F1W8 / Doxazosin
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29. Wenghoefer M, Pantelis A, Dommisch H, Reich R, Martini M, Allam JP, Novak N, Bergé S, Jepsen S, Winter J: Decreased gene expression of human beta-defensin-1 in the development of squamous cell carcinoma of the oral cavity. Int J Oral Maxillofac Surg; 2008 Jul;37(7):660-3
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  • [Title] Decreased gene expression of human beta-defensin-1 in the development of squamous cell carcinoma of the oral cavity.
  • The aim of this study was to investigate the gene expression of human beta-defensin-1, -2, -3 (hBD-1, -2, -3), interleukin-1beta, tumour necrosis factor-alpha and cyclooxygenase-2 in oral squamous cell carcinoma (OSCC) compared to benign and premalignant lesions as well as healthy controls.
  • RNA was extracted according to standard protocols and transcripts of hBD-1, -2, -3, interleukin-1beta, tumour necrosis factor-alpha and cyclooxygenase-2 were analysed by real-time polymerase chain reaction.
  • The loss of its function might contribute to the malignant progression of these tumours.
  • [MeSH-major] Anti-Infective Agents / analysis. Carcinoma, Squamous Cell / pathology. Mouth Neoplasms / pathology. beta-Defensins / analysis
  • [MeSH-minor] Cyclooxygenase 2 / analysis. Disease Progression. Fibroma / genetics. Fibroma / pathology. Gene Expression Regulation, Neoplastic / genetics. Gingiva / anatomy & histology. Humans. Interleukin-1beta / analysis. Leukoplakia, Oral / genetics. Leukoplakia, Oral / pathology. Precancerous Conditions / genetics. Precancerous Conditions / pathology. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / analysis

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  • (PMID = 18346877.001).
  • [ISSN] 0901-5027
  • [Journal-full-title] International journal of oral and maxillofacial surgery
  • [ISO-abbreviation] Int J Oral Maxillofac Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / DEFB1 protein, human; 0 / DEFB4A protein, human; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; 0 / beta-Defensins; 0 / beta-defensin 3, human; EC 1.14.99.1 / Cyclooxygenase 2
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30. Yamada M, Yanaba K, Hasegawa M, Matsushita Y, Horikawa M, Komura K, Matsushita T, Kawasuji A, Fujita T, Takehara K, Steeber DA, Tedder TF, Sato S: Regulation of local and metastatic host-mediated anti-tumour mechanisms by L-selectin and intercellular adhesion molecule-1. Clin Exp Immunol; 2006 Feb;143(2):216-27
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  • [Title] Regulation of local and metastatic host-mediated anti-tumour mechanisms by L-selectin and intercellular adhesion molecule-1.
  • Malignant melanoma is often accompanied by a host response of inflammatory cell infiltration that is highly regulated by multiple adhesion molecules.
  • This enhancement was associated generally with a reduced accumulation of natural killer (NK) cells, CD4+ T cells and CD8+ T cells and also with a diminished release of interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha but not interleukin (IL)-6.
  • Cytotoxicity against melanoma was not defective by the absence of ICAM-1, L-selectin or both, suggesting that the enhancement of tumour growth and metastasis caused by the loss of adhesion molecules results from an impaired migration of effector cells into the tissue rather than from a suppression of the cytotoxic response.
  • The results indicate that L-selectin and ICAM-1 contribute co-operatively to the anti-tumour reaction by regulating lymphocyte infiltration to the tumour.

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  • (PMID = 16412045.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA54464; United States / NCI NIH HHS / CA / CA81776
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Messenger; 126547-89-5 / Intercellular Adhesion Molecule-1; 126880-86-2 / L-Selectin
  • [Other-IDs] NLM/ PMC1809598
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31. Karmaniolas K, Dalamaga M, Liatis S, Kaskara A, Rigopoulos A, Migdalis IN: Hematological malignancies are associated with a lower interferon-a blocking activity than solid tumors. Res Commun Mol Pathol Pharmacol; 2005;117-118:65-75
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  • Interferon (IFN) and especially IFN-alpha exhibit clinical anti-tumor activity against various types of malignant diseases.
  • IFN inhibitors have been implicated for the ineffectiveness of IFN treatment in malignant neoplasias.
  • PATIENTS AND METHODS: Ninety patients with a clinically evident solid tumour and forty-six patients with haematological malignancies were included in the study.
  • Interferon-inhibiting activity as well as endogenous IFN-like activity were determined in all serum samples in a cell line highly sensitive to IFN.
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Line, Tumor. Cytopathogenic Effect, Viral / drug effects. Female. Humans. Interferon-alpha / antagonists & inhibitors. Interferon-alpha / blood. Male. Middle Aged. Recombinant Proteins

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  • (PMID = 18426079.001).
  • [ISSN] 1078-0297
  • [Journal-full-title] Research communications in molecular pathology and pharmacology
  • [ISO-abbreviation] Res. Commun. Mol. Pathol. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon Type I; 0 / Interferon-alpha; 0 / Recombinant Proteins
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32. Dallosso AR, Hancock AL, Szemes M, Moorwood K, Chilukamarri L, Tsai HH, Sarkar A, Barasch J, Vuononvirta R, Jones C, Pritchard-Jones K, Royer-Pokora B, Lee SB, Owen C, Malik S, Feng Y, Frank M, Ward A, Brown KW, Malik K: Frequent long-range epigenetic silencing of protocadherin gene clusters on chromosome 5q31 in Wilms' tumor. PLoS Genet; 2009 Nov;5(11):e1000745
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  • [Title] Frequent long-range epigenetic silencing of protocadherin gene clusters on chromosome 5q31 in Wilms' tumor.
  • Wilms' tumour (WT) is a pediatric tumor of the kidney that arises via failure of the fetal developmental program.
  • The methylated genes all belong to alpha-, beta-, and gamma-protocadherin (PCDH) gene clusters (Human Genome Organization nomenclature PCDHA@, PCDHB@, and PCDHG@, respectively).
  • Bisulfite polymerase chain reaction analysis showed that PCDH hypermethylation is a frequent event found in all Wilms' tumor subtypes.
  • WT precursor lesions showed no PCDH hypermethylation, suggesting that de novo PCDH hypermethylation occurs during malignant progression.
  • Importantly, we show that PCDHs negatively regulate canonical Wnt signalling, as short-interfering RNA-induced reduction of PCDHG@ encoded proteins leads to elevated beta-catenin protein, increased beta-catenin/T-cell factor (TCF) reporter activity, and induction of Wnt target genes.
  • Thus PCDHs are candidate tumor suppressors that modulate regulatory pathways critical in development and disease, such as canonical Wnt signaling.
  • [MeSH-major] Cadherins / genetics. Chromosomes, Human, Pair 5 / genetics. Epigenesis, Genetic. Gene Silencing. Multigene Family. Wilms Tumor / genetics

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  • [ErratumIn] PLoS Genet. 2009 Dec;5(12). doi: 10.1371/annotation/012d5a44-8239-4057-8c3b-3dc159ea3a02
  • (PMID = 19956686.001).
  • [ISSN] 1553-7404
  • [Journal-full-title] PLoS genetics
  • [ISO-abbreviation] PLoS Genet.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300415
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / PCDH1 protein, human; 0 / Wnt Proteins; 0 / beta Catenin
  • [Other-IDs] NLM/ PMC2776977
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33. Szlosarek PW, Grimshaw MJ, Wilbanks GD, Hagemann T, Wilson JL, Burke F, Stamp G, Balkwill FR: Aberrant regulation of argininosuccinate synthetase by TNF-alpha in human epithelial ovarian cancer. Int J Cancer; 2007 Jul 01;121(1):6-11
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  • [Title] Aberrant regulation of argininosuccinate synthetase by TNF-alpha in human epithelial ovarian cancer.
  • The pro-inflammatory cytokine, tumour necrosis factor-alpha, TNF-alpha, is dysregulated in malignant compared with normal ovarian surface epithelium (OSE).
  • Several epidemiological studies have associated inflammation with ovarian tumorigenesis, with TNF-alpha playing a key role in modulating invasion, angiogenesis and metastasis.
  • Here, we show that TNF-alpha also induces expression of arate-limiting enzyme in arginine synthesis, argininosuccinate synthetase (AS), thereby linking inflammation with several arginine-dependent metabolic pathways, implicated in accelerated carcinogenesis and tumour progression.
  • Having identified AS mRNA induction in TNF-alpha-treated IGROV-1 ovarian cancer cells, using RNA-arbitrarily primed-PCR, we then observed differential regulation of AS mRNA and protein in malignant, compared with normal, OSE cells.
  • A cDNA cancer profiling array with matched normal ovarian and ovarian tumour samples revealed increased expression of AS mRNA in the latter.
  • Moreover, AS protein co-localised with TNF-alpha in ovarian cancer cells, with significantly higher levels of AS in malignant compared with normal ovarian tissue.
  • Increased co-expression of AS and TNF-alpha mRNA was also observed in 2 other epithelial tumours, non-small cell lung and stomach cancer, compared with normal corresponding tissues.
  • In summary, high levels of AS expression, which may be required for several arginine-dependent processes in cancer, including the production of nitric oxide, proline, pyrimidines and polyamines, is regulated by TNF-alpha and may provide an important molecular pathway linking inflammation and metabolism to ovarian tumorigenesis.
  • [MeSH-major] Argininosuccinate Synthase / metabolism. Epithelial Cells / drug effects. Epithelial Cells / enzymology. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Ovarian Neoplasms / enzymology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Female. Health. Humans. RNA, Messenger / genetics. Tumor Cells, Cultured

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  • (PMID = 17354225.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501974; United Kingdom / Medical Research Council / / G0601867
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 6.3.4.5 / Argininosuccinate Synthase
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34. Darra E, Lenaz G, Cavalieri E, Fato R, Mariotto S, Bergamini C, Carcereri de Prati A, Perbellini L, Leoni S, Suzuki H: Alpha-bisabolol: unexpected plant-derived weapon in the struggle against tumour survival? Ital J Biochem; 2007 Dec;56(4):323-8
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  • [Title] Alpha-bisabolol: unexpected plant-derived weapon in the struggle against tumour survival?
  • Despite enormous scientific and economic effort tumour still is one of the most terrible pathologies among human population all over the world.
  • Here, we summarize the short story of the study of an extraordinary effect of one plant compound towards transformed cells derived from highly malignant tumours.
  • Alpha-bisabolol, a sesquiterpene widely present in plants, selectively kills transformed cells by apoptosis without affecting the viability of normal cells.
  • One of its intracellular targets seems to be situated on mitochondria and is possibly identified as the permeability transition pore, as judged from rapid mitochondrial membrane potential dissipation induced by alpha-bisabolol and the failure to kill cells in the presence of cyclosporine A.
  • Preferential adsorption of alpha-bisabolol into lipid rafts, rich in tumour cells, may explain the selective action of this compounds towards tumour cells.
  • Furthermore, Surface Plasmon Resonance analysis indicates that alpha-bisabolol directly interacts with Bid protein, a member of the Bcl2 family deeply involved in apoptosis, suggesting a possibility that Bid, or similar protein(s), may be involved in a putative intracellular transport system of alpha-bisabolol from plasma membrane to mitochondria.
  • Experiments with animals indicate that alpha-bisabolol is not toxic and is accumulated, through blood flow, in every tissues examined.
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Models, Biological. Signal Transduction

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  • (PMID = 19192636.001).
  • [ISSN] 0021-2938
  • [Journal-full-title] The Italian journal of biochemistry
  • [ISO-abbreviation] Ital. J. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Plant Extracts; 0 / Sesquiterpenes; 24WE03BX2T / bisabolol
  • [Number-of-references] 15
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35. Hungermann D, Buerger H, Oehlschlegel C, Herbst H, Boecker W: Adenomyoepithelial tumours and myoepithelial carcinomas of the breast--a spectrum of monophasic and biphasic tumours dominated by immature myoepithelial cells. BMC Cancer; 2005;5:92
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  • METHODS: A series of 27 adenomyoepithelial tumours of the breast was analysed immunohistochemically with antibodies directed against various cytokeratins, p63, smooth muscle alpha-actin (SMA) and vimentin.
  • With exception of one case diagnosed as myoepithelial carcinoma, all tested tumours expressed low molecular weight cytokeratin Ck18 in variable proportions of cells.
  • Double immunofluorescence revealed tumour cells exclusively staining for Ck5/Ck14 in the presence of other cell populations that co-expressed high molecular weight Ck5/Ck14 as well as either low molecular weight Ck8/18 or SMA.
  • Based on morphology, we assigned the series to three categories, benign, borderline and malignant.
  • Although categorisation of adenomyoepithelial tumours in benign, borderline and malignant was supported by results of CGH, any assessment of prognosis requires to be firmly based on morphological grounds.
  • [MeSH-major] Breast Neoplasms / diagnosis. Carcinoma / diagnosis. Epithelial Cells / cytology. Myoepithelioma / diagnosis
  • [MeSH-minor] Actins / biosynthesis. Adult. Aged. Aged, 80 and over. Cell Proliferation. DNA-Binding Proteins. Female. Genes, Tumor Suppressor. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. Immunophenotyping. Keratins / biosynthesis. Microscopy, Fluorescence. Middle Aged. Nucleic Acid Hybridization. Phosphoproteins / biosynthesis. Prognosis. Trans-Activators / biosynthesis. Transcription Factors. Tumor Suppressor Proteins. Vimentin / biosynthesis

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  • (PMID = 16050957.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / DNA-Binding Proteins; 0 / Phosphoproteins; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Vimentin; 68238-35-7 / Keratins
  • [Other-IDs] NLM/ PMC1187882
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36. Obi N, Katabami T, Obi R, Odanaka M, Sasano K, Tanaka Y: Primary malignant hepatic glucagonoma: an autopsy case. Endocr J; 2009;56(5):715-9
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  • [Title] Primary malignant hepatic glucagonoma: an autopsy case.
  • She displayed the signs and symptoms of glucagonoma syndrome, including necrolytic migratory erythema (NME), low aminoacidemia, and a marked increase of the serum glucagon level (4,940 pg/ ml).
  • Thus, we suspected a glucagonoma causing secondary diabetes.
  • However, we could not detect any mass in the pancreas or the gastrointestinal tract, and only found a liver lesion resembling a hemangioma.
  • At autopsy, the only tumor detected was the liver mass.
  • This was a large solid tumor (8 x 6 x 5 cm) with a pattern of white and dark brown stripes located in the left lobe, while two white nodules were also found in the right lobe.
  • Based on the histopathological and immunohistochemical findings, the liver lesion was shown to be a malignant glucagonoma with intrahepatic metastases.
  • Since primary malignant hepatic glucagonoma has not been reported before, we present this extremely rare case of primary malignant glucagonoma of the liver.
  • [MeSH-major] Diabetes Mellitus, Type 2 / etiology. Glucagonoma / pathology. Liver Neoplasms / pathology

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  • (PMID = 19367016.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Amino Acids
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37. Ranza E, Bertolotti A, Facoetti A, Mariotti L, Pasi F, Ottolenghi A, Nano R: Influence of imatinib mesylate on radiosensitivity of astrocytoma cells. Anticancer Res; 2009 Nov;29(11):4575-8
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  • Imatinib mesylate (STI571), an inhibitor of alpha- and beta-platelet-derived growth factor receptors (PDGFR) and other tyrosine kinases, is a well established treatment for chronic myeloid leukaemia and gastrointestinal stromal tumours.
  • Moreover, it is under investigation for the therapy of several other malignant tumours since protein kinases are frequently mutated or otherwise deregulated in human malignancies and they serve as a target for differentiating between tumour cells and normal tissues.
  • The objective of this study was to determine whether gamma radiation could sensitize astrocytoma cell lines to the effects of imatinib in vitro.
  • The clonogenic survival assays performed with the combination of imatinib with radiation demonstrated that the drug had an additive antiproliferative effect in both cell lines considered.
  • Imatinib confered greater radiosensitivity on the T98G tumour cells effecting a significant decrease in colony formation compared with radiation alone.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Benzamides. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / radiation effects. Combined Modality Therapy. Dose-Response Relationship, Drug. Gamma Rays. Glioblastoma / drug therapy. Glioblastoma / radiotherapy. Humans. Imatinib Mesylate

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  • (PMID = 20032406.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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38. Roesch-Ely M, Schnölzer M, Nees M, Plinkert PK, Bosch FX: Reference spectra from squamous epithelium and connective tissue allow whole section proteomics analysis. Arch Physiol Biochem; 2010 Oct-Dec;116(4-5):218-26
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  • We reasoned that micro-dissection of tumour cells for protein expression studies should be omitted since tumour-stroma interactions are an important part of the biology of solid tumours.
  • To study such interactions in head and neck squamous cell carcinoma (HNSCC) development, we generated reference protein spectra for normal squamous epithelium and connective tissue by SELDI-TOF-MS.
  • The alpha-defensins 1-3 and the haemoglobin subunits were identified in the connective tissue.
  • Tumour-distant epithelia, representing early pre-malignant lesions, showed up-regulated expression of the stromal alpha-defensins, whereas the epithelial Annexin 1 was down-regulated.
  • Thus, tumour microenvironment interactions occur very early in the carcinogenic process.
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. Head and Neck Neoplasms / metabolism. Neoplasm Proteins / metabolism. Protein Array Analysis. Proteomics. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization / methods. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization / standards
  • [MeSH-minor] Annexins / analysis. Calgranulin A / analysis. Cluster Analysis. Connective Tissue / chemistry. Connective Tissue / metabolism. Connective Tissue / pathology. Epithelium / chemistry. Epithelium / metabolism. Epithelium / pathology. Hemoglobins / analysis. Humans. Microdissection. Reference Standards. alpha-Defensins / analysis

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  • (PMID = 21080850.001).
  • [ISSN] 1744-4160
  • [Journal-full-title] Archives of physiology and biochemistry
  • [ISO-abbreviation] Arch. Physiol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexins; 0 / Calgranulin A; 0 / Hemoglobins; 0 / Neoplasm Proteins; 0 / alpha-Defensins
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39. Ammirante M, Luo JL, Grivennikov S, Nedospasov S, Karin M: B-cell-derived lymphotoxin promotes castration-resistant prostate cancer. Nature; 2010 Mar 11;464(7286):302-5
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  • [Title] B-cell-derived lymphotoxin promotes castration-resistant prostate cancer.
  • Prostate cancer (CaP) progresses from prostatic intraepithelial neoplasia through locally invasive adenocarcinoma to castration-resistant metastatic carcinoma.
  • Curiously, castration-resistant CaP remains androgen-receptor dependent, and potent androgen-receptor antagonists induce tumour regression in castrated mice.
  • The inflammation-responsive IkappaB kinase (IKK)-beta and its target NF-kappaB have important tumour-promoting functions within malignant cells and inflammatory cells.
  • The latter, including macrophages and lymphocytes, are important elements of the tumour microenvironment, but the mechanisms underlying their recruitment remain obscure, although they are thought to depend on chemokine and cytokine production.
  • We found that CaP progression is associated with inflammatory infiltration and activation of IKK-alpha, which stimulates metastasis by an NF-kappaB-independent, cell autonomous mechanism.
  • Here we show that androgen ablation causes infiltration of regressing androgen-dependent tumours with leukocytes, including B cells, in which IKK-beta activation results in production of cytokines that activate IKK-alpha and STAT3 in CaP cells to enhance hormone-free survival.


40. Jalving M, Koornstra JJ, De Jong S, De Vries EG, Kleibeuker JH: Review article: the potential of combinational regimen with non-steroidal anti-inflammatory drugs in the chemoprevention of colorectal cancer. Aliment Pharmacol Ther; 2005 Feb 15;21(4):321-39
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  • Non-steroidal anti-inflammatory drugs do not, however, offer complete protection against adenoma and carcinoma development.
  • There is increasing interest in combining non-steroidal anti-inflammatory drugs with agents that target specific cell signalling pathways in malignant and premalignant cells.
  • This review aims to describe the current knowledge regarding the efficacy of peroxisome proliferator-activated receptor-gamma ligands, cholesterol synthesis inhibitors (statins), epidermal growth factor signalling inhibitors and tumour necrosis factor-related apoptosis-inducing ligand against colorectal neoplasms and the rationale for combining these drugs with non-steroidal anti-inflammatory drugs to improve efficacy in the chemoprevention of colorectal cancer, a PUBMED computer search of the English language literature was conducted to identify relevant papers published before July 2004.
  • In vitro, tumour necrosis factor-related apoptosis-inducing ligand induces apoptosis in human colon cancer cells, but not in normal cells.
  • [MeSH-minor] Apoptosis Regulatory Proteins. Drug Therapy, Combination. Humans. Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use. Ligands. Membrane Glycoproteins / therapeutic use. PPAR gamma / agonists. Receptor, Epidermal Growth Factor / antagonists & inhibitors. TNF-Related Apoptosis-Inducing Ligand. Tumor Necrosis Factor-alpha / therapeutic use

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  • (PMID = 15709983.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / PPAR gamma; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Number-of-references] 190
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41. Lopes N, Sousa B, Martins D, Gomes M, Vieira D, Veronese LA, Milanezi F, Paredes J, Costa JL, Schmitt F: Alterations in Vitamin D signalling and metabolic pathways in breast cancer progression: a study of VDR, CYP27B1 and CYP24A1 expression in benign and malignant breast lesions. BMC Cancer; 2010;10:483
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  • [Title] Alterations in Vitamin D signalling and metabolic pathways in breast cancer progression: a study of VDR, CYP27B1 and CYP24A1 expression in benign and malignant breast lesions.
  • CONCLUSIONS: From this study, we conclude that there is a deregulation of the Vitamin D signalling and metabolic pathways in breast cancer, favouring tumour progression.
  • Thus, during mammary malignant transformation, tumour cells lose their ability to synthesize the active form of Vitamin D and respond to VDR-mediated Vitamin D effects, while increasing their ability to degrade this hormone.
  • [MeSH-major] 25-Hydroxyvitamin D3 1-alpha-Hydroxylase / metabolism. Breast / metabolism. Breast Neoplasms / metabolism. Receptors, Calcitriol / metabolism. Steroid Hydroxylases / metabolism. Vitamin D / metabolism
  • [MeSH-minor] Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Blotting, Western. Carcinoma, Ductal, Breast / metabolism. Carcinoma, Ductal, Breast / pathology. Carcinoma, Intraductal, Noninfiltrating / metabolism. Carcinoma, Intraductal, Noninfiltrating / pathology. Cohort Studies. Disease Progression. Female. Gene Expression Profiling. Humans. Immunoenzyme Techniques. Metabolic Networks and Pathways. Neoplasm Staging. Oligonucleotide Array Sequence Analysis. Prognosis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Vitamin D3 24-Hydroxylase

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  • (PMID = 20831823.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / Receptors, Calcitriol; 1406-16-2 / Vitamin D; EC 1.14.- / 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; EC 1.14.- / Steroid Hydroxylases; EC 1.14.13.126 / CYP24A1 protein, human; EC 1.14.13.126 / Vitamin D3 24-Hydroxylase
  • [Other-IDs] NLM/ PMC2945944
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42. Neuzil J, Dyason JC, Freeman R, Dong LF, Prochazka L, Wang XF, Scheffler I, Ralph SJ: Mitocans as anti-cancer agents targeting mitochondria: lessons from studies with vitamin E analogues, inhibitors of complex II. J Bioenerg Biomembr; 2007 Feb;39(1):65-72
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  • Recently mitochondria in cancer cells have emerged as the Achilles heel for tumour destruction.
  • Anti-cancer agents specifically targeting cancer cell mitochondria are referred to as 'mitocans'.
  • These compounds act by destabilising these organelles, unleashing their apoptogenic potential, resulting in the efficient death of malignant cells and suppression of tumour growth.
  • Importantly, at least some mitocans are selective for cancer cells, and these are represented by the group of redox-silent vitamin E analogues, epitomised by alpha-tocopheryl succinate (alpha-TOS).
  • Moreover, alpha-TOS is selective for cancer cells with their reduced anti-oxidant defenses and lower esterase activity than the normal (non-malignant) counterparts.
  • In this mini-review we discuss the emerging significance of mitocans, as exemplified by alpha-TOS.

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  • (PMID = 17294131.001).
  • [ISSN] 0145-479X
  • [Journal-full-title] Journal of bioenergetics and biomembranes
  • [ISO-abbreviation] J. Bioenerg. Biomembr.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Reactive Oxygen Species; 11062-77-4 / Superoxides; 1406-18-4 / Vitamin E; EC 1.3.5.1 / Electron Transport Complex II
  • [Number-of-references] 73
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43. Humphreys EH, Williams KT, Adams DH, Afford SC: Primary and malignant cholangiocytes undergo CD40 mediated Fas dependent apoptosis, but are insensitive to direct activation with exogenous Fas ligand. PLoS One; 2010 Nov 17;5(11):e14037
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  • [Title] Primary and malignant cholangiocytes undergo CD40 mediated Fas dependent apoptosis, but are insensitive to direct activation with exogenous Fas ligand.
  • We have shown that primary human cholangiocyte and hepatocyte survival is tightly regulated via co-operative interactions between two tumour necrosis family (TNF) receptor family members; CD40 and Fas (CD95).
  • AIMS: To determine whether malignant cholangiocytes display defects in CD40 mediated apoptosis.
  • By comparing CD40 and Fas-mediated apoptosis and intracellular signalling in primary human cholangiocytes and three cholangiocyte cell lines.
  • RESULTS: Primary cholangiocytes and cholangiocyte cell lines were relatively insensitive to direct Fas-mediated killing with exogenous FasL when compared with Jurkat cells, which readily underwent Fas-mediated apoptosis, but were extremely sensitive to CD154 stimulation.
  • The sensitivity of cells to CD40 activation was similar in magnitude in both primary and malignant cells and was STAT-3 and AP-1 dependent in both. CONCLUSIONS:.
  • 1) Both primary and malignant cholangiocytes are relatively resistant to Fas-mediated killing but show exquisite sensitivity to CD154, suggesting that the CD40 pathway is intact and fully functional in both primary and malignant cholangiocytes 2) The relative insensitivity of cholangiocytes to Fas activation demonstrates the importance of CD40 augmentation of Fas dependent death in these cells.
  • Agonistic therapies which target CD40 and associated intracellular signalling pathways may be effective in promoting apoptosis of malignant cholangiocytes.

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  • (PMID = 21103345.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/E017096/1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Antigens, CD95; 0 / Fas Ligand Protein; 0 / STAT3 Transcription Factor; 0 / Transcription Factor AP-1; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 147205-72-9 / CD40 Ligand
  • [Other-IDs] NLM/ PMC2984448
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44. Moriya T, Kozuka Y, Kanomata N, Tse GM, Tan PH: The role of immunohistochemistry in the differential diagnosis of breast lesions. Pathology; 2009 Jan;41(1):68-76
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  • [Title] The role of immunohistochemistry in the differential diagnosis of breast lesions.
  • Immunohistochemistry may be helpful in the diagnosis of various breast lesions.
  • It can be used to assist in distinguishing benign and malignant conditions, or to clarify the histological subtype of invasive carcinomas.
  • Myoepithelial markers (p63, alpha-SMA, smooth muscle myosin heavy chain, and others) are useful to highlight myoepithelial cells.
  • They are employed to verify myoepithelial cell lining in intraductal papillary lesions, or to recognise peripheral myoepithelial cells for non-invasive carcinoma, although their staining results are not always excellent.
  • High molecular weight cytokeratins (CK5/6, CK14, 34betaE12) typically show a mosaic-like pattern of expression in benign papillary/hyperplastic lesions, and are mostly negative in ductal in situ carcinoma, but some exceptions exist.
  • Negative E-cadherin staining is used for making confirmative diagnosis of lobular carcinoma, with a specificity and sensitivity of approximately 90%.
  • Cytokeratins, especially the antibody 34betaE12, are of value to differentiate spindle cell carcinoma from phyllodes tumour.
  • Nevertheless, for accurate diagnosis, it is essential to correlate the immmunohistochemical staining results with the histological findings.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Breast Neoplasms / diagnosis. Breast Neoplasms / metabolism. Immunohistochemistry / methods
  • [MeSH-minor] Carcinoma, Intraductal, Noninfiltrating / diagnosis. Carcinoma, Intraductal, Noninfiltrating / metabolism. Carcinoma, Intraductal, Noninfiltrating / pathology. Carcinoma, Lobular / diagnosis. Carcinoma, Lobular / metabolism. Carcinoma, Lobular / pathology. Carcinoma, Papillary / diagnosis. Carcinoma, Papillary / metabolism. Carcinoma, Papillary / pathology. Diagnosis, Differential. Female. Humans. Myoepithelioma / diagnosis. Myoepithelioma / metabolism. Myoepithelioma / pathology


45. Montesano R, Soulié P, Eble JA, Carrozzino F: Tumour necrosis factor alpha confers an invasive, transformed phenotype on mammary epithelial cells. J Cell Sci; 2005 Aug 1;118(Pt 15):3487-500
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  • [Title] Tumour necrosis factor alpha confers an invasive, transformed phenotype on mammary epithelial cells.
  • Although loss of cell-cell adhesion and gain of invasive properties play a crucial role in the malignant progression of epithelial tumours, the molecular signals that trigger these processes have not been fully elucidated.
  • In light of the well-established relationship between chronic inflammation and cancer, we hypothesized that pro-inflammatory cytokines disrupt epithelial-cell adhesion and promote cell migration.
  • Among the several cytokines examined, tumour necrosis factor alpha (TNF-alpha) caused a pronounced 3D scattering of preformed epithelial-cell colonies and induced 31EG4-2A4 cells grown on top of a collagen gel to invade the underlying matrix.
  • In addition, TNF-alpha abolished contact-mediated inhibition of cell proliferation and stimulated cell growth both in the absence of exogenous mitogens and under anchorage-independent conditions.
  • TNF-alpha induced the expression of matrix metalloproteinase 9 (MMP-9).
  • Addition of the MMP inhibitor BB-94 abrogated TNF-alpha-induced 3D scattering.
  • TNF-alpha also enhanced the attachment of 31EG4-2A4 cells to type-I collagen and markedly increased the expression of the alpha2 integrin subunit.
  • Addition of a blocking antibody to beta1-integrin or of rhodocetin (a specific alpha2beta1 antagonist) to collagen-gel cultures abrogated 3D scattering.
  • Collectively, these results demonstrate an essential role for MMPs and alpha2beta1 integrin in the invasive response of 31EG4-2A4 cells to TNF-alpha.
  • We propose that the biological activities described in this study contribute to the ability of TNF-alpha to promote tumour progression and cancer-cell dissemination.
  • [MeSH-major] Cell Movement / drug effects. Cell Proliferation / drug effects. Epithelial Cells / drug effects. Mammary Glands, Animal / drug effects. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Cell Line. Collagen / metabolism. Extracellular Matrix / metabolism. Integrin alpha2beta1 / metabolism. Metalloproteases / antagonists & inhibitors. Metalloproteases / metabolism. Mice. Phenotype. Protease Inhibitors / pharmacology. Receptors, Tumor Necrosis Factor, Type I / metabolism

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  • (PMID = 16079290.001).
  • [ISSN] 0021-9533
  • [Journal-full-title] Journal of cell science
  • [ISO-abbreviation] J. Cell. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Integrin alpha2beta1; 0 / Protease Inhibitors; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Tumor Necrosis Factor-alpha; 9007-34-5 / Collagen; EC 3.4.- / Metalloproteases
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51. Koehn H, Magan N, Isaacs RJ, Stowell KM: Differential regulation of DNA repair protein Rad51 in human tumour cell lines exposed to doxorubicin. Anticancer Drugs; 2007 Apr;18(4):419-25
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  • [Title] Differential regulation of DNA repair protein Rad51 in human tumour cell lines exposed to doxorubicin.
  • Radiotherapy and chemotherapy often induce DNA double-strand breaks in both normal and malignant cells.
  • The proteins involved in the repair of such lesions are central to cancer prognosis and treatment, as they can be overexpressed in many cancers, accelerating malignant transformation and increasing repair capacity, potentially leading to cellular resistance.
  • If malignant cells can be selectively targeted repair proteins could also be candidates for targeted therapy.
  • In this study, two keyplayers in eukaryotic DNA double-strand break repair, Rad51 and DNA-dependent protein kinase catalytic subunit, were analysed in noncancerous human breast cells (MCF12A) and the breast cancer cell lines (MDA MB 231 and MCF7) in response to treatment with doxorubicin.
  • A cell cycle-independent increase in Rad51 protein levels (a recombinase involved in homologous recombination repair) was observed 24 and 48 h after treatment in MDA MB 231 and MCF12A when exposed to low levels of doxorubicin, whereas MCF7 cells displayed a continuous decrease in Rad51 protein with increasing drug concentration.
  • Topoisomerase II-alpha protein, the primary target of doxorubicin, was upregulated at low concentrations of doxorubicin in all cell lines tested.
  • Here we show that Rad51 protein levels can be differentially regulated in normal and malignant breast cell lines in response to doxorubicin, independent of cell cycle state.
  • [MeSH-minor] Blotting, Western. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. DNA Damage. Dose-Response Relationship, Drug. Female. Flow Cytometry. Genes, p53 / genetics. Humans. Receptors, Estrogen / genetics. Receptors, Estrogen / physiology. Transforming Growth Factor beta / genetics. Transforming Growth Factor beta / physiology

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  • (PMID = 17351394.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Receptors, Estrogen; 0 / Transforming Growth Factor beta; 80168379AG / Doxorubicin; EC 2.7.7.- / Rad51 Recombinase
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52. Huang L, Verstrepen L, Heyninck K, Wullaert A, Revets H, De Baetselier P, Beyaert R: ABINs inhibit EGF receptor-mediated NF-kappaB activation and growth of EGF receptor-overexpressing tumour cells. Oncogene; 2008 Oct 16;27(47):6131-40
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  • [Title] ABINs inhibit EGF receptor-mediated NF-kappaB activation and growth of EGF receptor-overexpressing tumour cells.
  • The epidermal growth factor receptor (EGFR) is frequently overexpressed in various tumours of epidermal origin and is held responsible for tumourigenicity and tumour persistence.
  • Increased nuclear factor (NF)-kappaB activity has been suggested to be involved in the malignant behaviour of EGFR-overexpressing cells.
  • Moreover, EGF-induced NF-kappaB activation could be inhibited by overexpression of ABINs, which were previously identified as intracellular inhibitors of tumour necrosis factor, interleukin-1 and lipopolysaccharide-induced NF-kappaB activation.
  • Adenoviral gene transfer of ABINs reduced constitutive NF-kappaB activity as well as the proliferation of EGFR-overexpressing A431 and DU145 human carcinoma cells.
  • Altogether, these results demonstrate an important role for an ABIN-sensitive non-classical NF-kappaB signalling pathway in the proliferation of EGFR-overexpressing tumour cells, and indicate a potential use for ABIN gene therapy in the treatment of cancer.
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Cyclin D1 / genetics. Epidermal Growth Factor / pharmacology. Genetic Therapy. Humans. I-kappa B Proteins / metabolism. NF-kappa B p52 Subunit / metabolism. Phosphorylation. Protein Structure, Tertiary. RNA Interference. Signal Transduction

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  • (PMID = 18622428.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [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 / DNA-Binding Proteins; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / NF-kappa B p52 Subunit; 0 / TNIP1 protein, human; 0 / TNIP2 protein, human; 136601-57-5 / Cyclin D1; 139874-52-5 / NF-kappaB inhibitor alpha; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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53. Monteagudo C, Martin JM, Jorda E, Llombart-Bosch A: CXCR3 chemokine receptor immunoreactivity in primary cutaneous malignant melanoma: correlation with clinicopathological prognostic factors. J Clin Pathol; 2007 Jun;60(6):596-9
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  • [Title] CXCR3 chemokine receptor immunoreactivity in primary cutaneous malignant melanoma: correlation with clinicopathological prognostic factors.
  • BACKGROUND: A role for CXCR3, the receptor for chemokines Mig, IP-10 and interferon-inducible T cell alpha-chemoattractant, in tumour cell migration during melanoma progression has been proposed.
  • AIMS: To analyse CXCR3 expression in primary cutaneous malignant melanomas and its comparison with clinicopathological and prognostic factors.
  • Melanomas were categorised by age, sex, primary site, tumour thickness, growth phase, ulceration, lymphocytic infiltration, recurrence, lymph node and distant metastasis, and survival.
  • In univariate analysis, a significant association of CXCR3-positive tumour cell immunostaining with tumour thickness >1 mm (p = 0.003), absence of lymphocytic infiltration (p = 0.04) and the presence of distant metastasis (p = 0.048) was found.
  • Multivariate analysis found tumour thickness as the only independent factor with considerable association with distant metastases.
  • CONCLUSIONS: Our findings of a positive correlation of CXCR3 tumour cell immunoreactivity in human primary cutaneous melanoma with tumour thickness >1 mm and absence of intratumoral lymphocytic infiltration support the biological implication of CXCR3 in the tumour progression of cutaneous malignant melanoma.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Melanoma / metabolism. Receptors, Chemokine / metabolism. Skin Neoplasms / metabolism

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  • (PMID = 16522748.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CXCR3 protein, human; 0 / Neoplasm Proteins; 0 / Receptors, CXCR3; 0 / Receptors, Chemokine
  • [Other-IDs] NLM/ PMC1955073
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54. Baumeister P, Schwenk-Zieger S, Reiter M, Welz C, Harréus U: Transforming Growth Factor-alpha reduces carcinogen-induced DNA damage in mini-organ cultures from head-and-neck cancer patients. Mutat Res; 2009 Jun-Jul;677(1-2):42-5
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  • [Title] Transforming Growth Factor-alpha reduces carcinogen-induced DNA damage in mini-organ cultures from head-and-neck cancer patients.
  • EGFR is over-expressed in up to 90-100% of head-and-neck squamous cell carcinomas (HNSCC), and increased expression of EGFR and its ligand Transforming Growth Factor-alpha (TGF-alpha) is not limited to malignant cells, but also detected in histologically normal mucosa of HNSCC patients, supporting the hypothesis of field carcinogenesis.
  • Our study evaluates the impact of stimulation by TGF-alpha on carcinogen-induced and oxidative DNA damage in mucosa tissue cultures of macroscopically normal biopsies from tumour patients and controls.
  • Effects of TGF-alpha on DNA-repair capacity were investigated.
  • To assess DNA fragmentation, alkaline single-cell gel electrophoresis (comet assay) was used.
  • Stimulation of cultures during 24 h with TGF-alpha decreased benzo(a)pyrene diolepoxide (BPDE)-induced DNA damage by 36% in the tumour group (p < 0.001) and by 7% in controls (n = 30).
  • The exact mechanism by which TGF-alpha stimulation reduces BPDE-induced DNA fragmentation remains unclear.
  • However, our results show a strong DNA-stabilizing effect of stimulation by TGF-alpha in mucosa tissue cultures of tumour patients and may therefore be seen as a physiological response to continued carcinogenic impact on the epithelium of the upper aerodigestive tract.
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. DNA Damage / drug effects. Head and Neck Neoplasms / genetics. Transforming Growth Factor alpha / pharmacology

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  • (PMID = 19539778.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Transforming Growth Factor alpha; 55097-80-8 / 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide; BBX060AN9V / Hydrogen Peroxide
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55. Brennan PA, Mackenzie N, Quintero M: Hypoxia-inducible factor 1alpha in oral cancer. J Oral Pathol Med; 2005 Aug;34(7):385-9
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  • It contributes to local and systemic tumour progression as well as potentially compromising radiotherapy and chemotherapy.
  • It targets the transcription of over 60 genes involved in many aspects of cancer biology including cell survival, glucose metabolism, cell invasion and angiogenesis.
  • RESULTS: Although there are a few conflicting reports of its prognostic significance, over expression of HIF-1alpha seems to play an adverse role in the malignant progression of head and neck cancer by facilitating the adaptation of cells to hypoxia as well as contributing to the invasive properties and angiogenesis in these tumours.
  • The pharmacological manipulation of HIF-1alpha has marked effects on tumour growth, and it could prove to be an important target for drug therapy, both in oral cancer and in other hypoxia-dependent disease states.
  • [MeSH-major] Cell Hypoxia / physiology. Mouth Neoplasms / metabolism. Nitric Oxide / physiology. Transcription Factors / physiology
  • [MeSH-minor] Humans. Hypoxia-Inducible Factor 1, alpha Subunit

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  • (PMID = 16011605.001).
  • [ISSN] 0904-2512
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transcription Factors; 31C4KY9ESH / Nitric Oxide
  • [Number-of-references] 40
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56. Milicevic Z, Bogojevic D, Mihailovic M, Petrovic M, Krivokapic Z: Molecular characterization of hsp90 isoforms in colorectal cancer cells and its association with tumour progression. Int J Oncol; 2008 Jun;32(6):1169-78
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  • [Title] Molecular characterization of hsp90 isoforms in colorectal cancer cells and its association with tumour progression.
  • As determined by Western blot assay all hsp90 isoforms studied, alpha (84 kDa), beta (86 kDa) and hsp90N (75 kDa), were up-regulated and differentially expressed in various stages of colorectal carcinoma.
  • The expression of hsp90beta is definitely higher in poorly-differentiated carcinomas than in well-differentiated cancers, suggesting an involvement of hsp90beta in the inhibition of cancer cell differentiation.
  • Especially, the expression of cytosolic hsp90N isoform in malignant cells points to the possibility that induction or overexpression of hsp90N might be causally related to tumour formation.
  • In this way, the hsp90 would be at the crossroads of both signalling and cell migration events.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Blotting, Western. Cell Differentiation. Cell Membrane / metabolism. Cell Movement. Disease Progression. Female. Gene Expression Regulation, Neoplastic. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Invasiveness. Prognosis. Protein Isoforms. Signal Transduction

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  • (PMID = 18497978.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / HSP90 Heat-Shock Proteins; 0 / Protein Isoforms
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57. Jackson IL, Batinic-Haberle I, Sonveaux P, Dewhirst MW, Vujaskovic Z: ROS production and angiogenic regulation by macrophages in response to heat therapy. Int J Hyperthermia; 2006 Jun;22(4):263-73
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  • PURPOSE: It has been well established that inadequate blood supply combined with high metabolic rates of oxygen consumption results in areas of low oxygen tension (<1%) within malignant tumours and that elevating tumour temperatures above 39 degrees Celsius results in significant improvement in tumour oxygenation.
  • Macrophages play a dual role in tumour initiation and progression having both pro-tumour and anti-tumour effects.
  • [MeSH-minor] Animals. Cell Line. Cytokines / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / analysis. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Mice. Neoplasms / metabolism. Neoplasms / therapy. Oxygen Consumption / physiology. Respiratory Burst / physiology. Superoxides / metabolism. Temperature. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16754348.001).
  • [ISSN] 0265-6736
  • [Journal-full-title] International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
  • [ISO-abbreviation] Int J Hyperthermia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Reactive Oxygen Species; 0 / Vascular Endothelial Growth Factor A; 11062-77-4 / Superoxides
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58. Aggelis V, Craven RA, Peng J, Harnden P, Cairns DA, Maher ER, Tonge R, Selby PJ, Banks RE: Proteomic identification of differentially expressed plasma membrane proteins in renal cell carcinoma by stable isotope labelling of a von Hippel-Lindau transfectant cell line model. Proteomics; 2009 Apr;9(8):2118-30
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  • [Title] Proteomic identification of differentially expressed plasma membrane proteins in renal cell carcinoma by stable isotope labelling of a von Hippel-Lindau transfectant cell line model.
  • The von Hippel-Lindau (VHL) tumour suppressor gene plays a central role in development of clear cell renal cell carcinoma (RCC).
  • Using a cell line pair generated from the VHL-defective RCC cell line UMRC2 by transfection with vector control or VHL (-/+VHL) and stable isotope labelling with amino acids in cell culture (SILAC) followed by enrichment of plasma membrane proteins by cell surface biotinylation/avidin-affinity chromatography and analysis by GeLC-MS/MS, VHL-associated changes in plasma membrane proteins were analysed.
  • These included several proteins previously reported to be VHL targets, such as transferrin receptor 1 and the alpha 3 and beta1 integrin subunits and novel findings including upregulation of CD166 and CD147 in VHL-defective cells.
  • Analysis of patient-matched normal and malignant renal tissues confirmed these differences were also present in vivo in a subset of clear cell RCCs.
  • [MeSH-major] Carcinoma, Renal Cell / metabolism. Membrane Proteins / biosynthesis. Von Hippel-Lindau Tumor Suppressor Protein / physiology
  • [MeSH-minor] Antigens, CD / biosynthesis. Antigens, CD147 / biosynthesis. Biomarkers / metabolism. Cell Adhesion Molecules, Neuronal / biosynthesis. Cell Line, Tumor. Fetal Proteins / biosynthesis. Glycosylation. Humans. Isotope Labeling. Kidney Neoplasms / chemistry. Kidney Neoplasms / metabolism. Kidney Neoplasms / ultrastructure. Mass Spectrometry. Proteomics. Transfection. Up-Regulation

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  • (PMID = 19337990.001).
  • [ISSN] 1615-9861
  • [Journal-full-title] Proteomics
  • [ISO-abbreviation] Proteomics
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / ALCAM protein, human; 0 / Antigens, CD; 0 / Biomarkers; 0 / Cell Adhesion Molecules, Neuronal; 0 / Fetal Proteins; 0 / Membrane Proteins; 136894-56-9 / Antigens, CD147; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
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59. Katori H, Nozawa A, Tsukuda M: Markers of malignant transformation of sinonasal inverted papilloma. Eur J Surg Oncol; 2005 Oct;31(8):905-11
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  • [Title] Markers of malignant transformation of sinonasal inverted papilloma.
  • AIM: To measure HPV status, epidermal growth factor receptor (EGFR) and transforming growth factor-alpha (TGF-alpha) expression and Ki-67 index in exophytic papilloma (EP), inverted papilloma (IP) with dysplasia, IP with carcinoma and invasive squamous cell carcinoma (SCC).
  • The nasal tissues were stained with monoclonal antibodies to EGFR, TGF-alpha and Ki-67.
  • RESULTS: Significant increase of EGFR and TGF-alpha was observed in IP with severe dysplasia, IP with carcinoma and invasive SCC compared to IP with mild dysplasia and control nasal mucosa.
  • Among IP, HPV 6/11-positive was present in 42% tumour and HPV 16/18-positive was present in 31% of tumours.
  • CONCLUSION: Pre-cancerous lesions of IP exhibited elevated levels of EGFR and TGF-alpha and these expression may be associated with early events in IP carcinogenesis.
  • HPV infection may be an early event in a multistep process of malignant formation of IP.
  • [MeSH-major] Biomarkers, Tumor / analysis. Cell Transformation, Neoplastic / pathology. Nose Neoplasms / pathology. Papilloma, Inverted / pathology. Paranasal Sinus Neoplasms / pathology
  • [MeSH-minor] Antibodies, Monoclonal. Carcinoma / pathology. Carcinoma, Squamous Cell / pathology. Female. Humans. In Situ Hybridization. Ki-67 Antigen / analysis. Male. Middle Aged. Nasal Mucosa / pathology. Neoplasm Invasiveness. Papilloma / pathology. Papillomaviridae / classification. Papillomaviridae / isolation & purification. Precancerous Conditions / pathology. Receptor, Epidermal Growth Factor / analysis. Transforming Growth Factor alpha / analysis

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  • (PMID = 16005600.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Transforming Growth Factor alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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60. Przybyło M, Lityńska A, Pocheć E: Different adhesion and migration properties of human HCV29 non-malignant urothelial and T24 bladder cancer cells: role of glycosylation. Biochimie; 2005 Feb;87(2):133-42
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  • [Title] Different adhesion and migration properties of human HCV29 non-malignant urothelial and T24 bladder cancer cells: role of glycosylation.
  • In tumour cells, alterations in cellular glycosylation may play a key role in their metastatic behaviour.
  • This study used cell lines having very different behaviour in vivo: HCV29 non-malignant transitional epithelium and T24 bladder transitional cell carcinoma.
  • The functional role of carbohydrates was studied by treating these cells with swainsonine, an inhibitor of Golgi alpha-mannosidase II, and in vitro adhesion and migration assays.
  • Swainsonine treatment reduced the rate of T24 cell migration by 20%.
  • We concluded that beta1-6 branched tri- and tetraantennary complex-type glycans have an important function in adhesion and migration in the studied cell lines.
  • [MeSH-major] Cell Movement. Epithelial Cells / metabolism. Polysaccharides / biosynthesis. Ureter / metabolism. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Cell Adhesion / drug effects. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Female. Glycosylation / drug effects. Humans. Male. Species Specificity. Swainsonine / pharmacology

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  • (PMID = 15760705.001).
  • [ISSN] 0300-9084
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Polysaccharides; RSY4RK37KQ / Swainsonine
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61. Tajima N, Schönherr K, Niedling S, Kaatz M, Kanno H, Schönherr R, Heinemann SH: Ca2+-activated K+ channels in human melanoma cells are up-regulated by hypoxia involving hypoxia-inducible factor-1alpha and the von Hippel-Lindau protein. J Physiol; 2006 Mar 1;571(Pt 2):349-59
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  • Under chronic hypoxia, tumour cells undergo adaptive changes involving hypoxia-inducible factors (HIFs).
  • This increase involves the HIF system as confirmed by overexpression of HIF-1alpha or the von Hippel-Lindau tumour suppressor gene.
  • Hypoxia increased cell proliferation, but the K(Ca) channel blockers apamin and charybdotoxin slowed down cell growth, particularly under hypoxic conditions.
  • Similar results were obtained for the cell line IGR39 and for acutely isolated cells from a biopsy of a melanoma metastasis.
  • Thus, up-regulation of K(Ca) channels may be a novel mechanism by which HIFs can contribute to the malignant phenotype of human tumour cells.
  • [MeSH-major] Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Intermediate-Conductance Calcium-Activated Potassium Channels / metabolism. Melanoma / metabolism. Potassium Channels, Calcium-Activated / metabolism. Small-Conductance Calcium-Activated Potassium Channels / metabolism. Von Hippel-Lindau Tumor Suppressor Protein / physiology
  • [MeSH-minor] Apamin / pharmacology. Cell Hypoxia. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Transfection. Tumor Cells, Cultured. Up-Regulation

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  • (PMID = 16396931.001).
  • [ISSN] 0022-3751
  • [Journal-full-title] The Journal of physiology
  • [ISO-abbreviation] J. Physiol. (Lond.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Intermediate-Conductance Calcium-Activated Potassium Channels; 0 / Potassium Channels, Calcium-Activated; 0 / Small-Conductance Calcium-Activated Potassium Channels; 24345-16-2 / Apamin; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
  • [Other-IDs] NLM/ PMC1796787
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62. Woodward JK, Rennie IG, Elshaw SR, Burn JL, Sisley K: Invasive and noninvasive uveal melanomas have different adhesive properties. Eye (Lond); 2005 Mar;19(3):342-8
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  • METHODS: Cells from an invasive and noninvasive uveal melanoma cell line and hepatic and dermal microvascular endothelial cells were assessed by flow cytometry for adhesion molecule expression.
  • Tumour cell adhesion to ECM substrates (collagens I and IV, fibronectin, laminin, and vitronectin) and endothelial cells was also investigated using a commercially available assay or a fluorescence-based in vitro assay, respectively.
  • The significance of results comparing cell lines was determined using a Student's t-test, whereby P-values of less than 0.05 were taken as significant.
  • The invasive cell line also expressed higher levels of other integrins than the noninvasive line.
  • CONCLUSIONS: Successful attachment to and migration through the ECM, basement membrane, and endothelium are vital processes involved in malignant progression.
  • [MeSH-minor] Cell Adhesion. Cell Adhesion Molecules / metabolism. Endothelial Cells / pathology. Endothelium, Vascular / pathology. Extracellular Matrix / pathology. Extracellular Matrix Proteins / metabolism. Humans. Integrin alpha Chains / metabolism. Neoplasm Invasiveness. Neoplasm Proteins / metabolism. Tumor Cells, Cultured

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  • (PMID = 15258612.001).
  • [ISSN] 0950-222X
  • [Journal-full-title] Eye (London, England)
  • [ISO-abbreviation] Eye (Lond)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Extracellular Matrix Proteins; 0 / Integrin alpha Chains; 0 / Neoplasm Proteins
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63. Lansigan F, Foss FM: Current and emerging treatment strategies for cutaneous T-cell lymphoma. Drugs; 2010 Feb 12;70(3):273-86
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  • [Title] Current and emerging treatment strategies for cutaneous T-cell lymphoma.
  • Cutaneous T-cell lymphomas (CTCLs) are a rare group of mature T-cell lymphomas presenting primarily in the skin.
  • Other than an allogeneic stem cell transplant, there are no curative therapies for this disease.
  • These therapies include biological immune enhancers such as interferon alpha and extracorporeal photopheresis that exert their effect by stimulating an immune response to the tumour cells.
  • The fusion toxin denileukin diftitox targets the interleukin-2 receptor expressed on malignant T cells.
  • Forodesine is a novel inhibitor of purine nucleoside phosphorylase and leads to apoptosis of malignant T cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy / methods. Lymphoma, T-Cell, Cutaneous / drug therapy. Lymphoma, T-Cell, Cutaneous / therapy. Skin Neoplasms / drug therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Clinical Protocols. Drug Administration Routes. Hematopoietic Stem Cell Transplantation / methods. Humans

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  • (PMID = 20166766.001).
  • [ISSN] 1179-1950
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
  • [Number-of-references] 90
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64. Lau YS, Sabokbar A, Giele H, Cerundolo V, Hofstetter W, Athanasou NA: Malignant melanoma and bone resorption. Br J Cancer; 2006 May 22;94(10):1496-503
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  • [Title] Malignant melanoma and bone resorption.
  • The cellular and humoral mechanisms accounting for osteolysis in skeletal metastases of malignant melanoma are uncertain.
  • We isolated tumour-associated macrophages (TAMs) from metastatic (lymph node/skin) melanomas and cultured them in the presence and absence of osteoclastogenic cytokines and growth factors.
  • The effect of tumour-derived fibroblasts and melanoma cells on osteoclast formation and resorption was also analysed.
  • Tumour-associated macrophage-osteoclast differentiation also occurred via a RANKL-independent pathway when TAMs were cultured with tumour necrosis factor-alpha and interleukin (IL)-1alpha.
  • Our findings indicate that TAMs in metastatic melanomas can differentiate into osteoclasts and that melanoma fibroblasts and melanoma tumour cells can induce osteoclast formation by RANKL-dependent and RANKL-independent mechanisms, respectively.
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents / pharmacology. Carrier Proteins / metabolism. Cell Differentiation. Cells, Cultured. Culture Media, Conditioned / pharmacology. Female. Fibroblasts. Glycoproteins / pharmacology. Humans. Interleukin-1 / pharmacology. Lymphatic Metastasis. Male. Membrane Glycoproteins / metabolism. Middle Aged. Osteolysis / pathology. Osteoprotegerin. RANK Ligand. Receptor Activator of Nuclear Factor-kappa B. Receptors, Cytoplasmic and Nuclear. Receptors, Tumor Necrosis Factor. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16641914.001).
  • [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 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / Culture Media, Conditioned; 0 / Glycoproteins; 0 / Interleukin-1; 0 / Membrane Glycoproteins; 0 / Osteoprotegerin; 0 / RANK Ligand; 0 / Receptor Activator of Nuclear Factor-kappa B; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF11A protein, human; 0 / TNFRSF11B protein, human; 0 / TNFSF11 protein, human; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2361270
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65. Kang KB, Zhu C, Yong SK, Gao Q, Wong MC: Enhanced sensitivity of celecoxib in human glioblastoma cells: Induction of DNA damage leading to p53-dependent G1 cell cycle arrest and autophagy. Mol Cancer; 2009;8:66
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  • [Title] Enhanced sensitivity of celecoxib in human glioblastoma cells: Induction of DNA damage leading to p53-dependent G1 cell cycle arrest and autophagy.
  • BACKGROUND: Selective cyclooxygenase (COX)-2 inhibitors elicit anti-proliferative responses in various tumours, however the underlying anti-tumour mechanisms are unclear.
  • Mutational inactivation of the tumour suppressor p53 gene is frequent in malignant gliomas.
  • The role of p53 mutation in the anti-tumour responses of the selective COX-2 inhibitor celecoxib in human glioblastoma cells is unknown.
  • Inhibition of p53 was achieved in U87MG cells transfected with E6 oncoprotein (U87MG-E6) and treated with pifithrin-alpha, a reversible inhibitor of p53 (U87MG-PFT).
  • We investigated whether the anti-glioblastoma responses of celecoxib were p53-dependent, and whether celecoxib induced DNA damage leading to p53-dependent G1 cell cycle arrest, followed by autophagy or apoptosis.
  • RESULTS: Our findings demonstrated that celecoxib concentration-dependently reduced glioblastoma cell viability, following 24 and 72 hours of treatment.
  • Celecoxib induced G1-phase cell cycle arrest, accompanied with p21 activation in U87MG cells.
  • Cell cycle progression of U87MG-E6 and U87MG-PFT cells was not affected by celecoxib.
  • In parallel, celecoxib induced G1 cell cycle arrest in LN229 cells, but not in U373MG cells.
  • Celecoxib inhibits glioblastoma cell viability by induction of DNA damage, leading to p53-dependent G1 cell cycle arrest and p53-dependent autophagy, but not apoptosis.
  • [MeSH-major] Autophagy / drug effects. DNA Damage. G1 Phase / drug effects. Pyrazoles / pharmacology. Sulfonamides / pharmacology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Analysis of Variance. Benzothiazoles / pharmacology. Blotting, Western. Celecoxib. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Comet Assay. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclooxygenase Inhibitors / pharmacology. Dose-Response Relationship, Drug. G0 Phase / drug effects. Humans. Immunohistochemistry. Reverse Transcriptase Polymerase Chain Reaction. Toluene / analogs & derivatives. Toluene / pharmacology

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  • (PMID = 19706164.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzothiazoles; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Tumor Suppressor Protein p53; 0 / pifithrin; 3FPU23BG52 / Toluene; JCX84Q7J1L / Celecoxib
  • [Other-IDs] NLM/ PMC2741461
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66. Bircan S, Ensari A, Ozturk S, Erdogan N, Dundar I, Ortac F: Immunohistochemical analysis of c-myc, c-jun and estrogen receptor in normal, hyperplastic and neoplastic endometrium. Pathol Oncol Res; 2005;11(1):32-9
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  • [Title] Immunohistochemical analysis of c-myc, c-jun and estrogen receptor in normal, hyperplastic and neoplastic endometrium.
  • To evaluate the role of c-jun and c-myc proto-oncogenes in normal, hyperplastic and neoplastic endometrium in relation to estrogen receptor (ER) status and to investigate whether these genes can be related to other histopathological features of endometrial carcinoma, 32 endometrial carcinomas, 38 endometrial hyperplasias and 22 cyclic endometria (10 proliferative and 12 secretory) were evaluated histologically.
  • Endometrial carcinoma cases were subtyped according to the International Society of Gynecological Pathologists.
  • Immunohistochemical examination was performed using antibodies to ER-alpha, c-myc and c-jun with streptavidin-biotin-peroxidase technique.
  • The mean percentage of ER-alpha positive cells changed cyclically during the menstrual cycle, and it was the highest (96%) and the lowest (31.6%) in proliferative and carcinomatous endometrium, respectively.
  • There was a statistically significant difference between proliferative and secretory phases and proliferative and carcinomatous endometrium in relation to ER-alpha staining (p<0.05).
  • There was also a statistically significant difference with respect to ERalpha reactivity between secretory phase and each hyperplastic group, as well as between the carcinoma group and each hyperplastic group (p<0.05).
  • Although not significant, the mean percentage of c-myc expressing cells in the carcinoma group was higher (15.3%) than that of proliferative phase and hyperplastic groups.
  • The mean percentage of c-jun positive cells in proliferative endometrium was slightly higher than in secretory endometrium, and it was the highest in atypical hyperplastic endometrium (28.3%), but there was no statistically significant difference between the groups.
  • In carcinoma cases, a positive correlation was observed between c-jun positivity and tumor grade (p=0.027, r=0.3908), but such a correlation with c-myc was not found.
  • A positive correlation was detected between ER-alpha and c-myc expression (p=0.038, r=0.3686).
  • A progressive loss of ER seems to be correlated with increasing malignant transformation.
  • C-myc expression might play a role in the development of endometrial carcinoma via ER.
  • The association between c-jun and ER appears to be lost in endometrial carcinoma.
  • The relationship between c-myc, c-jun and ER appears to be altered in endometrial carcinoma compared to that of menstrual endometrium.
  • [MeSH-major] Endometrial Hyperplasia / metabolism. Endometrial Neoplasms / metabolism. Endometrium / metabolism. Estrogen Receptor alpha / metabolism. Proto-Oncogene Proteins c-jun / metabolism. Proto-Oncogene Proteins c-myc / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cell Proliferation. Female. Humans. Immunoenzyme Techniques. Menstrual Cycle / metabolism. Middle Aged. Prognosis

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  • (PMID = 15800680.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Estrogen Receptor alpha; 0 / Proto-Oncogene Proteins c-jun; 0 / Proto-Oncogene Proteins c-myc
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67. Kang KP, Kim DH, Jung YJ, Lee AS, Lee S, Lee SY, Jang KY, Sung MJ, Park SK, Kim W: Alpha-lipoic acid attenuates cisplatin-induced acute kidney injury in mice by suppressing renal inflammation. Nephrol Dial Transplant; 2009 Oct;24(10):3012-20
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  • [Title] Alpha-lipoic acid attenuates cisplatin-induced acute kidney injury in mice by suppressing renal inflammation.
  • BACKGROUND: Cisplatin is a chemotherapeutic agent used in treatment of malignant tumours.
  • Alpha-lipoic acid (alpha-LA) has anti-inflammatory effects that inhibit both adhesion molecule expression in human endothelial cells and monocyte adhesion by suppressing the nuclear factor-kappaB (NF-kappaB) signalling pathway.
  • The goals of this study were to investigate the anti-inflammatory effects of alpha-LA during cisplatin-induced renal injury and to examine the mechanisms of protection.
  • METHODS: C57BL/6 mice were given cisplatin (20 mg/kg) with or without alpha-LA treatment (100 mg/kg for 3 days).
  • Renal function, histological changes, adhesion molecule expression and inflammatory cell infiltration were examined.
  • The effect of alpha-LA on NF-kappaB activity was evaluated by examining nuclear translocation and phosphorylation of NF-kappaB p65 subunits in kidney tissue.
  • RESULTS: Cisplatin-induced decreases in renal function, measured by blood urea nitrogen, serum creatinine level and renal tubular injury scores, were attenuated by alpha-LA treatment. alpha-LA decreased the tissue levels of tumour necrosis factor-alpha, the expression of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1), and suppressed the infiltration of CD11b-positive macrophages. alpha-LA also attenuated the cisplatin-induced increases in the phosphorylation and nuclear translocation of NF- kappaB p65 subunits in kidney tissue.
  • CONCLUSIONS: These results suggest that alpha-LA treatment ameliorates cisplatin-induced acute kidney injury by reducing inflammatory adhesion molecule expression and NF-kappaB activity.

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  • (PMID = 19474282.001).
  • [ISSN] 1460-2385
  • [Journal-full-title] Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
  • [ISO-abbreviation] Nephrol. Dial. Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 73Y7P0K73Y / Thioctic Acid; Q20Q21Q62J / Cisplatin
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68. Setyono-Han B, Stürzebecher J, Schmalix WA, Muehlenweg B, Sieuwerts AM, Timmermans M, Magdolen V, Schmitt M, Klijn JG, Foekens JA: Suppression of rat breast cancer metastasis and reduction of primary tumour growth by the small synthetic urokinase inhibitor WX-UK1. Thromb Haemost; 2005 Apr;93(4):779-86
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  • [Title] Suppression of rat breast cancer metastasis and reduction of primary tumour growth by the small synthetic urokinase inhibitor WX-UK1.
  • The serine protease uPA (urokinase-type plasminogen activator) and its receptor uPAR (CD87) are often elevated in malignant tumours, hence, inhibition of this tumour-associated plasminogen activation system provides an attractive target for therapeutic strategies.
  • The anti-tumour and anti-metastatic (number of lung foci and weight of the axillary lymph nodes) properties were studied by subcutaneous administration of WX-UK1 to Brown Norwegian (BN) rats carrying orthotopically transplanted BN472 rat breast tumours.
  • WX-UK1 selectively inhibited tumour-related proteases from rats and humans such as uPA, plasmin, or thrombin in the sub or low micromolar range.
  • Chronical administration of the L-enantiomer of WXUK1 impaired primary tumour growth and metastasis of BN472 rat breast cancer in a dose-dependent manner.
  • In conclusion, our results provide evidence that WX-UK1 as a single agent inhibits breast tumour growth and metastasis in vivo, and thus is a promising candidate drug to treat human cancer.
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Evaluation, Preclinical. Female. Gene Expression Regulation, Neoplastic. Neoplasm Transplantation. Phenylalanine / analogs & derivatives. Phenylalanine / therapeutic use. Plasminogen Activator Inhibitor 1 / genetics. RNA, Neoplasm / analysis. Rats. Rats, Inbred BN. Receptors, Cell Surface / genetics. Receptors, Urokinase Plasminogen Activator

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  • (PMID = 15841327.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / PLAUR protein, human; 0 / Plasminogen Activator Inhibitor 1; 0 / Plaur protein, rat; 0 / RNA, Neoplasm; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator; 47E5O17Y3R / Phenylalanine; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; UJ925Q0P3B / WX-UK1
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69. Eyden B: The myofibroblast: a study of normal, reactive and neoplastic tissues, with an emphasis on ultrastructure. part 2 - tumours and tumour-like lesions. J Submicrosc Cytol Pathol; 2005 Nov;37(3-4):231-96
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  • [Title] The myofibroblast: a study of normal, reactive and neoplastic tissues, with an emphasis on ultrastructure. part 2 - tumours and tumour-like lesions.
  • This paper describes the ultrastructure of the commoner myofibroblastic tumours and tumour-like lesions.
  • The objective is to complement mainstream pathology texts, which have concentrated on the clinical and light microscopy features of these lesions and which have arguably but understandably somewhat neglected electron microscopy as an ancillary diagnostic tool and a technique for investigating tumour cell biology.
  • Ultrastructural features are described of nodular fasciitis, the myofibromatoses (including Dupuytren's disease), inflammatory myofibroblastic tumour, post-operative spindle cell nodule, fibroma of tendon sheath, fibrous pseudotumour, benign fibrous histiocytoma, atypical fibroxanthoma, dermatofibrosarcoma protuberans, myofibrosarcoma (myofibroblastic sarcoma), malignant fibrous histiocytoma (pleomorphic myofibrosarcoma), epithelioid sarcoma and spindle-cell carcinoma.
  • The fibronexus is emphasised as an important marker for the most confident diagnosis of myofibrosarcoma.
  • Some pathologists accept a light microscope definition, which includes alpha-smooth-muscle actin positivity, h-caldesmon negativity and, in some cases, desmin positivity.
  • Myofibroblastoma and angiomyofibroblastoma are examples of tumours argued on the basis of ultrastructural findings (sometimes in combination with desmin staining) to be primitively differentiated smooth-muscle cell rather than myofibroblastic proliferations.

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  • (PMID = 16612972.001).
  • [ISSN] 1122-9497
  • [Journal-full-title] Journal of submicroscopic cytology and pathology
  • [ISO-abbreviation] J. Submicrosc. Cytol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 344
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70. Vasiljeva O, Korovin M, Gajda M, Brodoefel H, Bojic L, Krüger A, Schurigt U, Sevenich L, Turk B, Peters C, Reinheckel T: Reduced tumour cell proliferation and delayed development of high-grade mammary carcinomas in cathepsin B-deficient mice. Oncogene; 2008 Jul 10;27(30):4191-9
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  • [Title] Reduced tumour cell proliferation and delayed development of high-grade mammary carcinomas in cathepsin B-deficient mice.
  • Expression levels of the papain-like cysteine protease cathepsin B (Ctsb) have been positively correlated with mammary tumour progression and metastasis; however, its roles in the hallmark processes of malignant growth remain poorly defined.
  • Using Ctsb-deficient mice we investigated tumour cell differentiation, proliferation and apoptosis in the Tg(MMTV-PyMT) mouse mammary cancer model.
  • Mice lacking Ctsb exhibited reduced cell proliferation in mammary carcinomas and their lung metastases.
  • Notably, intravenous injection of primarily isolated, Ctsb-expressing tumour cells into congenic Ctsb-deficient mice revealed impaired cell proliferation in the resulting experimental lung metastases, providing evidence for the involvement of Ctsb in paracrine regulation of cancer cell proliferation.
  • No Ctsb genotype-dependent difference in tumour cell death was observed in vivo or by treatment of isolated PyMT cancer cells with tumour necrosis factor-alpha.
  • [MeSH-major] Carcinoma / genetics. Cathepsin B / genetics. Cell Proliferation. Immunity, Innate / genetics. Mammary Neoplasms, Animal / genetics. Tumor Burden / genetics
  • [MeSH-minor] Animals. Cell Death / genetics. Disease Progression. Female. Lung Neoplasms / genetics. Lung Neoplasms / secondary. Mice. Mice, Knockout. Neoplasm Transplantation. Time Factors. Tumor Cells, Cultured


71. Boyd M, Sorensen A, McCluskey AG, Mairs RJ: Radiation quality-dependent bystander effects elicited by targeted radionuclides. J Pharm Pharmacol; 2008 Aug;60(8):951-8
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  • The efficacy of radiotherapy may be partly dependent on indirect effects, which can sterilise malignant cells that are not directly irradiated.
  • We determined bystander responses generated by the uptake of radioiodinated iododeoxyuridine ([*I]IUdR) and radiohaloanalogues of meta-iodobenzylguanidine ([*I]MIBG) by noradrenaline transporter (NAT) gene-transfected tumour cells.
  • Multicellular spheroids that consisted of 5% of NAT-expressing cells, capable of the active uptake of radiopharmaceutical, were sterilised by treatment with 20 kBqmL(-1) of the alpha-emitter meta-[211At]astatobenzylguanidine ([211At]MABG).
  • Similarly, in nude mice, retardation of the growth of tumour xenografts containing 5% NAT-positivity was observed after treatment with [131I]MIBG.
  • Cells exposed to media from [131I]MIBG- or [131I]IUdR-treated cells demonstrated a dose-response relationship with respect to clonogenic cell death.
  • It is concluded that radiopharmaceutical-induced bystander effects may depend on LET of the decay particles but are independent of site of intracellular concentration of radionuclide.
  • [MeSH-minor] Animals. Cell Death / radiation effects. Cell Line, Tumor. Culture Media, Conditioned / metabolism. Dose-Response Relationship, Radiation. Humans. Iodine Radioisotopes. Mice. Mice, Nude. Norepinephrine Plasma Membrane Transport Proteins / genetics. Norepinephrine Plasma Membrane Transport Proteins / metabolism. Radiation Dosage. Spheroids, Cellular. Transfection. Xenograft Model Antitumor Assays

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  • (PMID = 18644188.001).
  • [ISSN] 0022-3573
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Iodine Radioisotopes; 0 / Norepinephrine Plasma Membrane Transport Proteins; 0 / Radiopharmaceuticals; 35MRW7B4AD / 3-Iodobenzylguanidine; LGP81V5245 / Idoxuridine
  • [Number-of-references] 70
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72. Kuljaca S, Liu T, Tee AE, Haber M, Norris MD, Dwarte T, Marshall GM: Enhancing the anti-angiogenic action of histone deacetylase inhibitors. Mol Cancer; 2007;6:68
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  • BACKGROUND: Histone deacetylase inhibitors (HDACIs) have many effects on cancer cells, such as growth inhibition, induction of cell death, differentiation, and anti-angiogenesis, all with a wide therapeutic index.
  • RESULTS: Trichostatin A (TSA) and alpha-interferon (IFNalpha) were the most effective combination across a range of different cancer cell lines, while normal non-malignant cells did not respond in the same manner to the combination therapy.
  • Moreover, inhibition of p21WAF1 expression in a p21WAF1-expressing breast cancer cell line by a specific siRNA increased the cytotoxic effects of TSA and IFNalpha.
  • In vitro assays of endothelial cell function showed that TSA and IFNalpha decreased endothelial cell migration, invasion, and capillary tubule formation, without affecting endothelial cell viability.
  • Combination TSA and IFNalpha therapy markedly reduced tumour angiogenesis in neuroblastoma-bearing transgenic mice.
  • [MeSH-minor] Animals. Anoxia. Cell Movement. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Drug Synergism. Humans. Hydroxamic Acids / pharmacology. Interferon-alpha / metabolism. Mice. Models, Biological. Neoplasm Invasiveness. Neoplasm Transplantation

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  • (PMID = 17958916.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Interferon-alpha; 3X2S926L3Z / trichostatin A
  • [Other-IDs] NLM/ PMC2173905
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73. Dohi O, Ohtani H, Hatori M, Sato E, Hosaka M, Nagura H, Itoi E, Kokubun S: Histogenesis-specific expression of fibroblast activation protein and dipeptidylpeptidase-IV in human bone and soft tissue tumours. Histopathology; 2009 Oct;55(4):432-40
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  • The aim was to identify cell types that express FAP and DPP-IV in human bone and soft tissue tumours, and to determine whether there are any correlations between the expression of FAP and DPP-IV and the malignant potential of tumours.
  • METHODS AND RESULTS: This study analysed in situ expression in 25 malignant and 13 benign human bone and soft tissue tumours.
  • Immunohistochemistry using pre-fixed frozen sections revealed that FAP was positive in low-grade myofibroblastic sarcoma, the fibroblastic component of osteosarcomas, and malignant fibrous histiocytomas, but negative in Ewing's sarcomas and rhabdomyosarcomas.
  • Giant cells expressed DPP-IV in giant cell tumours.
  • CONCLUSIONS: Our data suggest that FAP and DPP-IV are consistently expressed in bone and soft tissue tumour cells that are histogenetically related to activated fibroblasts and/or myofibroblasts, irrespective of their malignancy.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Bone Neoplasms / metabolism. Bone Neoplasms / pathology. Dipeptidyl Peptidase 4 / metabolism. Gelatinases / metabolism. Membrane Proteins / metabolism. Serine Endopeptidases / metabolism. Soft Tissue Neoplasms / metabolism. Soft Tissue Neoplasms / pathology
  • [MeSH-minor] Fibroblasts / metabolism. Fibroblasts / pathology. Histiocytoma, Malignant Fibrous / metabolism. Histiocytoma, Malignant Fibrous / pathology. Humans. Macrophages / metabolism. Macrophages / pathology. Monocytes / metabolism. Monocytes / pathology. Osteosarcoma / metabolism. Osteosarcoma / pathology. Rhabdomyosarcoma / metabolism. Rhabdomyosarcoma / pathology. Sarcoma, Ewing / metabolism. Sarcoma, Ewing / pathology

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  • (PMID = 19817894.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Proteins; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
  • [Other-IDs] NLM/ PMC2784039
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74. Redpath M, Marques CM, Dibden C, Waddon A, Lalla R, Macneil S: Ibuprofen and hydrogel-released ibuprofen in the reduction of inflammation-induced migration in melanoma cells. Br J Dermatol; 2009 Jul;161(1):25-33
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  • OBJECTIVES: The aims of this study were: (i) to examine the effects of ibuprofen on the major proinflammatory cytokine tumour necrosis factor (TNF)-alpha induction of migration of C8161 and HBL human melanoma cells;.
  • METHODS: Melanoma cells were exposed to 300 U mL(-1) TNF-alpha for a 24-h period prior to making a scratch wound to which ibuprofen or ibuprofen-loaded hydrogels were then added.
  • The effects of relevant concentrations of ibuprofen on cell viability and apoptosis were examined.
  • RESULTS: Ibuprofen at 10(-3) mol L(-1) significantly reduced TNF-alpha-stimulated migration of both cell types to that of nonstimulated cells (P < 0.001).
  • TNF-alpha-unstimulated cell migration was not significantly affected.
  • CONCLUSIONS: These results demonstrate that TNF-alpha upregulated malignant melanoma migration in vitro and that this could be reduced by ibuprofen both in solution and delivered from a hydrogel.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Apoptosis / drug effects. Cell Movement / drug effects. Ibuprofen / pharmacology. Melanoma / pathology. Skin Neoplasms / pathology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Delayed-Action Preparations / pharmacology. Humans. Hydrogel / pharmacology. Inflammation / drug therapy. Tumor Cells, Cultured

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  • (PMID = 19438858.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0401428; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Delayed-Action Preparations; 0 / Tumor Necrosis Factor-alpha; 25852-47-5 / Hydrogel; WK2XYI10QM / Ibuprofen
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75. Lazer G, Idelchuk Y, Schapira V, Pikarsky E, Katzav S: The haematopoietic specific signal transducer Vav1 is aberrantly expressed in lung cancer and plays a role in tumourigenesis. J Pathol; 2009 Sep;219(1):25-34
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  • Physiological expression of Vav1 is restricted to the haematopoietic system, where its best-known function is as a GDP/GTP nucleotide exchange factor for Rho/RacGTPases, an activity strictly controlled by tyrosine phosphorylation downstream of cell surface receptors.
  • Here we find Vav1 expression in 42% of 78 lung cancer cell lines analysed.
  • Moreover, immunohistochemical analysis of primary human lung cancer tissue samples revealed Vav1 expression in 26/59 malignant samples, including adenocarcinoma, squamous cell carcinoma and bronchioloalveolar carcinoma.
  • Stronger Vav1 staining was associated with larger tumour size. siRNA-mediated knockdown of Vav1 in lung cancer cells reduced proliferation in agar and tumour growth in nude mice, while control siRNA had no effect, suggesting that Vav1 plays a critical role in the tumorigenicity of lung cancer cells.
  • [MeSH-major] Carcinoma / metabolism. Gene Expression Regulation, Neoplastic. Hematopoiesis / genetics. Lung Neoplasms / metabolism. Proto-Oncogene Proteins c-vav / metabolism. Signal Transduction / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Gene Expression. Glyceraldehyde-3-Phosphate Dehydrogenases / genetics. Humans. Immunohistochemistry / methods. Mice. Mice, Nude. RNA Interference. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction / methods. Transforming Growth Factor alpha / genetics. rac GTP-Binding Proteins / genetics

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  • (PMID = 19533802.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-vav; 0 / RNA, Small Interfering; 0 / Transforming Growth Factor alpha; 0 / VAV1 protein, human; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases; EC 3.6.5.2 / rac GTP-Binding Proteins
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76. Kasper G, Vogel A, Klaman I, Gröne J, Petersen I, Weber B, Castaños-Vélez E, Staub E, Mennerich D: The human LAPTM4b transcript is upregulated in various types of solid tumours and seems to play a dual functional role during tumour progression. Cancer Lett; 2005 Jun 16;224(1):93-103
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  • [Title] The human LAPTM4b transcript is upregulated in various types of solid tumours and seems to play a dual functional role during tumour progression.
  • LAPTM4b (lysosome associated protein transmembrane 4 beta) was recently identified as a gene overexpressed in human hepatocellular carcinoma and belongs to the mammalian LAPTM family.
  • By analysing genome-wide expression profiles of microdissected solid tumour samples by the means of Affymetrix GenChip hybridisation, we found LAPTM4b to be upregulated in 88% (23/26) of lung and in 67% (18/27) of colon carcinoma patients.
  • Other members of the LAPTM family were not overexpressed in the investigated tumour samples according to GeneChip hybridisation data.
  • Due to sequence analysis of bilaterian LAPTM proteins we suggests the presence of four transmembrane helices per protein, which are probably packed together by hydrophobic forces that are excerted by several evolutionary conserved aromatic residues within the alpha-helices.
  • We discuss an active role for LAPTM4b during disease progression of malignant cells and conclude that its putative dual functional involvement in tumour cell proliferation as well as in multidrug-resistance may represent LAPTM4b as a target suitable for development of novel therapeutic agents.
  • [MeSH-minor] Amino Acid Sequence. Blotting, Northern. Cell Proliferation. Cell Transformation, Neoplastic. Disease Progression. Female. Humans. Male. Molecular Sequence Data. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Tissue Distribution. Up-Regulation

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  • (PMID = 15911104.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / LAPTM4B protein, human; 0 / Membrane Proteins; 0 / Oncogene Proteins
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77. Escher N, Spies-Weisshart B, Kaatz M, Melle C, Bleul A, Driesch D, Wollina U, von Eggeling F: Identification of HNP3 as a tumour marker in CD4+ and CD4- lymphocytes of patients with cutaneous T-cell lymphoma. Eur J Cancer; 2006 Jan;42(2):249-55
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  • [Title] Identification of HNP3 as a tumour marker in CD4+ and CD4- lymphocytes of patients with cutaneous T-cell lymphoma.
  • Cutaneous T-cell lymphomas (CTCL) are characterized by malignant proliferation of skin homing T-cells.
  • Lymphocytes were separated in CD4+ and CD4- fractions by magnetic cell sorting (MACS).
  • For the generated combined rule base for the CD4- cell fraction, both the sensitivity and specificity for the prediction of CTCL reached 96%, while for the CD4+ fraction they were 92% and 84%, respectively, for sensitivity and specificity.
  • The most significant peak at 3489Da could be identified as HNP3, an alpha-defensin, by immunocapturing.
  • These results open up both the possibility for the use of this protein signature, especially HNP3, to more effectively monitor and screen CTCL, and the avenue to identify the other relevant peaks for a better understanding of the development of this tumour.
  • [MeSH-major] Biomarkers, Tumor / metabolism. CD4-Positive T-Lymphocytes / metabolism. Lymphoma, T-Cell, Cutaneous / diagnosis. Skin Neoplasms / diagnosis. alpha-Defensins / metabolism

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  • (PMID = 16338134.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Biomarkers, Tumor; 0 / alpha-Defensins; 0 / human neutrophil peptide 3
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78. Marini P, Schmid A, Jendrossek V, Faltin H, Daniel PT, Budach W, Belka C: Irradiation specifically sensitises solid tumour cell lines to TRAIL mediated apoptosis. BMC Cancer; 2005 Jan 14;5:5
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  • [Title] Irradiation specifically sensitises solid tumour cell lines to TRAIL mediated apoptosis.
  • BACKGROUND: TRAIL (tumor necrosis factor related apoptosis inducing ligand) is an apoptosis inducing ligand with high specificity for malignant cell systems.
  • Combined treatment modalities using TRAIL and cytotoxic drugs revealed highly additive effects in different tumour cell lines.
  • Little is known about the efficacy and underlying mechanistic effects of a combined therapy using TRAIL and ionising radiation in solid tumour cell systems.
  • METHODS: Tumour cell systems derived from breast- (MDA MB231), lung--(NCI H460) colorectal--(Colo 205, HCT-15) and head and neck cancer (FaDu, SCC-4) were treated with a combination of TRAIL and irradiation using two different time schedules.
  • RESULTS: The combined treatment of TRAIL with irradiation strongly increased apoptosis induction in all treated tumour cell lines compared to treatment with TRAIL or irradiation alone.
  • Upregulation of TRAIL receptor DR5 after irradiation was observed in four of six tumour cell lines but did not correlate to tumour cell sensitisation to TRAIL.
  • TRAIL did not show toxicity in normal tissue cell systems.
  • In addition, pre-irradiation did not sensitise all nine tested human normal tissue cell cultures to TRAIL.
  • Sequential application of ionising radiation followed by TRAIL is associated with an synergistic induction of cell death in a large panel of solid tumour cell lines.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis. Membrane Glycoproteins / therapeutic use. Neoplasms / therapy. Radiation, Ionizing. Tumor Necrosis Factor-alpha / therapeutic use
  • [MeSH-minor] Apoptosis Regulatory Proteins. Caspase 8. Caspases / metabolism. Cell Line, Tumor. Cells, Cultured. Combined Modality Therapy. Humans. Poly(ADP-ribose) Polymerases / metabolism. Receptors, Tumor Necrosis Factor / metabolism. TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 15651986.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC547906
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79. Orii T, Takeda H, Kawata S, Maeda K, Yamakawa M: Differential immunophenotypic analysis of dendritic cell tumours. J Clin Pathol; 2010 Jun;63(6):497-503
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  • [Title] Differential immunophenotypic analysis of dendritic cell tumours.
  • AIMS: The phenotypic and biological characteristics of dendritic cell (DC) tumours have not been fully elucidated.
  • The aim of this study was to compare the immunophenotypic characteristics of DC-related markers and cell-cycle-associated markers among DC tumours and finally to utilise them for differential diagnosis of DC tumours.
  • METHODS: Tissue sections from 28 patients with DC tumours were immunohistochemically examined using DC-related and cell-cycle-associated markers.
  • RESULTS: The Langerhans cell histiocytosis (LCH) and Langerhans cell sarcoma (LCS) samples were positive for S-100 protein, CD1a, Langerin, fascin, DEC-205 and DC-SIGN.
  • Interdigitating dendritic cell sarcoma (IDCS) was positive for S-100 protein and fascin and negative for Langerin.
  • Follicular dendritic cell sarcoma was distinguished from other DC tumours by the lack of DC-SIGN, Langerin and DCE-205.
  • CONCLUSIONS: These results suggest that Langerin can be used to distinguish LCS from IDCS, and DC-SIGN and DEC-205 can be used to identify DC tumour cells.
  • The frequency of cell-cycle-associated markers can be used for the differential diagnosis of malignant and benign DC tumours.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Dendritic Cell Sarcoma, Interdigitating / diagnosis. Histiocytosis, Langerhans-Cell / diagnosis. Langerhans Cell Sarcoma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Cycle Proteins / metabolism. Child. Dendritic Cells / immunology. Diagnosis, Differential. Female. Forkhead Transcription Factors / analysis. Histones / metabolism. Humans. Immunophenotyping. Interleukin-3 Receptor alpha Subunit / analysis. Male. Middle Aged. Neoplasm Proteins / metabolism. Tumor Suppressor Protein p53 / metabolism. Young Adult

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  • (PMID = 20439325.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Histones; 0 / IL3RA protein, human; 0 / Interleukin-3 Receptor alpha Subunit; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53
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80. Rago V, Romeo F, Giordano F, Ferraro A, Andò S, Carpino A: Identification of ERbeta1 and ERbeta2 in human seminoma, in embryonal carcinoma and in their adjacent intratubular germ cell neoplasia. Reprod Biol Endocrinol; 2009;7:56
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  • [Title] Identification of ERbeta1 and ERbeta2 in human seminoma, in embryonal carcinoma and in their adjacent intratubular germ cell neoplasia.
  • BACKGROUND: Estrogens exert a role on germ cell physiology of normal human testis through the mediation of the estrogen receptor (ER) beta subtypes.
  • Epidemiological studies evidenced an increased incidence of testicular germ cell cancer after elevated pre-natal estrogen exposure but the expression of estrogen receptors in these testicular neoplasms has not been well elucidated.
  • METHODS: Immunohistochemistry and Western blot analysis were used to investigate the expression of three distinct ER isoforms, ERalpha, ERbeta1, and ERbeta2 in paraffin-embedded tissues from seminomas and embryonal carcinomas, which are the most common testicular germ cell tumours.
  • A similar pattern of estrogen receptor immunostaining was also observed in the malignant germ cells of intratubular germ cell neoplasia, adjacent to testicular cancers.
  • Western blot analysis of tumour extracts revealed two immunoreactive bands, a 59 kDa band for ERbeta1 and a 53 kDa band for ERbeta2.
  • CONCLUSION: A variable ERbeta expression was previously reported in testicular germ cell tumours and, particularly, an ERbeta down-regulation was evidenced in seminoma and embryonal carcinoma.
  • Conversely, the current study has clearly identified ERbeta1 and ERbeta2 in the neoplastic cells of seminoma and embryonal carcinoma, as well as in the malignant cells of their common pre-invasive precursor, intratubular germ cell neoplasia.
  • [MeSH-major] Carcinoma, Embryonal / metabolism. Estrogen Receptor beta / metabolism. Neoplasms, Germ Cell and Embryonal / metabolism. Seminoma / metabolism. Testicular Neoplasms / metabolism
  • [MeSH-minor] Adult. Blotting, Western. Down-Regulation / physiology. Estrogen Receptor alpha / metabolism. Humans. Immunohistochemistry. Male. Young Adult

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  • (PMID = 19493328.001).
  • [ISSN] 1477-7827
  • [Journal-full-title] Reproductive biology and endocrinology : RB&E
  • [ISO-abbreviation] Reprod. Biol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta
  • [Other-IDs] NLM/ PMC2700117
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81. Charles J, Chaperot L, Salameire D, Di Domizio J, Aspord C, Gressin R, Jacob MC, Richard MJ, Beani JC, Plumas J, Leccia MT: Plasmacytoid dendritic cells and dermatological disorders: focus on their role in autoimmunity and cancer. Eur J Dermatol; 2010 Jan-Feb;20(1):16-23
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  • The presence of PDC, cells capable of producing large quantities of interferon alpha (IFN-alpha) in response to pathogenic agents or danger signals, seems to be closely related to pathological conditions.
  • PDC have been observed in inflammatory immunoallergic dermatological disorders, in malignant cutaneous tumours and in cutaneous lesions of infectious origin.
  • Their function within a tumour context is not as well known and is controversial.
  • They could have a tolerogenic role towards tumour cells in the absence of an activator but they also have the capacity to become activated in response to Toll-like receptor (TLR) ligands and could therefore be useful for therapeutic purposes.
  • [MeSH-minor] Humans. Interferon-alpha / immunology. Interferon-alpha / secretion

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  • (PMID = 19850548.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Interferon-alpha
  • [Number-of-references] 25
  • [Other-IDs] NLM/ HALMS471485; NLM/ PMC2881955
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82. Paraskeva PA, Ridgway PF, Olsen S, Isacke C, Peck DH, Darzi AW: A surgically induced hypoxic environment causes changes in the metastatic behaviour of tumours in vitro. Clin Exp Metastasis; 2006;23(2):149-57
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  • The use of laparoscopic techniques for curative resections of malignant tumours has been under scrutiny.
  • The potential benefits to the patient in the form of earlier recovery and less immune paresis are countered by the reports of increased tumour recurrence.
  • The biological sequelae of the hypoxic laparoscopic environment on tumour cells is unknown.
  • Components of the metastatic cascade were evaluated under in vitro laparoscopic conditions using a human colonic adenocarcinoma cell line (SW1222).
  • Exposure to the laparoscopic gases carbon dioxide and helium for 4 h, comparable to the duration of a laparoscopic colorectal resection, had no effect on cell viability.
  • The changes were reflected at the molecular level by significant down regulation of adhesion molecules known to be involved in tumour progression (E-cadherin, CD44 and beta1 sub-unit).
  • [MeSH-major] Adenocarcinoma / surgery. Cell Hypoxia. Colonic Neoplasms / surgery. Laparoscopy / adverse effects
  • [MeSH-minor] Cadherins / metabolism. Carbon Dioxide / adverse effects. Cell Adhesion. Cell Adhesion Molecules / metabolism. Extracellular Matrix Proteins / metabolism. Helium / adverse effects. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / analysis. Neoplasm Metastasis. Time Factors. Tumor Cells, Cultured