Salima Haque

Tulane University, New Orleans, Louisiana, United States

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Publications (13)40.43 Total impact

  • Tropical gastroenterology: official journal of the Digestive Diseases Foundation 01/2011; 32(3):242-3.
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    ABSTRACT: Reports of primary intraabdominal synovial sarcomas are extremely rare. A literature review using PubMed was performed. A retrospective review of the one known case at our institution was completed. Even the most experienced pathologists report that synovial sarcomas can be very difficult to diagnose correctly. One cytogenic abnormality that is common (> 90%) and pathognomonic for synovial sarcoma is a characteristic chromosomal translocation resulting in the SYT/SSX fusion gene. Wide regional excision has been performed for intraabdominal sarcoma, with improved results. Our patient is more than 24 months with no evidence of recurrent or metastatic disease. The prognosis for patients with intraabdominal synovial sarcoma remains poor. However, wide regional excision may allow for prolonged disease-free survival.
    JSLS: Journal of the Society of Laparoendoscopic Surgeons / Society of Laparoendoscopic Surgeons 07/2010; 14(3):421-5. DOI:10.4293/108680810X12924466006846 · 0.91 Impact Factor
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    ABSTRACT: Hepatocellular carcinoma with extension into the right heart is a recognized, albeit rare occurrence. Patients who present with tumors extending into the heart have generally been considered inoperable and had limited survival, many sustaining tumor embolism and/or sudden death. Resection has been fraught with intraoperative and perioperative mortality as well as considerable postoperative morbidity. We report an exceptional case of a patient with such a tumor successfully treated with an aggressive surgical approach and review the limited published experience.
    The American surgeon 11/2009; 75(11):1104-8. · 0.82 Impact Factor
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    ABSTRACT: Alpha interferon in combination with ribavirin is the standard therapy for hepatitis C virus infection. Unfortunately, a significant number of patients fail to eradicate their infection with this regimen. The mechanisms of IFN-resistance are unclear. The aim of this study was to determine the contribution of host cell factors to the mechanisms of interferon resistance using replicon cell lines. HCV replicons with high and low activation of the IFN-promoter were cultured for a prolonged period of time in the presence of interferon-alpha (IFN-alpha2b). Stable replicon cell lines with resistant phenotype were isolated and characterized by their ability to continue viral replication in the presence of IFN-alpha. Interferon resistant cell colonies developed only in replicons having lower activation of the IFN promoter and no resistant colonies arose from replicons that exhibit higher activation of the IFN promoter. Individual cell clones were isolated and nine IFN resistant cell lines were established. HCV RNA and protein levels in these cells were not altered by IFN- alpha2b. Reduced signaling and IFN-resistant phenotype was found in all Huh-7 cell lines even after eliminating HCV, suggesting that cellular factors are involved. Resistant phenotype in the replicons is not due to lack of interferon receptor expression. All the cell lines show defect in the JAK-STAT signaling and phosphorylation of STAT 1 and STAT 2 proteins were strongly inhibited due to reduced expression of Tyk2 and Jak-1 protein. This in vitro study provides evidence that altered expression of the Jak-Stat signaling proteins can cause IFN resistance using HCV replicon cell clones.
    Virology Journal 02/2007; 4(1):89. DOI:10.1186/1743-422X-4-89 · 2.18 Impact Factor
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    ABSTRACT: We present here a comprehensive review of the current literature plus our own findings about in vivo and in vitro analysis of hepatitis C virus (HCV) infection, viral pathogenesis, mechanisms of interferon action, interferon resistance, and development of new therapeutics. Chronic HCV infection is a major risk factor for the development of human hepatocellular carcinoma. Standard therapy for chronic HCV infection is the combination of interferon alpha and ribavirin. A significant number of chronic HCV patients who cannot get rid of the virus infection by interferon therapy experience long-term inflammation of the liver and scarring of liver tissue. Patients who develop cirrhosis usually have increased risk of developing liver cancer. The molecular details of why some patients do not respond to standard interferon therapy are not known. Availability of HCV cell culture model has increased our understanding on the antiviral action of interferon alpha and mechanisms of interferon resistance. Interferons alpha, beta, and gamma each inhibit replication of HCV, and the antiviral action of interferon is targeted to the highly conserved 5'UTR used by the virus to translate protein by internal ribosome entry site mechanism. Studies from different laboratories including ours suggest that HCV replication in selected clones of cells can escape interferon action. Both viral and host factors appear to be involved in the mechanisms of interferon resistance against HCV. Since interferon therapy is not effective in all chronic hepatitis C patients, alternative therapeutic strategies are needed to treat chronic hepatitis C patients not responding to interferon therapy. We also reviewed the recent development of new alternative therapeutic strategies for chronic hepatitis C, which may be available in clinical use within the next decade. There is hope that these new agents along with interferon will prevent the occurrence of hepatocellular carcinoma due to chronic persistent hepatitis C virus infection. This review is not inclusive of all important scientific publications due to space limitation.
    Microscopy Research and Technique 11/2005; 68(3-4):130-48. DOI:10.1002/jemt.20227 · 1.15 Impact Factor
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    ABSTRACT: Interferon-alpha (IFN(alpha)) binds to receptors on the cell surface, which initiate a cascade of signal transduction pathways that leads to transcription of selected genes. This transduction pathway involves binding of transcription factors to a common cis-acting DNA sequence called IFN-stimulated response element (ISRE). To test whether these signaling pathways are functional in hepatitis C virus (HCV)-replicating cells, we studied the regulation of ISRE-mediated transcription of firefly luciferase gene in stable replicon cell lines. A plasmid construct was prepared (pISRELuc) which contains four tandem repeats of 9-27 ISRE sequences positioned directly upstream of the herpes virus 1 thymidine kinase promoter TATA box that drives the expression of firefly luciferase. Regulation of ISRE-mediated expression of firefly luciferase by IFN(alpha) was studied by transfecting this clone into Huh-7 cells replicating HCV subgenomic HCV RNA. The significance of ISRE-mediated transcriptional activation was studied in a replicon cell line by pretreatment of cells with actinomycin D, which inhibits cellular DNA-dependent RNA transcription. IFN treatment activates ISRE-mediated expression of luciferase, indicating that this pathway is functional in Huh-7 cells. Activation of ISRE-mediated transcription of luciferase is relatively high in two Huh-7 stable cell lines replicating HCV subgenomic RNA. Inhibition of ISRE-mediated transcription of luciferase by actinomycin D also makes HCV replication totally resistant to IFN(alpha). These in vitro studies suggest that activation of IFN-inducible genes is important in mounting a successful antiviral response against HCV.
    Intervirology 09/2005; 48(5):301-11. DOI:10.1159/000085099 · 1.68 Impact Factor
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    ABSTRACT: Interferon (IFN)-alpha is the standard therapy for the treatment of chronic hepatitis C, but the mechanisms underlying its antiviral action are not well understood. In this report, we demonstrated that IFN-alpha, -beta and -gamma inhibit replication of the hepatitis C virus (HCV) in a cell culture model at concentrations between 10 and 100 IU/ml. We demonstrated that the antiviral actions each of each these IFNs are targeted to the highly conserved 5' untranslated region of the HCV genome, and that they directly inhibit translation from a chimeric clone between full-length HCV genome and green fluorescent protein (GFP). This effect is not limited to HCV internal ribosome entry site (IRES), since these IFNs also inhibit translation of the encephalomyocardititis virus (EMCV) chimeric mRNA in which GFP is expressed by IRES-dependent mechanisms (pCITE-GFP). These IFNs had minimal effects on the expression of mRNAs from clones in which translation is not IRES dependent. We conclude that IFN-alpha, -beta and -gamma inhibit replication of sub-genomic HCV RNA in a cell culture model by directly inhibiting two internal translation initiation sites of HCV- and EMCV-IRES sequences present in the dicistronic HCV sub-genomic RNA. Results of this in vitro study suggest that selective inhibition of IRES-mediated translation of viral polyprotein is a general mechanism by which IFNs inhibits HCV replication.
    Liver international: official journal of the International Association for the Study of the Liver 07/2005; 25(3):580-94. DOI:10.1111/j.1478-3231.2005.01082.x · 4.85 Impact Factor
  • C. E. Olmos · D. C. Lagarde · S. Haque ·

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    Natalia Buza · D C Lagarde · Srikanta Dash · Salima Haque ·
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    ABSTRACT: Langerhans cell histiocytosis is a rare disorder characterized by abnormal proliferation of Langerhans cells that can affect various organ systems. The disease usually presents as a unifocal lytic bone lesion and can affect any age group. Less frequently it presents as a disseminated disease with multisystem involvement. Hepatic manifestation in Langerhans cell histiocytosis is relatively rare and usually presents as a part of a disseminated process. We report a case of Langerhans cell histiocytosis involving only the liver in a 9-years-old child.
    Journal of Cellular and Molecular Medicine 07/2004; 8(3):397-401. DOI:10.1111/j.1582-4934.2004.tb00329.x · 4.01 Impact Factor
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    ABSTRACT: We have established a T7-based model system for hepatitis C virus (HCV) 1a strain, which involves the use of a replication-defective adenovirus that carries the gene for T7 RNA polymerase and a transcription plasmid containing full-length HCV cDNA clone. To facilitate high-level expression of HCV, sub-confluent Huh7 cells were first infected with adenovirus containing the gene for the T7 RNA polymerase and then transfected with the transcription plasmid. As a negative control, part of NS5B gene of this clone was deleted which abolishes the HCV RNA-dependent RNA polymerase and prevents replication of viral RNA. This model produces high levels of structural (core, E1, E2) and nonstructural proteins (NS5), which were detected by Western blot analysis and immunofluorescence assay. Negative-strand HCV RNA was detected only in the wild-type clone in the presence of actinomycin D, and no RNA was detected with the NS5B deleted mutant control. As a practical validation of this model, we showed that IFN alpha-2b selectively inhibits negative-strand RNA synthesis by blocking at the level of protein translation. The inhibitory effect of IFN alpha-2b is not due reduction of transcription by T7 polymerase or due to intracellular degradation of HCV RNA. This in vitro model provides an efficient and reliable means of assaying negative-strand RNA, protein processing, and testing the antiviral properties of interferon.
    Experimental and Molecular Pathology 07/2004; 76(3):242-52. DOI:10.1016/j.yexmp.2004.01.004 · 2.71 Impact Factor

  • Hepatology 12/2003; 38:625-625. DOI:10.1016/S0270-9139(03)81012-1 · 11.06 Impact Factor

  • Hepatology 12/2003; 38:633-633. DOI:10.1016/S0270-9139(03)81028-5 · 11.06 Impact Factor
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    ABSTRACT: BACKGROUND: Undifferentiated (embryonal) sarcoma (UES) of the liver is a malignant hepatic neoplasm accounting for 7% of pediatric hepatic tumors. Current use of multimodal therapy, including chemotherapy and surgery, has greatly improved survival. Tumor rupture is uncommon and, prior to the adjuvant use of sarcoma based chemotherapy regimens, was thought to be poor prognostic sign. CASE PRESENTATION AND DISCUSSION: A 10-year-old girl presented with acute worsening of abdominal pain while being worked up for liver mass. At surgery, she was found to have a ruptured, 20 x 15 x 5 centimeter (cm) UES, the largest reported ruptured UES to be resected primarily. The size and position of her tumor required very aggressive surgery for complete resection. She subsequently received adjuvant chemotherapy and radiation. Twenty-four months following surgery she is doing well with no evidence of disease. CONCLUSION: Despite tumor rupture, complete tumor resection gives the patient the best chance of long-term survival. Aggressive surgery is warranted if the tumor can be completely resected.
    The Journal of the Louisiana State Medical Society: official organ of the Louisiana State Medical Society 161(1):41-4.

Publication Stats

119 Citations
40.43 Total Impact Points


  • 2004-2007
    • Tulane University
      • Department of Pathology and Laboratory Medicine
      New Orleans, Louisiana, United States
  • 2005
    • Louisiana State University Health Sciences Center New Orleans
      • Department of Microbiology, Immunology & Parasitology
      New Orleans, Louisiana, United States