Exploiting the mutanome for tumor vaccination.
By J. Castle, S. Kreiter, Jan Diekmann, M. Löwer, Niels van de Roemer, J. de Graaf, Abderraouf Selmi, M. Diken, Sebastian Boegel, C. Paret and 6 more. Cancer Research, 2012
765 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology, Radiology, Nuclear Medicine and Imaging
View Paper: https://www.semanticscholar.org/paper/fe35b87a658fd2ca4e2641ba1d9828a88cd3bcb3
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In Immunology
In Molecular Biology
- Elaine R. Mardis
- Michael R. Stratton
- Maria Fischer
- Zlatko Trajanoski
- Stephan Pabinger
- R. Kerkhoven
- Michael R. Speicher
- Andreas Dander
Citations in the corpus
- pVAC-Seq: A genome-guided in silico approach to identifying tumor neoantigens (2016, background): “Several other studies have also characterized these neoantigens as being derived from somatically mutated genes in mouse [5] as well as in humans [6 – 9], and have shown that they can be recognized by T cells.”
- A survey of tools for variant analysis of next-generation genome sequencing data (2013, background): “finally, mutations are tested for their capability to elicit T-cell immunogenicity [22].”
- Genetic basis for clinical response to CTLA-4 blockade in melanoma. (2014, neutral): “Not available 1 (9) 1 (7) 14 (56) 2 (14)”
- T Cell Dysfunction in Cancer (2018, background): “These alterations distinguish cancer cells from normal cells, thereby frequently prompting the induction of tumor-reactive T cell responses in both mouse models and cancer patients (Castle et al., 2012; Matsushita et al., 2012; Robbins et al., 2013; van Rooij et al., 2013).”
- Tumor Exome Analysis Reveals Neoantigen-Specific T-Cell Reactivity in an Ipilimumab-Responsive Melanoma (2013, background): “Intriguingly, on the basis of animal model data it has recently been suggested that (therapy-induced) analysis of T cell reactivity against patient-specific neo-antigens may be feasible through exploitation of cancer genome data (11;12).”
- PGC-1α mediates mitochondrial biogenesis and oxidative phosphorylation to promote metastasis (2014, neutral): “Partial gene mutations reported for these lines are listed below (WT: wild-type: no mutation; * known mutations): 4T1 (P53*)(37), B16F10 (P53WT/KrasWT/cMycWT)(38) and MDA-MB-231 (P53*/Kras*/cMyc*)(39).”