Nourhan Essam Omran

Ms. Nourhan Essam Omran


Research Focus & Metrics

Academic Career Length

1Year (2026-Present)

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

Representative Publications

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30 January 2026 in Cancers
Verified
Journal Article
Open access
PDF file
SAShaimaa Alharbi
Shaimaa Alharbi
FMFarah Fawzi Mohammed
Farah Fawzi Mohammed
MTMahsa Taleb Talebi
Mahsa Taleb Talebi
NONourhan Essam Omran
Nourhan Essam Omran
Rifat HamoudiRifat Hamoudi
Rifat Hamoudi
RHRania Harati
Rania Harati
Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer characterized by high immunogenicity and specific immune signatures. Although these molecular features including elevated tumor-infiltrating lymphocytes (TILs) and programmed death-ligand 1 (PD-L1) expression provide a strong rationale for immunotherapy, clinical response remains limited due to multiple mechanisms of immune escape. This review summarizes current and emerging immunotherapeutic strategies in TNBC, including immune checkpoint inhibitors (PDL-1 and cytotoxic T-lymphocyte-associated protein 4 (CTL-4) blockade), adoptive cell therapy (ACT) (chimeric antigen receptor T-cell therapy (CAR-T) and TIL therapy), oncolytic virotherapy, and antibody-based approaches. We also discuss the mechanisms of resistance including DNA damage response alterations, anti-apoptotic signaling, and tumor microenvironment-mediated resistance. Finally, we highlight rational combination strategies, immunotherapy with chemotherapy, targeted therapy, or additional immunotherapies that aim to enhance response to immunotherapy. Ongoing advances in immunotherapy hold significant potential to improve outcomes for patients with TNBC.

Verified
Journal Article
Open access
PDF file
SFSalma Fayed
Salma Fayed
SASalma Amer
Salma Amer
MBMalak Badawy
Malak Badawy
LMLara J. Bou Malhab
Lara J. Bou Malhab
NONourhan Essam Omran
Nourhan Essam Omran
RHRania Harati
Rania Harati
Glioblastoma multiforme (GBM) remains the most aggressive and treatment-refractory form of primary brain tumor in adults, characterized by rapid proliferation, intratumoral heterogeneity and resistance to current therapies. Despite therapeutic advancements in surgical resection, radiotherapy and chemotherapy, clinical outcomes remain poor, underscoring the need for innovative molecular strategies. This review examines the therapeutic potential of CRISPR/Cas9 genome-editing technologies in GBM, highlighting their ability to model, dissect and potentially correct the genetic alterations that drive GBM tumorigenesis. Key molecular targets, such as EGFR, PTEN, TP53, NF1 and PIK3CA, are discussed within the context of GBM’s mutational and signaling landscape. We further outline emerging CRISPR applications in preclinical models, the current status of CRISPR-based clinical trials and the major barriers hindering translation, including off-target effects, immunogenicity and the challenge of delivering gene-editing systems across the blood–brain barrier. Particular emphasis is placed on delivery technologies, viral and non-viral vectors, including lipid nanoparticles, polymeric systems, inorganic nanocarriers and DNA nanostructures, which are rapidly evolving to improve precision, safety and CNS penetrance. Collectively, this review highlights CRISPR/Cas9 as a powerful tool whose integration with molecular neuro-oncology and precision medicine may ultimately shift GBM treatment toward more personalized and durable therapeutic interventions.

4 June 2026 in Neuroscience
Verified
Journal Article
Closed access
NONourhan Essam Omran
Nourhan Essam Omran
RZRuba A. Zenati
Ruba A. Zenati
LMLara J. Bou Malhab
Lara J. Bou Malhab
YBYasser Bustanji
Yasser Bustanji
KAKarem H. Alzoubi
Karem H. Alzoubi
MSMohammad H. Semreen
Mohammad H. Semreen