Basic steps in oncogene formation

Inhibiting signaling in a BCAN-TRK1 brain tumor

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. The use of  CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) to introduce

SCYL3-NTRK1, HEAT repeats with an active kinase

An exciting and perplexing new TrkA fusion: SCYL3-NTRK1. Yes, we have yet another chromosome 1 intra-chromosome rearrangement with NTRK1. This time it is with a rather poorly understood protein whose gene name is SCYL3 and protein name is PACE1 (Protein-associating

A brief history of NTRK fusions

NTRK fusions (Tropomyosin related kinase fusion proteins) were discovered thirty years ago in search for colon carcinoma associated oncogenes (Martin-Zanca 1986). In those days, fusion proteins were called chimeras, after a Greek mythological monster.  The syntax in most common usage

MYO5A-NTRK3, a motor fused to a kinase

Have motor, will travel. Lu Wang of  Memorial Sloan Kettering Cancer Center and a very large group of coworkers published an extremely interesting report of a MYO5A-NTRK3 gene rearrangement of the long arm of chromosome 5 in a childhood melanocytic

Identification of NTRK fusions in pediatric mesenchymal tumors

Breaking news Dean Pavlick  of Foundation Medicine, Inc. and coworkers profiled 2,031 advanced cancers from pediatric patients (< 21 years) with the goal of identifying NTRK fusions. The role of one NTRK gene rearrangement, ETV6-NTRK3, was mentioned in adult mammary analog

QKI-NTRK2, quaking with a kinase

The QKI-NTRK2 fusion was mentioned in a report of somatic mutations in pilocytic astrocytoma, the most common childhood brain tumor (Jones 2013). The protein quaking encoded by the QKI gene is an RNA-binding protein. The many splice variations of quaking are making

TPM3-NTRK1, an actin targeted kinase?

Tropomyosins bind to the cytoskeleton protein actin. They also modulate how other actin binding proteins bind to actin. Nemaline myopathy and Rod myopathy are diseases caused by variations in the TPM3 gene. Several splice variants of tropomyosin are coded for

LMNA-NTRK1, weaving kinase domains into a fabric

Lamins A and C are alternatively spliced products of the LMNA gene. Lamins are considered nuclear intermediate filaments. Lamins are components of the nuclear lamina. The nuclear lamina lines the nucleoplasmic side of the nuclear membrane. Diseases caused by variations

SQSTM1-NTRK1, a kinase gets fused with a garbage disposal protein

The SQSTM1 gene product, p62, is a scaffold protein involved in protein turnover and signaling. p62 is commonly found in dense protein bodies in eukaryotic cells. In autophagy, p62 (the protein) shuttles ubiquitnated proteins to the autophagosome for degradation (Ciuffa

Detecting Gene Rearrangements in Patient Populations

Detecting Gene Rearrangements in Patient Populations Through a 2-Step Diagnostic Test Comprised of Rapid IHC Enrichment Followed by Sensitive Next-Generation Sequencing (NGS). Murphy DA, Ely HA, Shoemaker R, Boomer A, Culver BP, Hoskins I, Haimes JD, Walters RD, Fernandez D,