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. 2017 Dec 21;7(12):660.
doi: 10.1038/s41408-017-0021-z.

Aggressive NK-cell leukemia: clinical subtypes, molecular features, and treatment outcomes

Y-T Tang  1 , D Wang  1 , H Luo  1 , M Xiao  1 , H-S Zhou  2 , D Liu  3 , S-P Ling  3 , N Wang  1 , X-L Hu  1 , Y Luo  1 , X Mao  1 , Q-L Ao  4 , J Huang  1 , W Zhang  1 , L-S Sheng  1 , L-J Zhu  1 , Z Shang  1 , L-L Gao  1 , P-L Zhang  1 , M Zhou  1 , K-G Zhou  1 , L-G Qiu  5 , Q-F Liu  2 , H-Y Zhang  6 , J-Y Li  7 , J Jin  8 , L Fu  9 , W-L Zhao  10 , J-P Chen  11 , X Du  12 , G Huang  13   14 , Q-F Wang  3   5   15 , J-F Zhou  1   5   16 , L Huang  17   18
Affiliations

Aggressive NK-cell leukemia: clinical subtypes, molecular features, and treatment outcomes

Y-T Tang et al. Blood Cancer J. .
No abstract available

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Conflict of interest statement

Competing interests

The authors declare that they have no competing interests.

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Figures

Fig. 1
Fig. 1. Outcomes and mutational patterns of ANKL subtypes
a Comparison of overall survival (OS) between subacute ANKL patients (N = 18) and classic ANKL patients (N = 95). OS was estimated from the onset of disease to the date of death or the end of the study. A marked survival advantage was revealed in subacute ANKL patients (left, P < 0.001), even if the patients receiving allo-HSCT (N = 7) were excluded (right, P < 0.001). b Somatic mutations identified by targeted sequencing in eight subacute ANKL patients and 29 classic ANKL patients were shown. The custom sequencing panel contained 18 candidate genes, including transcriptional factors (TP53 and MYC), JAK-STAT pathway genes (JAK2, JAK3, STAT3, STAT5A, STAT5B, and STAT6), other signaling pathway genes (PIK3CB, NFKB1, NFKBIA, MAP3K13, MAPK10, NRAS, and FGFR1), and epigenetic regulators (PRDM9, CREBBP, and TET2). Gene mutation patterns were similar between two subtypes, while TP53 gene mutations enriched in classic ANKL patients
See this image and copyright information in PMC

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