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  1. Article: Inflammation-associated regulation of the macrophage inhibitory cytokine (MIC-1) gene in prostate cancer.

    Dubey, Seema / Vanveldhuizen, Peter / Holzbeierlein, Jeffrey / Tawfik, Ossama / Thrasher, J Brantley / Karan, Dev

    Oncology letters

    2012  Volume 3, Issue 5, Page(s) 1166–1170

    Abstract: Macrophage inhibitory cytokine-1 (MIC-1), also known as prostate-derived factor (PDF), is a molecule of the TGF-β superfamily and has been associated with the progression of various types of diseases including prostate cancer. Initially identified from ... ...

    Abstract Macrophage inhibitory cytokine-1 (MIC-1), also known as prostate-derived factor (PDF), is a molecule of the TGF-β superfamily and has been associated with the progression of various types of diseases including prostate cancer. Initially identified from activated macrophages, the MIC-1 gene may provide a potential link between inflammation and prostate cancer. In this context, we performed MIC-1 expression analysis using mouse prostate tissues to determine whether there was any correlation with age and inflammation. Reverse transcription PCR analysis on RNA samples isolated from prostate lobes from prostate-specific antigen transgenic mice of varying ages revealed that MIC-1 gene expression is extremely low to non-detectable in the prostate tissues obtained from young mice, while its expression increases in the prostate tissues harvested from elderly mice. Increased MIC-1 gene expression in the mouse prostate was found to be associated with an increased level of infiltrating lymphocytes. To confirm this observation, we showed that inflammation-associated cytokines (IL-1β and TNF-α) significantly upregulate the secretion of the MIC-1 protein in a human prostate cancer cell line (LNCaP cells), while cytokines IL-6 and granulocyte macrophage colony-stimulating factor were less effective. Taken together, these data indicated that inflammation-associated cytokines may play a critical role in the functional regulation of the MIC-1 gene in the early stages of prostate cancer development. More studies are required to understand the biological activity of MIC-1 gene regulation in the development and progression of prostate cancer.
    Language English
    Publishing date 2012-03-06
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 2573196-8
    ISSN 1792-1082 ; 1792-1074
    ISSN (online) 1792-1082
    ISSN 1792-1074
    DOI 10.3892/ol.2012.635
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Biclonal post-transplant B-cell lymphoma: report of a case with two distinct cell populations, XX,t(14;18) and XY,t(11;14).

    Dennis, Katie L / Wallentine, Steven L / Vanveldhuizen, Peter J / Persons, Diane L / Mathur, Sharad C

    Cancer genetics and cytogenetics

    2007  Volume 173, Issue 2, Page(s) 150–153

    Abstract: Lymphoproliferative disorders are more likely to occur in transplant patients compared to the general population. Typically in these patients, lymphomas occur within 6-10 months following transplant and are Epstein-Barr virus (EBV) positive. We report a ... ...

    Abstract Lymphoproliferative disorders are more likely to occur in transplant patients compared to the general population. Typically in these patients, lymphomas occur within 6-10 months following transplant and are Epstein-Barr virus (EBV) positive. We report a biclonal apparently EBV negative lymphoma occurring in a patient ten years after renal transplant, with karyotypes XX,t(14;18) and XY,t(11;14). Though the biclonal populations also had different sex chromosome compositions, complete evaluation showed that both clones most likely evolved from the patient's native lymphocytes.
    MeSH term(s) Aged ; Chromosomes, Human, Pair 11 ; Chromosomes, Human, Pair 14 ; Chromosomes, Human, Pair 18 ; Chromosomes, Human, X ; Chromosomes, Human, Y ; Clone Cells/metabolism ; Clone Cells/pathology ; Humans ; In Situ Hybridization, Fluorescence ; Karyotyping ; Kidney Transplantation ; Lymphoma, B-Cell/genetics ; Lymphoma, B-Cell/pathology ; Male ; Sex Chromosome Aberrations ; Translocation, Genetic
    Language English
    Publishing date 2007-03
    Publishing country United States
    Document type Case Reports ; Journal Article
    ZDB-ID 800806-1
    ISSN 1873-4456 ; 0165-4608
    ISSN (online) 1873-4456
    ISSN 0165-4608
    DOI 10.1016/j.cancergencyto.2006.09.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1521: Show issues Location:
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  3. Article ; Online: Leiomyosarcoma of the inferior vena cava: a case report and review of the literature.

    Reddy, Venkataprasanth P / Vanveldhuizen, Peter J / Muehlebach, Gregory F / Dusing, Reginald W / Birkbeck, James P / Williamson, Stephen K / Krishnan, Leela / Meyers, David G

    Cases journal

    2010  Volume 3, Page(s) 71

    Abstract: A 68-year-old white female presented with two years of progressively worsening dyspnea. Echocardiography revealed a large right atrial mass and partial obstruction of the inferior vena cava. Further imaging revealed a cystic dense mass in the inferior ... ...

    Abstract A 68-year-old white female presented with two years of progressively worsening dyspnea. Echocardiography revealed a large right atrial mass and partial obstruction of the inferior vena cava. Further imaging revealed a cystic dense mass in the inferior vena cava and right atrium. Immunohistochemical stains were consistent with leiomyosarcoma. Intraoperatively, the tumor was noted to originate from the posterior aspect of the inferior vena cava. The patient underwent successful resection of the mass. Adjuvant radiation therapy was completed. The patient's dyspnea gradually improved and she continues to remain disease free five years post-resection.
    Language English
    Publishing date 2010-02-23
    Publishing country England
    Document type Journal Article
    ZDB-ID 2431132-7
    ISSN 1757-1626 ; 1757-1626
    ISSN (online) 1757-1626
    ISSN 1757-1626
    DOI 10.1186/1757-1626-3-71
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Gain of oncogenic function of p53 mutants induces invasive phenotypes in human breast cancer cells by silencing CCN5/WISP-2.

    Dhar, Gopal / Banerjee, Snigdha / Dhar, Kakali / Tawfik, Ossama / Mayo, Matthew S / Vanveldhuizen, Peter J / Banerjee, Sushanta K

    Cancer research

    2008  Volume 68, Issue 12, Page(s) 4580–4587

    Abstract: CCN5/WISP-2 is overexpressed in noninvasive breast cancer cells and tissue samples, whereas its expression is minimal or undetected in invasive conditions. CCN5/WISP-2 has been considered as an antiinvasive gene because CCN5/WISP-2 silencing augments the ...

    Abstract CCN5/WISP-2 is overexpressed in noninvasive breast cancer cells and tissue samples, whereas its expression is minimal or undetected in invasive conditions. CCN5/WISP-2 has been considered as an antiinvasive gene because CCN5/WISP-2 silencing augments the invasive phenotypes in vitro. However, the mechanism of silencing of CCN5 during the progression of the disease has been elusive. Because p53 mutations are associated with breast cancer progression and have been shown to correlate inversely with CCN5/WISP-2 expression in other cancer cell types, the objective of this study was to explore whether p53 mutants suppress CCN5 expression in breast tumor cells resulting in the progression of this disease. We found CCN5 expression is inversely correlated with the mutational activation of p53 in human breast tumor cells. The ectopic expression of p53 mutants in ER-positive noninvasive breast tumor cells silenced the CCN5/WISP-2 expression and enhanced invasive phenotypes, including the induction of morphologic changes from the epithelial-to-mesenchymal type along with the alterations of hallmark proteins of these cell types and an augmentation of the migration of these cells. The suppression of CCN5 by the p53 mutants can be nullified by estrogen signaling in these cells through the transcriptional activation of the CCN5 gene. Moreover, the invasive changes can be imitated by blocking the CCN5/WISP-2 expression through RNA interference or can be reversed by the addition of CCN5/WISP-2 recombinant protein in the culture. Thus, these studies suggest that CCN5 inactivation could be an essential molecular event for p53 mutant-induced invasive phenotypes.
    MeSH term(s) Blotting, Western ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; CCN Intercellular Signaling Proteins ; Carcinoma, Intraductal, Noninfiltrating/genetics ; Carcinoma, Intraductal, Noninfiltrating/metabolism ; Carcinoma, Intraductal, Noninfiltrating/pathology ; Cell Differentiation ; Cell Movement ; Chloramphenicol O-Acetyltransferase/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Intercellular Signaling Peptides and Proteins/genetics ; Intercellular Signaling Peptides and Proteins/metabolism ; Mutation/genetics ; Neoplasm Invasiveness ; Phenotype ; Promoter Regions, Genetic ; RNA Interference ; Receptors, Estrogen/metabolism ; Repressor Proteins ; Signal Transduction ; Transcription Factors/antagonists & inhibitors ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transfection ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances CCN Intercellular Signaling Proteins ; CCN5 protein, human ; Intercellular Signaling Peptides and Proteins ; Receptors, Estrogen ; Repressor Proteins ; Transcription Factors ; Tumor Suppressor Protein p53 ; Chloramphenicol O-Acetyltransferase (EC 2.3.1.28)
    Language English
    Publishing date 2008-06-16
    Publishing country United States
    Document 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.
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-08-0316
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.135/5: Show issues Location:
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  5. Article ; Online: 2-methoxyestradiol inhibits Barrett's esophageal adenocarcinoma growth and differentiation through differential regulation of the beta-catenin-E-cadherin axis.

    Kambhampati, Suman / Banerjee, Snigdha / Dhar, Kakali / Mehta, Smita / Haque, Inamul / Dhar, Gopal / Majumder, Monami / Ray, Gibanananda / Vanveldhuizen, Peter J / Banerjee, Sushanta K

    Molecular cancer therapeutics

    2010  Volume 9, Issue 3, Page(s) 523–534

    Abstract: The purpose of this study was to evaluate whether 2-methoxyestradiol (2-ME(2)), a promising anticancer agent, modulates Barrett's esophageal adenocarcinoma (BEAC) cell growth and behavior through a cellular pathway involving beta-catenin in partnership ... ...

    Abstract The purpose of this study was to evaluate whether 2-methoxyestradiol (2-ME(2)), a promising anticancer agent, modulates Barrett's esophageal adenocarcinoma (BEAC) cell growth and behavior through a cellular pathway involving beta-catenin in partnership with E-cadherin, which seems to play a critical role in the induction of antitumor responses in cancer cells. We found that 2-ME(2) markedly reduced the BEAC cell proliferation through regulating apoptotic machinery such as Bcl-2 and Bax. It may nullify the aggressive behavior of the cells by reducing the migratory behavior. Expressions of beta-catenin and E-cadherin and binding of these two proteins is activated in a 2-ME(2)-dependent fashion in Bic-1 cells. Moreover, overexpressions of these two proteins may be due to the stabilization of these proteins by 2-ME(2). We found that 2-ME(2)-induced antimigratory effects are mediated through the beta-catenin-E-cadherin signaling pathways. In view of these results, we determined whether 2-ME(2) reduces BEAC tumor growth. Administration of 2-ME2 significantly decreased the growth of BEAC cells xenografted on the flank of nude mice. The evidence presented points out that the effect of 2-ME(2) on beta-catenin-orchestrated signal transduction plausibly plays a multifaceted functional role to inhibit the proliferation and cell migration of 2-ME(2)-treated malignant cells and it could be a potential candidate in novel treatment strategies for Barrett's esophageal adenocarcinoma.
    MeSH term(s) 2-Methoxyestradiol ; Adenocarcinoma/drug therapy ; Adenocarcinoma/metabolism ; Adenocarcinoma/pathology ; Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Barrett Esophagus/drug therapy ; Barrett Esophagus/metabolism ; Barrett Esophagus/pathology ; Cadherins/metabolism ; Cadherins/physiology ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Cell Transformation, Neoplastic ; Esophageal Neoplasms/drug therapy ; Esophageal Neoplasms/metabolism ; Esophageal Neoplasms/pathology ; Estradiol/analogs & derivatives ; Estradiol/pharmacology ; Estradiol/therapeutic use ; Female ; Humans ; Male ; Mice ; Mice, Nude ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays ; beta Catenin/metabolism ; beta Catenin/physiology
    Chemical Substances Antineoplastic Agents ; Cadherins ; beta Catenin ; Estradiol (4TI98Z838E) ; 2-Methoxyestradiol (6I2QW73SR5)
    Language English
    Publishing date 2010-03-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2063563-1
    ISSN 1538-8514 ; 1535-7163
    ISSN (online) 1538-8514
    ISSN 1535-7163
    DOI 10.1158/1535-7163.MCT-09-0845
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5750: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  6. Article ; Online: The use of zoledronic acid in men receiving androgen deprivation therapy for prostate cancer with severe osteopenia or osteoporosis.

    Campbell, Steven C / Bhoopalam, Nirmala / Moritz, Thomas E / Pandya, Mona / Iyer, Padmini / Vanveldhuizen, Peter / Ellis, Nancy K / Thottapurathu, Lizy / Garewal, Harinder / Warren, Stuart R / Friedman, Nicholas / Reda, Domenic J

    Urology

    2010  Volume 75, Issue 5, Page(s) 1138–1143

    Abstract: Objectives: To study the effect of zoledronic acid on patients with pre-existing osteoporosis on androgen deprivation therapy (ADT), who are at highest risk for fracture. Zoledronic acid is a potent bisphosphonate that can prevent osteoporosis in ... ...

    Abstract Objectives: To study the effect of zoledronic acid on patients with pre-existing osteoporosis on androgen deprivation therapy (ADT), who are at highest risk for fracture. Zoledronic acid is a potent bisphosphonate that can prevent osteoporosis in patients with nonmetastatic (M0), prostate cancer (CaP) who are initiating ADT. The effect of zoledronic acid on patients with pre-existing osteoporosis on ADT, who are highest risk for fracture, has not been adequately studied.
    Methods: We enrolled 28 patients with M0 CaP on ADT with severe osteopenia or osteoporosis (baseline bone-mineral density (BMD) T score < -2.0) in this open-label, single-arm trial to assess the effect of zoledronic acid on BMD. All patients also received supplemental calcium and vitamin D, and were counseled about lifestyle modifications. Patients received zoledronic acid (4 mg) intravenously every 3 months for 4 treatments. BMD was measured by dual energy X-ray absorptiometry scan at enrollment, 6 and 12 months. Primary endpoint was percent change in lumbar spine BMD.
    Results: This was a high-risk patient population-primarily older Caucasians (mean age, 73 years), former smokers, and moderate users of alcohol. Mean duration of ADT was 2.4 years. Pre-existing osteopenia or osteoporosis was observed in a single site in 9 patients and multiple sites in 19 (68%). After 12 months of zoledronic acid, lumbar spine BMD increased 4.17% (P < .0001), and BMD increased significantly (P < .05) in both hips and the right femoral neck. Seven patients (25%) experienced improved BMD into the nonosteoporotic range (T score > -2.0). Zoledronic acid infusion was well tolerated and without substantial renal toxicity.
    Conclusions: Zoledronic acid improves BMD in men with M0 CaP on ADT with severe osteopenia or osteoporosis (T scores < 2.0). This novel finding identifies a high-risk patient population that can potentially benefit from bisphosphonate therapy.
    MeSH term(s) Aged ; Androgen Antagonists/therapeutic use ; Bone Density Conservation Agents/therapeutic use ; Bone Diseases, Metabolic/etiology ; Bone Diseases, Metabolic/prevention & control ; Diphosphonates/therapeutic use ; Gonadotropin-Releasing Hormone/analogs & derivatives ; Humans ; Imidazoles/therapeutic use ; Male ; Orchiectomy ; Osteoporosis/etiology ; Osteoporosis/prevention & control ; Prostatic Neoplasms/therapy ; Severity of Illness Index
    Chemical Substances Androgen Antagonists ; Bone Density Conservation Agents ; Diphosphonates ; Imidazoles ; Gonadotropin-Releasing Hormone (33515-09-2) ; zoledronic acid (6XC1PAD3KF)
    Language English
    Publishing date 2010-05
    Publishing country United States
    Document type Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov't
    ZDB-ID 192062-5
    ISSN 1527-9995 ; 0090-4295
    ISSN (online) 1527-9995
    ISSN 0090-4295
    DOI 10.1016/j.urology.2009.11.083
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1142: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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    Zs.MO 275: Show issues

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  7. Article: Differential expression of neuropilin-1 in malignant and benign prostatic stromal tissue.

    Vanveldhuizen, Peter J / Zulfiqar, Muhammad / Banerjee, Snigdha / Cherian, Rachel / Saxena, Neela K / Rabe, Amy / Thrasher, J Brantley / Banerjee, Sushanta K

    Oncology reports

    2003  Volume 10, Issue 5, Page(s) 1067–1071

    Abstract: Neuropilin-1 (NRP-1), a co-receptor for VEGF165, is overexpressed in various prostate cancer cell lines and in advanced prostate tumors. However, distribution of the NRP-1 in prostate tumors has not yet been evaluated. Using immunohistochemical analysis, ...

    Abstract Neuropilin-1 (NRP-1), a co-receptor for VEGF165, is overexpressed in various prostate cancer cell lines and in advanced prostate tumors. However, distribution of the NRP-1 in prostate tumors has not yet been evaluated. Using immunohistochemical analysis, we evaluated 21 archival prostate tumors and 5 benign glands for the expression of NRP-1. In addition, we utilized a quantitative RT-PCR method to examine mRNA expression in 9 additional prostate tumors obtained from radical prostatectomy specimens and compared this expression to the adjacent normal tissue. The RT-PCR analyses demonstrated overexpression of NRP-1 mRNA in malignant tissue samples by 10.0-fold as compared to adjacent normal tissue. By immunohistochemistry, NRP-1 protein was undetected or minimally detected in the epithelial tumor cells. However, NRP-1 immuno-reaction was detected in the surrounding tumor stroma. Variable immuno-reaction for NRP-1 was also seen in the adjacent normal tumor stroma and the stroma of the benign prostate samples. These observations suggest that neuropilin-1 is expressed in the prostatic stromal cells, not epithelial tumor cells, and this expression is significantly increased in the malignant phenotype.
    MeSH term(s) Aged ; Cell Line, Tumor ; DNA, Complementary/metabolism ; Epithelial Cells/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Neuropilin-1/biosynthesis ; Neuropilin-1/chemistry ; Neuropilin-1/metabolism ; Phenotype ; Prostate/metabolism ; Prostatic Neoplasms/metabolism ; RNA, Messenger/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Stromal Cells/metabolism
    Chemical Substances DNA, Complementary ; RNA, Messenger ; Neuropilin-1 (144713-63-3)
    Language English
    Publishing date 2003-09
    Publishing country Greece
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1222484-4
    ISSN 1791-2431 ; 1021-335X
    ISSN (online) 1791-2431
    ISSN 1021-335X
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4213: Show issues Location:
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