Julhash U. Kazi

ORCID: 0000-0002-0719-5336
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About
Contact & Profiles
Research Areas
  • Acute Myeloid Leukemia Research
  • Protein Degradation and Inhibitors
  • Cancer Immunotherapy and Biomarkers
  • Ferroptosis and cancer prognosis
  • Chronic Myeloid Leukemia Treatments
  • Chronic Lymphocytic Leukemia Research
  • PI3K/AKT/mTOR signaling in cancer
  • Protein Kinase Regulation and GTPase Signaling
  • Mast cells and histamine
  • Acute Lymphoblastic Leukemia research
  • Cancer-related Molecular Pathways
  • Ubiquitin and proteasome pathways
  • Radiomics and Machine Learning in Medical Imaging
  • Cell Adhesion Molecules Research
  • Advanced Biosensing Techniques and Applications
  • Computational Drug Discovery Methods
  • Medical Imaging Techniques and Applications
  • Cell death mechanisms and regulation
  • HER2/EGFR in Cancer Research
  • Genomics and Chromatin Dynamics
  • Cytokine Signaling Pathways and Interactions
  • Microtubule and mitosis dynamics
  • Histone Deacetylase Inhibitors Research
  • Peptidase Inhibition and Analysis
  • Cancer Genomics and Diagnostics

Lund University
2015-2024

Medicon Village
2013-2024

Skåne University Hospital
2012-2019

University of Barisal
2015-2017

Boston Biomedical Research Institute
2013-2014

Translational Research in Oncology
2014

Japan External Trade Organization
2011

Inha University
2007-2009

Columbia University
2007

Therapy directed against oncogenic FLT3 has been shown to induce response in patients with acute myeloid leukemia (AML), but these responses are almost always transient. To address the mechanism of inhibitor resistance, we generated two resistant AML cell lines by sustained treatment sorafenib. Parental carry FLT3-ITD (tandem duplication) mutation and highly responsive inhibitors, whereas display resistance multiple inhibitors. Sanger sequencing protein mass-spectrometry did not identify any...

10.1038/onc.2016.41 article EN cc-by Oncogene 2016-03-21

Acute myeloid leukemia (AML) is a heterogeneous disease with variable patient responses to therapy. Selinexor, an inhibitor of nuclear export, has shown promising clinical activity for AML. To identify the molecular context monotherapy sensitivity as well rational drug combinations, we profile selinexor signaling using phosphoproteomics in primary AML samples and cell lines. Functional phosphosite scoring reveals that p53 function required consistent enhanced efficacy combination MDM2...

10.1016/j.celrep.2022.111177 article EN cc-by Cell Reports 2022-08-01

Abstract Molecular targeted therapy using a drug that suppresses the growth and spread of cancer cells via inhibition specific protein is foundation precision medicine treatment. High expression proto-oncogene Bcl-3 promotes proliferation metastasis originating from tissues such as colon, prostate, breast, skin. The development novel drugs targeting alone or in combination with other therapies can cure these patients prolong their survival. As proof concept, present study, we focused on...

10.1186/s12885-023-11663-y article EN cc-by BMC Cancer 2024-01-18
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