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A549 has also been employed in viral research and associated protein expression changes as a consequence of viral infection. [10] Although A549 is a cancer cell line, it has also been studied for its response to tuberculosis, specifically the production of chemokines as it is induced by the invading bacteria. [11]
Database Institute / Organization Alteration Types Primary Source [t 1] Processed Data [t 2] Organisms Cell lines [t 3] Public Data [t 4] Restricted Data [t 5]; The BioExpress® Oncology Suite from Ocimum Bio Solutions contains gene expression data from primary, metastatic, and benign tumor samples, and normal samples, including matched adjacent controls.
The COSMIC (Catalogue of Somatic Mutations in Cancer) database was designed to collect and display information on somatic mutations in cancer. It was launched in 2004, with data from just four genes, HRAS, KRAS2, NRAS and BRAF. [6] These four genes are known to be somatically mutated in cancer. Since its creation, the database has expanded rapidly.
To further confirm that endogenous wild-type p53 is really causing the repression of survivin gene expression, the authors induced A549 (human lung cancer cell line with wild-type p53) and T47D (human breast cancer cell line with mutant p53) cells with DNA-damaging agent adriamycin to trigger the physiological p53 apoptotic response in these ...
The Cancer Genome Atlas (TCGA) is a project to catalogue the genomic alterations responsible for cancer using genome sequencing and bioinformatics. [1] [2] The overarching goal was to apply high-throughput genome analysis techniques to improve the ability to diagnose, treat, and prevent cancer through a better understanding of the genetic basis of the disease.
The Leiden Open Variation Database (LOVD) is a free, flexible web-based open source database developed in the Leiden University Medical Center in the Netherlands, designed to collect and display variants in the DNA sequence. [1] [2] The focus of an LOVD is usually the combination between a gene and a genetic (heritable) disease.
Lewis lung carcinoma is a hypermutated Kras/Nras–mutant cancer with extensive regional mutation clusters in its genome. A tumor that spontaneously developed as an epidermoid carcinoma in the lung of a C57BL mouse. It was discovered in 1951 by Dr. Margaret Lewis of the Wistar Institute and became one of the first transplantable tumors. [1]
Cancer occurs when a somatic cell that normally cannot divide undergoes mutations that cause deregulation of the normal cell cycle controls, leading to uncontrolled proliferation. Immortalised cell lines have undergone similar mutations, allowing a cell type that would normally not be able to divide to be proliferated in vitro .
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