Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2020 Feb;61(2):460-464.
doi: 10.1080/10428194.2019.1675876. Epub 2019 Oct 15.

Clonally-Related CD5+ CLL/SLL and CD10+ high grade B-cell lymphoma suggests common neoplastic progenitor with branched disease evolution, with therapeutic implications

Affiliations

Clonally-Related CD5+ CLL/SLL and CD10+ high grade B-cell lymphoma suggests common neoplastic progenitor with branched disease evolution, with therapeutic implications

Priyadarshini Kumar et al. Leuk Lymphoma. 2020 Feb.
No abstract available

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
(a) Low power view showing hypercellular marrow. (b) High power view showing “blastoid” morphology in high grade B-cell lymphoma (HGBCL). (c) High power view showing CLL/SLL. (d) Aspirate smear showing dimorphic population of small lymphocytes with mature chromatin and large lymphoid cells with dispersed chromatin and prominent nucleoli. (e) Flow cytometric plots showing immunophenotype of HGBCL (orange) and CLL/SLL (blue). (f) SNP array findings in HGBCL showing homozygous deletion at 13q14.2 (including RB1 and SETDB2) and CN-LOH of 17p terminal to 17p11.2 (including TP53). (g) SNP array findings in CLL/SLL showing a 13q14.2 hemizygous deletion for RB1 and homozygous deletion for SETDB2 and loss of 17p13.1 to 17p12 (including TP53).
Figure 2.
Figure 2.
FISH findings on flow-sorted cells. (a) Loss of TP53 in 85% cells in CLL/SLL component. (b) No loss of TP53 in HGBCL component. (c) No MYC rearrangement in CLL/SLL component. (d) MYC rearrangement in 98% of cells in HGBCL component. (a–b) TP53 (17p13) probe (Red) and CEP17 (chr. 17 centromere) probe (Green). (c–d) MYC (8q24) break-apart probes.

References

    1. Swerdlow SH, Campo E, Harris NL, et al. WHO classification of tumours of haematopoietic and lymphoid tissues. 4th ed. Lyon: International Agency for Research on Cancer (IARC); 2017. (Steven H Swerdlow MEC, MD, PhD; Lee Harris Nancy, MD; Jaffe Elaine S., MD; Pileri Stefani A., MD, PhD; Stein Harald, MD; Thiele Jurgen, MD, PhD, editor. World Health Organization Classification of Tumours; ).
    1. Tsimberidou AM, Keating MJ. Richter syndrome: biology, incidence, and therapeutic strategies. Cancer. 2005;103(2): 216–228. - PubMed
    1. Fabbri G, Khiabanian H, Holmes AB, et al. Genetic lesions associated with chronic lymphocytic leukemia transformation to Richter syndrome. J Exp Med. 2013;210(11):2273–2288. - PMC - PubMed
    1. Rossi D, Spina V, Deambrogi C, et al. The genetics of Richter syndrome reveals disease heterogeneity and predicts survival after transformation. Blood. 2011;117(12):3391–3401. - PubMed
    1. Chigrinova E, Rinaldi A, Kwee I, et al. Two main genetic pathways lead to the transformation of chronic lymphocytic leukemia to Richter syndrome. Blood. 2013;122(15):2673–2682. - PubMed

Publication types

MeSH terms

LinkOut - more resources