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Genetic architecture of Multiple Myeloma and its prognostic implications - An updated review.
Malays J Pathol
December 2024
Universiti Sains Malaysia, School of Medical Sciences, Human Genome Centre, Health Campus, Kelantan, Malaysia.
Multiple myeloma (MM), a clonal B-cell neoplasia, is an incurable and heterogeneous disease where survival ranges from a few months to more than 10 years. The clinical heterogeneity of MM arises from multiple genomic events that result in tumour development and progression. Recurring genomic abnormalities including cytogenetic abnormalities, gene mutations and abnormal gene expression profiles in myeloma cells have a strong prognostic power.
View Article and Find Full Text PDFThe Genetic and Molecular Drivers of Multiple Myeloma: Current Insights, Clinical Implications, and the Path Forward.
Pharmgenomics Pers Med
December 2024
Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: Multiple myeloma (MM) is a hematological malignancy characterized by the clonal proliferation of malignant plasma cells within the bone marrow. The disease's complexity is underpinned by a variety of genetic and molecular abnormalities that drive its progression.
Methods: This review was conducted through a state-of-The-art literature search, primarily utilizing PubMed to gather peer-reviewed articles.
c-JUN interacts with HDAC1 as a potential combinatorial therapeutic target in acute myeloid leukemia.
Int Immunopharmacol
December 2024
Department of Scientific Research, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, China. Electronic address:
Acute myeloid leukemia (AML) is a biologically heterogeneous disease originating from the clonal expansion of hematopoietic stem cells (HSCs). Clonal expansion of hematopoietic stem cell progenitors (HSC-Prog), along with a block in differentiation, are hallmark features of AML. The disease is characterized by poor clinical outcomes, highlighting the urgent need for effective therapeutic strategies and suitable drug targets.
View Article and Find Full Text PDFDecoding cancer etiology with cellular reprogramming.
Curr Opin Genet Dev
December 2024
Department of Integrative Biology and Pharmacology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA; The University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences, Houston, TX 77030, USA; Center for Precision Health, McWilliams School of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA. Electronic address:
Cancer research remains clinically unmet in many areas due to limited access to patient samples and the lack of reliable model systems that truly reflect human cancer biology. The emergence of patient-derived induced pluripotent stem cells and engineered human pluripotent stem cells (hPSCs) has helped overcome these challenges, offering a versatile alternative platform for advancing cancer research. These hPSCs are already proving to be valuable models for studying specific cancer driver mutations, offering insights into cancer origins, pathogenesis, tumor heterogeneity, clonal evolution, and facilitating drug discovery and testing.
View Article and Find Full Text PDFMenin inhibitors in the treatment of acute myeloid leukemia.
Blood
December 2024
University Medical Center Groningen, Groningen, Netherlands.
Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy characterized by the (oligo)clonal expansion of myeloid progenitor cells. Despite advances in treatment, AML remains challenging to cure, particularly in patients with specific genetic abnormalities. Menin inhibitors have emerged as a promising therapeutic approach, targeting key genetic drivers of AML such as KMT2A rearrangements and NPM1 mutations.
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