. Author manuscript; available in PMC: 2020 Apr 24.

Published in final edited form as: Leukemia. 2018 Dec 16;33(2):287–298. doi: 10.1038/s41375-018-0303-x

Table 2.

Biological and molecular features of the most common stereotyped subsets

Stereotyped subset	Subset #1	Subset #2	Subset #4	Subset #8
Frequency	˜2,4% ^{28, 67}	˜2.8% ^{28, 67}	˜1% ^{28, 67}	˜0.5 % ²⁸
IGHV/IGVL gene identity	Clan I IGHV genes/IGHD6–19 /IGHJ4/IGKV1[D]-39 ^{28, 29, 32}	IGHV3–21/ IGHJ6/ IGLV3–21 ^{28, 73}	γ-switched IGHV4–34/ IGHJ6/ IGKV2–30 ^{28, 29}	γ-switched IGHV4–39/ IGHD6–13/ IGHJ5/ IGKV1[D]-39 ^{28, 29, 83}
IGHV mutational status	Unmutated ^{28, 29}	Mutated (60%) Unmutated (40%) ^{28, 29, 74}	Mutated ^{28, 29, 33}	Unmutated ^{28, 29, 83}
BCR signaling properties	functional BCR signaling ^{36, 68}	functional BCR signaling ³⁶	anergic BCRs ⁸²	functional BCR signaling ³⁶
Predicted antigens	Vimentin; Calreticulin; MEACs; healthy Hep-2; apoptotic RAMOS; apoptotic Jurkat; oxidation markers; dsDNA; Insulin/LPS ^{36,50, 52, 89, 90}	cofilin-1; stomach chief cells; pancreatic exocrine glands ⁵³	intact anti-I/i motif; viable human memory B cells ^{33, 52,99}	MEACs; healthy Hep-2; apoptotic RAMOS; apoptotic Jurkat oxidation markers; extractable nuclear antigens; dsDNA microbial antigens/TLR ligands, calreticulin ^{36,50, 52, 90}
Genetic lesions in treatment-naïve CLL	deletion of 11q, 17p, NOTCH1, NFKBIE mutations ^{68, 70, 71, 76}	deletion of 13q, SF3B1 mutations ^{69, 70,75, 76}	deletion of 13q ^{69, 70,75}	trisomy 12, NOTCH1 mutations ^{69,70, 84}
Clinical course/ Risk of transformation	Aggressive (median TTFT of 1.6 yrs)³⁰	Aggressive (median TTFT of 1.9 yrs)³⁰	Indolent (median TTFT of 11 yrs)³⁰	Aggressive (median TTFT of 1.5 yrs),³⁰ increased risk of Richter’s transformation⁸⁴