Mosaic amplification of multiple receptor tyrosine kinase genes in glioblastoma.

By M. Snuderl, Ladan Fazlollahi, Long P. Le, Mai Nitta, Boryana H. Zhelyazkova, Christian J Davidson, S. Akhavanfard, D. Cahill, Kenneth D. Aldape, Rebecca A. Betensky and 2 more. Cancer Cell, 2011

708 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics, Oncology

View Paper: https://www.semanticscholar.org/paper/d6c19223eec8fa5bcbc25346d3e6497e13cbcfa6

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The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Nicholas McGranahan
2. Charles Swanton
3. Gad Getz
4. Eric S. Lander
5. Matthew Meyerson
6. Aviv Regev
7. Christopher Sander
8. Peter W. Laird

In Genetics

1. Charles Swanton
2. Jill S. Barnholtz-Sloan
3. Aviv Regev
4. Christopher Sander
5. Peter W. Laird
6. Richard A. Gibbs
7. David Haussler
8. Marco A. Marra

In Oncology

1. Nicholas McGranahan
2. Charles Swanton
3. John N. Weinstein
4. Christopher Sander
5. Peter W. Laird
6. Charles M. Perou
7. Gad Getz
8. Giovanni Ciriello

Citations in the corpus

• The Somatic Genomic Landscape of Glioblastoma (2013, background): “4%, 14/33), as did the majority of MET-altered tumors (3/4), reflecting a pattern of intratumoral heterogeneity that has been previously documented by in situ hybridization (Snuderl et al., 2011; Szerlip et al., 2012).”
• Intratumor heterogeneity in human glioblastoma reflects cancer evolutionary dynamics (2013, methodology): “In GB, intratumor heterogeneity at the level of the tyrosine kinases EGFR, PDGFRA, and MET was demonstrated previously using FISH (11).”
• Single-cell RNA-seq highlights intratumoral heterogeneity in primary glioblastoma (2014, background): “Mosaic RTK amplification and redundant signaling pathways contribute to targeted therapy resistance in glioblastoma (11, 30, 31).”
• Glioblastoma: pathology, molecular mechanisms and markers (2015, background): “More importantly, activating genetic alterations can occur simultaneously in multiple RTKs within individual GBMs, with distinct cellular subpopulations containing amplified receptor genes [151, 158].”
• Clonal status of actionable driver events and the timing of mutational processes in cancer evolution (2015, background): “For instance, in colorectal cancer, subclonal RAS mutations have been shown to precipitate resistance to cetuximab (8), and in glioblastomas, individual driver events can be present in distinct populations of cancer cells or subclones (9, 10).”
• Cancer heterogeneity: implications for targeted therapeutics (2013, background): “For this reason, it is routine for pathologists to examine multiple sections from the same tumour, but to report only the highest grade.”