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Items 1 to 100 of about 1435
1. Paula LC, Zen VL, Czepielewski MA: [Granulosa-stromal tumor of the ovary: a case of mixed germ cell-cord stromal tumor of the ovary with endocrinological considerations]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):776-83
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  • [Title] [Granulosa-stromal tumor of the ovary: a case of mixed germ cell-cord stromal tumor of the ovary with endocrinological considerations].
  • [Transliterated title] Puberdade precoce associada a tumor misto ovariano (células germinativas- estroma-cordão sexual): aspectos clínicos, diagnósticos e manejo de um caso.
  • We report a case of mixed germ cell-cord stromal tumor of ovary in a 7.2 years old girl, who presented with isosexual pseudo-precocious puberty of progressive outcome.
  • Unilateral salpingo-oophorectomy was performed with complete resection of the tumor.
  • The patient is well 7 years after surgery with normal pubertal and growth development and no signs of tumor relapse.
  • We review the clinical manifestations of ovarian tumors, classification and staging of sex cord-stromal tumors, follow-up, tumor markers, treatment and prognosis.
  • [MeSH-major] Granulosa Cell Tumor / complications. Mixed Tumor, Malignant / complications. Ovarian Neoplasms / complications. Puberty, Precocious / etiology
  • [MeSH-minor] 17-alpha-Hydroxyprogesterone / blood. Biomarkers, Tumor / blood. Child. Estradiol / blood. Female. Humans. Ovariectomy / methods. Testosterone / blood. Treatment Outcome

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  • (PMID = 16444360.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 68-96-2 / 17-alpha-Hydroxyprogesterone
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2. Stathopoulos GT, Kollintza A, Moschos C, Psallidas I, Sherrill TP, Pitsinos EN, Vassiliou S, Karatza M, Papiris SA, Graf D, Orphanidou D, Light RW, Roussos C, Blackwell TS, Kalomenidis I: Tumor necrosis factor-alpha promotes malignant pleural effusion. Cancer Res; 2007 Oct 15;67(20):9825-34
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  • [Title] Tumor necrosis factor-alpha promotes malignant pleural effusion.
  • Tumor necrosis factor (TNF)-alpha is present in the microenvironment of human tumors, including malignant pleural effusion (MPE).
  • Although the cytokine is produced in the pleural cavity by both tumor and host cells, its effects on MPE formation are unknown.
  • In these studies, we sought to determine the role of TNF-alpha in the pathogenesis of MPE and to assess the therapeutic effects of its neutralization in a preclinical model.
  • The roles of tumor- and host-derived TNF-alpha were assessed using combined experimentation with TNF-alpha gene-deficient mice and in vivo TNF-alpha neutralization.
  • To expand the scope of preclinical data, TNF-alpha and vascular endothelial growth factor (VEGF) expression were determined in human cancer cell lines and human MPE.
  • In the MPE model, TNF-alpha of host and tumor origin was present.
  • TNF-alpha neutralization significantly limited tumor dissemination, effusion formation, vascular hyperpermeability, TNF-alpha and VEGF expression, and angiogenesis, thereby improving survival.
  • In contrast, these variables were not different between TNF-alpha gene-sufficient and TNF-alpha gene-deficient mice.
  • In mouse cancer cells, TNF-alpha functioned via nuclear factor-kappaB- and neutral sphingomyelinase-dependent pathways to induce TNF-alpha and VEGF, respectively.
  • These results were recapitulated in human cancer cells, and a correlation was detected between TNF-alpha and VEGF content of human MPE.
  • We conclude that tumor-derived TNF-alpha is important in the development of MPE in mice, and provide preclinical evidence supporting the efficacy of TNF-alpha blockade against malignant pleural disease.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology. Pleural Effusion, Malignant / pathology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Animals. Capillary Permeability. Cell Line, Tumor. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Knockout. NF-kappa B / metabolism. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / pathology. Prostatic Neoplasms / blood supply. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. Sphingomyelin Phosphodiesterase / metabolism. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 17942913.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL61419; United States / NHLBI NIH HHS / HL / HL66196
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; EC 3.1.4.12 / Sphingomyelin Phosphodiesterase
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3. Chen PY, Chen WY, Ho DM, Pan CC: Malignant ganglioneuroma arising from mediastinal mixed germ cell tumor. J Chin Med Assoc; 2007 Feb;70(2):76-9
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  • [Title] Malignant ganglioneuroma arising from mediastinal mixed germ cell tumor.
  • Mixed germ cell tumors with non-germ cell malignant components rarely occur in the anterior mediastinum.
  • We report a case of a 34-year-old man who presented with an anterior mediastinum mass.
  • Mixed germ cell tumor was initially diagnosed based on the pathologic findings of germinoma on thoracoscopic biopsy and clinical findings of elevated serum alpha-fetoprotein and beta-human chorionic gonadotropin.
  • The patient received preoperative chemotherapy and subsequent complete resection of the residual tumor.
  • Pathologic examination of the excised specimen showed predominantly malignant ganglioneuroma and small residual foci of teratoma.
  • To our knowledge, this is the first reported case of a malignant ganglioneuroma arising from mediastinal mixed germ cell tumor.
  • [MeSH-major] Ganglioneuroma / etiology. Mediastinal Neoplasms / complications. Neoplasms, Germ Cell and Embryonal / complications

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  • (PMID = 17339149.001).
  • [ISSN] 1726-4901
  • [Journal-full-title] Journal of the Chinese Medical Association : JCMA
  • [ISO-abbreviation] J Chin Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
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4. Szlosarek PW, Grimshaw MJ, Kulbe H, Wilson JL, Wilbanks GD, Burke F, Balkwill FR: Expression and regulation of tumor necrosis factor alpha in normal and malignant ovarian epithelium. Mol Cancer Ther; 2006 Feb;5(2):382-90
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  • [Title] Expression and regulation of tumor necrosis factor alpha in normal and malignant ovarian epithelium.
  • The proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) and both its receptors (TNFRI and TNFRII) are expressed in biopsies of this malignancy.
  • Here, we tested the hypothesis that TNF-alpha is a regulator of the proinflammatory microenvironment of ovarian cancer.
  • A cancer profiling array showed higher expression of TNF-alpha in ovarian tumors compared with normal ovarian tissue, and cultured ovarian cancer cells expressed up to 1,000 times more TNF-alpha mRNA than cultured normal ovarian surface epithelial cells; TNF-alpha protein was only detected in the supernatant of tumor cell cultures.
  • Treatment with TNF-alpha induced TNF-alpha mRNA via TNFRI in both malignant and normal cells with evidence for enhanced TNF-alpha mRNA stability in tumor cells.
  • TNF-alpha induced TNF-alpha protein in an autocrine fashion in tumor but not in normal ovarian surface epithelial cells.
  • The TNF-alpha neutralizing antibody infliximab reduced the constitutive levels of TNF-alpha mRNA in tumor cell lines capable of autocrine TNF-alpha production.
  • Apart from TNF-alpha mRNA expression, several other proinflammatory cytokines were constitutively expressed in malignant and normal ovarian surface epithelial cells, including interleukin (IL)-1alpha, IL-6, CCL2, CXCL8, and M-CSF.
  • TNF-alpha treatment further induced these cytokines with de novo transcription of IL-6 mRNA contrasting with the increased stability of CCL2 mRNA.
  • RNA interference directed against TNF-alpha was highly effective in abolishing constitutive IL-6 production by ovarian tumor cells.
  • In summary, we show that TNF-alpha is differentially regulated in ovarian cancer cells compared with untransformed cells and modulates production of several cytokines that may promote ovarian tumorigenesis.
  • Infliximab treatment may have a role in suppressing the TNF-alpha-driven inflammatory response associated with ovarian cancer.
  • [MeSH-major] Cytokines / metabolism. Ovarian Neoplasms / metabolism. Ovary / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Cell Line, Tumor. Chemokine CCL2 / metabolism. Epithelium / drug effects. Epithelium / metabolism. Female. Humans. Infliximab. Interleukin-6 / metabolism. RNA Interference. RNA Stability. RNA, Messenger / analysis. RNA, Messenger / metabolism

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  • (PMID = 16505113.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501974
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / CCL2 protein, human; 0 / Chemokine CCL2; 0 / Cytokines; 0 / Interleukin-6; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab
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5. Appetecchia M, Ferretti E, Carducci M, Izzo F, Carpanese L, Marandino F, Terzoli E: Malignant glucagonoma. New options of treatment. J Exp Clin Cancer Res; 2006 Mar;25(1):135-9
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  • [Title] Malignant glucagonoma. New options of treatment.
  • Few cases of malignant glucagonomas have been described in the literature.
  • In this paper we present a case of a 77-year-old woman with necrolytic migratory erythema and high plasma glucagon and chromogranin A levels caused by a neuroendocrine tumour.
  • An abdominal CT scan suggested a pancreatic lesion and two liver metastases.
  • The patient underwent pancreatic debulking and liver metastasectomy.
  • Histological and immunohistochemical investigations revealed a well differentiated neuroendocrine tumour with vascular invasion and scattered immunopositivity for somatostatin receptors.
  • The patient was treated with octreotide (30 mg i.m. every 28 days) and interferon-alpha (6 MU s.cc 3 times per week) plus three cycles of hepatic chemoembolisation.
  • The patient is now asymptomatic with persistent hepatic disease and normal serum glucagon levels forty months after primary treatment.
  • So far, only few immunohistochemical studies are reported on malignant glucagonoma and combined treatment schedules.
  • We demonstrated, for the first time, a scattered immunopositivity for somatostatin receptors in a malignant glucagonoma.
  • A combined antiproliferative medical treatment and the hepatic chemoembolization have been able to control tumor growth and disease symptoms for a long time after surgery.
  • [MeSH-major] Glucagonoma / therapy
  • [MeSH-minor] Aged. Chromogranin A. Chromogranins / blood. Female. Glucagon / blood. Humans. Immunohistochemistry. Interferon-alpha / metabolism. Neuroendocrine Tumors / blood. Octreotide / pharmacology. Proglucagon / metabolism. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 16761630.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Interferon-alpha; 55963-74-1 / Proglucagon; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide
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6. Williams LE, DeNardo GL, Meredith RF: Targeted radionuclide therapy. Med Phys; 2008 Jul;35(7Part1):3062-3068

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Targeted radionuclide therapy (TRT) seeks molecular and functional targets within patient tumor sites.
  • A number of agents have been constructed and labeled with beta, alpha, and Auger emitters.
  • Uptake, in percent-injected dose per gram of malignant tissue, is used to evaluate the specificity of the targeting vehicle.
  • Lymphoma (B-cell) has been the primary clinical application.

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  • [Copyright] © 2008 American Association of Physicists in Medicine.
  • (PMID = 28513035.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Anatomy / Auger effect / Cancer / Computed tomography / Conformal radiation treatment / Dosimetry / Medical imaging / Positron emission tomography / Positron emission tomography (PET) / Proteins / Single photon emission computed tomography / Single photon emission computed tomography (SPECT) / Tissue engineering / Tissues / absorbed dose / alpha-particle sources / antibodies / beta-ray sources / blood / cellular biophysics / positron emission tomography / radiation therapy / radioisotopes / radionuclide therapy / single photon emission computed tomography / tumours
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7. Werther M, Schmelz HU, Schwerer M, Sparwasser C: [Sclerosing Sertoli cell tumor of the testis: a rare tumor. Case report and review of the literature on the subtypes of Sertoli-cell tumor]. Urologe A; 2007 Nov;46(11):1551-6
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  • [Title] [Sclerosing Sertoli cell tumor of the testis: a rare tumor. Case report and review of the literature on the subtypes of Sertoli-cell tumor].
  • [Transliterated title] Sklerosierender Sertoli-Zell-Tumor des Hodens - ein seltener Tumor : Fallvorstellung und Literaturübersicht über die Subtypen des Sertoli-Zell-Tumors.
  • Sertoli cell tumors of the testis are extremely rare (0.4-1.5% of all testicular neoplasms) and have a heterogeneous pathology.
  • Histopathologically classic, large cell calcifying and sclerosing subtypes are differentiated.Up to now, 14 cases of sclerosing Sertoli cell tumor are known.
  • The subtypes differ in particular in age of onset, malignant potential, prognosis, and therapy.
  • While no cases of sclerosing Sertoli cell tumor with a malignant course have been reported, both other subtypes have been found to be potentially malignant.
  • In the case of malignancy the prognosis is very poor, and it is difficult to select the best treatment because there is so little experience with this type of tumor.
  • Once the diagnosis of a Sertoli cell tumor has been confirmed, exact determination of the histological subtype is essential to allow appropriate risk-adapted therapy.
  • [MeSH-major] Sertoli Cell Tumor / diagnosis. Testicular Neoplasms / diagnosis
  • [MeSH-minor] Adult. Biomarkers, Tumor / blood. Biopsy. Diagnosis, Differential. Fatty Liver, Alcoholic / blood. Humans. Male. Neoplasm Staging. Sclerosis. Testis / pathology. Ultrasonography. alpha-Fetoproteins

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  • (PMID = 17898983.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / alpha-Fetoproteins
  • [Number-of-references] 20
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8. Suh KS, Crutchley JM, Koochek A, Ryscavage A, Bhat K, Tanaka T, Oshima A, Fitzgerald P, Yuspa SH: Reciprocal modifications of CLIC4 in tumor epithelium and stroma mark malignant progression of multiple human cancers. Clin Cancer Res; 2007 Jan 1;13(1):121-31
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  • [Title] Reciprocal modifications of CLIC4 in tumor epithelium and stroma mark malignant progression of multiple human cancers.
  • PURPOSE: CLIC4, a member of a family of intracellular chloride channels, is regulated by p53, c-Myc, and tumor necrosis factor-alpha.
  • Regulation by factors involved in cancer pathogenesis, together with the previously shown proapoptotic activity of CLIC4, suggests that the protein may have a tumor suppressor function.
  • To address this possibility, we characterized the expression profile, subcellular localization, and gene integrity of CLIC4 in human cancers and determined the functional consequences of CLIC4 expression in tumor epithelium and stromal cells.
  • CLIC4 expression, as a consequence of crosstalk between stroma and epithelium, was tested in vitro by coculture of breast epithelial tumor cells and normal fibroblasts, and the functional consequences of CLIC4 expression was tested in vivo in xenografts of human breast tumor cell lines reconstituted with CLIC4 or mixed with fibroblasts that overexpress CLIC4 transgenically.
  • RESULTS: In cDNA arrays of matched human normal and tumor tissues, CLIC4 expression was reduced in renal, ovarian, and breast cancers.
  • However, CLIC4 protein levels were variable in tumor lysate arrays.
  • Transcript sequences of CLIC4 from the human expressed sequence tag database and manual sequencing of cDNA from 60 human cancer cell lines (NCI60) failed to reveal deletion or mutations in the CLIC4 gene.
  • With advancing malignant progression, CLIC4 staining became undetectable in tumor cells, but expression increased in stromal cells coincident with up-regulation of alpha-smooth muscle actin, suggesting that CLIC4 is up-regulated in myofibroblasts.
  • Coculture of cancer cells and fibroblasts induced the expression of both CLIC4 and alpha-smooth muscle actin in fibroblasts adjacent to tumor nests.
  • Introduction of CLIC4 or nuclear targeted CLIC4 via adenovirus into human breast cancer xenografts inhibited tumor growth, whereas overexpression of CLIC4 in stromal cells of xenografts enhanced tumor growth.
  • CONCLUSION: Loss of CLIC4 in tumor cells and gain in tumor stroma is common to many human cancers and marks malignant progression.
  • Up-regulation of CLIC4 in tumor stroma is coincident with myofibroblast conversion, generally a poor prognostic indicator.
  • Reactivation and restoration of CLIC4 in tumor cells or the converse in tumor stromal cells could provide a novel approach to inhibit tumor growth.
  • [MeSH-minor] Actins / metabolism. Animals. Cell Line, Tumor. DNA Mutational Analysis. Disease Progression. Epithelium / metabolism. Fibroblasts / metabolism. Genes, Tumor Suppressor. Humans. Mice. Neoplasm Transplantation. Proto-Oncogene Proteins c-myc / metabolism. Tumor Necrosis Factor-alpha / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 17200346.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / CLIC4 protein, human; 0 / Chloride Channels; 0 / Proto-Oncogene Proteins c-myc; 0 / TP53 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53
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9. Gu Y, Li H, Miki J, Kim KH, Furusato B, Sesterhenn IA, Chu WS, McLeod DG, Srivastava S, Ewing CM, Isaacs WB, Rhim JS: Phenotypic characterization of telomerase-immortalized primary non-malignant and malignant tumor-derived human prostate epithelial cell lines. Exp Cell Res; 2006 Apr 1;312(6):831-43
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  • [Title] Phenotypic characterization of telomerase-immortalized primary non-malignant and malignant tumor-derived human prostate epithelial cell lines.
  • In vitro human prostate cell culture models are critical for clarifying the mechanism of prostate cancer progression and for testing preventive and therapeutic agents.
  • Cell lines ideal for the study of human primary prostate tumors would be those derived from spontaneously immortalized tumor cells; unfortunately, explanted primary prostate cells survive only short-term in culture, and rarely immortalize spontaneously.
  • Therefore, we recently have generated five immortal human prostate epithelial cell cultures derived from both the benign and malignant tissues of prostate cancer patients with telomerase, a gene that prevents cellular senescence.
  • Examination of these cell lines for their morphologies and proliferative capacities, their abilities to grow in low serum, to respond to androgen stimulation, to grow above the agar layer, to form tumors in SCID mice, suggests that they may serve as valid, useful tools for the elucidation of early events in prostate tumorigenesis.
  • Furthermore, the chromosome alterations observed in these immortalized cell lines expressing aspects of the malignant phenotypes imply that these cell lines accurately recapitulate the genetic composition of primary tumors.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. Telomerase / metabolism. Tumor Cells, Cultured
  • [MeSH-minor] Adult. Aged. Animals. Cell Aggregation / physiology. Cell Proliferation. Chromosomes, Human / genetics. Cytogenetic Analysis. Dihydrotestosterone / pharmacology. Gene Expression Profiling. Humans. Immunohistochemistry. Male. Mice. Mice, SCID. Middle Aged. Neoplasm Transplantation. Neoplasms, Experimental / metabolism. Phenotype. Racemases and Epimerases / genetics. Receptors, Androgen / drug effects. Receptors, Androgen / genetics. Reverse Transcriptase Polymerase Chain Reaction. Xenograft Model Antitumor Assays

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  • (PMID = 16413016.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AR protein, human; 0 / DNA-Binding Proteins; 0 / Receptors, Androgen; 08J2K08A3Y / Dihydrotestosterone; EC 2.7.7.49 / Telomerase; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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10. Darra E, Abdel-Azeim S, Manara A, Shoji K, Maréchal JD, Mariotto S, Cavalieri E, Perbellini L, Pizza C, Perahia D, Crimi M, Suzuki H: Insight into the apoptosis-inducing action of alpha-bisabolol towards malignant tumor cells: involvement of lipid rafts and Bid. Arch Biochem Biophys; 2008 Aug 15;476(2):113-23

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  • [Title] Insight into the apoptosis-inducing action of alpha-bisabolol towards malignant tumor cells: involvement of lipid rafts and Bid.
  • In a precedent report we showed that alpha-bisabolol, a sesquiterpene present widely in the plant kingdom, exerts a rapid and efficient apoptosis-inducing action selectively towards human and murine malignant glioblastoma cell lines through mitochondrial damage.
  • The present study extends these data demonstrating the apoptosis-inducing action of alpha-bisabolol towards highly malignant human pancreatic carcinoma cell lines without affecting human fibroblast viability.
  • The present study further shows the preferential incorporation of alpha-bisabolol to transformed cells through lipid rafts on plasma membranes and, thereafter, direct interaction between alpha-bisabolol and Bid protein, one of pro-apoptotic Bcl-2 family proteins, analyzed either by Surface Plasmon Resonance method or by intrinsic fluorescence measurement.
  • Notions that lipid rafts are rich in plasma membranes of transformed cells and that Bid, richly present in lipid rafts, is deeply involved in lipid transport make highly credible the hypothesis that the molecular mechanism of alpha-bisabolol action may include its capacity to interact with Bid protein.
  • [MeSH-minor] Caspase 3 / analysis. Caspase 3 / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Humans. Membrane Potentials / drug effects. Mitochondria / metabolism. Models, Molecular. Molecular Structure. Pancreatic Neoplasms / pathology. Recombinant Proteins / chemistry. Recombinant Proteins / metabolism. Surface Plasmon Resonance. Time Factors

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  • (PMID = 18291090.001).
  • [ISSN] 1096-0384
  • [Journal-full-title] Archives of biochemistry and biophysics
  • [ISO-abbreviation] Arch. Biochem. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BH3 Interacting Domain Death Agonist Protein; 0 / Recombinant Proteins; 0 / Sesquiterpenes; 24WE03BX2T / bisabolol; EC 3.4.22.- / Caspase 3
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11. Sanersak S, Prueksritanond N: Regression pattern of alpha fetoprotein level changed after treatment of malignant germ cell tumor. J Med Assoc Thai; 2008 Mar;91(3):287-94
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  • [Title] Regression pattern of alpha fetoprotein level changed after treatment of malignant germ cell tumor.
  • OBJECTIVE: To identify the regression pattern of serum alpha fetoprotein in malignant germ cell tumors after initial chemotherapy MATERIAL AND METHOD: This was a retrospective descriptive study.
  • All patients with malignant germ cell tumor who had elevated serum alpha fetoprotein (AFP) and received adjuvant chemotherapy in Rajavithi Hospital between January 1984 and May 2007 were included.
  • RESULTS: Sixty patients with malignant germ cell tumor that met the study criteria were included.
  • CONCLUSION: The regression of AFP is an independent prognostic factor in malignant germ cell tumor and may be a useful tool in the therapeutic management of these patients.
  • [MeSH-major] Neoplasms, Germ Cell and Embryonal / physiopathology. alpha-Fetoproteins / analysis

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  • (PMID = 18575279.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / alpha-Fetoproteins
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12. Phuphanich S, Rudnick J, Chu R, Mazer M, Wang H, Serrano N, Francisco M, Wheeler C, Singh M, Yu JS: A phase I trial of tumor-associated antigen-pulsed dendritic cell immunotherapy for patients with brain stem glioma and glioblastoma. J Clin Oncol; 2009 May 20;27(15_suppl):2032

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  • [Title] A phase I trial of tumor-associated antigen-pulsed dendritic cell immunotherapy for patients with brain stem glioma and glioblastoma.
  • : 2032 Background: Previous immunotherapy trials for malignant glioma (Yu, J.,et al, Cancer Res.
  • 2001;61:842-7 and 2004;64;4973-9) have demonstrated efficacy in generating a tumor specific immune response.
  • METHODS: The goal of this study is to use tumor associated antigens (TAA) known to be expressed on gliomas and pulse dendritic cells with these antigens in an MHC compatible fashion using epitopes of HER-2, TRP-2, gp100, MAGE-1, IL13R alpha, and AIM-3.
  • Leukapheresis was used to isolate mononuclear cells which were differentiated into dendritic cells in culture, pulsed with tumor peptide, and then administered intradermally three times at 2-week intervals.
  • Our data on 19 patients and 54 courses of dendritic cell vaccines demonstrate zero grade 3 /4 toxicities that were attributable to the vaccination.
  • Thirteen patients continue to have stable disease (ranging from 15 to 115 weeks), six patients have demonstrated tumor progression.
  • Of 15 patients tested to date, six patients demonstrated an antigen-specific cytotoxic T-cell response to at least one antigen after vaccination.
  • Only 17% of CTL responders (1/6) demonstrated tumor progression compared to 56% (5/9) of nonresponders to date.
  • CONCLUSIONS: This phase I study demonstrated the feasibility, safety, and bioactivity of a TAA-pulsed dendritic cell vaccine for patients with glioblastoma progression free survival correlated with CTL response.

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  • (PMID = 27964632.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Pollak MN, Blouin M, Zakikhani M, Zhao Y, Algire C: Dependence of malignant proliferation associated with loss of PTEN on glucose concentration in the hyperglycemic range: Relevance to population studies linking hyperglycemia to unfavorable cancer prognosis. J Clin Oncol; 2009 May 20;27(15_suppl):11113

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dependence of malignant proliferation associated with loss of PTEN on glucose concentration in the hyperglycemic range: Relevance to population studies linking hyperglycemia to unfavorable cancer prognosis.
  • : 11113 Background: Loss of function of the tumor suppressor PTEN enhances malignant proliferation, but effects on cellular energy metabolism are less well characterized.
  • METHODS: We used a tetracycline-inducible PTEN expression vector in the PTEN-null U251 glioma cell line to characterize effects of PTEN on cellular energy metabolism.
  • RESULTS: Forced expression of PTEN led to decreased phospho-AKT<sup>Ser473</sup>, decreased hexokinase II and HIF-1 alpha levels, and increased p53 levels.

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  • (PMID = 27963493.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Sundstedt A, Celander M, Hedlund G: Combining tumor-targeted superantigens with interferon-alpha results in synergistic anti-tumor effects. Int Immunopharmacol; 2008 Mar;8(3):442-52

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combining tumor-targeted superantigens with interferon-alpha results in synergistic anti-tumor effects.
  • In this study we explored the possibility of improving the anti-tumor potency of tumor-targeted superantigens (TTS) by combination treatment with interferon-alpha (IFN-alpha).
  • TTS utilizes the powerful T cell activating property of the superantigen staphylococcal enterotoxin A (SEA) in fusion with an anti-tumor Fab-fragment to target this T cell activity against tumor cells.
  • TTS fusion proteins have shown anti-tumor efficacy in a number of experimental tumor models including the B16 mouse melanoma transfected with a human tumor-associated antigen recognized by the C215 monoclonal antibody.
  • IFN-alpha is approved for the treatment of solid tumors such as renal cell carcinoma and malignant melanoma and exerts immunomodulatory effects, which make it an appropriate candidate to combine with immunotherapy against cancer.
  • Here we report that daily administration of IFN-alpha (20 000 U i.p.) enhances and sustains CD8+ T cell activation induced by the TTS C215Fab-SEA (10 microg i.v.) in C57Bl/6 mice, as reflected by increased and prolonged cell-mediated cytotoxicity against tumor cells ex vivo as well as by augmented serum IFN-gamma levels.
  • C215Fab-SEA synergized with IFN-alpha in reducing the number of lung tumors in B16-C215 melanoma bearing mice as compared to mono therapy.
  • In a long term tumor survival experiment, the prolonged median survival time of the combination treatment was 3.5 and 7.7 times the prolonged median survival times of C215Fab-SEA and IFN-alpha monotherapies, respectively.
  • Hence, the combination treatment provoked synergistic anti-tumor effects as measured by the number of lung tumors and markedly prolonged survival.
  • The enhanced therapeutic efficacy correlated with a striking and sustained increase of CD8- and perforin-expressing tumor-infiltrating cells.
  • These results suggest significant potential of combining TTS with IFN-alpha for human cancer therapy.
  • [MeSH-major] Enterotoxins / administration & dosage. Immunoglobulin Fab Fragments / administration & dosage. Interferon-alpha / administration & dosage. Melanoma, Experimental / therapy. Superantigens / administration & dosage
  • [MeSH-minor] Animals. Cell Line, Tumor. Cytotoxicity, Immunologic. Female. Interferon-gamma / biosynthesis. Lymphocytes, Tumor-Infiltrating / immunology. Mice. Mice, Inbred C57BL. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 18279798.001).
  • [ISSN] 1567-5769
  • [Journal-full-title] International immunopharmacology
  • [ISO-abbreviation] Int. Immunopharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Enterotoxins; 0 / Immunoglobulin Fab Fragments; 0 / Interferon-alpha; 0 / Superantigens; 37337-57-8 / enterotoxin A, Staphylococcal; 82115-62-6 / Interferon-gamma
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15. Wu TT, Hsieh YH, Hsieh YS, Liu JY: Reduction of PKC alpha decreases cell proliferation, migration, and invasion of human malignant hepatocellular carcinoma. J Cell Biochem; 2008 Jan 1;103(1):9-20
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  • [Title] Reduction of PKC alpha decreases cell proliferation, migration, and invasion of human malignant hepatocellular carcinoma.
  • However, the exact role of these enzymes in human hepatocellular carcinoma (HCC) has not been well established.
  • Using the RT-PCR and Western blotting to analyze the levels of PKC isoforms mRNA and protein in the five different differentiated hepatoma cell lines, we found that PKC alpha was highly expressed in the poor-differentiated HCC cell lines (SK-Hep-1 and HA22T/VGH) as compared with that in the well-differentiated HCC cell lines (PLC/PRF/5, Hep3B, and HepG2).
  • When treated with PKC alpha antisense oligonucleotides (ODN), both HA22T/VGH and SK-Hep-1 cells lines showed the reduction of PKC alpha expression, as well as a deceleration in the growth rate and in the level of cyclin D1, but the increase in the levels of p53 and p21(WAF1/CIP1).
  • Moreover, the reduction of PKC alpha expression also inhibited the migratory and invasive potential of both HA22T/VGH and SK-Hep-1 cells lines, and revealed a down-regulation of several migration/invasion-related genes (MMP-1, u-PA, u-PAR, and FAK).
  • These phenomenon were also confirmed by DNA-based small interfering RNA (siRNA) PKC alpha and PKC alpha/beta specific inhibitor Go6976.
  • Thus, the results indicated that PKC alpha may be associated with regulation of cell proliferation/migration/invasion in human poorly differentiated HCC cells, suggesting a role for the PKC alpha in the malignant progression of human HCC.
  • [MeSH-major] Carcinoma, Hepatocellular / enzymology. Carcinoma, Hepatocellular / pathology. Cell Movement. Protein Kinase C-alpha / metabolism
  • [MeSH-minor] Carbazoles / pharmacology. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. DNA, Antisense / genetics. Gene Expression Regulation, Neoplastic. Humans. Indoles / pharmacology. Isoenzymes / genetics. Isoenzymes / metabolism. Neoplasm Invasiveness / pathology. Protein Kinase Inhibitors / pharmacology. RNA, Small Interfering / genetics. Tumor Suppressor Protein p53 / metabolism

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  • [Copyright] Copyright (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17486587.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Carbazoles; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA, Antisense; 0 / Indoles; 0 / Isoenzymes; 0 / Protein Kinase Inhibitors; 0 / RNA, Small Interfering; 0 / Tumor Suppressor Protein p53; 136194-77-9 / Go 6976; 136601-57-5 / Cyclin D1; EC 2.7.11.13 / Protein Kinase C-alpha
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16. Wong JM, Chi SN, Marcus KJ, Levine BS, Ullrich NJ, MacDonald S, Lechpammer M, Goumnerova LC: Germinoma with malignant transformation to nongerminomatous germ cell tumor. J Neurosurg Pediatr; 2010 Sep;6(3):295-8
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  • [Title] Germinoma with malignant transformation to nongerminomatous germ cell tumor.
  • The authors describe the case of a young girl with suprasellar germinoma.
  • Six weeks after this diagnosis, just prior to initiation of therapy, serum and CSF marker analysis revealed sudden and marked elevation of alpha-fetoprotein, indicating transformation of her germinoma to a nongerminomatous germ cell tumor.
  • She underwent chemotherapy and radiation therapy per the national treatment approach for the new diagnosis, with subsequent return of her serum and CSF tumor markers to normal levels.
  • To the authors' knowledge, this is the first case in the English-language literature of a nongerminomatous germ cell tumor resulting from conversion of germinoma at the original site of presentation.
  • [MeSH-major] Brain Neoplasms / diagnosis. Germinoma / diagnosis. Neoplasms, Germ Cell and Embryonal / diagnosis
  • [MeSH-minor] Adolescent. Biomarkers / blood. Child. Female. Humans. alpha-Fetoproteins / analysis


17. Suzuki S, Maeda S, Sasajima K, Yoshida H, Yokoyama T, Maruyama H, Matsutani T, Liu A, Hosone M, Tanno M, Uchida E: Malignant granular cell tumor in the gluteal region with unusual pathologic features. Int Surg; 2010 Oct-Dec;95(4):360-5

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  • [Title] Malignant granular cell tumor in the gluteal region with unusual pathologic features.
  • Malignant granular cell tumors (MGCTs) are very rare soft tissue sarcomas.
  • Definite criteria for pathologic diagnosis and the optimal treatment strategy have not been fully established.
  • Here, we describe a 76-year-old woman with a huge MGCT in the right gluteal region, who developed a local recurrence and died from that tumor 14 months after undergoing an operation for the primary tumor.
  • Although microscopic examination revealed that round and granular tumor cells staining for S-100 protein were dominant, components of the spindle cell sarcoma reacting with alpha smooth muscle actin were partially observed.
  • [MeSH-major] Buttocks / pathology. Granular Cell Tumor / pathology. Granular Cell Tumor / surgery. Soft Tissue Neoplasms / pathology. Soft Tissue Neoplasms / surgery

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  • (PMID = 21309422.001).
  • [ISSN] 0020-8868
  • [Journal-full-title] International surgery
  • [ISO-abbreviation] Int Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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18. Vogt AP, Chen Z, Osunkoya AO: Rete testis invasion by malignant germ cell tumor and/or intratubular germ cell neoplasia: what is the significance of this finding? Hum Pathol; 2010 Sep;41(9):1339-44
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  • [Title] Rete testis invasion by malignant germ cell tumor and/or intratubular germ cell neoplasia: what is the significance of this finding?
  • Pathologic stage and postsurgical treatment guidelines of malignant germ cell tumors, currently take into account angiolymphatic invasion, degree of extra testicular invasion, and serum tumor marker levels.
  • The significance of rete testis invasion by malignant germ cell tumors or intratubular germ cell neoplasia however remains controversial.
  • A search through the surgical pathology and expert consultation files at our institution from 2002 to 2009 was made for malignant germ cell tumors and intratubular germ cell neoplasia in orchiectomy specimens.
  • One hundred thirty-six were associated with malignant germ cell tumors.
  • The mean greatest tumor dimension was 4.1 cm (range, 0.8-18 cm).
  • Fifty-six were pure seminoma (40%), 50 were nonseminomatous malignant germ cell tumors (35%), and 35 were mixed malignant germ cell tumors including a seminoma component (25%).
  • Intratubular germ cell neoplasia was identified in 99 cases (70%).
  • Intratubular germ cell neoplasia was present in patients with rete testis invasion in 18 cases (90%), compared to only 13 cases (57%) in patients without rete testis invasion, P = .02.
  • The combination of rete testis invasion and angiolymphatic invasion were present in 8 cases and were found to be associated with elevated serum tumor markers in 7 (88%) of the 8 cases, compared to the combination of no invasion of the rete testis and angiolymphatic invasion showing elevated serum tumor markers in 3 (38%) of 8 cases.
  • Rete testis status should be documented in orchiectomy specimens with malignant germ cell tumors.
  • Intratubular germ cell neoplasia may be the only component of a malignant germ cell tumor involving the rete testis.
  • In this series, elevated tumor markers were more likely associated with angiolymphatic invasion and positive rete testis status.
  • [MeSH-major] Carcinoma in Situ / pathology. Germinoma / secondary. Rete Testis / pathology. Seminoma / secondary. Testicular Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / metabolism. Chorionic Gonadotropin, beta Subunit, Human / blood. Humans. Male. Middle Aged. Neoplasm Invasiveness. Orchiectomy. Young Adult. alpha-Fetoproteins / metabolism

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20573373.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AFP protein, human; 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / alpha-Fetoproteins
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19. Price KL, Herlyn M, Dent CL, Gewert DR, Linge C: The prevalence of interferon-alpha transcription defects in malignant melanoma. Melanoma Res; 2005 Apr;15(2):91-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The prevalence of interferon-alpha transcription defects in malignant melanoma.
  • The type I interferons, interferon-alpha (IFN-alpha) and interferon-beta (IFN-beta), are situated on the short arm of chromosome 9, specifically 9p21-22.
  • Recent evidence has demonstrated that metastatic melanoma cell lines have a specific loss of IFN-alpha gene expression, a defect that appears to occur at the level of transcription.
  • In this study, we examined the expression of IFN-alpha in cell lines isolated from the various stages of melanoma progression, with a view to determine the prevalence of the IFN-alpha transcription defects exhibited by malignant melanoma, and to assess whether the loss of IFN-alpha expression was particular to a certain stage of melanoma progression.
  • We showed that all the melanoma cell lines tested (n=20) demonstrated an inability to express IFN-alpha, a defect that was reflected in the apparent inactivity of the IFN-alpha promoter.
  • These defects were found to occur in cells isolated from early melanomas, lending support to the hypothesis that IFN-alpha has a role in the aetiology of malignant melanoma.
  • [MeSH-major] Antineoplastic Agents. Gene Expression Regulation, Neoplastic. Interferon-alpha / genetics. Melanoma / genetics. Skin Neoplasms / genetics. Transcription, Genetic
  • [MeSH-minor] Cell Line, Tumor. Chromosomes, Human, Pair 9. DNA-Binding Proteins. Enzyme-Linked Immunosorbent Assay. Genes, Tumor Suppressor. Humans. Melanocytes. Polymerase Chain Reaction. Prevalence. Promoter Regions, Genetic / physiology. RNA, Messenger / metabolism. RNA, Neoplasm / metabolism. Sendai virus. Transfection

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  • (PMID = 15846141.001).
  • [ISSN] 0960-8931
  • [Journal-full-title] Melanoma research
  • [ISO-abbreviation] Melanoma Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Interferon-alpha; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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20. Yokota T, Kouno J, Adachi K, Takahashi H, Teramoto A, Matsumoto K, Sugisaki Y, Onda M, Tsunoda T: Identification of histological markers for malignant glioma by genome-wide expression analysis: dynein, alpha-PIX and sorcin. Acta Neuropathol; 2006 Jan;111(1):29-38
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  • [Title] Identification of histological markers for malignant glioma by genome-wide expression analysis: dynein, alpha-PIX and sorcin.
  • Glioblastoma multiforme (GBM), the most malignant class of glial neoplasm (grade IV in WHO criteria), carries the worst clinical prognosis among primary brain tumors in adults.
  • Immunohistochemical staining for 3 of the respective gene products, dynein (product of DNCH2), alpha-PIX (product of ARHGEF6), and sorcin (product of SRI) indicated that this technique might be useful for histological grading of glial tumors.
  • To establish criteria for this diagnostic approach, we scored glial tumor tissues of different histological grades according to the staining results; the scores were significantly higher in anaplastic astrocytomas and GBMs than in diffuse astrocytomas or normal brain tissues.
  • These findings indicated that levels of these three proteins might serve as histological markers for malignant glioma classification.
  • [MeSH-major] Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Calcium-Binding Proteins / genetics. Cell Cycle Proteins / genetics. Dyneins / genetics. Glioblastoma / genetics. Guanine Nucleotide Exchange Factors / genetics

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  • (PMID = 16320026.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / ARHGEF6 protein, human; 0 / Biomarkers, Tumor; 0 / Calcium-Binding Proteins; 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / Guanine Nucleotide Exchange Factors; 0 / Rho Guanine Nucleotide Exchange Factors; 0 / SRI protein, human; EC 3.6.4.2 / Dyneins
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21. Thyrell L, Sangfelt O, Zhivotovsky B, Pokrovskaja K, Wang Y, Einhorn S, Grandér D: The HPV-16 E7 oncogene sensitizes malignant cells to IFN-alpha-induced apoptosis. J Interferon Cytokine Res; 2005 Feb;25(2):63-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The HPV-16 E7 oncogene sensitizes malignant cells to IFN-alpha-induced apoptosis.
  • There is a great variability in sensitivity to IFN treatment depending on both tumor type and the individual patient.
  • The fact that several IFN-induced anticellular effects are exerted through modulation of proto-oncogenes and tumor suppressor genes may indicate that the malignant genotype may be decisive in the cell's sensitivity to IFN.
  • To determine if a deregulated oncogene could alter the cellular response to IFN, a mouse lymphoma cell line (J3D) was stably transfected with the viral human papillomavirus-16 (HPV-16) E7 oncogene.
  • The E7-transfected cells and their respective mock-transfected sister clones were treated with IFN-alpha and examined for possible IFN-induced anticellular effects.
  • We found that the E7-transfected clones were greatly sensitized to IFN-alpha-induced apoptosis compared with their mock-transfected counterparts.
  • In summary, our data suggest that transfection of malignant cells with the E7 oncogene can sensitize them to IFN-alpha-induced apoptosis.
  • [MeSH-major] Apoptosis / drug effects. Interferon-alpha / pharmacology. Oncogene Proteins, Viral / metabolism. Papillomaviridae
  • [MeSH-minor] Animals. Caspases / metabolism. Cell Line, Transformed. Cell Line, Tumor. Cell Transformation, Viral. Enzyme Activation / drug effects. Flow Cytometry. Membrane Proteins / metabolism. Mice. Papillomavirus E7 Proteins. Proto-Oncogene Proteins c-bcl-2 / metabolism. Retroviridae / genetics. Transfection. bcl-2 Homologous Antagonist-Killer Protein

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  • (PMID = 15695927.001).
  • [ISSN] 1079-9907
  • [Journal-full-title] Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • [ISO-abbreviation] J. Interferon Cytokine Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bak1 protein, mouse; 0 / Interferon-alpha; 0 / Membrane Proteins; 0 / Oncogene Proteins, Viral; 0 / Papillomavirus E7 Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2 Homologous Antagonist-Killer Protein; 0 / oncogene protein E7, Human papillomavirus type 16; EC 3.4.22.- / Caspases
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22. Ohnuma A, Yoshida T, Takahashi N, Akema S, Kumagai M, Chiba Y, Kashimoto Y, Kuwahara M, Nakashima N, Harada T: Malignant Leydig cell tumor with spindle-shaped cells in a male CD-1 mouse. J Vet Med Sci; 2010 May;72(5):661-4

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  • [Title] Malignant Leydig cell tumor with spindle-shaped cells in a male CD-1 mouse.
  • Leydig cell tumors with spindle-shaped cells are very rare in humans and animals.
  • We report that an 84-week-old male CD-1 mouse had a malignant Leydig cell tumor characterized by proliferation of oval to spindle-shaped cells with or without fat deposition, and with a storiform pattern.
  • This differentiation from Leydig cells was further confirmed by the immunopositivity of these cells for nestin and alpha-smooth muscle actin, both of which are known to be expressed in the stem/progenitor cells that differentiate into Leydig cells.
  • These findings suggest that the tumor is most probably a malignant spindle-cell-type Leydig cell tumor.

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  • (PMID = 20075603.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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23. Barocas DA, Kawamoto H, Dreizin DF, Howard ME, Choi J, Pitts WR, You X, Tickoo SK, Boorjian SA, Scherr DS: Five-alpha-reductase expression in benign and malignant urothelium: correlation with disease characteristics and outcome. Urology; 2005 Nov;66(5):1134-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Five-alpha-reductase expression in benign and malignant urothelium: correlation with disease characteristics and outcome.
  • OBJECTIVES: To evaluate 5-alpha-reductase (5alphaR) expression in benign and malignant urothelium and to assess the relationship between 5alphaR expression and tumor stage, tumor grade, and clinical outcome in patients with urothelial carcinoma/transitional cell carcinoma.
  • METHODS: We performed immunohistochemistry for 5alphaR on 53 urothelial specimens from 36 patients with transitional cell carcinoma treated at our institution between June 2002 and July 2003.
  • For each tumor and the adjacent nontumor urothelium, a semiquantitative staining score was calculated.
  • Nontumor urothelium had greater mean staining scores than did tumor specimens (160.1 versus 105.5, P <0.01).
  • CONCLUSIONS: We demonstrated 5alphaR expression in human urothelium and found that expression is decreased in transitional cell carcinoma in relation to tumor grade and stage.
  • [MeSH-major] Carcinoma, Transitional Cell / enzymology. Cholestenone 5 alpha-Reductase / biosynthesis. Urologic Diseases / enzymology. Urologic Neoplasms / enzymology. Urothelium / enzymology

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  • (PMID = 16286153.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.3.1.22 / Cholestenone 5 alpha-Reductase
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24. Kinoshita Y, Tajiri T, Souzaki R, Tatsuta K, Higashi M, Izaki T, Takahashi Y, Taguchi T: Diagnostic value of lectin reactive alpha-fetoprotein for neoinfantile hepatic tumors and malignant germ cell tumors: preliminary study. J Pediatr Hematol Oncol; 2008 Jun;30(6):447-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnostic value of lectin reactive alpha-fetoprotein for neoinfantile hepatic tumors and malignant germ cell tumors: preliminary study.
  • BACKGROUND AND PURPOSE: The serum alpha-fetoprotein (AFP) level has been used as a tumor marker for hepatoblastoma, and malignant germ cell tumors in pediatric patients.
  • The AFP has 3 isoforms (L1, L2, L3), and the usefulness of the L3 fraction as a diagnostic marker for the adult hepatocellular carcinoma is well known.
  • However, there are few reports dealing with various pediatric malignant tumors.
  • MATERIALS AND METHODS: From 2003 to 2006, two cases of hepatoblastoma, and 5 cases of germ cell tumor, all of which were neoinfantile, were treated in our department.
  • RESULTS: In all cases of hepatoblastoma and yolk sac tumor, both the total AFP and the L3 fraction were high, either before treatment or in the presence of malignant tumors.
  • Only 1 case of the immature teratoma demonstrated malignant transformation, when the patient was 8 months old.
  • DISCUSSION: Our results indicated that the level of the L3 fraction accurately confirmed the existence, or the malignant potential of hepatic tumor or germ cell tumor.
  • The L3 fraction is useful as a tumor marker during the neoinfantile period.
  • [MeSH-major] Biomarkers, Tumor / blood. Hepatoblastoma / blood. Liver Neoplasms / blood. Neoplasms, Germ Cell and Embryonal / blood. alpha-Fetoproteins / analysis

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  • (PMID = 18525461.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Lectins; 0 / Protein Isoforms; 0 / alpha-Fetoproteins
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25. Kuphal S, Wallner S, Bosserhoff AK: Loss of nephronectin promotes tumor progression in malignant melanoma. Cancer Sci; 2008 Feb;99(2):229-33
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  • [Title] Loss of nephronectin promotes tumor progression in malignant melanoma.
  • POEM has several characteristics of a matrix protein including an arg-gly-asp binding domain site that is recognized by integrins.
  • We therefore speculate that deregulation of POEM expression plays a role in the development or progression of malignant melanoma.
  • Thus, we evaluated melanoma cell lines and tissue samples of malignant melanoma for POEM transcription.
  • We found that POEM expression was reduced or lost in most cell lines and in all tumor samples analyzed.
  • Functional assays with stable POEM transfected cell lines revealed that POEM expression increased cell adhesion and decreased cell migration and invasion supporting a role of POEM in tumor progression.
  • Interestingly, integrin alpha-8 expression, which was described as a receptor for POEM, is enhanced in malignant melanoma.
  • [MeSH-minor] Animals. Cell Line, Tumor. Down-Regulation. Humans. Immunohistochemistry. Mice. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 18271919.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Extracellular Matrix Proteins; 0 / RNA, Messenger; 0 / nephronectin
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26. Fox SA, Kusmiaty, Loh SS, Dharmarajan AM, Garlepp MJ: Cisplatin and TNF-alpha downregulate transcription of Bcl-xL in murine malignant mesothelioma cells. Biochem Biophys Res Commun; 2005 Nov 25;337(3):983-91
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  • [Title] Cisplatin and TNF-alpha downregulate transcription of Bcl-xL in murine malignant mesothelioma cells.
  • Malignant mesothelioma (MM) is an aggressive and highly chemo-resistant tumour.
  • All of the four mouse MM cell lines examined expressed Bax, Bcl-xL, c-Myc, and caspase-3 but not Bcl-2.
  • Cisplatin-induced apoptosis characterised by DNA fragmentation and cell death while caspase-3/7 was activated in 3 of 4 cell lines.
  • In the AC29 and AB1 models, both cisplatin and TNF-alpha downregulated Bcl-xL gene expression, indicating that this gene was a common transcriptional target in these cells.
  • [MeSH-major] Apoptosis / drug effects. Cisplatin / administration & dosage. Mesothelioma / metabolism. Tumor Necrosis Factor-alpha / administration & dosage. bcl-X Protein / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Cell Line, Tumor. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Gene Expression Regulation, Neoplastic. Mice. Transcription Factors / drug effects

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  • (PMID = 16225850.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bcl2l1 protein, mouse; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / bcl-X Protein; Q20Q21Q62J / Cisplatin
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27. Kobayashi T, Kawakita M, Terachi T, Habuchi T, Ogawa O, Kamoto T: Significance of elevated preoperative alpha-fetoprotein in postchemotherapy residual tumor resection for the disseminated germ cell tumors. J Surg Oncol; 2006 Dec 1;94(7):619-23
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  • [Title] Significance of elevated preoperative alpha-fetoprotein in postchemotherapy residual tumor resection for the disseminated germ cell tumors.
  • BACKGROUND AND OBJECTIVES: The purpose of the study is to determine the significance of elevated serum alpha-fetoprotein (AFP) in the setting prior to residual tumor resection (RTR) following chemotherapy for metastatic germ cell tumor in terms of the prediction of histology of the specimen and postoperative survival.
  • METHODS: We conducted a retrospective review of 68 patients undergoing RTR for metastatic nonseminomatous germ cell tumor or extragonadal germ cell tumor after at least a first-line chemotherapy.
  • Rates of presence of residual malignant cell in RTR specimen were similar between patients with normal AFP (7/28 or 25%) and with mildly elevated (10-30 ng/ml) AFP (3/11 or 27%).
  • [MeSH-major] Biomarkers, Tumor / blood. Chorionic Gonadotropin, beta Subunit, Human / blood. Neoplasms, Germ Cell and Embryonal / surgery. Testicular Neoplasms / surgery. alpha-Fetoproteins / metabolism

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  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 17111392.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / alpha-Fetoproteins
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28. Matsuo Y, Kamitani T: Parkinson's disease-related protein, alpha-synuclein, in malignant melanoma. PLoS One; 2010;5(5):e10481
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  • [Title] Parkinson's disease-related protein, alpha-synuclein, in malignant melanoma.
  • Parkinson's disease is a neurodegenerative disorder that is caused by mutation of alpha-synuclein or other genes.
  • METHODOLOGY/PRINCIPAL FINDINGS: Recently, we found that human melanoma cell lines highly express alpha-synuclein, whereas the protein is undetectable in the non-melanoma cancer cell lines tested.
  • To investigate the expression of alpha-synuclein in human melanoma tissues, we immunostained sections of melanoma, nevus, non-melanocytic cutaneous carcinoma, and normal skin. alpha-Synuclein was positively detected in 86% of the primary and 85% of the metastatic melanoma sections, as well as in 89% of nevus sections.
  • However, alpha-synuclein was undetectable in non-melanocytic cutaneous carcinoma and normal skin.
  • CONCLUSIONS/SIGNIFICANCE: The Parkinson's disease-related protein, alpha-synuclein, is expressed in both malignant and benign melanocytic lesions, such as melanomas and nevi.
  • Although alpha-synuclein cannot be used to distinguish between malignant and benign melanocytic skin lesions, it might be a useful biomarker for the diagnosis of metastatic melanoma.
  • [MeSH-major] Melanoma / metabolism. Parkinson Disease / metabolism. alpha-Synuclein / metabolism
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / metabolism. Biomarkers, Tumor / metabolism. Brain Neoplasms / metabolism. Brain Neoplasms / pathology. Cell Line, Tumor. Female. Humans. MART-1 Antigen. Male. Melanins / metabolism. Middle Aged. Neoplasm Proteins / metabolism. Nevus / metabolism. Nevus / pathology. Pigmentation. Retinoblastoma / metabolism. Retinoblastoma / pathology. Skin Neoplasms / metabolism. Skin Neoplasms / pathology

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  • [Cites] J Clin Pathol. 2001 Mar;54(3):196-200 [11253130.001]
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  • (PMID = 20463956.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R01 AG024497
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / MART-1 Antigen; 0 / MLANA protein, human; 0 / Melanins; 0 / Neoplasm Proteins; 0 / alpha-Synuclein
  • [Other-IDs] NLM/ PMC2864738
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29. Johansson D, Johansson A, Behnam-Motlagh P: alpha-Toxin of Staphylococcus aureus overcomes acquired cisplatin-resistance in malignant mesothelioma cells. Cancer Lett; 2008 Jun 28;265(1):67-75
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  • [Title] alpha-Toxin of Staphylococcus aureus overcomes acquired cisplatin-resistance in malignant mesothelioma cells.
  • alpha-Toxin (alpha-hemolysin) of Staphylococcus aureus is a pore-forming bacterial toxin which after caveolin-1-dependent assembly induces apoptosis in eukaryotic cells.
  • We investigated if a sub-toxic concentration of staphylococcal alpha-toxin could enhance cisplatin-induced apoptosis and overcome acquired cisplatin-resistance in cultured malignant pleural mesothelioma (MPM) cells.
  • MPM cells (P31wt) and a cisplatin-resistant sub-line (P31res) was incubated with alpha-toxin and/or cisplatin followed by determination of cell viability, apoptosis, and signaling pathways.
  • P31res cells were more sensitive to alpha-toxin than P31 wt cells due to induction of apoptosis.
  • A low-toxic concentration of alpha-toxin re-sensitized cisplatin P31res cytotoxicity by apoptosis-induced through the mitochondrial pathway without detectable activation of common up-stream apoptosis signaling proteins.
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Cell Survival / drug effects. Humans. Mesothelioma. Pleural Neoplasms. Signal Transduction

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  • (PMID = 18362050.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bacterial Toxins; 0 / Hemolysin Proteins; 0 / staphylococcal alpha-toxin; Q20Q21Q62J / Cisplatin
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30. Kuroda H, Moritake H, Sawada K, Kuwahara Y, Imoto I, Inazawa J, Sugimoto T: Establishment of a cell line from a malignant rhabdoid tumor of the liver lacking the function of two tumor suppressor genes, hSNF5/INI1 and p16. Cancer Genet Cytogenet; 2005 Apr 15;158(2):172-9
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  • [Title] Establishment of a cell line from a malignant rhabdoid tumor of the liver lacking the function of two tumor suppressor genes, hSNF5/INI1 and p16.
  • Malignant rhabdoid tumors (MRT) of the liver are rare.
  • A few liver MRT cell lines have been established but none has been characterized in detail.
  • Here we describe a new MRT cell line from the liver, which is designated MP-MRT-AN, and describe it in detail.
  • Immunohistochemical assays detected the expression of vimentin and cytokeratin but they were negative for neurofilament, desmin, alpha-smooth muscle actin, alpha-sarcomeric actin, and smooth muscle myosin heavy chains SM1 and SM2.
  • RT-PCR assays revealed that this cell line did not express smooth muscle myosin heavy chain isoforms or MyoD1.
  • No aberration was identified in 22q by G-banded analysis; however, the hSNF5/INI1 gene, a suppressor gene of MRT that maps to 22q11.2, was homozygously deleted from exons 1 to 5 in this cell line.
  • Furthermore, the expression of another tumor suppressor gene, p16 (CDKN2A), was not detected by RT-PCR.
  • This raises the possibility that the aggressive phenotype of malignant rhabdoid tumors is caused by the loss of two or more tumor suppressor genes.
  • [MeSH-major] DNA-Binding Proteins / genetics. Gene Deletion. Genes, Tumor Suppressor. Genes, p16. Liver Neoplasms / pathology. Rhabdoid Tumor / genetics. Transcription Factors / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Chromosomal Proteins, Non-Histone. Chromosome Banding. Chromosome Mapping. Chromosomes, Human, Pair 22. Female. Homozygote. Humans. Immunohistochemistry. Infant. Keratins / metabolism. Mice. Mice, Nude. Neoplasm Transplantation. Reverse Transcriptase Polymerase Chain Reaction. Vimentin / metabolism

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  • (PMID = 15796965.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromosomal Proteins, Non-Histone; 0 / DNA-Binding Proteins; 0 / SMARCB1 protein, human; 0 / Smarcb1 protein, mouse; 0 / Transcription Factors; 0 / Vimentin; 68238-35-7 / Keratins
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31. Koga M, Kai H, Egami K, Murohara T, Ikeda A, Yasuoka S, Egashira K, Matsuishi T, Kai M, Kataoka Y, Kuwano M, Imaizumi T: Mutant MCP-1 therapy inhibits tumor angiogenesis and growth of malignant melanoma in mice. Biochem Biophys Res Commun; 2008 Jan 11;365(2):279-84
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  • [Title] Mutant MCP-1 therapy inhibits tumor angiogenesis and growth of malignant melanoma in mice.
  • We investigated whether blocking of monocyte chemoattractant-1 (MCP-1) function would inhibit recruitment of tumor-associated macrophages (TAMs) and prevent tumor angiogenesis and tumor growth of human malignant melanoma.
  • 7ND treatment inhibited TAM recruitment and partially reduced tumor angiogenesis and tumor growth.
  • Also, 7ND treatment attenuated inductions of tumor necrosis factor-alpha (TNFalpha), interleukin-1alpha (IL-1alpha), and vascular endothelial growth factor (VEGF) in the stroma and tumor.
  • Accordingly, it was suggested that MCP-1 would enhance tumor angiogenesis and early tumor growth in the early stages by inducing TNFalpha, IL-1alpha, and VEGF through TAM recruitment and probably the direct autocrine/paracrine effects on melanoma cells.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Humans. Mice. Mice, Inbred C57BL. Mutation

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  • (PMID = 17991428.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCL2 protein, human; 0 / Chemokine CCL2
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32. Matsuura Y, Kitajima M, Hachisuga T, Tanimoto A, Okura N, Kihara I: Malignant mixed müllerian tumor with malignant neuroectodermal components (teratoid carcinosarcoma) of the ovary: Report of a case with clinicopathologic findings. J Obstet Gynaecol Res; 2010 Aug;36(4):907-11
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  • [Title] Malignant mixed müllerian tumor with malignant neuroectodermal components (teratoid carcinosarcoma) of the ovary: Report of a case with clinicopathologic findings.
  • Malignant mixed müllerian tumor (MMMT) or carcinosarcoma of the female genital tract is a rare neoplasm.
  • Malignant ovarian tumor composed of müllerian epithelial tumor and malignant germ cell tumor is also rare, with most cases composed of endometrioid adenocarcinoma and yolk sac tumor.
  • Ovarian MMMT with malignant neuroectodermal components resembling immature teratoma is extremely rare.
  • The resected tumor measuring over 20 cm in diameter consisted of cystic and solid components and was very fragile.
  • Microscopic examination showed a heterogenous mixed tumor composed of malignant epithelial, malignant mesodermal and malignant neuroectodermal components.
  • There was no tumor immunoreactivity to alpha-fetoprotein, carcinoembryonic antigen, human chorionic gonadotropin, and inhibin.
  • This quite rare ovarian tumor closely resembled nasopharyngeal tumors described as 'teratoid carcinosarcoma' is biologically aggressive.
  • Further cases need to be accumulated to make diagnosis and to determine a successful treatment modality.
  • [MeSH-major] Carcinosarcoma / pathology. Mixed Tumor, Mullerian / pathology. Ovarian Neoplasms / pathology. Teratoma / pathology

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  • (PMID = 20666968.001).
  • [ISSN] 1447-0756
  • [Journal-full-title] The journal of obstetrics and gynaecology research
  • [ISO-abbreviation] J. Obstet. Gynaecol. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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33. Werbowetski-Ogilvie TE, Agar NY, Waldkircher de Oliveira RM, Faury D, Antel JP, Jabado N, Del Maestro RF: Isolation of a natural inhibitor of human malignant glial cell invasion: inter alpha-trypsin inhibitor heavy chain 2. Cancer Res; 2006 Feb 1;66(3):1464-72
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  • [Title] Isolation of a natural inhibitor of human malignant glial cell invasion: inter alpha-trypsin inhibitor heavy chain 2.
  • Malignant central nervous system (CNS) tumors, such as glioblastoma multiforme, invade the brain and disrupt normal tissue architecture, making complete surgical removal virtually impossible.
  • Here, we have developed and optimized a purification strategy to isolate and identify natural inhibitors of glioma cell invasion in a three-dimensional collagen type I matrix.
  • Inter alpha-trypsin inhibitor heavy chain 2 (ITI H2) was identified from the most inhibitory fractions and its presence was confirmed both as a single protein and in a bikunin-bound form.
  • Stable overexpression in U251 glioma cells validated ITI H2's strong inhibition of human glioma cell invasion together with significant inhibition of cell proliferation and promotion of cell-cell adhesion.
  • These findings suggest that reduction of ITI H2 expression correlates with brain tumor progression and that targeting factors responsible for its loss or restoring the ITI supply exogenously may serve as potential therapeutic strategies for a variety of CNS tumors.
  • [MeSH-major] Alpha-Globulins / isolation & purification. Brain Neoplasms / chemistry. Glioma / chemistry
  • [MeSH-minor] Animals. Blotting, Western. Cell Adhesion / physiology. Cell Movement / physiology. Down-Regulation. Humans. Immunohistochemistry. Membrane Glycoproteins / biosynthesis. Membrane Glycoproteins / genetics. Mice. Neoplasm Invasiveness. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Recombinant Fusion Proteins / biosynthesis. Recombinant Fusion Proteins / genetics. Trypsin Inhibitor, Kunitz Soybean / biosynthesis. Trypsin Inhibitor, Kunitz Soybean / genetics

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  • (PMID = 16452202.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alpha-Globulins; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / Recombinant Fusion Proteins; 0 / SPINT2 protein, human; 39346-44-6 / inter-alpha-inhibitor; 9088-41-9 / Trypsin Inhibitor, Kunitz Soybean; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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34. Mattarollo SR, Kenna T, Nieda M, Nicol AJ: Chemotherapy pretreatment sensitizes solid tumor-derived cell lines to V alpha 24+ NKT cell-mediated cytotoxicity. Int J Cancer; 2006 Oct 1;119(7):1630-7
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  • [Title] Chemotherapy pretreatment sensitizes solid tumor-derived cell lines to V alpha 24+ NKT cell-mediated cytotoxicity.
  • There is an increasing awareness of the therapeutic potential for combining immune-based therapies with chemotherapy in the treatment of malignant diseases, but few published studies evaluate possible cytotoxic synergies between chemotherapy and cytotoxic immune cells.
  • Human V alpha 24+/V beta 11+ NKT cells are being evaluated for use in cell-based immunotherapy of malignancy because of their immune regulatory functions and potent cytotoxic potential.
  • The cytotoxicity of NKT cells was tested against solid-tumor derived cell lines NCI-H358, DLD-1, HT-29, DU-145, TSU-Pr1 and MDA-MB231, with or without prior treatment of these target cells, with a range of chemotherapy agents.
  • Low concentrations of chemotherapeutic agents led to sensitization of cell lines to NKT-mediated cytotoxicity, with the greatest effect being observed for prostate cancer cells.
  • Synergistic cytotoxicity occurred in an NKT cell in a dose-dependent manner.
  • Chemotherapy agents induced upregulation of cell surface TRAIL-R2 (DR5) and Fas (CD95) expression, increasing the capacity for NKT cells to recognize and kill via TRAIL- and FasL-mediated pathways.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cytotoxicity, Immunologic / immunology. Neoplasms / drug therapy. Neoplasms / immunology. Receptors, Antigen, T-Cell / immunology. Receptors, Antigen, T-Cell / metabolism. T-Lymphocytes, Regulatory / immunology
  • [MeSH-minor] Apoptosis Regulatory Proteins / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Fas Ligand Protein. Humans. Membrane Glycoproteins / metabolism. Receptors, Tumor Necrosis Factor / metabolism. TNF-Related Apoptosis-Inducing Ligand. Tumor Necrosis Factor-alpha / metabolism. Tumor Necrosis Factors / metabolism. Up-Regulation

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16646079.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Necrosis Factors
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35. Heiss MM, Ströhlein MA, Jäger M, Kimmig R, Burges A, Schoberth A, Jauch KW, Schildberg FW, Lindhofer H: Immunotherapy of malignant ascites with trifunctional antibodies. Int J Cancer; 2005 Nov 10;117(3):435-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunotherapy of malignant ascites with trifunctional antibodies.
  • These trifunctional antibodies (trAb) lead to efficient specific killing of targeted tumor cells without any pre- or co-stimulation.
  • This concept was investigated in vivo in patients with malignant ascites in a clinical situation that allowed monitoring of tumor cell elimination and correlation with clinical effects.
  • In a prospective study, 8 patients with malignant ascites due to peritoneal carcinomatosis were treated with intraperitoneal application of trAb, which bound either the EpCAM- or Her2/neu-antigen on tumor cells.
  • Tumor cell monitoring showed a complete elimination of tumor cells in ascites already at total doses as low as 40-140 microg.
  • Clinical response with disappearance of ascites accumulation was seen in all patients, which was correlated with elimination of tumor cells (p = 0.0014).
  • Intraperitoneal immunotherapy with trAb showed convincing efficacy in patients with malignant ascites.
  • [MeSH-minor] Cytokines / blood. DNA Primers. Humans. Leukocyte Count. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / immunology. Tumor Necrosis Factor-alpha / analysis

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15906359.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / DNA Primers; 0 / Tumor Necrosis Factor-alpha
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36. Eckert JM, Byer SJ, Clodfelder-Miller BJ, Carroll SL: Neuregulin-1 beta and neuregulin-1 alpha differentially affect the migration and invasion of malignant peripheral nerve sheath tumor cells. Glia; 2009 Nov 1;57(14):1501-20
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  • [Title] Neuregulin-1 beta and neuregulin-1 alpha differentially affect the migration and invasion of malignant peripheral nerve sheath tumor cells.
  • Malignant peripheral nerve sheath tumors (MPNSTs) are the most common malignancy associated with neurofibromatosis Type 1 (NF1).
  • These Schwann cell lineage-derived sarcomas aggressively invade adjacent nerve and soft tissue, frequently precluding surgical resection.
  • We have shown that MPNSTs express neuregulin-1 (NRG-1) beta isoforms, which promote Schwann cell migration during development, and NRG-1 alpha isoforms, whose effects on Schwann cells are poorly understood.
  • Hypothesizing that NRG-1 beta and/or NRG-1 alpha promote MPNST invasion, we found that NRG-1 beta promoted MPNST migration in a substrate-specific manner, markedly enhancing migration on laminin but not on collagen type I or fibronectin.
  • NRG-1 beta stimulated human and murine MPNST cell migration and invasion in a concentration-dependent manner in three-dimensional migration assays, acting as a chemotactic factor.
  • In contrast, NRG-1 alpha had no effect on the migration and invasion of some MPNST lines and inhibited the migration of others.
  • While NRG-1 beta potently and persistently activated Erk 1/2, SAPK/JNK, Akt and Src family kinases, NRG-1 alpha did not activate Akt and activated these other kinases with kinetics distinct from those evident in NRG-1 beta-stimulated cells.
  • These findings suggest that NRG-1 beta enhances MPNST migration and that NRG-1 beta and NRG-1 alpha differentially modulate this process.

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
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  • (PMID = 19306381.001).
  • [ISSN] 1098-1136
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P30 NS047466; United States / NINDS NIH HHS / NS / NS057098-03; United States / NINDS NIH HHS / NS / R01 NS048353-05; United States / NINDS NIH HHS / NS / P30 NS057098; United States / NCI NIH HHS / CA / R01 CA122804-02; United States / NINDS NIH HHS / NS / R01 NS048353; United States / PHS HHS / / 35294-0017; United States / NINDS NIH HHS / NS / P30 NS057098-03; United States / NINDS NIH HHS / NS / NS047466-04; United States / NCI NIH HHS / CA / R01 CA122804; United States / NINDS NIH HHS / NS / P30 NS047466-04; United States / NCI NIH HHS / CA / CA122804-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD29; 0 / Collagen Type I; 0 / Fibronectins; 0 / Laminin; 0 / NRG1 protein, human; 0 / Neuregulin-1; 0 / Nrg1 protein, mouse; 0 / Protein Isoforms; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Erbb4 protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-3; EC 2.7.10.1 / Receptor, ErbB-4
  • [Other-IDs] NLM/ NIHMS95134; NLM/ PMC2744852
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37. Takano S, Kamiyama H, Mashiko R, Osuka S, Ishikawa E, Matsumura A: Metronomic treatment of malignant glioma xenografts with irinotecan (CPT-11) inhibits angiogenesis and tumor growth. J Neurooncol; 2010 Sep;99(2):177-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metronomic treatment of malignant glioma xenografts with irinotecan (CPT-11) inhibits angiogenesis and tumor growth.
  • Irinotecan (CPT-11) has shown emerging promise in the treatment of malignant gliomas.
  • We found that metronomic administration of CPT-11 significantly inhibited malignant glioma growth by inhibiting angiogenesis; this treatment procedure reduced the number of tumor vessels and the area of hypoxic lesions and reduced expression of VEGF and HIF-1alpha, the most important angiogenic factors in gliomas.
  • These angiosuppressive effects of CPT-11 show promise for another use of CPT-11 in metronomic and scheduled angiosuppressive chemotherapy with low dose and long-term administration for malignant gliomas without systemic side effects.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Brain Neoplasms / prevention & control. Camptothecin / analogs & derivatives. Cell Proliferation / drug effects. Glioma / prevention & control. Neovascularization, Pathologic / prevention & control
  • [MeSH-minor] Angiogenesis Inhibitors / therapeutic use. Animals. Hypoxia / drug therapy. Hypoxia / genetics. Hypoxia / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Immunoenzyme Techniques. Male. Mice. Mice, SCID. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Tumor Cells, Cultured. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 20066473.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents, Phytogenic; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 0H43101T0J / irinotecan; XT3Z54Z28A / Camptothecin
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38. Hsiao HH, Liu YC, Tsai HJ, Tsai KB, Cheng YJ, Chou SH, Chong IW, Yang WC, Liu TC, Lin SF: Poor outcomes in patients with primary malignant mediastinal germ-cell tumors. Kaohsiung J Med Sci; 2005 Dec;21(12):561-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Poor outcomes in patients with primary malignant mediastinal germ-cell tumors.
  • Primary mediastinal germ-cell tumors (GCTs) without gonadal involvement are rare and can be divided into benign mature teratoma and malignant seminoma or nonseminoma.
  • We describe our experience of malignant mediastinal GCTs and compare the presentations and outcome with those of benign teratomas.
  • Four malignant GCTs (1 seminoma, 1 choriocarcinoma, and 2 yolk-sac tumors) have been treated in our hospital.
  • All patients were men with obvious symptoms before diagnosis.
  • Two patients died, one with extended pulmonary metastasis and the other with relapsed disease and high levels of tumor markers.
  • Compared with the nine cases of benign teratomas, the four malignant GCTs showed overwhelming male dominance, advanced symptoms at presentation, and poor outcome.
  • These cases highlight the important role of disease staging and tumor-marker levels in malignant GCTs, and suggest that new treatment strategies for malignant GCTs await further investigation.
  • [MeSH-major] Mediastinal Neoplasms / therapy. Neoplasms, Germ Cell and Embryonal / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Humans. Infant. Male. Retrospective Studies. Survival Rate. Treatment Outcome. alpha-Fetoproteins / analysis

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  • (PMID = 16670048.001).
  • [ISSN] 1607-551X
  • [Journal-full-title] The Kaohsiung journal of medical sciences
  • [ISO-abbreviation] Kaohsiung J. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China (Republic : 1949- )
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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39. Colombo G, Sordi A, Turcatti F, Carlin A, Rossi C, Lonati C, Santambrogio L, Gatti S, Catania A: Change in gene expression profile induced by alpha-melanocyte stimulating hormone in a malignant mesothelioma cell line. Cell Mol Biol (Noisy-le-grand); 2006;52(2):69-74
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  • [Title] Change in gene expression profile induced by alpha-melanocyte stimulating hormone in a malignant mesothelioma cell line.
  • We have previously reported that the peptide a-melanocyte stimulating hormone (alpha-MSH) has antiproliferative effects in human malignant mesothelioma cells.
  • To determine the molecular mechanisms underlying such effects, we investigated the changes in gene expression profile induced by the alpha-MSH analog [Nle4 -DPhe7 ]-alpha-MSH (NDP-alpha-MSH) in a human malignant mesothelioma cell line.
  • The cDNA macroarray technique revealed changes in expression of genes involved in cell growth, adhesion, signal transduction, and transcription.
  • In particular, NDP-alpha-MSH down-regulated expression of B-Myb and Myc, two oncogenes considered of paramount importance for cell proliferation and cancer.
  • Further, NDP-alpha-MSH exerted a favorable transcriptional regulation of certain integrins and their signaling pathways.
  • Finally, peptide treatment was associated with a prominent inhibition of IL-13, a cytokine with tumor-promoting effects.
  • The data indicate that the influences of alpha-MSH extend beyond the established anti-inflammatory effects in normal cells to include cell cycle regulatory properties in malignant cells.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / drug effects. alpha-MSH / pharmacology
  • [MeSH-minor] Cell Cycle Proteins / genetics. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin A / genetics. Cyclin A2. Cyclin B / genetics. Cyclin B1. DNA-Binding Proteins / genetics. Gene Expression Profiling. Humans. Interleukin-13 / genetics. Mesothelioma / genetics. Mesothelioma / metabolism. Mesothelioma / pathology. Oligonucleotide Array Sequence Analysis / methods. Proto-Oncogene Proteins c-myc / genetics. Reverse Transcriptase Polymerase Chain Reaction. Trans-Activators / genetics

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  • (PMID = 16914089.001).
  • [ISSN] 1165-158X
  • [Journal-full-title] Cellular and molecular biology (Noisy-le-Grand, France)
  • [ISO-abbreviation] Cell. Mol. Biol. (Noisy-le-grand)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / CCNA2 protein, human; 0 / CCNB1 protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin A; 0 / Cyclin A2; 0 / Cyclin B; 0 / Cyclin B1; 0 / DNA-Binding Proteins; 0 / Interleukin-13; 0 / MYBL2 protein, human; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc; 0 / Trans-Activators; 581-05-5 / alpha-MSH; 75921-69-6 / MSH, 4-Nle-7-Phe-alpha-
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40. Aoki M, Nabeshima K, Koga K, Hamasaki M, Suzumiya J, Tamura K, Iwasaki H: Imatinib mesylate inhibits cell invasion of malignant peripheral nerve sheath tumor induced by platelet-derived growth factor-BB. Lab Invest; 2007 Aug;87(8):767-79
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imatinib mesylate inhibits cell invasion of malignant peripheral nerve sheath tumor induced by platelet-derived growth factor-BB.
  • Malignant peripheral nerve sheath tumor (MPNST) is rare, highly aggressive, resistant to radiochemotherapy, and associated with poor prognosis.
  • This study was designed to identify motogenic factor(s) involved in MPNST cell invasion and inhibitor(s) of such invasive activity.
  • We profiled the invasion-inducing activities of eight motogenic growth factors on two human MPNST cell lines, FU-SFT8611 and 9817, using in vitro Matrigel invasion assays.
  • Platelet-derived growth factor-BB (PDGF-BB) was identified as the most effective MPNST cell invasion-inducing factor.
  • Epidermal growth factor (EGF) and hepatocyte growth factor (HGF) also stimulated invasion in one MPNST cell line.
  • In both MPNST cell lines, PDGF-BB induced tyrosine phosphorylation of PDGFR-beta but not of PDGFR-alpha, and specific PDGFR-beta inhibition by small interfering RNA to the receptor inhibited PDGF-BB-stimulated MPNST cell invasion, suggesting the predominant role of PDGFR-beta.
  • Inhibition of PDGFR-beta phosphorylation by pretreatment with herbimycin A and imatinib mesylate effectively suppressed basement membrane invasion and cell growth in vitro.
  • No mutations were present in exons 12 and 18 of PDGFR-beta in both MPNST cell lines and 10 human MPNST tissues examined.
  • [MeSH-minor] Adult. Benzamides. Cell Line, Tumor. Female. Humans. Imatinib Mesylate. Intercellular Signaling Peptides and Proteins / pharmacology. Intercellular Signaling Peptides and Proteins / physiology. Male. Middle Aged. Mutation. Neoplasm Invasiveness. Phosphorylation. Proto-Oncogene Proteins c-sis. RNA, Messenger / metabolism. Receptor, Platelet-Derived Growth Factor beta / antagonists & inhibitors. Receptor, Platelet-Derived Growth Factor beta / genetics. Receptor, Platelet-Derived Growth Factor beta / metabolism. Receptors, Growth Factor / genetics. Receptors, Growth Factor / metabolism

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  • (PMID = 17558420.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Intercellular Signaling Peptides and Proteins; 0 / Piperazines; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / Receptors, Growth Factor; 0 / platelet-derived growth factor BB; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
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41. Gordon GJ, Mani M, Mukhopadhyay L, Dong L, Yeap BY, Sugarbaker DJ, Bueno R: Inhibitor of apoptosis proteins are regulated by tumour necrosis factor-alpha in malignant pleural mesothelioma. J Pathol; 2007 Mar;211(4):439-46
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  • [Title] Inhibitor of apoptosis proteins are regulated by tumour necrosis factor-alpha in malignant pleural mesothelioma.
  • Inhibitor of apoptosis proteins (IAPs) are overexpressed by most neoplasms and promote tumour cell survival after a wide variety of apoptotic stimuli elicited via intrinsic (ie mitochondrial) and extrinsic (ie death receptor) pathways.
  • It has previously been reported that one of these proteins, IAP-1(MIHC/cIAP2), is overexpressed in malignant pleural mesothelioma (MPM) and is responsible for a large degree of the resistance of cultured MPM cells to cisplatin.
  • In the present study, potential regulatory mechanisms of IAP genes in MPM were investigated and it was found that tumour necrosis factor-alpha (TNF-alpha) can increase mRNA and protein levels of IAP-1, IAP-2, and XIAP, but not livin or survivin in MPM cell lines (n=4).
  • Co-incubation of MPM cells with TNF-alpha and pyrrolidine dithiocarbamate (PDTC), an NF-kappaB inhibitor, prevented TNF-mediated up-regulation of IAP gene expression levels.
  • In survival studies, TNF-alpha was not toxic to MPM cells at any concentration examined.
  • However, MPM cells exposed to TNF-alpha were twice as resistant to cisplatin in dose response survival assays compared with unstimulated controls and were found to have a significantly greater fraction of surviving cells at multiple cisplatin concentrations (p<0.0087).
  • Finally, it was found that levels of circulating TNF-alpha were statistically significantly (p=0.031) (median 312.5 pg/ml) higher in MPM patients (n=6) prior to surgical tumour debulking compared with those after surgery (median 0 pg/ml).
  • These results when combined with previous observations by our laboratory and others strongly suggest that IAPs act synergistically with TNF family members to promote survival of MPM tumour cells after exposure to cisplatin and possibly other chemotherapeutic drugs.
  • [MeSH-major] Inhibitor of Apoptosis Proteins / genetics. Mesothelioma / genetics. Neoplasm Proteins / genetics. Pleural Neoplasms / genetics. Tumor Necrosis Factor-alpha / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / analysis. Adaptor Proteins, Signal Transducing / genetics. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Cisplatin / pharmacology. Gene Expression Regulation, Neoplastic / genetics. Humans. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / genetics. NF-kappa B / genetics. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Transcription, Genetic / genetics. Up-Regulation / genetics. X-Linked Inhibitor of Apoptosis Protein / analysis. X-Linked Inhibitor of Apoptosis Protein / genetics

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  • [Copyright] Copyright (c) 2007 Pathological Society of Great Britain and Ireland.
  • (PMID = 17253597.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-100315; United States / NCI NIH HHS / CA / CA-102591; United States / NCI NIH HHS / CA / CA-105249
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / BIRC5 protein, human; 0 / BIRC7 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Tumor Necrosis Factor-alpha; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human; Q20Q21Q62J / Cisplatin
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42. Netto CD, da Silva AJ, Salustiano EJ, Bacelar TS, Riça IG, Cavalcante MC, Rumjanek VM, Costa PR: New pterocarpanquinones: synthesis, antineoplasic activity on cultured human malignant cell lines and TNF-alpha modulation in human PBMC cells. Bioorg Med Chem; 2010 Feb 15;18(4):1610-6
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  • [Title] New pterocarpanquinones: synthesis, antineoplasic activity on cultured human malignant cell lines and TNF-alpha modulation in human PBMC cells.
  • These compounds showed to be active against human leukemic cell lines and human lung cancer cell lines.
  • Even multidrug resistant cells were sensitive to 5a, which presented low toxicity toward peripheral blood mononuclear cells (PBMC) cells and decreased the production of TNF-alpha by these cells.
  • [MeSH-major] Antineoplastic Agents / chemical synthesis. Antineoplastic Agents / pharmacology. Monocytes / drug effects. Pterocarpans / chemical synthesis. Pterocarpans / pharmacology. Quinones / chemical synthesis. Quinones / pharmacology. Tumor Necrosis Factor-alpha / drug effects
  • [MeSH-minor] Cell Line, Tumor. Humans. Magnetic Resonance Spectroscopy. Spectrometry, Mass, Electrospray Ionization

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20117936.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pterocarpans; 0 / Quinones; 0 / Tumor Necrosis Factor-alpha
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43. Drimal D, Drimal J, Drimal J Jr: The regulation of human adrenomedullin (AM) and tumor necrosis factor alpha (TNF-alpha) receptors on human epithelial carcinoma (HeLa) cells. The role of AM secretion in tumor cell sensitivity. Neoplasma; 2006;53(2):144-9

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  • [Title] The regulation of human adrenomedullin (AM) and tumor necrosis factor alpha (TNF-alpha) receptors on human epithelial carcinoma (HeLa) cells. The role of AM secretion in tumor cell sensitivity.
  • The cytostatic cytokine tumor necrosis factor-alpha (TNF-alpha) and proliferative hormone adrenomedullin (AM) are abundantly expressed in human tumors.
  • However, little is known about mechanism (s) through which TNF-alpha and AM exert their regulatory effects, especially in the regulation of proliferative activity in malignant cells.
  • Also the role played by TNF-alpha in pathogenesis and treatment of cancer (targeted cancer therapy) remains less understood.
  • The purpose of this study was therefore to characterize the significance of TNF-alpha induced apoptosis with down-regulation of plasma-membrane TNF-alpha receptors and up-regulation of AM receptors with increased production of human AM mRNA, i.e. mechanisms that subsequently control aberrant cellular proliferation in malignant cells.
  • Cytotoxicity, and the whole cell ligand binding assays for TNF-alpha and AM receptors, and RIA-assays of AM production were accomplished in control experiments using pharmacologically pretreated HeLa cells.
  • TNF-alpha inhibitor of cell growth actinomycin-D significantly increased cytotoxicity of TNF-alpha in HeLa cells.
  • Hypoxia increased TNF-alpha production and increased surface-membrane [125I]AM binding.
  • Tumor promotor PMA and histamine down-regulated specific binding of [125I]TNF- alpha on HeLa cells.
  • BAY11-7082 at concentrations that inhibited IkappaB phosphorylation and thus nuclear translocation and surface membrane TNF-alpha expression increased AM specific binding.
  • These results suggest relative and contradictory TNF-alpha and AM surface-membrane receptor signaling in HeLa cells and findings reveal a novel proliferative mechanisms that control AM production and thus oncogenic signaling in cells.
  • This implies that several putative inhibitors of TNF-alpha and AM signaling may be considered in oncology for treatment of tumors otherwise nonresponding to cytostatic therapy.
  • [MeSH-major] Neoplasms / metabolism. Peptides / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Adrenomedullin. Cell Death / drug effects. Cell Proliferation / drug effects. Enzyme-Linked Immunosorbent Assay. HeLa Cells. Humans. Radioimmunoassay

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  • (PMID = 16575470.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Peptides; 0 / Tumor Necrosis Factor-alpha; 148498-78-6 / Adrenomedullin
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44. Rubinstein DB, Karmely M, Ziv R, Benhar I, Leitner O, Baron S, Katz BZ, Wreschner DH: MUC1/X protein immunization enhances cDNA immunization in generating anti-MUC1 alpha/beta junction antibodies that target malignant cells. Cancer Res; 2006 Dec 1;66(23):11247-53
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  • [Title] MUC1/X protein immunization enhances cDNA immunization in generating anti-MUC1 alpha/beta junction antibodies that target malignant cells.
  • MUC1 has generated considerable interest as a tumor marker and potential target for tumor killing.
  • To date, most antibodies against MUC1 recognize epitopes within the highly immunogenic alpha chain tandem repeat array.
  • A major shortcoming of such antibodies is that the MUC1 alpha chain is shed into the peripheral circulation, sequesters circulating antitandem repeat array antibodies, and limits their ability to even reach targeted MUC1-expressing cells.
  • Antibodies recognizing MUC1 epitopes tethered to the cell surface would likely be more effective.
  • MUC1 alpha subunit binding the membrane-tethered beta subunit provides such an epitope.
  • By use of a novel protocol entailing immunization with cDNA encoding full-length MUC1 (MUC1/TM) followed by boosting with the alternatively spliced MUC1/X isoform from which the tandem repeat array has been deleted, we generated monoclonal antibodies, designated DMC209, which specifically bind the MUC1 alpha/beta junction.
  • DMC209 is exquisitely unique for this site; amino acid mutations, which abrogate MUC1 cleavage, also abrogate DMC209 binding.
  • Additionally, DMC209 specifically binds the MUC1 alpha/beta junction on full-length MUC1/TM expressed by breast and ovarian cancer cell lines and on freshly obtained, unmanipulated MUC1-positive malignant plasma cells of multiple myeloma.
  • Moreover, the novel immunization procedure used in generating DMC209 can be used to generate additional anti-MUC1 alpha/beta junction antibodies, which may, analogously to Herceptin, have cytotoxic activity.
  • [MeSH-minor] Animals. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / metabolism. Antibody Specificity / immunology. Bone Marrow Cells / immunology. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cell Line. Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Genetic Vectors / administration & dosage. Genetic Vectors / genetics. Humans. Immunization / methods. Mice. Multiple Myeloma / immunology. Multiple Myeloma / metabolism. Multiple Myeloma / pathology. Mutation / genetics. Neoplasms / blood. Neoplasms / immunology. Neoplasms / pathology. Protein Binding

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  • (PMID = 17145869.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antibodies, Monoclonal; 0 / DNA, Complementary; 0 / Epitopes; 0 / Mucin-1
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45. Yamate J, Fumimoto S, Kuwamura M, Kotani T, Lamarre J: Characterization of a rat subcutaneous malignant fibrous histiocytoma and its tumor lines, with reference to histiocytic features. Vet Pathol; 2007 Mar;44(2):151-60
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  • [Title] Characterization of a rat subcutaneous malignant fibrous histiocytoma and its tumor lines, with reference to histiocytic features.
  • Malignant fibrous histiocytoma (MFH) is regarded as soft tissue-derived undifferentiated pleomorphic sarcoma, of which the histogenesis remains to be proven.
  • To investigate the cellular characteristics, a homotransplantable tumor line (KJ) was established from a spontaneous MFH that developed in the subcutis of an aged F344 rat.
  • A cloned cell line (KJ-A) was isolated from a KJ tumor.
  • Lipopolysaccharide (LPS) treatment increased the number of ED1-positive cells and the expression of tumor necrosis factor-alpha mRNA by reverse transcription-polymerase chain reaction.
  • Because tumor lines are useful for in vivo and in vitro studies concerning different characteristics of the original neoplasms.
  • [MeSH-major] Cell Line, Tumor. Histiocytoma, Malignant Fibrous / pathology
  • [MeSH-minor] Acid Phosphatase / metabolism. Animals. Carboxylesterase / metabolism. Immunohistochemistry / veterinary. Lipopolysaccharides / pharmacology. Male. Microscopy, Electron / veterinary. Polymerase Chain Reaction / veterinary. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Rats. Rats, Inbred F344. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 17317792.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 3.1.1.1 / Carboxylesterase; EC 3.1.3.2 / Acid Phosphatase
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46. Seno T, Harada H, Kohno S, Teraoka M, Inoue A, Ohnishi T: Downregulation of SPARC expression inhibits cell migration and invasion in malignant gliomas. Int J Oncol; 2009 Mar;34(3):707-15
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  • [Title] Downregulation of SPARC expression inhibits cell migration and invasion in malignant gliomas.
  • The secreted protein acidic and rich in cysteine (SPARC) is a secreted glycoprotein that plays an essential role in promoting the motility of invasive tumor cells.
  • Introduction of SPARC-targeted small interfering RNA (siRNA) into glioma cell lines resulted in downregulation of SPARC expression, and significantly suppressed glioma cell migration in vitro.
  • In addition, intracerebral injection of glioma cells transfected with SPARC siRNA in nude mice resulted in the formation of a non-invasive tumor, whereas injection of cells transfected with control siRNA resulted in diffuse invasive tumors.
  • Since SPARC was exclusively expressed in the invasive zone of the tumor margin and the area surrounding tumor necrosis, we investigated the relationship between SPARC expression and hypoxic stress.
  • Downregulation of SPARC may be a novel anti-invasion therapeutic strategy for malignant gliomas.
  • [MeSH-major] Brain Neoplasms / pathology. Cell Movement / physiology. Glioma / pathology. Osteonectin / biosynthesis
  • [MeSH-minor] Animals. Cell Hypoxia / genetics. Cell Line, Tumor. Cell Survival / physiology. Down-Regulation. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Mice. Mice, Nude. Neoplasm Invasiveness. RNA, Small Interfering / genetics. Rats. Transfection

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  • (PMID = 19212676.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Osteonectin; 0 / RNA, Small Interfering
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47. Craig DH, Downey C, Basson MD: SiRNA-mediated reduction of alpha-actinin-1 inhibits pressure-induced murine tumor cell wound implantation and enhances tumor-free survival. Neoplasia; 2008 Mar;10(3):217-22
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  • [Title] SiRNA-mediated reduction of alpha-actinin-1 inhibits pressure-induced murine tumor cell wound implantation and enhances tumor-free survival.
  • Viable cancer cells can commonly be recovered from surgical sites and venous blood during tumor resection.
  • Iatrogenic exposure to increased extracellular pressure modulates integrin binding affinity and stimulates colon cancer cell adhesion in vitro through an alpha-actinin-1-dependent signaling pathway.
  • We hypothesized that preoperative small interfering RNA-mediated silencing of alpha-actinin-1 in tumor tissue could disrupt pressure-stimulated cancer cell adhesion to murine surgical wounds and thereby enhance subsequent tumor-free survival.
  • Reducing alpha-actinin-1 in CT26 murine adenocarcinoma cells blocked cell adhesion to collagen in vitro and similarly inhibited pressure-induced CT26 implantation in murine surgical wounds in vivo.
  • Surgical wound contamination with pressure-activated CT26 cells significantly reduced tumor-free survival compared to contamination with tumor cells maintained under ambient pressure.
  • However, mice treated with pressure-activated CT26 cells preoperatively transfected with alpha-actinin-1-specific small interfering RNA displayed reduced surgical site implantation and increased tumor-free survival compared to mice exposed to pressure-activated cells expressing normal levels of alpha-actinin-1 protein.
  • These results suggest that pressure activation of malignant cells promotes tumor development and impairs tumor-free survival. alpha-Actinin-1 may be an effective therapeutic target to inhibit perioperative pressure-stimulated tumor cell implantation.

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  • (PMID = 18320066.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01DK06771
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actn1 protein, mouse; 0 / RNA, Small Interfering; 11003-00-2 / Actinin
  • [Other-IDs] NLM/ PMC2259451
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48. Suh KS, Mutoh M, Gerdes M, Crutchley JM, Mutoh T, Edwards LE, Dumont RA, Sodha P, Cheng C, Glick A, Yuspa SH: Antisense suppression of the chloride intracellular channel family induces apoptosis, enhances tumor necrosis factor {alpha}-induced apoptosis, and inhibits tumor growth. Cancer Res; 2005 Jan 15;65(2):562-71
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  • [Title] Antisense suppression of the chloride intracellular channel family induces apoptosis, enhances tumor necrosis factor {alpha}-induced apoptosis, and inhibits tumor growth.
  • mtCLIC/CLIC4 is a p53 and tumor necrosis factor alpha (TNFalpha) regulated intracellular chloride channel protein that localizes to cytoplasm and organelles and induces apoptosis when overexpressed in several cell types of mouse and human origin.
  • CLIC4 is elevated during TNFalpha-induced apoptosis in human osteosarcoma cell lines.
  • Cell lines expressing an inducible CLIC4-antisense construct that also reduces the expression of several other chloride intracellular channel (CLIC) family proteins were established in the human osteosarcoma lines SaOS and U2OS cells and a malignant derivative of the mouse squamous papilloma line SP1.
  • Moreover, CLIC4-antisense induction increased TNFalpha-mediated apoptosis in both the SaOS and U2OS derivative cell lines without altering TNFalpha-induced NFkappaB activity.
  • Reducing CLIC proteins in tumor grafts of SP1 cells expressing a tetracycline-regulated CLIC4-antisense substantially inhibited tumor growth and induced tumor apoptosis.
  • [MeSH-major] Apoptosis / physiology. Bone Neoplasms / pathology. Chloride Channels / antagonists & inhibitors. DNA, Antisense / genetics. NF-kappa B / antagonists & inhibitors. Osteosarcoma / pathology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Cattle. Cell Growth Processes / genetics. Cell Line, Tumor. Humans. Mice. Mice, Nude. Transfection. Xenograft Model Antitumor Assays

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  • (PMID = 15695400.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CLIC4 protein, human; 0 / Chloride Channels; 0 / DNA, Antisense; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha
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49. Miki J, Furusato B, Li H, Gu Y, Takahashi H, Egawa S, Sesterhenn IA, McLeod DG, Srivastava S, Rhim JS: Identification of putative stem cell markers, CD133 and CXCR4, in hTERT-immortalized primary nonmalignant and malignant tumor-derived human prostate epithelial cell lines and in prostate cancer specimens. Cancer Res; 2007 Apr 1;67(7):3153-61
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  • [Title] Identification of putative stem cell markers, CD133 and CXCR4, in hTERT-immortalized primary nonmalignant and malignant tumor-derived human prostate epithelial cell lines and in prostate cancer specimens.
  • Normal and cancer stem cells in prostate have recently been identified with a CD44(+)/alpha(2)beta(1)(high)/CD133(+) phenotype.
  • Stromal cell-derived factor-1 (SDF-1) and its receptor, CXCR4, have multiple essential functions, including homing of stem cells and metastasis of cancer cells.
  • We show here that human telomerase reverse transcriptase (hTERT)-immortalized primary nonmalignant (RC-165N/hTERT) and malignant (RC-92a/hTERT) tumor-derived human prostate epithelial cell lines retain stem cell properties with a CD133(+)/CD44(+)/alpha(2)beta(1)(+)/34betaE12(+)/CK18(+)/p63(-)/androgen receptor (AR)(-)/PSA(-) phenotype.
  • The CD133(+) cells from these immortalized cell lines had high proliferative potential and were able to differentiate into AR(+) phenotype.
  • CXCR4/SDF-1 may sustain tumor chemotaxis in cancer stem cells.
  • [MeSH-minor] Cell Adhesion / physiology. Cell Differentiation / physiology. Cell Growth Processes / physiology. Cell Movement / physiology. Epithelial Cells / metabolism. Epithelial Cells / pathology. Humans. Male. Peptides. Tumor Cells, Cultured


50. Petersson F, Bulimbasic S, Sima R, Michal M, Hora M, Malagon HD, Matoska J, Hes O: Large cell calcifying Sertoli cell tumor: a clinicopathologic study of 1 malignant and 3 benign tumors using histomorphology, immunohistochemistry, ultrastructure, comparative genomic hybridization, and polymerase chain reaction analysis of the PRKAR1A gene. Hum Pathol; 2010 Apr;41(4):552-9
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  • [Title] Large cell calcifying Sertoli cell tumor: a clinicopathologic study of 1 malignant and 3 benign tumors using histomorphology, immunohistochemistry, ultrastructure, comparative genomic hybridization, and polymerase chain reaction analysis of the PRKAR1A gene.
  • Four cases of large cell calcifying Sertoli cell tumor, 3 benign and 1 malignant, with no clinical signs of Carney complex or Peutz-Jeghers syndrome are reported with results of histologic, immunohistochemical, ultrastructural, and comparative genomic hybridization studies.
  • The patient with a malignant large cell calcifying Sertoli cell tumor died of disease 4 years after surgery.
  • All tumors were well circumscribed, unencapsulated, and composed of solid sheets, irregular cords, tubular structures, and nests in a fibrous and/or myxoid stroma with cellular atypia in the malignant case.
  • Tumors were negative for CAM 5.2, Mic-2, Melan-A laminin, placental alkaline phosphatase, and alpha-fetoprotein.
  • The proliferation index was 5% and 10% for 2 of the benign tumors and 30% for the malignant tumor.
  • Although the combination of large cell calcifying Sertoli cell tumor and PRKAR1A mutation fulfills the criteria for establishing a diagnosis of Carney complex, the clinical relevance of finding a PRKAR1A gene mutation in a patient without any clinical signs of Carney complex or Peutz-Jeghers syndrome remains to be established.
  • [MeSH-major] Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / metabolism. Sertoli Cell Tumor / metabolism. Testicular Neoplasms / metabolism

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  • [Copyright] Copyright 2010 Elsevier Inc.
  • (PMID = 20004940.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human
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51. Horinaka M, Yoshida T, Shiraishi T, Nakata S, Wakada M, Sakai T: The dietary flavonoid apigenin sensitizes malignant tumor cells to tumor necrosis factor-related apoptosis-inducing ligand. Mol Cancer Ther; 2006 Apr;5(4):945-51
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  • [Title] The dietary flavonoid apigenin sensitizes malignant tumor cells to tumor necrosis factor-related apoptosis-inducing ligand.
  • Dietary flavonoid apigenin is expected to have preventive and therapeutic potential against malignant tumors.
  • In this report, we show for the first time that apigenin markedly induces the expression of death receptor 5 (DR5) and synergistically acts with exogenous soluble recombinant human tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) to induce apoptosis in malignant tumor cells.
  • These results suggest that this combined treatment with apigenin and TRAIL might be promising as a new therapy against malignant tumors.
  • [MeSH-major] Apigenin / pharmacology. Apoptosis / drug effects. Apoptosis Regulatory Proteins / physiology. Membrane Glycoproteins / physiology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Cell Line, Tumor. Colonic Neoplasms. Humans. Jurkat Cells. Male. Prostatic Neoplasms. RNA, Messenger / genetics. Receptors, TNF-Related Apoptosis-Inducing Ligand. Receptors, Tumor Necrosis Factor / drug effects. Receptors, Tumor Necrosis Factor / genetics. TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 16648565.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10B protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 7V515PI7F6 / Apigenin
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52. Ageely HM, Dawoud HA, Heiba AA: Anemia, interleukin-10, tumor necrosis factor alpha, and erythropoietin levels in children with acute, complicated and uncomplicated malignant malaria in Jazan, Saudi Arabia. J Egypt Soc Parasitol; 2008 Aug;38(2):359-70
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  • [Title] Anemia, interleukin-10, tumor necrosis factor alpha, and erythropoietin levels in children with acute, complicated and uncomplicated malignant malaria in Jazan, Saudi Arabia.
  • To gain insight into potential relationships between tumor necrosis factor alpha (TNF-alpha), interleukin 10 (IL-10), erythropoietin (EPO), and anemia in acute malaria, 90 children 3 to 11 years with acute malaria were studied.
  • Good marrow response was in G1 & G2 showed by elevation of serum EPO and soluble transferring receptors (sTfR) and increased red cell distribution width (RDW).
  • TNF-alpha level was significantly higher G2 and G3 (P.05).
  • The mean IL-10 to TNF-alpha ratio in G2 (4.64) was significantly higher (P<.005) than in G3 (mean ratio, 1.77).
  • [MeSH-major] Anemia / blood. Erythropoietin / blood. Interleukin-10 / blood. Malaria, Falciparum / blood. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 18853611.001).
  • [ISSN] 1110-0583
  • [Journal-full-title] Journal of the Egyptian Society of Parasitology
  • [ISO-abbreviation] J Egypt Soc Parasitol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / Tumor Necrosis Factor-alpha; 11096-26-7 / Erythropoietin; 130068-27-8 / Interleukin-10
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53. Motohashi S, Nakayama T: Natural killer T cell-mediated immunotherapy for malignant diseases. Front Biosci (Schol Ed); 2009;1:108-16

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  • [Title] Natural killer T cell-mediated immunotherapy for malignant diseases.
  • Human invariant Valpha24 Natural Killer T (NKT) cells are unique lymphocyte subsets, characterized by an invariant T-cell receptor Valpha24 chain paired with Vbeta11.
  • Recent findings have highlighted the role of NKT cells in tumor immunity.
  • Valpha24 NKT cells are activated by a specific glycolipid ligand, alpha-Galactosylceramide and rapidly produce high levels of cytokines upon stimulation, thereby modulating other immune cells such as NK cells antigen-specific CD4+ and CD8+ T cells and dendritic cells.
  • Abnormalities in the numbers and functions of Valpha24 NKT cells have been observed in patients with various malignant diseases.
  • The quantitative alteration and functional impairment of circulating Valpha24 NKT cells are herein reviewed in various cancer-bearing patients and the progress to date in the clinical applications of NKT cell-based tumor immunotherapy is summarized.

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  • (PMID = 19482686.001).
  • [ISSN] 1945-0524
  • [Journal-full-title] Frontiers in bioscience (Scholar edition)
  • [ISO-abbreviation] Front Biosci (Schol Ed)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 41
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54. Stapelberg M, Gellert N, Swettenham E, Tomasetti M, Witting PK, Procopio A, Neuzil J: Alpha-tocopheryl succinate inhibits malignant mesothelioma by disrupting the fibroblast growth factor autocrine loop: mechanism and the role of oxidative stress. J Biol Chem; 2005 Jul 8;280(27):25369-76
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  • [Title] Alpha-tocopheryl succinate inhibits malignant mesothelioma by disrupting the fibroblast growth factor autocrine loop: mechanism and the role of oxidative stress.
  • We have studied the potential effect against human malignant mesotheliomas (MM) of alpha-tocopheryl succinate (alpha-TOS), a redox-silent vitamin E analog with strong pro-apoptotic and anti-cancer activity. alpha-TOS at sub-apoptotic levels inhibited proliferation of MM cell lines, while being nontoxic to nonmalignant mesothelial cells.
  • Because MM cells are typified by a highly metastatic phenotype, we investigated the effect of alpha-TOS on genes playing a major role in MM progression.
  • Of these, alpha-TOS down regulated fibroblast growth factor (FGF)-1 and, in particular, FGF-2 on the transcriptional level in MM cells, and this was not observed in their nonmalignant counterparts.
  • Down-regulation of FGF-2 was likely because of inhibition of the egr-1 transcription activity that was decreased in MM cells via oxidative stress induced by alpha-TOS, as evidenced by EPR spectroscopy, whereas nonmalignant cells did not show this response.
  • An analog of coenzyme Q targeted to mitochondria and superoxide dismutase overrode inhibition of MM cell proliferation by alpha-TOS as well as alpha-TOS-induced inhibition of egr-1-dependent transactivation.
  • Finally, alpha-TOS significantly suppressed experimental MM in immunocompromised mice.
  • Our data suggest that alpha-TOS suppresses MM cell proliferation by disrupting the FGF-FGF receptor autocrine signaling loop by generating oxidative stress and point to the agent as a selective drug against thus far fatal mesotheliomas.
  • [MeSH-minor] Cell Division / drug effects. Cell Line, Tumor. DNA, Single-Stranded / metabolism. Down-Regulation / drug effects. Fibroblast Growth Factor 1 / antagonists & inhibitors. Fibroblast Growth Factor 1 / genetics. Fibroblast Growth Factor 1 / metabolism. Gene Expression / drug effects. Humans. Reactive Oxygen Species / metabolism. Signal Transduction / drug effects. Tocopherols

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  • (PMID = 15878867.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA enzyme ED5; 0 / DNA, Single-Stranded; 0 / Reactive Oxygen Species; 103107-01-3 / Fibroblast Growth Factor 2; 104781-85-3 / Fibroblast Growth Factor 1; 1406-18-4 / Vitamin E; 1406-66-2 / Tocopherols
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55. Clairotte A, Ringenbach F, Laithier V, Aubert D, Kantelip B: [Malignant rhabdoid tumor of the liver with spontaneous rupture: a case report]. Ann Pathol; 2006 Apr;26(2):122-5
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  • [Title] [Malignant rhabdoid tumor of the liver with spontaneous rupture: a case report].
  • [Transliterated title] Tumeur rhabdoïde hépatique maligne avec rupture spontanée: à propos d'un cas.
  • We report the case of an 8-year-old child, presenting a rhabdoid tumor of the liver with spontaneous rupture, revealed by an intra-abdominal bleeding with rapidly fatal course.
  • This clinical and pathological report raises the problem of the differential diagnosis of primary malignant hepatic tumors of the child with no alpha-foetoprotein increase.
  • [MeSH-major] Liver Neoplasms / pathology. Rhabdoid Tumor / pathology. Rupture, Spontaneous / pathology
  • [MeSH-minor] Cell Division. Child. Diagnosis, Differential. Humans. Immunohistochemistry. Keratins / analysis. Male

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  • (PMID = 16791124.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 68238-35-7 / Keratins
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56. Zins K, Abraham D, Sioud M, Aharinejad S: Colon cancer cell-derived tumor necrosis factor-alpha mediates the tumor growth-promoting response in macrophages by up-regulating the colony-stimulating factor-1 pathway. Cancer Res; 2007 Feb 1;67(3):1038-45
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  • [Title] Colon cancer cell-derived tumor necrosis factor-alpha mediates the tumor growth-promoting response in macrophages by up-regulating the colony-stimulating factor-1 pathway.
  • The interplay between malignant and stromal cells is essential in tumorigenesis.
  • Profiling of tumor cell cytokine expression in SW620 tumor xenografts in nude mice showed increased human tumor necrosis factor (TNF)-alpha mRNA expression with tumor growth.
  • Incubation of macrophages with small interfering (si) RNAs directed against TNF-alpha or TNF-alpha-depleted SW620 cell conditioned medium versus SW620 cell conditioned medium failed to support mouse macrophage proliferation, migration, and expression of CSF-1, VEGF-A, and MMP-2 mRNAs.
  • Consistent with these results, human TNF-alpha gene silencing decreased mouse macrophage TNF-alpha, CSF-1, MMP-2, and VEGF-A mRNA expression in macrophages cocultured with human cancer cells.
  • In addition, inhibition of human TNF-alpha or mouse CSF-1 expression by siRNA reduced tumor growth in SW620 tumor xenografts in mice.
  • These results suggest that colon cancer cell-derived TNF-alpha stimulates TNF-alpha and CSF-1 production by macrophages, and that CSF-1, in turn, induces macrophage VEGF-A and MMP-2 in an autocrine manner.
  • Thus, interrupting tumor cell-macrophage communication by targeting TNF-alpha may provide an alternative therapeutic approach for the treatment of colon cancer.
  • [MeSH-major] Colonic Neoplasms / metabolism. Macrophage Colony-Stimulating Factor / biosynthesis. Macrophages / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Growth Processes / physiology. Cell Line, Tumor. Gene Expression. Humans. Male. Matrix Metalloproteinase 2 / biosynthesis. Matrix Metalloproteinase 2 / genetics. Mice. Mice, Inbred BALB C. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Small Interfering / genetics. Transplantation, Heterologous. Up-Regulation. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics

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  • (PMID = 17283136.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 3.4.24.24 / Matrix Metalloproteinase 2
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57. Tangjitgamol S, Hanprasertpong J, Manusirivithaya S, Wootipoom V, Thavaramara T, Buhachat R: Malignant ovarian germ cell tumors: clinico-pathological presentation and survival outcomes. Acta Obstet Gynecol Scand; 2010;89(2):182-9
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  • [Title] Malignant ovarian germ cell tumors: clinico-pathological presentation and survival outcomes.
  • OBJECTIVE: To evaluate clinico-pathological features, treatment, survival, and prognostic factors of patients with malignant ovarian germ cell tumors.
  • POPULATION: Malignant ovarian germ cell tumor patients treated between January 1996 and December 2007.
  • Patients with malignant tumors arising from benign cystic teratoma were excluded.
  • Only preoperative tumor marker elevation was a significant poor prognostic factor for PFS.
  • CONCLUSIONS: Malignant ovarian germ cell tumors have a good prognosis with conservative surgical treatment.
  • Elevated preoperative serum tumor markers are a poor prognostic factor for PFS.
  • [MeSH-major] Neoplasms, Germ Cell and Embryonal / mortality. Neoplasms, Germ Cell and Embryonal / pathology. Ovarian Neoplasms / mortality. Ovarian Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Age Factors. Biomarkers, Tumor / blood. Chemotherapy, Adjuvant. Child. Child, Preschool. Chorionic Gonadotropin, beta Subunit, Human / blood. Disease-Free Survival. Female. Humans. L-Lactate Dehydrogenase / blood. Neoplasm Recurrence, Local / pathology. Prognosis. Radiotherapy, Adjuvant. Survival Rate. Young Adult. alpha-Fetoproteins / analysis

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  • (PMID = 19961281.001).
  • [ISSN] 1600-0412
  • [Journal-full-title] Acta obstetricia et gynecologica Scandinavica
  • [ISO-abbreviation] Acta Obstet Gynecol Scand
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / alpha-Fetoproteins; EC 1.1.1.27 / L-Lactate Dehydrogenase
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58. Micchelli ST, Vivekanandan P, Boitnott JK, Pawlik TM, Choti MA, Torbenson M: Malignant transformation of hepatic adenomas. Mod Pathol; 2008 Apr;21(4):491-7
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  • [Title] Malignant transformation of hepatic adenomas.
  • They have a small but poorly characterized risk of malignant degeneration.
  • Immunohistochemistry for p53, beta-catenin and alpha-fetoprotein (AFP) were performed on those cases with malignant transformation and exon 3 of beta-catenin was amplified and sequenced.
  • A total of 17 hepatic adenomas were resected and 3 showed malignant transformation.
  • Histologically, the malignant transformation occurred within otherwise typical hepatic adenomas.
  • The hepatocellular carcinoma arose as distinct nodules directly within the adenomas, effectively ruling out synchronous lesions.
  • The hepatocellular carcinomas were unifocal in two cases and multifocal in one case with the greatest dimensions of the hepatocellular carcinoma being 2.5, 2.2, and 1 cm.
  • Immunostains for AFP and beta-catenin were negative in both the hepatic adenomas and areas of hepatocellular carcinoma. p53 immunostaining was positive within the areas of malignant transformation in one case.
  • No mutations or deletions were seen in exon 3 of the beta-catenin gene for either the adenomas or the carcinoma.
  • [MeSH-major] Adenoma, Liver Cell / pathology. Carcinoma, Hepatocellular / pathology. Cell Transformation, Neoplastic / pathology. Liver Neoplasms / pathology
  • [MeSH-minor] Adult. Contraceptives, Oral, Hormonal / adverse effects. Female. Humans. Immunohistochemistry. Tumor Suppressor Protein p53 / biosynthesis. alpha-Fetoproteins / biosynthesis. beta Catenin / genetics

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  • (PMID = 18246041.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contraceptives, Oral, Hormonal; 0 / Tumor Suppressor Protein p53; 0 / alpha-Fetoproteins; 0 / beta Catenin
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59. Liu SY, Chang LC, Pan LF, Hung YJ, Lee CH, Shieh YS: Clinicopathologic significance of tumor cell-lined vessel and microenvironment in oral squamous cell carcinoma. Oral Oncol; 2008 Mar;44(3):277-85
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  • [Title] Clinicopathologic significance of tumor cell-lined vessel and microenvironment in oral squamous cell carcinoma.
  • Oral squamous cell carcinoma (SCC) can be vascularized through a process called "tumor cell-lined vessels".
  • Currently, the tumor microenvironment, which is recognized as hypoxic and orchestrated largely by inflammatory cells and defective blood vessels, is considered an important participant in the neoplastic process.
  • Vascular structure was investigated by multistaining with pan-cytokeratin, CD34, and alpha-smooth actin/type IV collagen.
  • Immunohistochemical staining of the hypoxia inducible factor-1 alpha (HIF-1 alpha) and CD68 was used to reflect hypoxia and tumor-associated macrophages (TAM).
  • Significant association between the integrity of vascular structure and lymph node involvement and presence of tumor cell-lined vessel was found.
  • HIF-1 alpha overexpression was frequently observed in cancer cells (78/112) and correlated with tumor progress index.
  • There was a significant correlation between TAM and lymph node involvement (P=0.004) and tumor size (P=0.004).
  • In addition, survival analysis revealed that tumor cell-lined vessels (P=0.001), HIF-1 alpha expression (P=0.004), and TAM (P=0.001) correlated significantly with poor survival.
  • We conclude that in the cancer microenvironment, HIF-1 alpha expression and the TAM are induced and contributed to malignant behavior of tumor cells.
  • Furthermore, the presence of tumor cell-lined vessel, HIF-1 alpha overexpression, and high TAM could be the potential markers of prognosis for patients with oral SCC.
  • [MeSH-major] Blood Vessels / pathology. Carcinoma, Squamous Cell / blood supply. Mouth Neoplasms / blood supply. Neovascularization, Pathologic


60. 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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61. Yasui Y, Toyoda K, Imai K: A primary hepatic malignant mesenchymal tumor with myofibrogenic differentiation in a B6C3F1 mouse. Toxicol Pathol; 2009 Feb;37(2):244-8
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  • [Title] A primary hepatic malignant mesenchymal tumor with myofibrogenic differentiation in a B6C3F1 mouse.
  • We found a malignant mesenchymal tumor with myofibrogenic differentiation in the liver of a 110-week-old female B6C3F1 mouse used for a carcinogenicity study.
  • Histologically, the tumor was composed of interlacing fascicles of spindle-shaped cells with oval or elongated nuclei and lightly eosinophilic cytoplasm.
  • Tumor cells metastasized to the lung, parapancreatic lymph node, and spleen.
  • Special staining revealed individual tumor cells surrounded by reticulin fibers and an abundant collagenous matrix.
  • Immunohistochemically, the tumor cells were positive for vimentin, alpha-smooth muscle actin, and desmin, but were negative for von Willebrand factor, Mac-2, S-100, and cytokeratin.
  • Electron microscopic examination revealed that the tumor cells contained prominent rough endoplasmic reticulum and thin filaments in the cytoplasm, although they lacked basal lamina, focal densities, or lipid droplets.
  • Thus, detailed histopathological examination suggested the origin of the present tumor to possibly be Ito cells within the fibrous stroma.
  • This report provides additional histopathological evidence of malignant hepatic nonepithelial tumors in mice.
  • [MeSH-major] Cell Differentiation. Liver Neoplasms / pathology. Myofibrils / physiology. Soft Tissue Neoplasms / pathology

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  • (PMID = 19332665.001).
  • [ISSN] 1533-1601
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Desmin; 0 / Vimentin
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62. Kulbe H, Thompson R, Wilson JL, Robinson S, Hagemann T, Fatah R, Gould D, Ayhan A, Balkwill F: The inflammatory cytokine tumor necrosis factor-alpha generates an autocrine tumor-promoting network in epithelial ovarian cancer cells. Cancer Res; 2007 Jan 15;67(2):585-92
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  • [Title] The inflammatory cytokine tumor necrosis factor-alpha generates an autocrine tumor-promoting network in epithelial ovarian cancer cells.
  • Constitutive expression of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) is characteristic of malignant ovarian surface epithelium.
  • We investigated the hypothesis that this autocrine action of TNF-alpha generates and sustains a network of other mediators that promote peritoneal cancer growth and spread.
  • When compared with two ovarian cancer cell lines that did not make TNF-alpha, constitutive production of TNF-alpha was associated with greater release of the chemokines CCL2 and CXCL12, the cytokines interleukin-6 (IL-6) and macrophage migration-inhibitory factor (MIF), and the angiogenic factor vascular endothelial growth factor (VEGF).
  • TNF-alpha production was associated also with increased peritoneal dissemination when the ovarian cancer cells were xenografted.
  • We next used RNA interference to generate stable knockdown of TNF-alpha in ovarian cancer cells.
  • Tumor growth and dissemination in vivo were significantly reduced when stable knockdown of TNF-alpha was achieved.
  • Tumors derived from TNF-alpha knockdown cells were noninvasive and well circumscribed and showed high levels of apoptosis, even in the smallest deposits.
  • This was reflected in reduced vascularization of TNF-alpha knockdown tumors.
  • Furthermore, culture supernatants from such cells failed to stimulate endothelial cell growth in vitro.
  • We conclude that autocrine production of TNF-alpha by ovarian cancer cells stimulates a constitutive network of other cytokines, angiogenic factors, and chemokines that may act in an autocrine/paracrine manner to promote colonization of the peritoneum and neovascularization of developing tumor deposits.
  • [MeSH-major] Ovarian Neoplasms / pathology. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Animals. Cell Growth Processes / physiology. Cell Line, Tumor. Chemokine CXCL12. Chemokines, CXC / metabolism. Female. Humans. Mice. Mice, Nude. Neoplasm Invasiveness. Neovascularization, Pathologic / immunology. Neovascularization, Pathologic / metabolism. Receptors, CXCR4 / metabolism. Transfection. Transplantation, Heterologous

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  • (PMID = 17234767.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Arthritis Research UK / / 17208; 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 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse; 0 / Receptors, CXCR4; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2679985; NLM/ UKMS4487
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63. Devoogdt N, Revets H, Kindt A, Liu YQ, De Baetselier P, Ghassabeh GH: The tumor-promoting effect of TNF-alpha involves the induction of secretory leukocyte protease inhibitor. J Immunol; 2006 Dec 1;177(11):8046-52
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  • [Title] The tumor-promoting effect of TNF-alpha involves the induction of secretory leukocyte protease inhibitor.
  • According to the cancer immunoediting concept, inflammatory mediators play not only a critical role in promoting host protection against cancer but also contribute to cancer cell growth and survival.
  • TNF-alpha is a critical factor in this network.
  • However, the mechanisms underlying the tumor-promoting effect of TNF-alpha have not been fully elucidated yet.
  • We previously reported that in vitro culture of Lewis lung carcinoma 3LL cells with TNF-alpha-producing macrophages resulted in enhanced resistance toward TNF-alpha-mediated lysis and increased malignancy of the 3LL cells.
  • In this study, we analyzed the effects of endogenous TNF-alpha on TNF-alpha resistance and malignant behavior in vivo of low-malignant/TNF-alpha-sensitive 3LL-S cells and cancer cells derived from 3LL-S tumors that developed in wild-type or TNF-alpha(-/-) mice.
  • Interestingly, 3LL-S cells acquired a malignant phenotype in vivo depending on the presence of host TNF-alpha, whereas acquisition of TNF-alpha resistance was TNF-alpha-independent.
  • This result suggested that malignancy-promoting characteristics of 3LL-S cells other than TNF-alpha resistance are influenced in vivo by TNF-alpha.
  • In this study, we show that SLPI, but not S100A4, was induced in 3LL-S cells both in vitro and in vivo by TNF-alpha, and that silencing of in vivo induced 3LL-S SLPI expression using RNA interference abrogated in vivo progression but did not influence TNF-alpha resistance.
  • These data indicate that SLPI induction may be one mechanism whereby TNF-alpha acts as an endogenous tumor promoter.
  • [MeSH-major] Carcinoma, Lewis Lung / immunology. Cytotoxicity, Immunologic. Neoplasm Invasiveness / immunology. Secretory Leukocyte Peptidase Inhibitor / metabolism. Tumor Necrosis Factor-alpha / immunology

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  • (PMID = 17114478.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / Secretory Leukocyte Peptidase Inhibitor; 0 / Slpi protein, mouse; 0 / Tumor Necrosis Factor-alpha
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64. Pozharisskiĭ KM, Leenman EE, Arzumanov AA: [Achievements in morphological diagnosis of prostatic cancer: alpha-methylacyl-coenzyme-A-racemase--a new marker of malignant cell transformation]. Arkh Patol; 2005 Sep-Oct;67(5):15-9
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  • [Title] [Achievements in morphological diagnosis of prostatic cancer: alpha-methylacyl-coenzyme-A-racemase--a new marker of malignant cell transformation].
  • Gene P504S is considered as the most specific for prostatic carcinoma and its protein (alpha-methylacyl coenzyme A racemaze (AMACR/P504S) is higly sensitive and specific marker not only for adenocarcinoma cells but also for preceding changes - prostatic intraepithelial neoplasm (PIN).
  • AMACR/P504S seems to be the first marker of malignant transformation and tumor progression.
  • Use of immunohistochemical method for revealing this marker together with methods of basal prostatic cells observation (cytokeratin of a high molecular weight, cytokeratin 5/6, p63) improves morphological diagnosis of prostatic carcinoma, particularly on the material of needle biopsies.
  • [MeSH-major] Biomarkers, Tumor / analysis. Cell Transformation, Neoplastic. Prostatic Intraepithelial Neoplasia / diagnosis. Prostatic Neoplasms / diagnosis. Racemases and Epimerases / analysis

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  • (PMID = 16323473.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] Editorial; English Abstract
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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65. Ringel J, Jesnowski R, Moniaux N, Lüttges J, Ringel J, Choudhury A, Batra SK, Klöppel G, Löhr M: Aberrant expression of a disintegrin and metalloproteinase 17/tumor necrosis factor-alpha converting enzyme increases the malignant potential in human pancreatic ductal adenocarcinoma. Cancer Res; 2006 Sep 15;66(18):9045-53
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  • [Title] Aberrant expression of a disintegrin and metalloproteinase 17/tumor necrosis factor-alpha converting enzyme increases the malignant potential in human pancreatic ductal adenocarcinoma.
  • To understand the role of ADAM17/tumor necrosis factor-alpha (TNF-alpha) converting enzyme (TACE) in pancreatic ductal adenocarcinoma (PDAC), we investigated its expression, function, and in vitro regulation.
  • ADAM17/TACE mRNA was expressed in 3 of 10 normal pancreatic tissues, 6 of 8 samples from patients with chronic pancreatitis, 10 of 10 PDAC tissues, and 9 of 9 pancreatic cancer cell lines, but it was absent in primary duct epithelial cells.
  • Immunohistochemical staining revealed positive cancer cells in 8 of 10 PDACs but no staining of ducts in normal pancreas.
  • ADAM17/TACE was found in 0 of 16 pancreatic intraepithelial neoplasia (PanIN)-1A lesions, 1 of 30 PanIN-1B lesions, 2 of 13 PanIN-2 lesions but, in 13 of 15 PanIN-3 lesions, associated with PDAC.
  • Western blot, flow cytometry, and confocal microscopy analyses showed the aberrant expression of ADAM17/TACE protein in pancreatic cancer cell lines.
  • The proteolytic activity of ADAM17/TACE, assessed by the release of TNF-alpha, was inhibited by TNF-alpha protease inhibitor.
  • Furthermore, ADAM17/TACE mRNA expression was down-regulated in pancreatic cancer cells arrested in G2-M phase as well as in a time-dependent manner after TNF-alpha and interleukin-6 incubation.
  • [MeSH-major] ADAM Proteins / biosynthesis. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / enzymology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Cycle / genetics. Cell Growth Processes / genetics. Cell Line, Tumor. Disease Progression. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. Immunohistochemistry. Neoplasm Invasiveness. Pancreatitis, Chronic / enzymology. Pancreatitis, Chronic / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 16982746.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA772712
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / tumor necrosis factor-alpha convertase
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66. Indra AK, Castaneda E, Antal MC, Jiang M, Messaddeq N, Meng X, Loehr CV, Gariglio P, Kato S, Wahli W, Desvergne B, Metzger D, Chambon P: Malignant transformation of DMBA/TPA-induced papillomas and nevi in the skin of mice selectively lacking retinoid-X-receptor alpha in epidermal keratinocytes. J Invest Dermatol; 2007 May;127(5):1250-60
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  • [Title] Malignant transformation of DMBA/TPA-induced papillomas and nevi in the skin of mice selectively lacking retinoid-X-receptor alpha in epidermal keratinocytes.
  • Retinoid-X-receptor alpha (RXRalpha), a member of the nuclear receptor (NR) superfamily, is a ligand-dependent transcriptional regulatory factor.
  • We investigated the role of RXRalpha and its partners on mouse skin tumor formation and malignant progression upon topical DMBA/TPA treatment.
  • As keratinocyte-selective peroxisome proliferator-activated receptor gamma (PPARgamma) ablation had similar effects, RXRalpha/PPARgamma heterodimers most probably mediate epidermal tumor suppression.
  • Distinct RXRalpha-mediated molecular events appear therefore to be involved, in keratinocytes, in cell-autonomous suppression of epidermal tumorigenesis and malignant progression, and in non-cell-autonomous suppression of nevi formation and progression.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Epidermis / metabolism. Keratinocytes / metabolism. Nevus, Pigmented / pathology. Papilloma / pathology. Retinoid X Receptor alpha / metabolism. Skin Neoplasms / pathology


67. Lehner M, Bailo M, Stachel D, Roesler W, Parolini O, Holter W: Caspase-8 dependent apoptosis induction in malignant myeloid cells by TLR stimulation in the presence of IFN-alpha. Leuk Res; 2007 Dec;31(12):1729-35
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  • [Title] Caspase-8 dependent apoptosis induction in malignant myeloid cells by TLR stimulation in the presence of IFN-alpha.
  • We have previously reported that IFN-alpha can sensitize human monocytes to apoptosis induction by lipopolysaccharide (LPS).
  • Based on these results we investigated whether similarly apoptosis can be cooperatively induced in myeloid tumor cells.
  • When testing established acute myeloid leukemia (AML) cell lines we found the monocytic cell line THP-1 to be sensitive to IFN-alpha plus LPS induced apoptosis, which was partially dependent on caspase-8 and was associated with an enhanced expression of Fas/CD95.
  • We extended our study to 29 short term blast lines from patients with AML and observed additive effects of IFN-alpha and LPS on cell death only with few samples indicating that sensitivity to IFN-alpha plus LPS inducible apoptosis is present in a fraction of AML samples only with no obvious correlation with certain FAB phenotypes.
  • [MeSH-major] Apoptosis. Caspase 8 / physiology. Interferon-alpha / pharmacology. Leukemia, Myeloid, Acute / pathology. Toll-Like Receptors / physiology
  • [MeSH-minor] Cell Line. Cell Line, Tumor. Humans. Lipopolysaccharides / pharmacology. Monocytes. Myeloid Cells

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  • (PMID = 17572490.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Lipopolysaccharides; 0 / Toll-Like Receptors; EC 3.4.22.- / Caspase 8
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68. Li B, Vincent A, Cates J, Brantley-Sieders DM, Polk DB, Young PP: Low levels of tumor necrosis factor alpha increase tumor growth by inducing an endothelial phenotype of monocytes recruited to the tumor site. Cancer Res; 2009 Jan 1;69(1):338-48
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  • [Title] Low levels of tumor necrosis factor alpha increase tumor growth by inducing an endothelial phenotype of monocytes recruited to the tumor site.
  • Microenvironmental cues instruct infiltrating tumor-associated myeloid cells to drive malignant progression.
  • A subpopulation of tumor-associated myeloid cells coexpressing endothelial and myeloid markers, although rare in peripheral blood, are primarily associated with tumors where they enhance tumor growth and angiogenesis.
  • These biphenotypic vascular leukocytes result from the endothelial differentiation of myeloid progenitors, a process regulated by tumor necrosis factor (TNF)alpha in vitro.
  • An in vivo increase in tumor-derived TNFalpha expression promoted tumor growth and vascularity of mouse melanoma, lung cancer, and mammary tumors.
  • Notably, tumor growth was accompanied by a significant increase in myeloid/endothelial biphenotypic populations.
  • TNFalpha-associated tumor growth, vascularity, and generation of tumor vascular leukocytes in mouse melanoma tumors were dependent on intact host TNFalpha receptors.
  • Our studies suggest that TNFalpha constitutes a tumor microenvironment signal that biases recruited monocytes toward a proangiogenic/provasculogenic myeloid/endothelial phenotype.

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  • (PMID = 19118019.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL088424-01A1; United States / NHLBI NIH HHS / HL / R01 HL088424-01A1; United States / NIDDK NIH HHS / DK / DK056008-10; United States / NIDDK NIH HHS / DK / R01 DK056008-10; United States / NHLBI NIH HHS / HL / R01 HL088424; United States / NHLBI NIH HHS / HL / HL 088424; United States / NIDDK NIH HHS / DK / DK 56008; United States / NIDDK NIH HHS / DK / R01 DK056008; United States / NIDDK NIH HHS / DK / Z01 DK056008
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ NIHMS86128; NLM/ PMC2651676
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69. Rizk S, Maalouf K, Baydoun E: The antiproliferative effect of kefir cell-free fraction on HuT-102 malignant T lymphocytes. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S198-203

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  • [Title] The antiproliferative effect of kefir cell-free fraction on HuT-102 malignant T lymphocytes.
  • Kefir is produced by adding kefir grains (a mass of proteins, polysaccharides, bacteria, and yeast) to pasteurized milk; it has been shown to control several cellular types of cancer, such as Sarcoma 180 in mice, Lewis lung carcinoma, and human mammary cancer.
  • Human T-cell lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia, which is a fatal disease with no effective treatment.
  • The current study aims at investigating the effect of a cell-free fraction of kefir on HuT-102 cells, which are HTLV-1-positive malignant T-lymphocytes.
  • The effect of all the noncytotoxic concentrations of kefir cell-free fraction on the proliferation of HuT-102 cells was then assessed.
  • The levels of transforming growth factor (TGF)-alpha mRNA upon kefir treatment were then analyzed using reverse transcriptase polymerase chain reaction.
  • Finally, the growth inhibitory effects of kefir on cell cycle progression and/or apoptosis were assessed by flow cytometry.
  • Kefir cell-free fraction caused the downregulation of TGF-alpha, which is a cytokine that induces the proliferation and replication of cells.
  • Finally, a marked increase in cell cycle distribution was noted in the pre-G1 phase.
  • In conclusion, kefir is effective in inhibiting proliferation and inducing apoptosis of HTLV-1-positive malignant T-lymphocytes.
  • [MeSH-major] Cultured Milk Products / metabolism. Gene Expression Regulation, Leukemic. Leukemia, T-Cell / drug therapy. T-Lymphocytes / drug effects
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Apoptosis. Cell Cycle. Cell Line, Tumor. Cell-Free System. Down-Regulation. Human T-lymphotropic virus 1 / metabolism. Humans. Milk. RNA, Messenger / metabolism. Transforming Growth Factor alpha / metabolism

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  • (PMID = 19778841.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / Transforming Growth Factor alpha
  • [Number-of-references] 26
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70. Lu H, Li Y, Shu M, Tang J, Huang Y, Zhou Y, Liang Y, Yan G: Hypoxia-inducible factor-1alpha blocks differentiation of malignant gliomas. FEBS J; 2009 Dec;276(24):7291-304
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  • [Title] Hypoxia-inducible factor-1alpha blocks differentiation of malignant gliomas.
  • Here we show that rat C6 and primary human malignant glioma cells can be induced to differentiate into astrocytes by the well-known adenylate cyclase activator forskolin.
  • Importantly, knockdown of hypoxia inducible factor-1alpha by RNA interference restores the differentiation capabilities of the cells, even in the presence of cobalt chloride, whereas stabilization of hypoxia-inducible factor-1alpha through retarded ubiquitination by von Hippel-Lindau tumor suppressor gene silence abrogates the induced differentiation.
  • Administration of chetomin in combination with forskolin significantly suppresses malignant glioma growth in an in vivo xenograft model.
  • Analysis of 95 human glioma tissues revealed an increase of hypoxia-inducible factor-1alpha protein expression with progressing tumor grade.
  • Taken together, these findings suggest a key signal transduction pathway involving hypoxia-inducible factor-1alpha that contributes to a differentiation defect in malignant gliomas and sheds new light on the differentiation therapy of solid tumors by targeting hypoxia-inducible factor-1alpha.
  • [MeSH-major] Cell Differentiation / drug effects. Glioma / pathology. Hypoxia-Inducible Factor 1, alpha Subunit / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Transformation, Neoplastic / drug effects. Cobalt / antagonists & inhibitors. Cobalt / pharmacology. Colforsin / pharmacology. Deferoxamine / pharmacology. Disulfides / pharmacology. Gene Expression Regulation, Neoplastic. Humans. Indole Alkaloids / pharmacology. Male. Mice. Rats. Tumor Cells, Cultured

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  • (PMID = 19912340.001).
  • [ISSN] 1742-4658
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Disulfides; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Indole Alkaloids; 1403-36-7 / chetomin; 1F7A44V6OU / Colforsin; 3G0H8C9362 / Cobalt; EVS87XF13W / cobaltous chloride; J06Y7MXW4D / Deferoxamine
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71. Stathopoulos GT, Zhu Z, Everhart MB, Kalomenidis I, Lawson WE, Bilaceroglu S, Peterson TE, Mitchell D, Yull FE, Light RW, Blackwell TS: Nuclear factor-kappaB affects tumor progression in a mouse model of malignant pleural effusion. Am J Respir Cell Mol Biol; 2006 Feb;34(2):142-50
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  • [Title] Nuclear factor-kappaB affects tumor progression in a mouse model of malignant pleural effusion.
  • We developed a novel mouse model of malignant pleural effusion (MPE) by injecting Lewis lung cancer (LLC) cells directly into the pleural space of syngeneic C57B/6 mice.
  • Implantation and growth of pleural tumors triggers a host inflammatory response characterized by a mixed inflammatory cell influx into the pleural fluid.
  • LLC cells exhibited high basal nuclear factor (NF)-kappaB activity in vitro and in vivo, which we used to drive expression of a NF-kappaB-dependent green fluorescent protein-firefly luciferase fusion reporter construct.
  • Inhibition of NF-kappaB in LLC cells did not affect cell viability in culture; however, injection of LLC cells expressing a dominant NF-kappaB inhibitor resulted in decreased tumor burden, decreased pleural effusion volume, and decreased pleural effusion TNF-alpha levels.
  • These studies indicate that tumor NF-kappaB activity regulates pleural tumor progression.
  • This reproducible model of MPE can be used to further study the influence of specific host and tumor factors on the pathogenesis of MPE and evaluate new therapeutic strategies.

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  • (PMID = 16210694.001).
  • [ISSN] 1044-1549
  • [Journal-full-title] American journal of respiratory cell and molecular biology
  • [ISO-abbreviation] Am. J. Respir. Cell Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL61419; United States / NHLBI NIH HHS / HL / HL66196
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ccl2 protein, mouse; 0 / Chemokine CCL2; 0 / I-kappa B Proteins; 0 / MCP-5 protein, rat; 0 / Monocyte Chemoattractant Proteins; 0 / NF-kappa B; 147336-22-9 / Green Fluorescent Proteins; EC 1.1.1.27 / L-Lactate Dehydrogenase
  • [Other-IDs] NLM/ PMC2644178
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72. Sen S, Dong M, Kumar S: Isoform-specific contributions of alpha-actinin to glioma cell mechanobiology. PLoS One; 2009 Dec 23;4(12):e8427
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  • [Title] Isoform-specific contributions of alpha-actinin to glioma cell mechanobiology.
  • Glioblastoma Multiforme (GBM) is a malignant astrocytic tumor associated with low survival rates because of aggressive infiltration of tumor cells into the brain parenchyma.
  • Expression of the actin binding protein alpha-actinin has been strongly correlated with the invasive phenotype of GBM in vivo.
  • To probe the cellular basis of this correlation, we have suppressed expression of the nonmuscle isoforms alpha-actinin-1 and alpha-actinin-4 and examined the contribution of each isoform to the structure, mechanics, and motility of human glioma tumor cells in culture.
  • Mechanistic studies reveal a relationship between alpha-actinin and non-muscle myosin II in which depletion of either alpha-actinin isoform reduces myosin expression and maximal cell-ECM tractional forces.
  • Our results demonstrate that both alpha-actinin-1 and alpha-actinin-4 make critical and distinct contributions to cytoskeletal organization, rigidity-sensing, and motility of glioma cells, thereby yielding mechanistic insight into the observed correlation between alpha-actinin expression and GBM invasiveness in vivo.

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  • (PMID = 20037648.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIH HHS / OD / DP2 OD004213; United States / NIH HHS / OD / 1DP2OD004213
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 11003-00-2 / Actinin; 125361-02-6 / Vinculin; EC 3.6.4.1 / Myosins
  • [Other-IDs] NLM/ PMC2793025
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73. Katori H, Nozawa A, Tsukuda M: Expression of epidermal growth factor receptor, transforming growth factor-alpha and Ki-67 in relationship to malignant transformation of pleomorphic adenoma. Acta Otolaryngol; 2007 Nov;127(11):1207-13
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  • [Title] Expression of epidermal growth factor receptor, transforming growth factor-alpha and Ki-67 in relationship to malignant transformation of pleomorphic adenoma.
  • The data support the hypothesis that increased epidermal growth factor receptor (EGFR) and transforming growth factor (TGF)-alpha expression is associated with early events in malignant transformation of pleomorphic adenoma (PA).
  • OBJECTIVE: In the present study, we attempted to identify EGFR and TGF-alpha expression and Ki-67 index in carcinoma ex-pleomorphic adenoma (Ca ex-PA) and PA.
  • We also compared the presence of EGFR and TGF-alpha and Ki-67 index with clinical data.
  • MATERIALS AND METHODS: The tissues were stained with monoclonal antibodies to EGFR, TGF-alpha and Ki-67.
  • In the immunohistochemical analysis of EGFR and TGF-alpha and Ki67 index, a significant increase was observed in Ca ex-PA, especially with adenocarcinoma, compared with PA and sialadenitis.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. Biomarkers, Tumor / biosynthesis. Cell Transformation, Neoplastic. Ki-67 Antigen / genetics. Receptor, Epidermal Growth Factor / biosynthesis. Salivary Gland Neoplasms / metabolism. Transforming Growth Factor alpha / biosynthesis

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  • (PMID = 17851915.001).
  • [ISSN] 0001-6489
  • [Journal-full-title] Acta oto-laryngologica
  • [ISO-abbreviation] Acta Otolaryngol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 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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74. Kammertoens T, Willebrand R, Erdmann B, Li L, Li Y, Engels B, Uckert W, Blankenstein T: CY15, a malignant histiocytic tumor that is phenotypically similar to immature dendritic cells. Cancer Res; 2005 Apr 1;65(7):2560-4
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  • [Title] CY15, a malignant histiocytic tumor that is phenotypically similar to immature dendritic cells.
  • The origin and pathogenesis of histiocytic malignancies and the biology of the tumor cells are poorly understood.
  • We have isolated a murine histiocytic tumor cell line (CY15) from a BALB/c IFNgamma(-/-) mouse and characterized it in terms of phenotype and function.
  • The cells form tumors in BALB/c mice and metastasize to spleen, liver, lung, kidney, and to a lesser extend to lymph nodes and bone marrow, as judged by the growth of green fluorescent protein transfected tumor cells in mice.
  • Lipopolysaccharide induces the cells to up-regulate B7.1 and B7.2 and to secrete tumor necrosis factor alpha and IL-12.
  • Based on these data, CY15 is a dendritic cell-like tumor cell line and may serve as a transplantable tumor model for histiocytosis in humans.
  • [MeSH-major] Dendritic Cells / pathology. Histiocytes / pathology. Histiocytic Disorders, Malignant / pathology
  • [MeSH-minor] Animals. Cell Growth Processes. Cell Line, Tumor. Flow Cytometry. Interferon-gamma / deficiency. Interferon-gamma / genetics. Lymphocyte Activation. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Microscopy, Electron. Neoplasm Metastasis. Neoplasm Transplantation. T-Lymphocytes / immunology. T-Lymphocytes / pathology

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  • (PMID = 15805249.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 82115-62-6 / Interferon-gamma
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75. Chetaille B, Massard G, Falcoz PE: [Mediastinal germ cell tumors: anatomopathology, classification, teratomas and malignant tumors]. Rev Pneumol Clin; 2010 Feb;66(1):63-70

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Mediastinal germ cell tumors: anatomopathology, classification, teratomas and malignant tumors].
  • Mediastinal germ cell tumors are rare tumors.
  • It is classic to divide those tumors into two categories, seminomas and nonseminomatous germ cell tumors: teratomas (mature or immature), embryonal carcinomas, yolk sac tumors, and choriocarcinomas.
  • Each histological sub-type can be associated to another sub-type that realise a so-called mixed germ cell tumor.
  • Diagnosis strategy is currently well codified for malignant mediastinal germ cell tumors.
  • It greatly benefits from tumoral markers (alpha-fetoprotein and beta human chorionic gonadotrophin).
  • The treatment of seminomatous tumors is standardised--chemotherapy/surgery on residual tumor greater than 3 cm/radiotherapy on viable persistent residual tumors--and provides very satisfying results.
  • As for the nonseminomatous germ cell tumors, the situation is dramatically different.
  • [MeSH-major] Mediastinal Neoplasms / pathology. Neoplasms, Germ Cell and Embryonal / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Combined Modality Therapy. Humans. Mediastinum / pathology. Neoplasm Invasiveness. Prognosis. Seminoma / classification. Seminoma / pathology. Seminoma / therapy. Teratoma / classification. Teratoma / pathology. Teratoma / therapy. Tomography, X-Ray Computed

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  • [Copyright] Copyright (c) 2009 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20207298.001).
  • [ISSN] 0761-8417
  • [Journal-full-title] Revue de pneumologie clinique
  • [ISO-abbreviation] Rev Pneumol Clin
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 18
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76. Li H, Gu Y, Miki J, Hukku B, McLeod DG, Hei TK, Rhim JS: Malignant transformation of human benign prostate epithelial cells by high linear energy transfer alpha-particles. Int J Oncol; 2007 Sep;31(3):537-44
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  • [Title] Malignant transformation of human benign prostate epithelial cells by high linear energy transfer alpha-particles.
  • In the present study, we examined the oncogenic transforming potency of alpha-particles using non-tumorigenic, telomerase-immortalized human benign prostate epithelial cells.
  • We report the malignant transformation of human benign prostate epithelial cells after a single exposure to 0.6 Gy dose of alpha-particles.
  • The cell line derived from tumor (SCID 5015), like the unirradiated cells, expressed cytokeratin 5, 8 and 18, NKX3.1 and AMACR.
  • The malignant cells showed increased secretion of MMP2.
  • Prominent changes in chromosomes 6, 11 and 16, as well as mutations and deletions of the p53 gene were observed in the tumor outgrowth and tumor cells.
  • These findings provide the first evidence of malignant transformation of human benign prostate epithelial cells exposed to a single dose of alpha-particles.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / etiology. Alpha Particles. Cell Transformation, Neoplastic. Linear Energy Transfer. Neoplasms, Radiation-Induced / etiology. Prostate / pathology. Prostatic Neoplasms / diagnosis. Prostatic Neoplasms / etiology
  • [MeSH-minor] Animals. Cell Line, Transformed. Chromosome Aberrations. Humans. Male. Mice. Mice, SCID. Neoplasm Transplantation

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  • (PMID = 17671680.001).
  • [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; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Greece
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77. Calaminus G, Schneider DT, Weissbach L, Schönberger S, Okpanyi V, Leuschner I, Poremba C, Göbel U: Survival after an antiangiogenetic therapy and surgery in a wide spread growing teratoma originating from a testicular mixed malignant germ cell tumor. Klin Padiatr; 2009 May-Jun;221(3):136-40
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  • [Title] Survival after an antiangiogenetic therapy and surgery in a wide spread growing teratoma originating from a testicular mixed malignant germ cell tumor.
  • Growing teratoma is still an often unsolved problem especially in male with mixed malignant GCTs of the testis or the mediastinum.
  • This specific situation with progressive tumor growth and simultaneous normalization of tumor markers during or after treatment of malignant GCTs with teratomatous elements is judged as a fatal situation if this situation can not be controlled by extensive surgery, as teratoma are not sensible to chemotherapy or irradiation.
  • Here, we report the case history of a 17-year old male patient with a testicular malignant GCT and wide spread lymph node metastases, who developed a rapidly progressive growing teratoma within the lymph node metastases.
  • Within the molecular profile of the tumor we could find a cytogenetic picture typically found in malignant adult GCTs.
  • In view of the bulky abdominal, thoracic and cervical metastases and the uncontrolled tumor progression, the situation was considered incurable.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Endodermal Sinus Tumor / drug therapy. Endodermal Sinus Tumor / surgery. Lymph Node Excision. Lymphatic Metastasis. Neoplasms, Germ Cell and Embryonal / drug therapy. Neoplasms, Germ Cell and Embryonal / surgery. Neoplasms, Multiple Primary / drug therapy. Neoplasms, Multiple Primary / surgery. Teratoma / drug therapy. Teratoma / surgery. Testicular Neoplasms / drug therapy. Testicular Neoplasms / surgery
  • [MeSH-minor] Adolescent. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / adverse effects. Antibodies, Monoclonal, Humanized. Bevacizumab. Combined Modality Therapy. Dose-Response Relationship, Drug. Drug Administration Schedule. Follow-Up Studies. Humans. Interferon-alpha / administration & dosage. Interferon-alpha / adverse effects. Lymph Nodes / blood supply. Lymph Nodes / pathology. Magnetic Resonance Imaging. Male. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / surgery. Neoplasm Staging. Recombinant Proteins. Reoperation. Salvage Therapy. Survival Rate. Thalidomide / administration & dosage. Thalidomide / adverse effects. Tomography, X-Ray Computed. Vinblastine / administration & dosage. Vinblastine / adverse effects

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  • [CommentIn] Klin Padiatr. 2009 May-Jun;221(3):134-5 [19437359.001]
  • (PMID = 19437360.001).
  • [ISSN] 1439-3824
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Interferon-alpha; 0 / Recombinant Proteins; 2S9ZZM9Q9V / Bevacizumab; 4Z8R6ORS6L / Thalidomide; 5V9KLZ54CY / Vinblastine; 76543-88-9 / interferon alfa-2a
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78. Nishio S, Yamada N, Ohyama H, Yamanegi K, Nakasho K, Hata M, Nakamura Y, Fukunaga S, Futani H, Yoshiya S, Ueda H, Taniguchi M, Okamura H, Terada N: Enhanced suppression of pulmonary metastasis of malignant melanoma cells by combined administration of alpha-galactosylceramide and interleukin-18. Cancer Sci; 2008 Jan;99(1):113-20
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  • [Title] Enhanced suppression of pulmonary metastasis of malignant melanoma cells by combined administration of alpha-galactosylceramide and interleukin-18.
  • alpha-Galactosylceramide (alpha-GalCer) shows antitumor effects by activating natural killer (NK) cells indirectly through stimulation of the secretion of cytokines by NKT cells, whereas interleukin (IL)-18 shows antitumor effects by activating NK cells directly.
  • In the present study, we examined the antitumor effect of the combined administration of alpha-GalCer and IL-18.
  • An injection of NK cell-sensitive mouse B16 melanoma cells into a mouse tail vein produced pulmonary metastasis.
  • The daily administration of alpha-GalCer or IL-18 alone for 4 days starting 1 day after the injection of B16 melanoma cells markedly suppressed the number of pulmonary metastatic foci, and their combined administration enhanced the antitumor effect compared with single administration.
  • Combined administration of alpha-GalCer and IL-18 enhanced the cytotoxicity of NK cells and increased the number of NK cells in the lung.
  • Analysis of NKT cell-dependent and NK cell-independent secretion of cytokines, to which NK cells can respond, showed that the administration of alpha-GalCer increased the secretion of IL-2, IL-4, interferon-gamma, IL-12, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-alpha, and IL-10, and the combined administration of alpha-GalCer and IL-18 enhanced the secretion of IL-2, IL-4, interferon-gamma, and granulocyte-macrophage colony-stimulating factor further but only slightly.
  • These results show that IL-18 in combination with alpha-GalCer exerts an antitumor effect on NK cell-sensitive tumors primarily by the direct stimulation of NK cells by IL-18 and the indirect stimulation of NK cells by alpha-GalCer through its activation of NKT cells.
  • [MeSH-minor] Animals. Cell Growth Processes / drug effects. Cytokines / immunology. Cytokines / secretion. Female. Galactosylceramides / administration & dosage. Galactosylceramides / pharmacology. Interleukin-15 / blood. Interleukin-15 / immunology. Interleukin-18 / administration & dosage. Interleukin-18 / pharmacology. Killer Cells, Natural / immunology. Mice. Mice, Inbred C57BL

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  • (PMID = 17949451.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-amino-1-galactopyranosyloxy-3,4-dihydroxyoctadecane; 0 / Cytokines; 0 / Galactosylceramides; 0 / Interleukin-15; 0 / Interleukin-18
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79. Estevam FR, Augusto SF, Rodrigues SA, Pinheiro MR, Monteiro AF: Apoptosis and production of TNF-alpha by tumor-associated inflammatory cells in histological grade III breast cancer. Cancer Immunol Immunother; 2005 Jul;54(7):671-6
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  • [Title] Apoptosis and production of TNF-alpha by tumor-associated inflammatory cells in histological grade III breast cancer.
  • Tumor necrosis factor alpha (TNF-alpha) is a cytokine that acts as an important mediator of the apoptotic process that also demonstrates selective citotoxicity against malignant breast tumor cells.
  • In the present study, the presence of apoptotic tumor cells and the synthesis of TNF-alpha by inflammatory cells were investigated in tissue samples from grade III invasive breast cancer with long-term follow-up.
  • In situ detection of tumor apoptotic cells was investigated by direct immuno-peroxidase of digoxigenin-labeled genomic DNA.
  • The production of TNF-alpha and tumor cell proliferation were investigated by immunohistochemical procedures.
  • Our data demonstrated that patients with a clinical history of cancer recurrence and metastasis presented a lower number of cancerous apoptotic cells, higher tumor proliferation rates, and lower TNF-alpha expression rates by inflammatory cells than what is observed among patients diagnosed with the same histopathological breast cancer type but in the absence of tumor recurrence and metastasis.
  • [MeSH-major] Apoptosis. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology. Lymphocytes, Tumor-Infiltrating / immunology. Tumor Necrosis Factor-alpha / biosynthesis
  • [MeSH-minor] Female. Gene Expression Regulation, Neoplastic. Humans. Inflammation. Neoplasm Recurrence, Local / immunology. Neoplasm Recurrence, Local / pathology. Neoplasm Staging. Tumor Cells, Cultured

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  • (PMID = 15625605.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha
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80. Nutt JE, Razak AR, O'Toole K, Black F, Quinn AE, Calvert AH, Plummer ER, Lunec J: The role of folate receptor alpha (FRalpha) in the response of malignant pleural mesothelioma to pemetrexed-containing chemotherapy. Br J Cancer; 2010 Feb 2;102(3):553-60
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  • [Title] The role of folate receptor alpha (FRalpha) in the response of malignant pleural mesothelioma to pemetrexed-containing chemotherapy.
  • BACKGROUND: The standard treatment of choice for malignant pleural mesothelioma is chemotherapy with pemetrexed and platinum, but the clinical outcome is poor.
  • This study investigates the response to pemetrexed in a panel of eight mesothelioma cell lines and the clinical outcome for patients treated with pemetrexed in relation to folate receptor alpha (FRalpha).
  • METHODS: Cell lines were treated with pemetrexed to determine the concentration that reduced growth to 50% (GI(50)).
  • RESULTS: A wide range of GI(50) values was obtained for the cell lines, H2452 cells being the most sensitive (GI(50) 22 nM) and RS5 cells having a GI(50) value greater than 10 microM.
  • No FRalpha protein was detected in any cell line, and there was no relationship between sensitivity and expression of folate transporters.
  • FRalpha was detected in 39% of tumour samples, generally in a small percentage of cells.

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  • (PMID = 20051956.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Folate Receptors, GPI-Anchored; 0 / Folic Acid Antagonists; 0 / Glutamates; 0 / Receptors, Cell Surface; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine
  • [Other-IDs] NLM/ PMC2822938
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81. Chang GC, Lan HC, Juang SH, Wu YC, Lee HC, Hung YM, Yang HY, Whang-Peng J, Liu KJ: A pilot clinical trial of vaccination with dendritic cells pulsed with autologous tumor cells derived from malignant pleural effusion in patients with late-stage lung carcinoma. Cancer; 2005 Feb 15;103(4):763-71
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  • [Title] A pilot clinical trial of vaccination with dendritic cells pulsed with autologous tumor cells derived from malignant pleural effusion in patients with late-stage lung carcinoma.
  • BACKGROUND: The authors conducted a pilot clinical trial to explore the vaccination of patients with late-stage lung carcinoma with dendritic cells (DCs) pulsed with necrotic tumor cells derived from malignant pleural effusion specimens, and to evaluate the antitumor immune response induced by this therapy.
  • Day-7 DCs were cocultured overnight with autologous necrotic tumor cells derived from pleural effusion specimens to allow internalization of tumor antigens.
  • DCs were then treated with tumor necrosis factor-alpha for 16 hours.
  • Eight patients with late-stage nonsmall cell lung carcinoma were treated in this manner.
  • Minor to moderate increases in T-cell responses against tumor antigens were observed after DC vaccination in six of eight patients.
  • One patient had minor tumor response and two patients had stable disease.
  • The two patients who had longer disease control also had better T-cell responses.
  • CONCLUSIONS: The results indicated that it was feasible to immunize patients with lung carcinoma intranodally with DCs pulsed with necrotic tumor cells enriched from pleural effusion specimens, and this approach may generate T-cell responses and provide clinical benefit in some patients.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Carcinoma, Non-Small-Cell Lung / therapy. Dendritic Cells / transplantation. Lung Neoplasms / therapy. Pleural Effusion, Malignant / cytology
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / immunology. Coculture Techniques. Female. Flow Cytometry. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Humans. Interleukin-4 / pharmacology. Lymphocyte Culture Test, Mixed. Male. Middle Aged. Pilot Projects. T-Lymphocytes / immunology. Tumor Necrosis Factor-alpha / pharmacology

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  • [Copyright] Copyright (c) 2005 American Cancer Society.
  • (PMID = 15637694.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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82. Mathsson L, Tejde A, Carlson K, Höglund M, Nilsson B, Nilsson-Ekdahl K, Rönnelid J: Cryoglobulin-induced cytokine production via FcgammaRIIa: inverse effects of complement blockade on the production of TNF-alpha and IL-10. Implications for the growth of malignant B-cell clones. Br J Haematol; 2005 Jun;129(6):830-8
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  • [Title] Cryoglobulin-induced cytokine production via FcgammaRIIa: inverse effects of complement blockade on the production of TNF-alpha and IL-10. Implications for the growth of malignant B-cell clones.
  • Complement blockade resulted in increased IgG CG-induced interleukin (IL)-10 production that was inversely correlated with decreased production of tumour necrosis factor-alpha.
  • CG-induced IL-10 might be a growth factor for malignant B-lymphocytes in CG-associated lymphoproliferative diseases with constant complement consumption.
  • [MeSH-minor] Aged. Cells, Cultured. Complement Inactivator Proteins / immunology. Complement Pathway, Classical / immunology. Female. Humans. Hydrogen-Ion Concentration. Immunoglobulin G / immunology. Immunoglobulin M / immunology. Interleukin-10 / biosynthesis. Male. Middle Aged. Monocytes / immunology. Neoplastic Stem Cells / pathology. Temperature. Tumor Necrosis Factor-alpha / biosynthesis

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  • (PMID = 15953012.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Complement Inactivator Proteins; 0 / Cryoglobulins; 0 / Cytokines; 0 / Fc gamma receptor IIA; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Receptors, IgG; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10
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83. Perrone F, Da Riva L, Orsenigo M, Losa M, Jocollè G, Millefanti C, Pastore E, Gronchi A, Pierotti MA, Pilotti S: PDGFRA, PDGFRB, EGFR, and downstream signaling activation in malignant peripheral nerve sheath tumor. Neuro Oncol; 2009 Dec;11(6):725-36
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  • [Title] PDGFRA, PDGFRB, EGFR, and downstream signaling activation in malignant peripheral nerve sheath tumor.
  • We investigated the activation of platelet-derived growth factor (PDGF) receptor A (PDGFRA), PDGF receptor B (PDGFRB), epidermal growth factor receptor (EGFR), and their downstream pathways in malignant peripheral nerve sheath tumors (MPNSTs).
  • The activation of the downstream receptor pathways was also studied by means of v-akt murine thymoma viral oncogene homolog (AKT), extracellular signal-regulated kinase (ERK), and mammalian target of rapamycin (mTOR) Western blotting experiments, as well as rat sarcoma viral oncogene homolog (RAS), v-raf murine sarcoma viral oncogene homolog B1 (BRAF), phosphoinositide-3-kinase, catalytic, alpha polypeptide (PI3KCA), and phosphatase and tensin homolog deleted on chromosome ten (PTEN) mutational analysis and fluorescence in situ hybridization.
  • [MeSH-major] Nerve Sheath Neoplasms / metabolism. Receptor, Epidermal Growth Factor / metabolism. Receptor, Platelet-Derived Growth Factor alpha / metabolism. Receptor, Platelet-Derived Growth Factor beta / metabolism. Signal Transduction

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  • (PMID = 19246520.001).
  • [ISSN] 1523-5866
  • [Journal-full-title] Neuro-oncology
  • [ISO-abbreviation] Neuro-oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Nuclear Proteins; 0 / PI3KCA protein, human; 0 / RNA, Messenger; 0 / Transcription Factors; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, rat; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-ret; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC2802393
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84. Akahane T, Sekizawa A, Okuda T, Kushima M, Saito H, Okai T: Disappearance of steroid hormone dependency during malignant transformation of ovarian clear cell cancer. Int J Gynecol Pathol; 2005 Oct;24(4):369-76
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  • [Title] Disappearance of steroid hormone dependency during malignant transformation of ovarian clear cell cancer.
  • Ovarian clear-cell carcinoma (OCCA) and ovarian endometrioid carcinoma (OEMC) are often associated with endometriosis.
  • Pathological progression from endometriosis to atypical endometriosis to carcinoma was identified in 4 of 22 OCCAs and 4 of 16 OEMCs.
  • A gradual reduction in ERalpha and PRA expression was observed with malignant transformation from endometriosis to atypical endometriosis to OCCA.
  • In OEMC, ERalpha expression increased with malignant transformation.
  • Disappearance of hormone dependency might therefore be associated with malignant transformation to OCCA.
  • [MeSH-major] Adenocarcinoma, Clear Cell / chemistry. Adenocarcinoma, Clear Cell / pathology. Ovarian Neoplasms / chemistry. Ovarian Neoplasms / pathology. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis
  • [MeSH-minor] Animals. Antibodies, Monoclonal. Cell Transformation, Neoplastic. Endometriosis / pathology. Estrogen Receptor alpha / analysis. Female. Humans. Immunohistochemistry. Ki-67 Antigen / analysis. Mice. Receptor, ErbB-2 / analysis. Tumor Suppressor Protein p53 / analysis

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  • (PMID = 16175084.001).
  • [ISSN] 0277-1691
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Estrogen Receptor alpha; 0 / Ki-67 Antigen; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / Tumor Suppressor Protein p53; 0 / progesterone receptor A; EC 2.7.10.1 / Receptor, ErbB-2
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85. Salonen J, Butzow R, Palvimo JJ, Heikinheimo M, Heikinheimo O: Oestrogen receptors and small nuclear ring finger protein 4 (RNF4) in malignant ovarian germ cell tumours. Mol Cell Endocrinol; 2009 Aug 13;307(1-2):205-10
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  • [Title] Oestrogen receptors and small nuclear ring finger protein 4 (RNF4) in malignant ovarian germ cell tumours.
  • The peak incidence of malignant ovarian germ cell tumours occurs soon after puberty.
  • While ERbeta and SNURF are down-regulated in testicular germ cell tumours, their role in the ovarian germ cell tumours remains unknown.
  • We herein studied the different subtypes of malignant ovarian germ cell tumours, and found that they all express ERalpha, ERbeta, and SNURF.
  • Our results suggest that oestrogen signalling has a role in malignant ovarian germ cell tumours.
  • [MeSH-major] Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / metabolism. Neoplasms, Germ Cell and Embryonal / metabolism. Nuclear Proteins / metabolism. Ovarian Neoplasms / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Adolescent. Adult. Cell Line, Tumor. Child. Estradiol / pharmacology. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunohistochemistry. Middle Aged. Oocytes / drug effects. Oocytes / metabolism. Ovary / cytology. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 19524139.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / RNF4 protein, human; 0 / Transcription Factors; 4TI98Z838E / Estradiol
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86. Najy AJ, Day KC, Day ML: ADAM15 supports prostate cancer metastasis by modulating tumor cell-endothelial cell interaction. Cancer Res; 2008 Feb 15;68(4):1092-9
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  • [Title] ADAM15 supports prostate cancer metastasis by modulating tumor cell-endothelial cell interaction.
  • Using human tumor and cDNA microarray technology, we have recently shown that the ADAM15 disintegrin is significantly overexpressed during the metastatic progression of human prostate cancer.
  • In the current study, we used lentiviral-based short hairpin RNA (shRNA) technology to down-regulate ADAM15 in the metastatic prostate cancer cell line, PC-3.
  • ADAM15 down-regulation dramatically attenuated many of the malignant characteristics of PC-3 cells in vitro and prevented the s.c. growth of PC-3 cells in severe combined immunodeficient (SCID) mice.
  • By inhibiting the expression of ADAM15 in PC-3 cells, we showed decreased cell migration and adhesion to specific extracellular matrix proteins.
  • This was accompanied by a reduction in the cleavage of N-cadherin by ADAM15 at the cell surface.
  • Fluorescence-activated cell sorting analysis revealed reduced cell surface expression of the metastasis-associated proteins alpha(v) integrin and CD44.
  • In an in vitro model of vascular invasion, loss of ADAM15 reduced PC-3 adhesion to, and migration through, vascular endothelial cell monolayers.
  • Taken together, these data strongly support a functional role for ADAM15 in prostate tumor cell interaction with vascular endothelium and the metastatic progression of human prostate cancer.
  • [MeSH-major] ADAM Proteins / physiology. Cell Communication / physiology. Endothelial Cells / pathology. Membrane Proteins / physiology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Animals. Antigens, CD44 / metabolism. Bone Neoplasms / secondary. Cell Adhesion / physiology. Cell Movement / physiology. Humans. Male. Matrix Metalloproteinase 9 / metabolism. Mice. Mice, SCID. Neoplasm Metastasis. RNA, Small Interfering / genetics

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  • [CommentIn] Future Oncol. 2008 Jun;4(3):351-4 [18518760.001]
  • (PMID = 18281484.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK56137
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Membrane Proteins; 0 / RNA, Small Interfering; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / ADAM15 protein, human; EC 3.4.24.35 / Matrix Metalloproteinase 9
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87. Cheng X, Shimizu I, Yuan Y, Wei M, Shen M, Huang H, Urata M, Sannomiya K, Fukuno H, Hashimoto-Tamaoki T, Ito S: Effects of estradiol and progesterone on tumor necrosis factor alpha-induced apoptosis in human hepatoma HuH-7 cells. Life Sci; 2006 Oct 19;79(21):1988-94
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  • [Title] Effects of estradiol and progesterone on tumor necrosis factor alpha-induced apoptosis in human hepatoma HuH-7 cells.
  • Preventing apoptosis may thereby induce a malignant transformation of liver tumor cells.
  • We examined the proapoptotic role of progesterone as well as the antiapoptotic role of E2 in human hepatoma HuH-7 cells in a state of early apoptosis induced by tumor necrosis factor (TNF) alpha.
  • The TNF alpha-induced ROS generation, lipid peroxidation, antioxidant enzyme consumption, a proapoptotic predominant expression of Bcl-2 family proteins, and a disruption of mitochondrial membrane potential were all inhibited by E2, and then they were further stimulated by progesterone in HuH-7 cells.
  • Treatment with the progesterone receptor antagonist RU486 led to the blockage of the progesterone-mediated responses to E2 pretreatment in TNF alpha-induced apoptosis.
  • These findings demonstrate that E2 inhibits the TNF alpha-induced early apoptosis in hepatoma cells, by suppressing the oxidative stress processes, whereas progesterone acts in a manner opposite from the effects of E2, and the inhibitory effects of E2 were blocked by progesterone, thus leading to the apoptosis of hepatoma cells.
  • [MeSH-major] Apoptosis / drug effects. Estradiol / pharmacology. Progesterone / pharmacology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Antioxidants / metabolism. Cell Line, Tumor. Drug Interactions. Estrogen Receptor alpha / biosynthesis. Estrogen Receptor beta / biosynthesis. Glutathione Peroxidase / metabolism. Humans. Intracellular Membranes / drug effects. Lipid Peroxidation / drug effects. Membrane Potentials / drug effects. Mitochondria / drug effects. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Reactive Oxygen Species / metabolism. Receptors, Progesterone / biosynthesis. Recombinant Proteins / pharmacology. Superoxide Dismutase / metabolism

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  • (PMID = 16860828.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antioxidants; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Reactive Oxygen Species; 0 / Receptors, Progesterone; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 4G7DS2Q64Y / Progesterone; 4TI98Z838E / Estradiol; EC 1.11.1.9 / Glutathione Peroxidase; EC 1.15.1.1 / Superoxide Dismutase
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88. Bricard G, Cesson V, Devevre E, Bouzourene H, Barbey C, Rufer N, Im JS, Alves PM, Martinet O, Halkic N, Cerottini JC, Romero P, Porcelli SA, Macdonald HR, Speiser DE: Enrichment of human CD4+ V(alpha)24/Vbeta11 invariant NKT cells in intrahepatic malignant tumors. J Immunol; 2009 Apr 15;182(8):5140-51
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  • [Title] Enrichment of human CD4+ V(alpha)24/Vbeta11 invariant NKT cells in intrahepatic malignant tumors.
  • Invariant NKT cells (iNKT cells) recognize glycolipid Ags via an invariant TCR alpha-chain and play a central role in various immune responses.
  • Although human CD4(+) and CD4(-) iNKT cell subsets both produce Th1 cytokines, the CD4(+) subset displays an enhanced ability to secrete Th2 cytokines and shows regulatory activity.
  • We performed an ex vivo analysis of blood, liver, and tumor iNKT cells from patients with hepatocellular carcinoma and metastases from uveal melanoma or colon carcinoma.
  • Frequencies of Valpha24/Vbeta11 iNKT cells were increased in tumors, especially in patients with hepatocellular carcinoma.
  • The proportions of CD4(+), double negative, and CD8alpha(+) iNKT cell subsets in the blood of patients were similar to those of healthy donors.
  • However, we consistently found that the proportion of CD4(+) iNKT cells increased gradually from blood to liver to tumor.
  • Furthermore, CD4(+) iNKT cell clones generated from healthy donors were functionally distinct from their CD4(-) counterparts, exhibiting higher Th2 cytokine production and lower cytolytic activity.
  • Thus, in the tumor microenvironment the iNKT cell repertoire is modified by the enrichment of CD4(+) iNKT cells, a subset able to generate Th2 cytokines that can inhibit the expansion of tumor Ag-specific CD8(+) T cells.
  • Because CD4(+) iNKT cells appear inefficient in tumor defense and may even favor tumor growth and recurrence, novel iNKT-targeted therapies should restore CD4(-) iNKT cells at the tumor site and specifically induce Th1 cytokine production from all iNKT cell subsets.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. Liver Neoplasms / immunology. Natural Killer T-Cells / immunology. Receptors, Antigen, T-Cell / immunology

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  • [CommentIn] Immunotherapy. 2009 Sep;1(5):733-6 [20636016.001]
  • (PMID = 19342695.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD1d; 0 / Antigens, CD3; 0 / CD1D protein, human; 0 / Receptors, Antigen, T-Cell
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89. Qian ZY, Miao Y, Dai CC, Xu ZK, Liu XL: [Combined multiple organ resection in 16 patients with adenocarcinoma of the body or tail of the pancreas]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao; 2005 Oct;27(5):572-4
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  • [Title] [Combined multiple organ resection in 16 patients with adenocarcinoma of the body or tail of the pancreas].
  • OBJECTIVE: To investigate the feasibility and therapeutic results of multiple organ resection in patients with tumor of the body and tail of pancreas.
  • METHODS: The clinical and pathological data were analysed in 16 consecutive patients with neoplasm of the body and tail of pancreas from 1999 to 2004 retrospectively.
  • RESULTS: Multiple organ resection was performed in 6 cases of primary pancreatic adenocarcinoma of the body and tail (3 cases of pancreatic cancer, 2 cases of malignant glucagonoma, and 1 case of well-differentiated pancreatic stromal sarcoma) and 10 cases of extrapancreatic malignancy (4 cases of gastric cancer, 2 cases of gastric leiomyosarcoma, 1 case of duodenal cancer, and 3 cases of colon cancer of hepatic flexure).
  • Patients with primary pancreatic cancer or pancreatic stromal sarcoma died within 1 year.
  • Two patients with malignant glucagonoma died 51 and 39 months later.
  • [MeSH-major] Adenocarcinoma / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery

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  • (PMID = 16274034.001).
  • [ISSN] 1000-503X
  • [Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
  • [ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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90. Yamini B, Yu X, Pytel P, Galanopoulos N, Rawlani V, Veerapong J, Bickenbach K, Weichselbaum RR: Adenovirally delivered tumor necrosis factor-alpha improves the antiglioma efficacy of concomitant radiation and temozolomide therapy. Clin Cancer Res; 2007 Oct 15;13(20):6217-23
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  • [Title] Adenovirally delivered tumor necrosis factor-alpha improves the antiglioma efficacy of concomitant radiation and temozolomide therapy.
  • PURPOSE: Treatment of malignant glioma involves concomitant temozolomide and ionizing radiation (IR).
  • This study was designed to evaluate if addition of Ad.Egr-tumor necrosis factor (TNF), a replication defective adenovector encoding a cDNA for TNF-alpha, to temozolomide and IR can improve overall antiglioma effect.
  • Pathologic examination shows that triple therapy leads to a complete response with formation of a collagenous scar.
  • CONCLUSION: This work shows that the addition of adenoviral TNF-alpha gene delivery to temozolomide and IR significantly improves antiglioma efficacy and illustrates a potential new treatment regimen for use in patients with malignant glioma.
  • [MeSH-major] Adenoviridae / metabolism. Antineoplastic Agents, Alkylating / administration & dosage. Brain Neoplasms / radiotherapy. Brain Neoplasms / therapy. Dacarbazine / analogs & derivatives. Gene Transfer Techniques. Glioma / radiotherapy. Glioma / therapy. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Combined Modality Therapy. DNA, Complementary / metabolism. Female. Genetic Therapy / methods. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Time Factors. Treatment Outcome

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  • (PMID = 17947489.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097247; United States / NCI NIH HHS / CA / R01 CA111423-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / DNA, Complementary; 0 / Tumor Necrosis Factor-alpha; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
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91. Murugaesu N, Schmid P, Dancey G, Agarwal R, Holden L, McNeish I, Savage PM, Newlands ES, Rustin GJ, Seckl MJ: Malignant ovarian germ cell tumors: identification of novel prognostic markers and long-term outcome after multimodality treatment. J Clin Oncol; 2006 Oct 20;24(30):4862-6
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  • [Title] Malignant ovarian germ cell tumors: identification of novel prognostic markers and long-term outcome after multimodality treatment.
  • PURPOSE: Malignant ovarian germ cell tumors are rare and knowledge about prognostic parameters currently is limited.
  • This study was undertaken to evaluate long-term outcome of patients with malignant ovarian germ cell tumors (MOGCTs) after chemotherapy and to assess prognostic parameters.
  • Univariate and multivariate analyses demonstrated that initial stage of disease (relative risk [RR], 5.96; 95% CI, 3.47 to 10.22; P = .03) and elevation of serum markers beta-human chorionic gonadotropin and alpha-fetoprotein (RR, 3.90; 95% CI, 1.40 to 10.9; P = .009) were significant predictors of overall survival, whereas age at diagnosis was of no prognostic value.
  • CONCLUSION: This is the first study to identify stage and tumor markers as prognostic parameters for patients with MOGCTs.
  • [MeSH-major] Biomarkers, Tumor / blood. Neoplasms, Germ Cell and Embryonal / blood. Neoplasms, Germ Cell and Embryonal / therapy. Ovarian Neoplasms / blood. Ovarian Neoplasms / therapy. alpha-Fetoproteins / analysis

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  • (PMID = 17050871.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / alpha-Fetoproteins
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92. Fujiwara S, Nakagawa K, Harada H, Nagato S, Furukawa K, Teraoka M, Seno T, Oka K, Iwata S, Ohnishi T: Silencing hypoxia-inducible factor-1alpha inhibits cell migration and invasion under hypoxic environment in malignant gliomas. Int J Oncol; 2007 Apr;30(4):793-802
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  • [Title] Silencing hypoxia-inducible factor-1alpha inhibits cell migration and invasion under hypoxic environment in malignant gliomas.
  • Malignant gliomas are characterized by active invasiveness, necrosis, and vascular proliferation.
  • Although many studies have described the relationship between tumor angiogenesis and hypoxic environment, the roles of HIF-1 in cell invasion have been barely elucidated in malignant gliomas.
  • Four malignant glioma cell lines, U87MG, U251MG, U373MG, and LN18, were cultured under 21 and 1% oxygen concentration.
  • Expression of HIF-1alpha under hypoxia was observed to be much higher than that under normoxia in all cell lines.
  • Introducing HIF-1alpha-targeted small interfering RNA (HIF-1alpha siRNA) into the glioma cell lines resulted in downregulation of HIF-1alpha expression, and significantly suppressed glioma cell migration in vitro.
  • In addition, under hypoxic conditions, the level of matrix metalloproteinase (MMP)-2 mRNA was upregulated, and that of tissue inhibitor of metalloproteinase (TIMP)-2 was downregulated in all glioma cell lines.
  • These findings suggest that overexpression of HIF-1alpha induced by hypoxic stress is an essential event in the activation of glioma cell motility through alteration of invasion-related molecules.
  • Targeting the HIF-1alpha molecule may be a novel therapeutic strategy for malignant gliomas.
  • [MeSH-major] Anoxia / metabolism. Brain Neoplasms / pathology. Cell Movement / genetics. Glioma / pathology. Hypoxia-Inducible Factor 1, alpha Subunit / antagonists & inhibitors

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  • (PMID = 17332917.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Small Interfering; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
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93. Bilandzic M, Chu S, Farnworth PG, Harrison C, Nicholls P, Wang Y, Escalona RM, Fuller PJ, Findlay JK, Stenvers KL: Loss of betaglycan contributes to the malignant properties of human granulosa tumor cells. Mol Endocrinol; 2009 Apr;23(4):539-48
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  • [Title] Loss of betaglycan contributes to the malignant properties of human granulosa tumor cells.
  • Previous studies have suggested that betaglycan acts as a tumor suppressor in certain human epithelial cancers.
  • However, the roles of betaglycan in ovarian granulosa cell tumors (GCTs) are poorly understood.
  • The objective of this study was to determine whether human GCTs exhibit betaglycan expression and, if so, what impact this receptor has on tumor biology.
  • Similarly, two human GCT cell lines, KGN and COV434, exhibited low betaglycan expression and poor responsiveness to TGFbeta and inhibin A in luciferase reporter assays, which was restored by stable transfection of wild-type betaglycan.
  • Expression of mutant forms of betaglycan that are defective in TGFbeta and/or inhibin binding in each GCT cell line revealed that the inhibitory effects of betaglycan on wound healing were most strongly linked to the inhibin-binding region of betaglycan.
  • [MeSH-major] Granulosa Cell Tumor / pathology. Ovarian Neoplasms / pathology. Proteoglycans / metabolism. Receptors, Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Activins / genetics. Activins / metabolism. Cell Adhesion / physiology. Cell Line, Tumor. Female. Gene Silencing. Humans. Inhibins / genetics. Inhibins / metabolism. Ligands. Neoplasm Invasiveness. Transforming Growth Factor beta / genetics. Transforming Growth Factor beta / metabolism

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  • (PMID = 19164448.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Proteoglycans; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; 0 / inhibin-alpha subunit; 104625-48-1 / Activins; 145170-29-2 / betaglycan; 57285-09-3 / Inhibins
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94. Anraku M, Tagawa T, Wu L, Yun Z, Keshavjee S, Zhang L, Johnston MR, de Perrot M: Synergistic antitumor effects of regulatory T cell blockade combined with pemetrexed in murine malignant mesothelioma. J Immunol; 2010 Jul 15;185(2):956-66
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  • [Title] Synergistic antitumor effects of regulatory T cell blockade combined with pemetrexed in murine malignant mesothelioma.
  • CD4(+)CD25(+) regulatory T cells (Tregs) can promote the growth of some tumors, but it is unknown whether this is true for all tumors, including malignant pleural mesothelioma.
  • We have previously shown that the existence of Tregs was associated with poor survival in patients with malignant pleural mesothelioma.
  • In this study, using an intrathoracic murine model of malignant mesothelioma (MM), we provide evidence suggesting that Treg blockade could enhance survival when combined with pemetrexed in established tumor.
  • AC29 murine MM cells were injected into the right pleural cavity of CBA mice for tumor development.
  • Four days after the tumor injection, tumor-bearing mice were then treated with pemetrexed alone, Treg blockade alone, or a combination of pemetrexed and Treg blockade.
  • The combination of Treg blockade and pemetrexed was associated with decreased tumor-infiltrating Tregs, increased IL-2 production, dendritic cell maturation, and increased CD3(+)CD8(+)IFN-gamma(+) tumor-infiltrating T cells when compared with mice treated with pemetrexed alone or Treg blockade alone.
  • Therefore, this study suggests that Treg blockade combined with pemetrexed can suppress mesothelioma growth in established tumor in vivo through an immune-mediated process.
  • This study also validates a new intrathoracic tumor model of pleural effusion to explore the role of antitumor immunity in murine MM.
  • [MeSH-minor] Animals. Antigens, CD4 / immunology. Antigens, CD8 / immunology. Cell Line, Tumor. Drug Synergism. Female. Glutamates / administration & dosage. Guanine / administration & dosage. Guanine / analogs & derivatives. Interleukin-2 Receptor alpha Subunit / immunology. Mice. Mice, Inbred BALB C. Mice, Inbred CBA. Mice, Inbred NOD. Mice, SCID. Pemetrexed. Survival Analysis. Treatment Outcome

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  • (PMID = 20548032.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Glutamates; 0 / Interleukin-2 Receptor alpha Subunit; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine
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95. Said HM, Staab A, Hagemann C, Vince GH, Katzer A, Flentje M, Vordermark D: Distinct patterns of hypoxic expression of carbonic anhydrase IX (CA IX) in human malignant glioma cell lines. J Neurooncol; 2007 Jan;81(1):27-38
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  • [Title] Distinct patterns of hypoxic expression of carbonic anhydrase IX (CA IX) in human malignant glioma cell lines.
  • The hypoxia-inducible enzyme carbonic anhydrase IX (CA IX) has recently been discussed as a surrogate marker of tumor hypoxia, an indicator of prognosis and a potential therapeutic target in malignant glioma.
  • To characterize patterns of expression of CA IX in human malignant glioma cells, we studied CA IX protein, CA9 mRNA and hypoxia-inducible factor-1alpha (HIF-1alpha) protein levels in U87-MG, U251, U373 and GaMG cells exposed to in vitro hypoxia (1, 6 or 24 h at 5%, 1% or 0.1% O(2)).
  • All cell lines displayed a strong hypoxic induction of CA9 mRNA in response to prolonged severe hypoxia with cell-line specific patterns at moderate to mild hypoxia and shorter treatment times.
  • In U251 and GaMG cell lines, a marked induction of CA IX protein in response to severe hypoxia was seen.
  • Therefore, immunohistochemical CA IX staining in human malignant glioma specimens can result from low oxygen concentrations or constitutive, oncogene-related, overexpression both of which may be prognostically relevant.
  • [MeSH-minor] Biomarkers, Tumor. Carbonic Anhydrase IX. Cell Line, Tumor. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Isoenzymes. RNA, Messenger / analysis

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  • (PMID = 16944313.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Isoenzymes; 0 / RNA, Messenger; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrase IX; EC 4.2.1.1 / Carbonic Anhydrases
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96. Yan B, Wang H, Rabbani ZN, Zhao Y, Li W, Yuan Y, Li F, Dewhirst MW, Li CY: Tumor necrosis factor-alpha is a potent endogenous mutagen that promotes cellular transformation. Cancer Res; 2006 Dec 15;66(24):11565-70
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  • [Title] Tumor necrosis factor-alpha is a potent endogenous mutagen that promotes cellular transformation.
  • Tumor necrosis factor-alpha (TNF-alpha) is an important inflammation cytokine without known direct effect on DNA.
  • In this study, we found that TNF-alpha can cause DNA damages through reactive oxygen species.
  • The mutagenic effect of TNF-alpha is comparable with that of ionizing radiation.
  • TNF-alpha treatment in cultured cells resulted in increased gene mutations, gene amplification, micronuclei formation, and chromosomal instability.
  • Antioxidants significantly reduced TNF-alpha-induced genetic damage.
  • TNF-alpha also induced oxidative stress and nucleotide damages in mouse tissues in vivo.
  • Moreover, TNF-alpha treatment alone led to increased malignant transformation of mouse embryo fibroblasts, which could be partially suppressed by antioxidants.
  • As TNF-alpha is involved in chronic inflammatory diseases, such as chronic hepatitis, ulcerative colitis, and chronic skin ulcers, and these diseases predispose the patients to cancer development, our results suggest a novel pathway through which TNF-alpha promotes cancer development through induction of gene mutations, in addition to the previously reported mechanisms, in which nuclear factor-kappaB activation was implicated.
  • [MeSH-major] Cell Transformation, Neoplastic. DNA Damage. Mutagens. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Colonic Neoplasms. Cytochalasin B / pharmacology. Fluoresceins. Gene Amplification. Humans. Mice. Mutation. Oxidative Stress / drug effects. Plasmids. Reactive Oxygen Species / metabolism


97. Elsawa SF, Novak AJ, Grote DM, Ziesmer SC, Witzig TE, Kyle RA, Dillon SR, Harder B, Gross JA, Ansell SM: B-lymphocyte stimulator (BLyS) stimulates immunoglobulin production and malignant B-cell growth in Waldenstrom macroglobulinemia. Blood; 2006 Apr 1;107(7):2882-8
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  • [Title] B-lymphocyte stimulator (BLyS) stimulates immunoglobulin production and malignant B-cell growth in Waldenstrom macroglobulinemia.
  • Waldenström macroglobulinemia (WM) is a serious and frequently fatal B-cell malignancy associated with an elevated monoclonal IgM protein in the serum.
  • B-lymphocyte stimulator (BLyS) is a TNF family member that is critical for maintenance of normal B-cell development and homeostasis.
  • BLyS is overexpressed in a variety of B-cell malignancies and has been shown to inhibit apoptosis in malignant B cells.
  • Malignant B cells were found to bind soluble BLyS and variably express the receptors BAFF-R, TACI, and BCMA.
  • BLyS, alone or in combination with cytokines that induce immunoglobulin production, was found to increase IgM secretion by malignant B cells.
  • Furthermore, BLyS was found to increase the viability and proliferation of malignant B cells from WM patients.

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  • (PMID = 16304043.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA92104; United States / NCI NIH HHS / CA / CA97274
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell Activating Factor; 0 / Immunoglobulins; 0 / Membrane Proteins; 0 / TNFSF13B protein, human; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC1895377
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98. Park CK, Kim JH, Moon MJ, Jung JH, Lim SY, Park SH, Kim JH, Kim DG, Jung HW, Cho BK, Paek SH: Investigation of molecular factors associated with malignant transformation of oligodendroglioma by proteomic study of a single case of rapid tumor progression. J Cancer Res Clin Oncol; 2008 Feb;134(2):255-62
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  • [Title] Investigation of molecular factors associated with malignant transformation of oligodendroglioma by proteomic study of a single case of rapid tumor progression.
  • PURPOSE: Frozen tumor tissues from a patient who showed rapid progression to anaplastic oligodendroglioma after near total resection of oligodendroglioma were used to examine differential expression of proteins to gain better understanding of the pathogenesis of malignant transformation.
  • RESULTS: Among 23 differentially expressed spots, overexpression of peroxiredoxin 6 and underexpression of rho GDP dissociation inhibitor alpha were confirmed to be valid after western blot and immunocytochemical analysis of oligodendroglioma tissue.
  • CONCLUSIONS: Abnormal expression of peroxiredoxin 6 and rho GDP dissociation inhibitor alpha may be associated with malignant transformation in oligodendroglioma and these proteins might be candidates of molecular predictive factors.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Cell Transformation, Neoplastic. Neoplasm Proteins / metabolism. Oligodendroglioma / metabolism

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  • (PMID = 17653765.001).
  • [ISSN] 1432-1335
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Guanine Nucleotide Dissociation Inhibitors; 0 / Neoplasm Proteins; 0 / rho-Specific Guanine Nucleotide Dissociation Inhibitors; EC 1.11.1.15 / PRDX6 protein, human; EC 1.11.1.15 / Peroxiredoxin VI
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99. Granata OM, Cocciadiferro L, Miceli V, Polito LM, Campisi I, Carruba G: Metabolic profiles of androgens in malignant human liver cell lines. Ann N Y Acad Sci; 2006 Nov;1089:262-7
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  • [Title] Metabolic profiles of androgens in malignant human liver cell lines.
  • In this study we have investigated androgen (testosterone and androstenedione) metabolism in malignant HepG2, Huh-7, and HA22T human liver cell lines.
  • [MeSH-minor] Androgens / metabolism. Aromatase / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Sulfotransferases / metabolism

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  • (PMID = 17261773.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Estrogens; 3XMK78S47O / Testosterone; 409J2J96VR / Androstenedione; EC 1.14.14.1 / Aromatase; EC 2.8.2.- / Sulfotransferases; EC 2.8.2.- / ethinylestradiol-17 alpha sulfotransferase
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100. Wenke AK, Kjellman C, Lundgren-Akerlund E, Uhlmann C, Haass NK, Herlyn M, Bosserhoff AK: Expression of integrin alpha10 is induced in malignant melanoma. Cell Oncol; 2007;29(5):373-86
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  • [Title] Expression of integrin alpha10 is induced in malignant melanoma.
  • However, by array studies we detected integrin alpha10 also to be upregulated in malignant melanoma compared to primary melanocytes.
  • Subsequent analysis of melanoma cell lines and melanoma tumor samples confirmed this finding.
  • Proliferation assays and colony forming assays revealed no differences comparing antisense integrin alpha10 cell clones with control and wild type melanoma cells, respectively.
  • However, antisense integrin alpha10 cell clones and Mel Im cells treated with an inhibitory antibody against integrin alpha10 showed a reduced migratory potential.
  • In summary, these data indicate that AP-2 and Ets-1 regulated expression of integrin alpha10 plays a role in migration of malignant melanoma cells.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Integrin alpha Chains / genetics. Integrin alpha Chains / metabolism. Melanoma / genetics. Melanoma / metabolism
  • [MeSH-minor] Cell Adhesion. Cell Line, Tumor. Cell Movement. Clone Cells. Humans. Melanocytes / metabolism. Neoplasm Invasiveness. Promoter Regions, Genetic / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Transcription, Genetic

  • MedlinePlus Health Information. consumer health - Melanoma.
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  • (PMID = 17726260.001).
  • [ISSN] 1570-5870
  • [Journal-full-title] Cellular oncology : the official journal of the International Society for Cellular Oncology
  • [ISO-abbreviation] Cell. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Integrin alpha Chains; 0 / RNA, Messenger; 0 / integrin alpha 10
  • [Other-IDs] NLM/ PMC4617990
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