Isocitrate dehydrogenases (IDH1/2) are central molecular markers for glioblastoma. Providing in vitro or in vivo models with mutated IDH1/2 can help prepare facilities to understand the biology of these mutated genes as glioma markers, as well as help, improve therapeutic strategies. In this review, we first summarize the biology principles of IDH and its mutations and outline the core primary findings in the clinical context of neuro-oncology. Given the extensive research interest and exciting developments in current stem cell biology and genome editing, the central part of the manuscript is dedicated to introducing various routes of disease modeling strategies of IDH mutation (IDH) glioma and comparing the scientific-technological findings from the field using different engineering methods. Lastly, by giving our perspective on the benefits and limitations of patient-derived and donor-derived disease modeling respectively, we aim to propose leading research questions to be answered in the context of IDH1 and glioma.
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http://dx.doi.org/10.1038/s41419-020-03196-0 | DOI Listing |
Ann Afr Med
November 2024
Department of Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India.
Genet Res (Camb)
October 2024
Department of Neurosurgery LiaoCheng People's Hospital, Liaocheng 252000, Shandong, China.
Backgrounds: Glioma stands as one of the most formidable brain tumor types, with patient outcomes remaining bleak even in the face of advancements in treatment modalities. FBXW4, a constituent of the F-box and WD repeat domain-containing protein family, is recognized for its participation in diverse cellular activities, including those related to tumor dynamics. Yet, the therapeutic relevance and specific role of FBXW4 in the context of glioma are not well defined.
View Article and Find Full Text PDFPLoS One
September 2024
Department of Surgery, Aga Khan University Hospital, Karachi, Pakistan.
Genome Med
August 2024
Department of Medical Informatics, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Background: Determining the impact of somatic mutations requires understanding the functional relationship of genes acquiring mutations; however, it is largely unknown how mutations in functionally related genes influence each other.
Methods: We employed non-synonymous-to-synonymous or dNdS ratios to evaluate the evolutionary dependency (ED) of gene pairs, assuming a mutation in one gene of a gene pair can affect the evolutionary fitness of mutations in its partner genes as mutation context. We employed PanCancer- and tumor type-specific mutational profiles to infer the ED of gene pairs and evaluated their biological relevance with respect to gene dependency and drug sensitivity.
Sci Rep
June 2024
Department of Neurosurgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
PTBP1 is an oncogene that regulates the splicing of precursor mRNA. However, the relationship between PTBP1 expression and gene methylation, cancer prognosis, and tumor microenvironment remains unclear. The expression profiles of PTBP1 across various cancers were derived from the TCGA, as well as the GTEx and CGGA databases.
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