Although with the majority of the specimens there was no obvious correlation between the morphologic cell type of lymphoma/leukemia and the c-onc RNA levels, interestingly two of the three samples diagnosed as chronic lymphocytic leukemia, B-cell type, showed considerably increased transcription of the c-myc gene relative to the other B-cell neoplasms.
We propose that altered expression of the c-myc gene, induced by translocation to an immunoglobulin locus, is a critical oncogenic event for these B lymphoid tumors.
N-myc is a DNA sequence which shares limited homology to the proto-oncogene c-myc and has been found to be amplified in both primary tissue and cell lines from neuroblastoma, a childhood tumour of neuroectodermal origin.
When 96 neoplastic lesions from 45 patients were examined, these lesions could be grouped into three categories: high copy (tumors with greater than 3 copies of the N-myc or c-myc gene per haploid genome), middle copy (1.5 to 3 copies per genome), and normal copy.
This finding further supports the common association of the myc gene family in neurogenic tumors and provides evidence of myc gene amplification in human brain cancer.
To determine the position of the gene encoding the alpha chain of the T-cell receptor and of the protooncogene MYC (formerly c-myc) in relation to the breakpoint junction and to evaluate their possible role in the pathogenesis of T-cell neoplasia, we applied the techniques of in situ chromosomal hybridization, Southern blot analysis, and molecular cloning to MOLT-16 cells.
Consequently, the levels of c-myc gene expression observed in primary tumor tissue did not help to define those individuals at higher or lower risk for recurrence of disease and did not point to the likelihood of increased or decreased survival in individuals undergoing surgery for adenocarcinoma of the colon.
Quantitation of c-myc protein levels in these tumor cell lines by ELISA assay indicates that they are 8- to 37-fold higher than the levels of protein in normal cells.
Comparative densitometry of Northern blot analyses demonstrated enhanced level of c-myc gene expression, i.e., greater than threefold increase over normal kidney tissues, in 11 of 15 (73%) of the tumors examined.
A significant increase in the mRNA levels of neuron-specific enolase was detected in BEAS-2B cells containing both the c-raf-1 and c-myc genes and derived tumor cell lines.
In contrast with most AIDS-associated NHLs, each of these three neoplasmslackedc-myc gene rearrangements and contained Epstein-Barr virus (EBV) proteins and/or sequences.
Elevation of c-myc transcript level in human liver during surgical resection of hepatocellular carcinoma: possible cause for underestimation of c-myc gene activation in the tumor.
Although no statistical correlation was found between different clinicopathological parameters (patient age, sex, TNM staging, number of lymph nodes invaded, extracapsular rupture of the tumour, its histopathological differentiation, or its site), the survival periods of patients with tumours possessing elevated levels of c-myc protein were found to be statistically shorter than those with lower levels of c-myc expression, (P less than 0.02).