Malik, Ihtzaz Ahmed

[["dc.bibliographiccitation.artnumber","257"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Cancer"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Bosio, Patrizia"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Malik, Ihtzaz A."],["dc.date.accessioned","2019-07-09T11:45:17Z"],["dc.date.available","2019-07-09T11:45:17Z"],["dc.date.issued","2018"],["dc.description.abstract","BACKGROUND: After orthotopic liver transplantation (OLT) for hepatocellular carcinoma (HCC), recurrent HCC mostly develops within 2 years. All cases of de novo HCC described so far occurred later than 2 years after OLT. Prevention of post-transplantation HCC has usually been tried to achieve by curing or controlling recurrent liver disease. This has been rationale for treatment with interferon (IFN)/ribavirin of HCV-recurrence in patients after OLT, transplanted for advanced HCV-induced liver disease and/or HCC. The availability of new and more efficient drugs has improved chances also for previously difficult-to-treat HCV-positive patients. CASE PRESENTATION: A 75 year-old male patient who had undergone OLT for decompensated HCV-cirrhosis in 2009, and bilio-digestive surgery in 2011 under tracrolimus (0.5 mg/day) and prednisone (5 mg/day) immunosuppressive therapy, started to receive antiviral treatment for recurrent HCV-infection of graft with 200 mg/day ribavirin in combination with ledipasvir and sofosbuvir by the end of October 2015. Because of multiple side effects (anemia, asthenia, infections, and reduction of kidney functions - palliated by treatment with erythropoietin), treatment was stopped after 16 weeks. At the third control, a minimal increase in alpha-fetoprotein (AFP) serum level to 10 μg/L was measured 8 months after therapy, whereas both liver sonography and serum transaminases were normal. The patient's general condition; however, remained poor, and a magnetic resonance imaging (MRI) of abdomen was performed 2 months later. A nodule of 3 cm in diameter with a pseudocapsule was found centrally in the liver. The patient had to be hospitalized for recurrent infections of the lung, overt ascites and peritonitis. Rapid tumor growth (10 cm) was detected during last stay in hospital (April 2017), concomitant with a rise of AFP-serum levels to 91 μg/L. The family decided to take the patient home, and best supportive care was provided by a general practitioner, local nurses and the patient's dedicated wife until his death. CONCLUSION: Before treating OLT patients with HCV graft reinfection one should not only consider possible advantages of newly effective antiviral-therapies, but also life expectancy and possible side effects (difficult to manage at an outpatient service basis), including severe disadvantages such as the development of HCC."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2018"],["dc.identifier.doi","10.1186/s12885-018-4175-2"],["dc.identifier.pmid","29510685"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15129"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15090"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59200"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1471-2407"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Case report: 8 years after liver transplantation: de novo hepatocellular carcinoma 8 months after HCV clearance through IFN-free antiviral therapy."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1801"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","1815"],["dc.bibliographiccitation.volume","176"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Dudas, Jozsef"],["dc.contributor.author","Mansuroglu, Tuemen"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T08:44:15Z"],["dc.date.available","2018-11-07T08:44:15Z"],["dc.date.issued","2010"],["dc.description.abstract","Liver damage is a serious clinical complication of gamma-irradiation. We therefore exposed rats to single-dose gamma-irradiation (25 Gy) that was focused on the liver. Three to six hours after irradiation, an increased number of neutrophils (but not mononuclear phagocytes) was observed by immunohistochemistry to be attached to portal vessels between and around the portal (myo)fibroblasts (smooth muscle actin and Thy-1(+) cells). MCP-1/CCL2 staining was also detected in the portal vessel walls, including some cells of the portal area. CC-chemokine (MCP-1/CCL2 and MCP-3/CCL7) and CXC-chemokine (KC/CXCL1, MIP-2/CXCL2, and LIX/CXCL5) gene expression was significantly induced in total RNA from irradiated livers. In laser capture microdissected samples, an early (1 to 3 hours) up-regulation of CCL2, CXCL1, CXCL8, and CXCR2 gene expression was detected in the portal area but not in the parenchyma; with the exception of CXCL1 gene expression. In addition, treatment with an antibody against MCP-1/CCL2 before irradiation led to an increase in gene expression of interferon-gamma and IP-10/CXCL10 in liver tissue without influencing the recruitment of granulocytes. Indeed, the CCL2, CXCL1, CXCL2, and CXCL5 genes were strongly expressed and further up-regulated in liver (myo)fibroblasts after irradiation (8 Gy). Taken together, these results suggest that gamma-irradiation of the liver induces a transient accumulation of granulocytes within the portal area and that (myo)fibroblasts of the portal vessels may be one of the major sources of the chemokines involved in neutrophil recruitment. Moreover, inhibition of more than one chemokine (eg, CXCL1 and CXCL8) may be necessary to reduce leukocytes recruitment. (Am J Pathol 2010, 176:1801-1815; DOI. 10.2353/ajpath.2010.090505)"],["dc.description.sponsorship","Deutsche Krebshilfe [108774]; Bundesamt fur Strahlenschutz [StSch4546]"],["dc.identifier.doi","10.2353/ajpath.2010.090505"],["dc.identifier.isi","000276471500027"],["dc.identifier.pmid","20185578"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6274"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20155"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Investigative Pathology, Inc"],["dc.relation.issn","0002-9440"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Single-Dose Gamma-Irradiation Induces Up-Regulation of Chemokine Gene Expression and Recruitment of Granulocytes into the Portal Area but Not into Other Regions of Rat Hepatic Tissue"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","353106"],["dc.bibliographiccitation.journal","BioMed Research International"],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Cameron, Silke"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Rave-Fraenk, Margret"],["dc.contributor.author","Christiansen, Hans"],["dc.contributor.author","Hess, Clemens Friedrich"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.date.accessioned","2018-11-07T09:29:26Z"],["dc.date.available","2018-11-07T09:29:26Z"],["dc.date.issued","2013"],["dc.description.abstract","The current study aimed to investigate radiation-induced regulation of iron proteins including ferritin subunits in rats. Rat livers were selectively irradiated in vivo at 25 Gy. This dose can be used to model radiation effects to the liver without inducing overt radiation-induced liver disease. Sham-irradiated rats served as controls. Isolated hepatocytes were irradiated at 8 Gy. Ferritin light polypeptide (FTL) was detectable in the serum of sham-irradiated rats with an increase after irradiation. Liver irradiation increased hepatic protein expression of both ferritin subunits. A rather early increase (3 h) was observed for hepatic TfR1 and Fpn-1 followed by a decrease at 12 h. The increase in TfR2 persisted over the observed time. Parallel to the elevation of AST levels, a significant increase (24 h) in hepatic iron content was measured. Complete blood count analysis showed a significant decrease in leukocyte number with an early increase in neutrophil granulocytes and a decrease in lymphocytes. In vitro, a significant increase in ferritin subunits at mRNA level was detected after irradiation which was further induced with a combination treatment of irradiation and acute phase cytokine. Irradiation can directly alter the expression of ferritin subunits and this response can be strongly influenced by radiation-induced proinflammatory cytokines. FTL can be used as a serum marker for early phase radiation-induced liver damage."],["dc.description.sponsorship","DFG [MA-5488/2-1]"],["dc.identifier.doi","10.1155/2013/353106"],["dc.identifier.isi","000328832300001"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10734"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31028"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Hindawi Publishing Corporation"],["dc.relation.issn","2314-6141"],["dc.relation.issn","2314-6133"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Differential Regulation of Ferritin Subunits and Iron Transport Proteins: An Effect of Targeted Hepatic X-Irradiation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","261"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell and Tissue Research"],["dc.bibliographiccitation.lastpage","272"],["dc.bibliographiccitation.volume","342"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Baumgartner, Bernhard G."],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T08:37:22Z"],["dc.date.available","2018-11-07T08:37:22Z"],["dc.date.issued","2010"],["dc.description.abstract","Non-thyroidal illness is characterized by low triiodothyronine (T3) serum level under acute-phase conditions. We studied hepatic gene expression of the newly identified thyroid hormone receptor (TR) cofactor DOR/TP53INP2 together with TRs in a rat model of aseptic abscesses induced by injecting intramuscular turpentine-oil into each hind limb. A fast (4-6 h) decrease in the serum level of free thyroxine and free T3 was observed. By immunohistology, abundant DOR protein expression was detected in the nuclei of hepatocytes and ED-1(+) (mononuclear phagocytes), CK-19(+) (biliary cells), and SMA(+) (mesenchymal cells of the portal tract) cells. DOR signal was reduced with a minimum at 6-12 h after the acute-phase reaction (APR). Immunohistology also showed a similar pattern of protein expression in TR alpha 1 but without a significant change during APR. Transcripts specific for DOR, nuclear receptor corepressor 1 (NCoR-1), and TR beta 1 were down-regulated with a minimum at 6-12 h, whereas expression for TR alpha 1 and TR alpha 2 was slightly and significantly up-regulated, respectively, with a maximum at 24 h after APR was initiated. In cultured hepatocytes, acute-phase cytokines interleukin-1 beta (1L-1 beta) and IL-6 down-regulated DOR and TR beta 1 at the mRNA level. Moreover, gene expression of DOR and TRs (TR alpha 1, TR alpha 2, and TR beta 1) was up-regulated in hepatocytes by adding 13 to the culture medium; this upregulation was almost completely blocked by treating the cells with IL-6. Thus, TR beta 1, NCoR-1, and the recently identified DOR/TP53INP2 are abundantly expressed and down-regulated in liver cells during APR. Their downregulation is attributable to the decreased serum level of thyroid hormones and most probably also to the direct action of the main acute-phase cytokines."],["dc.identifier.doi","10.1007/s00441-010-1067-4"],["dc.identifier.isi","000284665200012"],["dc.identifier.pmid","20949361"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5980"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18515"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-0878"],["dc.relation.issn","0302-766X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Changes in gene expression of DOR and other thyroid hormone receptors in rat liver during acute-phase response"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","299"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell and Tissue Research"],["dc.bibliographiccitation.lastpage","312"],["dc.bibliographiccitation.volume","344"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Sheikh, Nadeem"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2018-11-07T08:56:30Z"],["dc.date.available","2018-11-07T08:56:30Z"],["dc.date.issued","2011"],["dc.description.abstract","The \"acute phase\" is clinically characterized by homeostatic alterations such as somnolence, adinamia, fever, muscular weakness, and leukocytosis. Dramatic changes in iron metabolism are observed under acute-phase conditions. Rats were administered turpentine oil (TO) intramuscularly to induce a sterile abscess and killed at various time points. Tissue iron content in the liver and brain increased progressively after TO administration. Immunohistology revealed an abundant expression of transferrin receptor-1 (TfR1) in the membrane and cytoplasm of the liver cells, in contrast to almost only nuclear expression of TfR1 in brain tissue. The expression of TfR1 increased at the protein and RNA levels in both organs. Gene expression of hepcidin, ferritin-H, iron-regulatory protein-1, and heme oxygenase-1 was also upregulated, whereas that of hemojuvelin, ferroportin-1, and the hemochromatosis gene was significantly downregulated at the same time points in both the brain and the liver at the RNA level. However, in contrast to observations in the liver, gene expression of the main acute-phase cytokine (interleukin-6) in the brain was significantly upregulated. In vitro experiments revealed TfR1 membranous protein expression in the liver cells, whereas nuclear and cytoplasmic TfR1 protein was detectable in brain cells. During the non-bacterial acute phase, iron content in the liver and brain increased together with the expression of TfR1. The iron metabolism proteins were regulated in a way similar to that observed in the liver, possibly by locally produced acute-phase cytokines. The significance of the presence of TfR1 in the nucleus of the brain cells has to be clarified."],["dc.identifier.doi","10.1007/s00441-011-1152-3"],["dc.identifier.isi","000290167600012"],["dc.identifier.pmid","21437659"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6628"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23171"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0302-766X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Comparison of changes in gene expression of transferrin receptor-1 and other iron-regulatory proteins in rat liver and brain during acute-phase response"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2979"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","World Journal of Gastroenterology"],["dc.bibliographiccitation.lastpage","2994"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Cameron, Silke"],["dc.contributor.author","Blaschke, Martina"],["dc.contributor.author","Moriconi, Federico"],["dc.contributor.author","Naz, Naila"],["dc.contributor.author","Amanzada, Ahmad"],["dc.contributor.author","Ramadori, Giuliano"],["dc.contributor.author","Malik, Ihtzaz Ahmed"],["dc.date.accessioned","2018-11-07T09:42:27Z"],["dc.date.available","2018-11-07T09:42:27Z"],["dc.date.issued","2014"],["dc.description.abstract","AIM: To study KRAS/BRAF mutations in colorectalcancer (CRC) that influences the efficacy of treatment. To develop strategies for overcoming combination of treatment. METHODS: Five colonic cell-lines were investigated: DLD-1 with KRAS (G13D) mutation, HT 29 and Colo 205 with BRAF (V600E) mutation as well as the wild type (Wt) cell-lines Caco2 and Colo-320. DLD-1 (KRAS), HT-29 (BRAF) and Caco2 (Wt) cell lines were treated with cytokines (TNF alpha 50 ng, IL-1 beta 1 ng and IFN. 50 ng) and harvested at different time points (1-24 h). KRAS inhibition was performed by the siRNA-approach. Two colorectal cancer cells DLD-1 and Caco2 were used for KRAS inhibition. About 70% confluency were confirmed before transfection with small interferring RNA (siRNA) oligonucleotides. All the synthetic siRNA sequences were designed in our laboratory. Total RNA and protein was isolated from the cells for RT-PCR and Western blotting. Densitometry of the Western blotting was analyzed with the Image J software (NIH). Results are shown as mean +/- SD. RESULTS: RT-PCR analysis in non-stimulated cells showed a low basal expression of TNFa and IL-1 beta in the DLD-1 KRAS -mutated cell-line, compared to Caco2 wild type. No detection was found for IL-6 and IFN. in any of the studied cell lines. In contrast, pro-angiogenic chemokines (CXCL1, CXCL8) showed a high constitutive expression in the mutated cell-lines DLD-1 (KRAS), HT-29 and Colo205 (BRAF), compared to wild type (Caco2). The anti-angiogenic chemokine (CXCL10) showed a high basal expression in wild-type, compared to mutated cell-lines. KRAS down-regulation by siRNA showed a significant decrease in CXCL1 and CXCL10 gene expression in the DLD-1 (KRAS) cell-line in comparison to wild type (Caco2) at 72 h after KRAS silencing. In contrast, the specific KRAS inhibition resulted in an up-regulation of CXCL1 and CXCL10. The results of our study show a higher expression of pro-angiogenic chemokines at basal level in mutated cell-lines, which was further increased by cytokine treatment. CONCLUSION: To summarize, basal chemokine gene expression for pro-angiogenic chemokines was high in mutated as compared to wild type cell-lines. This reflects the likely existence of a different microenvironment in tumours consistent of wild type or mutated cells. This may help to rationalize the choice of molecular targets for suitable therapeutic investigation in clinical studies. c 2014 Baishideng Publishing Group Co., Limited. All rights reserved."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2014"],["dc.identifier.doi","10.3748/wjg.v20.i11.2979"],["dc.identifier.isi","000333667200026"],["dc.identifier.pmid","24659889"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10180"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33957"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Baishideng Publ Grp Co Ltd"],["dc.relation.issn","2219-2840"],["dc.relation.issn","1007-9327"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Differential gene expression of chemokines in KRAS and BRAF mutated colorectal cell lines: Role of cytokines"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]