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| 1 | Hepatitis B virus,HBx mutants and their role in hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC)is one of the leading causes of death induced by cancer in the modern world and majority of the cases are related to chronic hepatitis B virus(HBV)infection.HBV-encoded X protein(HBx)is known to play a pivotal role in the pathogenesis of viral induced HCC.HBx is a multifunctional protein of17 kDa which modulates several cellular processes by direct or indirect interaction with a repertoire of host factors resulting in HCC.HBX might interfere with several cellular processes such as oxidative stress,DNA repair,signal transduction,transcription,protein degradation,cell cycle progression and apoptosis.A number of reports have indicated that HBx is one of the most common viral ORFs that is often integrated into the host genome and its sequence variants play a crucial role in HCC.By mutational or deletion analysis it was shown that carboxy terminal of HBx has a likely role in protein-protein interactions,transcriptional transactivation,DNA repair,cell,signaling and pathogenesis of HCC.The accumulated evidence thus far suggests that it is difficult to understand the mechanistic nature of HBx associated HCC,and HBx mediated transcriptional transactivation and signaling pathways may be a major determinant.This article addresses the role of HBx in the development of HCC with particular emphasis on HBx mutants and their putative targets. | Ashraf Ali Hany Abdel-Hafiz Mohd Suhail Amany Al-Mars Mohammad Khalid Zakaria Kaneez Fatima Sultan Ahmad Esam Azhar Adeel Chaudhary Ishtiaq Qadri | 2014 | World Journal of Gastroenterology2014，20，30： | 29 |
| 2 | Potential mechanisms of hepatitis B virus induced liver injury显示文摘Chronic active hepatitis(CAH) is acknowledged as an imperative risk factor for the development of liver injury and hepatocellular carcinoma.The histological end points of CAH are chronic inflammation,fibrosis and cirrhosis which are coupled with increased DNA synthesis in cirrhotic vs healthy normal livers.The potential mechanism involved in CAH includes a combination of processes leading to liver cell necrosis,inflammation and cytokine production and liver scaring(fibrosis).The severity of liver damage is regulated by Hepatitis B virus genotypes and viral components.The viral and cellular factors that contribute to liver injury are discussed in this article.Liver injury caused by the viral infection affects many cellular processes such as cell signaling,apoptosis,transcription,DNA repair which in turn induce radical effects on cell survival,growth,transformation and maintenance.The consequence of such perturbations is resulted in the alteration of bile secretion,gluconeogenesis,glycolysis,detoxification and metabolism of carbohydrates,proteins,fat and balance of nutrients.The identification and elucidation of the molecular pathways perturbed by the viral proteins are important in order to design effective strategy to minimize and/or restore the hepatocytes injury. | Mohd Suhail Hany Abdel-Hafiz Ashraf Ali Kaneez Fatima Ghazi A Damanhouri Esam Azhar Adeel GA Chaudhary Ishtiaq Qadri | 2014 | World Journal of Gastroenterology2014，20，35： | 12 |
| 3 | Hepatitis C virus in Pakistan:A systematic review of prevalence,genotypes and risk factors显示文摘In Pakistan more than 10 million people are living with Hepatitis C virus (HCV), with high morbidity and mortality. This article reviews the prevalence, genotypes and factors associated with HCV infection in the Pakistani population. A literature search was performed by using the keywords; HCV prevalence, genotypes and risk factors in a Pakistani population, in Pubmed, PakMediNet and Google scholar. Ninetyone different studies dating from 1994 to May 2009 were included in this study, and weighted mean and standard error of each population group was calculated. Percentage prevalence of HCV was 4.95% ± 0.53% in the general adult population, 1.72% ± 0.24% in the pediatric population and 3.64% ± 0.31% in a young population applying for recruitment, whereas a very high 57% ± 17.7% prevalence was observed in injecting drug users and 48.67% ± 1.75% in a multi-transfused population. Most prevalent genotype of HCV was 3a. HCV prevalence was moderate in the general population but very high in injecting drug users and multi-transfused populations. This data suggests that the major contributing factors towards increased HCV prevalence include unchecked blood transfusions and reuse of injection syringes. Awareness programs are required to decrease the future burden of HCV in the Pakistani population. | Yasir Waheed Talha Shafi Sher Zaman Safi Ishtiaq Qadri | 2009 | World Journal of Gastroenterology2009，15，45： | 12 |
| 4 | Host nucleotide polymorphism in hepatitis B virusassociated hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC) is etiologically linked with hepatitis B virus(HBV) and is the leading cause of death amongst 80% of HBV patients. Among HBV affected patients, genetic factors are also involved in modifying the risk factors of HCC. However, the genetic factors that regulate progression to HCC still remain to be determined. In this review, we discuss several single nucleotide polymorphisms(SNPs) which were reportedly associated with increased or reduced risk of HCC occurrence in patients with chronic HBV infection such as cyclooxygenase(COX)-2 expression specifically at COX-2-1195G/A in Chinese, Turkish and Egyptian populations, tumor necrosis factor α and the three most commonly studied SNPs: PAT-/+, Lys939Gln(A33512C, rs2228001) and Ala499Val(C21151T, rs2228000). In genome-wide association studies, strong associations have also been found at loci 1p36.22, 11q22.3, 6p21(rs1419881, rs3997872, rs7453920 and rs7768538), 8p12(rs2275959 and rs37821974) and 22q11.21. The genes implicated in these studies include HLA-DQB2, HLA-DQA1, TCF19, HLA-C, UBE2L3, LTL, FDX1, MICA, UBE4 B and PG. The SNPs found to be associated with the above-mentioned genes still require validation in association studies in order to be considered good prognostic candidates for HCC. Screening of these polymorphisms is very beneficial in clinical experiments to stratify the higher or lower risk for HCC and may help in designing effective and efficient HCC surveillance programs for chronic HBV-infected patients if further genetic vulnerabilities are detected. | Shilu Mathew Hany Abdel-Hafiz Abbas Raza Kaneez Fatima Ishtiaq Qadri | 2016 | World Journal of Hepatology2016，8，10： | 4 |
| 5 | Hepatitis C virus and neurological damage显示文摘Chronic hepatitis C virus(HCV) infection exhibits a wide range of extrahepatic complications, affecting various organs in the human body. Numerous HCV patients suffer neurological manifestations, ranging from cognitive impairment to peripheral neuropathy. Overexpression of the host immune response leads to the production of immune complexes, cryoglobulins, as well as autoantibodies, which is a major pathogenic mechanism responsible for nervous system dysfunction. Alternatively circulating inflammatory cytokines and chemokines and HCV replication in neurons is another factor that severely affects the nervous system. Furthermore, HCV infection causes both sensory and motor peripheral neuropathy in the mixed cryoglobulinemia as well as known as an important risk aspect for stroke. These extrahepatic manifestations are the reason behind underlying hepatic encephalopathy and chronic liver disease. The brain is an apt location for HCV replication, where the HCV virus may directly wield neurotoxicity. Other mechanisms that takes place by chronic HCV infection due the pathogenesis of neuropsychiatric disorders includes derangement of metabolic pathways of infected cells, autoimmune disorders, systemic or cerebral inflammation and alterations in neurotransmitter circuits. HCV and its pathogenic role is suggested by enhancement of psychiatric and neurological symptoms in patients attaining a sustained virologic response followed by treatment with interferon; however, further studies are required to fully assess the impact of HCV infection and its specific antiviral targets associated with neuropsychiatric disorders. | shilu mathew muhammed faheem sara m ibrahim waqas iqbal bisma rauff kaneez fatima ishtiaq qadri | 2016 | World Journal of Hepatology2016，8，12： | 3 |
| 6 | Notch signalling pathway in development of cholangiocarcinoma显示文摘Cholangiocarcinoma(CCA)comprises of extra-hepatic cholangiocarcinoma and intrahepatic cholangiocarcinoma cancers as a result of inflammation of epithelium cell lining of the bile duct.The incidence rate is increasing dramatically worldwide with highest rates in Eastern and South Asian regions.Major risk factors involve chronic damage and inflammation of bile duct epithelium from primary sclerosing cholangitis,chronic hepatitis virus infection,gallstones and liver fluke infection.Various genetic variants have also been identified and as CCA develops on the background of biliary inflammation,diverse range of molecular mechanisms are involved in its progression.Among these,the Notch signalling pathway acts as a major driver of cholangiocarcinogenesis and its components(receptors,ligands and downstream signalling molecules)represent a promising therapeutic targets.Gamma-Secretase Inhibitors have been recognized in inhibiting the Notch pathway efficiently.A comprehensive knowledge of the molecular pathways activated by the Notch signalling cascade as well as its functional crosstalk with other signalling pathways provide better approach in developing innovative therapies against CCA. | Bisma Rauff Arif Malik Yasir Ali Bhatti Shafiq Ahmad Chudhary Ishtiaq Qadri Shafquat Rafiq | 2020 | World Journal of Gastrointestinal Oncology2020，12，9： | 2 |
| 7 | Additional Glycosylation Within a Specific Hypervariable Region of Subtype 3a of Hepatitis C Virus Protects Against Virus Neutralization显示文摘 | Sadia Anjum Ahmed Wahid Muhammad Sohail Afzal Anna Albecka Khaled Alsaleh Tahir Ahmad Thomas F. Baumert Czeslaw Wychowski Ishtiaq Qadri Fran?ois Penin Jean Dubuisson | 2013 | Journal of Infectious Diseases2013，，11： | 1 |
| 8 | Biomarkers for virus-induced hepatocellular carcinoma (HCC)显示文摘 | Shilu Mathew Ashraf Ali Hany Abdel-Hafiz Kaneez Fatima Mohd Suhail Govindaraju Archunan Nargis Begum Syed Jahangir Muhammad Ilyas Adeel G.A. Chaudhary Mohammad Al Qahtani Salem Mohamad Bazarah Ishtiaq Qadri | 2014 | Infection, Genetics and Evolution2014，，： | 1 |
| 9 | Hepatitis B virus X protein impedes the DNA repair via its association with transcription factor, TFIIH 显示文摘 | ISHTIAQ QADRI KANEEZ FATIMA HANY ABDEL-HAFIZ | 2011 | BMC Microbiology2011，11，48： | 1 |
| 10 | Isolation and Partial Characterization of a Virulent Bacteriophage IHQ1 Specific for Aeromonas punctata from Stream Water显示文摘 | Irshad Haq Waqas Chaudhry Saadia Andleeb Ishtiaq Qadri | 2012 | Microbial Ecology2012，，4： | 1 |
| 11 | C/EBPβ is AMP kinase sensitive and up-regulates PEPCK in response to ER stress in hepatoma cells显示文摘 | Mahua Choudhury Ishtiaq Qadri Shaikh Mizanoor Rahman Jill Schroeder-Gloeckler Rachel C. Janssen Jacob E. Friedman | 2010 | Molecular and Cellular Endocrinology2010，，1： | 1 |
| 12 | Upregulated hepatic expression of mitochondrial PEPCK triggers initial gluconeogenic reactions in the HCV-3 patients显示文摘Objective: To identify the differential expression of candidate gluconeogenic genes which may initiate hepatitis C virus(HCV) related metabolic disorder during early stages of disease. Methods: Patients of diverse age and sex, with positive HCV genotype 3(HCV-3) RNA in serum and with no history of other related infections, co-infections, alcoholism, diabetes or chemotherapeutic treatments were considered for this study. Semi-quantitative reverse transcriptase PCR analysis and quantitative fold change analysis of the fresh liver biopsies of eight chronically infected HCV-3 patients and six healthy individuals were evaluated for three potential biomarkers involved in glucose homeostasis induction, namely mitochondrial phosphoenolpyruvate carboxykinase 2(PCK2), glucose-6-phosphatase catalytic subunit(G6PC) and associated forkhead box protein 01(FOXO1). Results: Symptomatic evaluation, clinical history and blood test were conducted according to general disease prognosis procedures and reported here. Significantly upregulated expression of PCK2 independent of age, sex and viral infectivity levels in all HCV patients was observed, whereas no significant changes in the expression of G6 PC and FOXO1 were found. Conclusions: PCK2 triggers initial gluconeogenic reactions which ultimately result in the accumulation of glycogen in the liver hepatocytes. We therefore suggest that the overproduction of PCK2 has important physiological role in the onset of metabolic disorder in the HCV-3 patients. | Taimoor Islam Sheikh Tashfeen Adam Ishtiaq Qadri | 2015 | Asian Pacific Journal of Tropical Medicine2015，8，8： | 0 |
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