We examine the immunoreactivity of the non-
receptor tyrosine kinase,
c-Src kinase and its downstream molecule,
signal transducer and activator of transcription 3 (pStat3) in
retinoblastoma (RB), and correlation with invasiveness and differentiation.
Tumor samples from 40 patients with RB were available for the study. There were 18
tumors in group 1 (non-invasive) and 22
tumors in group 2 (invasive). The immunoreactivity of
c-Src kinase and pStat3 was compared in the two groups of
tumors. Group 1 (non-invasive) RB showed intermediate
c-Src kinase immunoreactivity (Allred score 4-5) in 14/18
tumors and low immunoreactivity (Allred score 2-3) in 4/18
tumors. pStat3 was intermediate (Allred score 4-5) in 6/18
tumors and negative (Allred score 0) in 12/18
tumors. Group 2 (invasive) RB showed high
c-Src kinase immunoreactivity (Allred score 6-8) in 22/22
tumors and high pStat3 (Allred score 6-8) in 19/22
tumors. The expression of
c-Src kinase (P<0.001) and pStat3 (P<0.001) was significantly higher in group 2 RB.
Src kinase expression (P<0.05) and pStat3 expression (P<0.05) was higher in the poorly differentiated
tumors compared to moderately- and well-differentiated
tumors. The increased expression of
c-Src kinase and pStat3 expression could play a role in the invasiveness of group 2
tumors. Further characterization of the pathways involved in the pathogenesis of RB will shed light on fundamental mechanisms of
tumorigenesis.