Experiments were undertaken to investigate a genetic event involved in leukemogenesis in adult T-cell leukemia (ATL). For this purpose, the p53 gene was chosen for study, since alteration of the gene has been found in a wide variety of human cancers. Structures and expression of the p53 gene in ATL cells were investigated by Southern and Northern blot analyses and a polymerase-chain-reaction single-strand conformation-polymorphism (PCR-SSCP) analysis. Either subtle alterations of the p53 gene or the absence of detectable level of p53 mRNA were found in 2 of 3 acute ATL cell lines and 2 of 12 acute ATL fresh samples. In contrast, no mutation was detected in 4 cases with less aggressive types of ATL (3 chronic and 1 smoldering ATL cases). Mutations found in acute ATL cells occurred in regions highly conserved in evolution and all the cells carrying p53 mutation showed loss of the other p53 allele. These results suggests that alteration of the p53 gene may contribute to progression of the disease in some cases of ATL.
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http://dx.doi.org/10.1002/ijc.2910490614 | DOI Listing |
Turk J Med Sci
December 2024
Department of Microbiology, Faculty of Medicine, Ankara University, Ankara, Turkiye.
Background/aim: The p53 protein, a crucial tumor suppressor, governs cell cycle regulation and apoptosis. Similarly, p63, a member of the p53 family, exhibits traits of both tumor suppression and oncogenic behavior through its isoforms. However, the functional impact of ΔNp63β, an isoform of the p63 protein, on human glioma cancer cells like T98G cells remains poorly understood, representing the novelty of this study in the current literature.
View Article and Find Full Text PDFTurk J Med Sci
December 2024
Department of Medical Biology, Faculty of Medicine, Kocaeli University, Kocaeli, Turkiye.
Background/aim: Lung cancer, a predominant contributor to cancer mortality, is characterized by diverse etiological factors, including tobacco smoking and genetic susceptibilities. Despite advancements, particularly in nonsmall-cell lung cancer (NSCLC), therapeutic options for lung squamous cell carcinoma (LUSC) are limited. Transposable elements (TEs) and their regulatory proteins, such as tigger transposable element derived (TIGD) family proteins, have been implicated in cancer development.
View Article and Find Full Text PDFAsian Pac J Cancer Prev
December 2024
Center of Excellence in Applied Medical Virology, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
Objective: This study aimed to identify upregulated genes in HPV16-positive cervical cancer cells and investigate the impact of downregulating NAD(P) H:quinone oxidoreductase 1 (NQO1) on the survival of these cells.
Methods: Transcriptomic sequencing (RNA-seq) was utilized to pinpoint upregulated genes and associated cancer-related pathways in HPV16-positive cervical cancer cells, comparing them to HPV-negative cervical cancer cells. NQO1 gene knockdown was performed in HPV16-positive cervical cancer cell lines to assess its effect on cell survival, including parameters such as cell proliferation, migration, invasion, cell cycle progression, apoptosis, and the expression of key proteins in the PI3K/AKT pathway, p53, and RECK.
Cell Death Differ
December 2024
Georgetown University Medical Center, Lombardi Comprehensive Cancer Center, Washington, D.C., USA.
Germline inactivating mutations of the SLC25A1 gene contribute to various human disorders, including Velocardiofacial (VCFS), DiGeorge (DGS) syndromes and combined D/L-2-hydroxyglutaric aciduria (D/L-2HGA), a severe systemic disease characterized by the accumulation of 2-hydroxyglutaric acid (2HG). The mechanisms by which SLC25A1 loss leads to these syndromes remain largely unclear. Here, we describe a mouse model of SLC25A1 deficiency that mimics human VCFS/DGS and D/L-2HGA.
View Article and Find Full Text PDFProstate Cancer Prostatic Dis
December 2024
Department of Radiation Oncology, Peking University First Hospital, 100034, Beijing, China.
Background: Metastatic prostate cancer (PCa) has much lower survival and ultimately develops castration resistance, which expects novel targets and therapeutic approaches. As a result of iron-dependent lipid peroxidation, ferroptosis triggers programmed cell death and has been associated with castration-resistant prostate cancer (CRPC).
Subjects: To better understand how ferroptosis can be used to treat CRPC, we reviewed the following: First, ferroptosis mechanisms and characteristics.
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