Engineered BCAN-TRK1 drives glioma formation

This post only covers a small portion of a very in depth study of Peter Cook and coworkers of Memorial Sloan Kettering Cancer Center in New York City. This group used a new genetic engineering technique called CRISPR (Clustered Regularly

Trk Mutations in Pediatric Glioma

The following is a gleaning of Trk mutations from a very comprehensive whole genome sequencing study of a very devastating childhood disease: pediatric high grade glioma (Wu 2014). This is not meant to be a comprehensive review of the study

Simple Trk Mutations in Colorectal Carcinoma

The discovery of the NTRK gene fusion by way of it’s colon cancer driving fusion protein is covered on another site.  The NTRK genes were discovered before the sparingly expressed kinases.  It is rather ironic that scientists looked at simple

TrkAIII and SOD2 in neuroblastoma:

When a splice variant like TrkAIII behaves differently than the canonical TrkAII variant, one has to ask what this could mean for Trk  fusion proteins. Pierdomenico Ruggeri and coworkers tested the hypothesis that not only are neuroblastoma associated proteins TrkAIII

NACC2-TRK2 in astrocytoma

Browsing NGS databases for TRK gene rearrangements can lead to more profound questions regarding their origin. In our sister website we had only one example of an TRK2 gene rearrangement, QKI-TRK2. The COSMIC database was searched revealing one more TRK2

Trk kinase domain nonsense mutations

A non-concern:  nonsense mutations in the TRK kinase domain? As we have reviewed earlier, nonsense mutations create premature translation stop condons. The end result is a truncated Trk that may or may not involve the active site. Toffalini and Demoulin

Trk activation loop mutations

In search of mutations that mimic autophosphorylation Toffalini and Demoulin (2010)  had some interesting comments on the need of phosphorylation of the 1-3 tyrosines on the Trk activation loop.  The most obvious effect of posphorylation would be the introduction of

Trk juxta membrane mutations

The Trk juxta membrane domain is coming out of the shadows and maybe telling us something about Trk fusion proteins In many structural reviews of the Trk family of receptor tyrosine kinases, the extracellular domains that bind growth factors are

Trk gene copy number variations and methylation

CNV – Overview In this overview we will show a tumor from the COSMIC database with a TRK3 gene amplification. In our search of TRK gene copy number variations, the first study on the list was COSU331. Apparently, only one

TRK3 copy number, what does it mean?

Predicting mRNA expression from copy number:  It’s not working! Total TRK3 copy number is a weak predictor of the copies of the “minor allele” but not a predictor of the mRNA transcripts. Amplified TRK3 gene copies do not take up