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A stain showing that a lymphoma makes a lot of both the growth protein MYC and the survival protein BCL2, without the genes being rearranged. It predicts a worse course, but on its own it does not change the treatment.
Protein co-expression is several times commoner than rearrangement and is not the same thing. In a 167-patient training cohort treated with R-CHOP, MYC protein was detected in 29% and BCL2 protein in 44%, with both together in 21%; MYC protein correlated with high MYC messenger RNA and with MYC translocation, but the translocation was present in only 11%. MYC protein predicted inferior overall and progression-free survival only when BCL2 protein was present as well, and the finding held in an independent cohort of 140 patients after adjustment for other risk factors (Johnson 2012). In the 442-patient RICOVER series, MYC protein above the 40% threshold was found in 31.8% of tumours, BCL2 in 79.6% and BCL6 in 82.8% (Horn 2013).
The thresholds are not standardised across laboratories, the antibodies differ, and reading is subjective, which is the main reason this remains a prognostic observation rather than a decision point.
In plain words · MYC (Myc proto-oncogene protein) is a protein that switches other genes on and off. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Skin cancer, Multiple myeloma and 5 more.
This is a prognostic label, not a different disease. It does not by itself mean a stronger regimen, and it is not the same as a double hit, which is found by a different test and does change the plan. It is worth asking which of the two a report means, because the names are easy to confuse.
Written only from the label or guideline text cited on this page. Not medical advice; your own report and the reading your team gives it come first.
Immunohistochemistry for MYC and BCL2 read as the percentage of tumour nuclei or cytoplasm staining, with commonly used cut-offs of 40% for MYC and 50% for BCL2; a double expressor is positive for both. The thresholds are not harmonised between laboratories and the stains are read by eye, so two centres can call the same block differently.
“MYC protein expression was only associated with inferior overall and progression-free survival when BCL2 protein was coexpressed (P < .001).”
Johnson et al., Journal of Clinical Oncology 2012No approval uses this readout as a threshold. It is defined by Johnson et al., J Clin Oncol 2012: concurrent MYC and BCL2 protein expression in diffuse large B-cell lymphoma treated with R-CHOP.
Shares BCL2 rearrangement, t(14;18), BCL-2, Non-Hodgkin lymphoma (all types), Diffuse large B-cell lymphoma and the tags biomarker, lymphoma.
Shares Cell of origin (GCB vs ABC), Non-Hodgkin lymphoma (all types), Diffuse large B-cell lymphoma and the tags biomarker, lymphoma.
Shares Non-Hodgkin lymphoma (all types), Diffuse large B-cell lymphoma and the tags biomarker, lymphoma.
Shares Non-Hodgkin lymphoma (all types) and the tags biomarker, lymphoma.
Shares Non-Hodgkin lymphoma (all types) and the tags biomarker, lymphoma.
Shares BCL2 rearrangement, t(14;18), Intrinsic apoptosis (BCL-2 family), BCL-2, Non-Hodgkin lymphoma (all types) and the tags biomarker, lymphoma.
Shares BCL2 rearrangement, t(14;18), Cell of origin (GCB vs ABC), Double-hit and triple-hit: MYC with BCL2 and BCL6 rearrangement, Intrinsic apoptosis (BCL-2 family) and the tag lymphoma.
Shares Non-Hodgkin lymphoma (all types) and the tags biomarker, lymphoma.