Table 1.
B‐cell malignancy | Major prosurvival proteins expressed | Level of BCL2 expression | Variability | Comment on mechanism |
---|---|---|---|---|
CLL | BCL2 > MCL >> BCLxL12, 14 | High | Some variability, but always high | BCL2: loss of repression by miRNA 15/1610; MCL1 & BCLxL induced by CD40 ligation and microenvironmental stimuli12, 15 |
Follicular lymphoma | BCL21; BCLxL16; MCL117, 18 | High | Rare to not be expressed | t(14;18) leads to constitutive expression from IgH promotor1; CD40L stimulates BCLxL expression16; MCL1 in centroblasts17 |
Diffuse large B‐cell lymphoma | BCL2 or MCL118 | High in GC type; low in many ABC type | High; where MYC‐driven MCL1 > BCL2 | Varies: including gene amplification,19 t(14;18) in double‐hit lymphoma, consequence of MYC dysregulation20 |
MCL | BCL2 > MCL118, 21 | High | Minor | Consequence of Cyclin D1 dysregulation22; MCL1 high in blastoid21 |
Myeloma | BCL2, MCL1, BCLxL13, 23 | High, especially t(11;14) | Moderate | BCL2 consequence of Cyclin dysregulation24; MCL1 constitutively expressed by plasma cells25; BCLxL increased through microenvironmental stimulation13 |
ALL | BCL2, MCL1, BCLxL26, 27 | Variable | Significant26 | Appears to mimic expression pattern of precursor cell; patterned by oncogenic driver |
ABC, activated B‐cell or origin subtype; ALL, acute lymphoblastic leukemia; BCL2, B‐cell‐lymphoma‐2; GC, germinal center cell of origin subtype; MCL, mantle cell lymphoma.