Iman Waheed Khan

Iman Waheed Khan


Research Focus & Metrics

Academic Career Length

6Years (2021-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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11 January 2025 in Gastroenterology Report
Verified
Journal Article
Open access
FUFatima Usama
Fatima Usama
RRRohullah Rasikh
Rohullah Rasikh
KHKhawaja Hassam
Khawaja Hassam
MRMansoor Rahman
Mansoor Rahman
FRFnu Khalil Ur Rehman
Fnu Khalil Ur Rehman
DLDaryl T-Y Lau
Daryl T-Y Lau
Gastrointestinal stromal tumors (GISTs) originate from mesenchymal cells and account for ∼1% of primary malignant tumors in the digestive system. They are diagnosed based on characteristic immunohistochemical staining pattern, including CD117 and DOG1, as well as genetic analysis for mutations in the KIT and platelet-derived growth factor receptor α genes. Extragastrointestinal stromal tumors (EGISTs) share very similar morphology with GISTs but arise outside the gastrointestinal tract. The most common locations for EGISTs are the omentum, mesentery, retroperitoneum, and pancreas, followed by the liver, vagina, and prostate. The mean age of presentation of these tumors is in the sixth decade of life and tumor dimensions at different locations typically range from 7 to 15.8 cm. Most of these tumors are unifocal and of the spindle cell type. GISTs generally have a better prognosis than EGISTs, with cumulative 5-year survival rates of 85% for GISTs and 38%–60.9% for EGISTs. Among EGISTs, omental tumors have higher overall survival than mesenteric or retroperitoneal tumors. Additionally, age of >60 years, male sex, larger tumor size, higher mitotic rate, and nuclear pleomorphism are associated with worse prognosis in EGISTs.

17 December 2021 in Microorganisms
Verified
Journal Article
Open access
PDF file
IKIman Waheed Khan
Iman Waheed Khan
MUMati Ullah Dad Ullah
Mati Ullah Dad Ullah
MCMina Choudhry
Mina Choudhry
Mukarram Jamat AliMukarram Jamat Ali
Mukarram Jamat Ali
MAMuhammad Ali
Muhammad Ali
DLDaryl T-Y Lau
Daryl T-Y Lau
Hepatitis B virus (HBV) infection is a global public health issue and is a major cause of cirrhosis and hepatocellular carcinoma (HCC). Hepatitis D virus (HDV) requires the hepatitis B surface antigen (HBsAg) to replicate. The eradication of HBV, therefore, can also cure HDV. The current therapies for chronic hepatitis B and D are suboptimal and cannot definitely cure the viruses. In order to achieve functional or complete cure of these infections, novel therapeutic agents that target the various sites of the viral replicative cycle are necessary. Furthermore, novel immunomodulatory agents are also essential to achieve viral clearance. Many of these new promising compounds such as entry inhibitors, covalently closed circular DNA (cccDNA) inhibitors, small interfering RNAs (siRNAs), capsid assembly modulators and nucleic acid polymers are in various stages of clinical developments. In this review article, we provided a comprehensive overview of the structure and lifecycle of HBV, the limitations of the current therapies and a summary of the novel therapeutic agents for both HDV and HBV infection.