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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 | 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 |
| 4 | 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 |
| 5 | Pulsed low intensity ultrasound enhances mineralisation in preosteoblast cells显示文摘 | Unswortb J Kaneez S Harris S | | 0，，09： | 1 |
| 6 | Pulsed low intensity ultrasound enhances mineralisation in preosteoblast cells 显示文摘 | Unsworth J Kaneez S Harris S | 2007 | Ultrasound in medicine & biology2007，33，9： | 1 |
| 7 | Perceived Social Support: Impact on Quality of Life in Diabetics 显示文摘 | Tahir Saeedl Nur Naha Abu Mansor Farah Naz Kaneez Fatima Hafiz Muhammad Ishaq | 2012 | International Journal of Academic Research2012，4，3： | 1 |
| 8 | Amino acid analysis of Intellan,a herbalproduct used in enhancing brain function显示文摘 | Ahmad Shahmuz Rahman Atiq-ur Fatima kaneez et a1 | 1994 | Pak Pharm Sci1994，7，2： | 1 |
| 9 | Diagnostic performance of the upper gastrointestinal series in the evaluation of children with clinically suspected malrotation显示文摘 | Alecia W. Sizemore Kaneez Z. Rabbani Alan Ladd Kimberly E. Applegate | 2008 | Pediatric Radiology2008，，5： | 1 |
| 10 | Some new prospects in the understanding of the molecular basis of the pathogenesis of stroke 显示文摘 | Sheikh AS Kaneez FS Taimur S | 2007 | Exp Brain Res2007，182，7： | 1 |
| 11 | A Student-Centred Model显示文摘 | Mihyar Hesson Kaneez Fatima Shad | 2007 | American Journal of Applied Science2007，4，9： | 1 |
| 12 | Characterization of the biocide polyhexamethylene biguanide bymatrix-assisted laser desorption ionization time-of-flight mass spectrometry显示文摘 | Leon P O Kaneez Z H Helen B Neil J Andrew N C | 2006 | Journal of Applied Polymer Science2006，，102： | 1 |
| 13 | Some new prospects in theunderstanding of the molecular basis of the pathogenesis of stroke显示文摘 | Sheikh Arshad Saeed Kaneez Fatima Shad Taimur Saleem | 2007 | Exp Brain Res2007，182，1： | 1 |
| 14 | Pulsed low in-tensity ultrasound enhances mineralisation in preosteo-blast cells显示文摘 | Unsworth J Kaneez S Harris S | | 0，，09： | 1 |
| 15 | 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 |
| 16 | Some new prospects in the understanding of the molecular basis of the pathogenesis of stroke 显示文摘 | Sheikh AS Kaneez FS Taimur S | 2007 | Exp Brain Res2007，182，1： | 1 |
| 17 | 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 |
| 18 | Diagnostic performance of the upper gastrointestinal series显示文摘 | Alecia W Sizemore Kaneez Z | 2008 | Pediatr Radio12008，38，： | 1 |
| 19 | Some new prospects in the understanding of the molecular basis of the pathogenesis of stroke显示文摘 | Sheikh AS Kaneez FS Taimur S | 2007 | Exp Brain Res2007，182，1： | 1 |
| 20 | Some new prospects in the un- derstanding of the molecular basis of the pathogenesis of stroke显示文摘 | Sheikh AS Kaneez FS Talmur S | 2007 | Exp Brain Res2007，182，1： | 1 |
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