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Molecular heterogeneity in peripheral T-cell lymphoma, not otherwise specified revealed by comprehensive genetic profiling

Watatani, Yosaku, Sato, Yasuharu, Miyoshi, Hiroaki, Sakamoto, Kana, Nishida, Kenji, Gion, Yuka, Nagata, Yasunobu, Shiraishi, Yuichi, Chiba, Kenichi, Tanaka, Hiroko, Zhao, Lanying, Ochi, Yotaro, Takeuchi, Yasuhide, Takeda, June, Ueno, Hiroo, Kogure, Yasunori, Shiozawa, Yusuke, Kakiuchi, Nobuyuki, Yoshizato, Tetsuichi, Nakagawa, Masahiro M., Nanya, Yasuhito, Yoshida, Kenichi, Makishima, Hideki, Sanada, Masashi, Sakata-Yanagimoto, Mamiko, Chiba, Shigeru, Matsuoka, Ryota, Noguchi, Masayuki, Hiramoto, Nobuhiro, Ishikawa, Takayuki, Kitagawa, Junichi, Nakamura, Nobuhiko, Tsurumi, Hisashi, Miyazaki, Tatsuhiko, Kito, Yusuke, Miyano, Satoru, Shimoda, Kazuya, Takeuchi, Kengo, Ohshima, Koichi, Yoshino, Tadashi, Ogawa, Seishi, Kataoka, Keisuke·2019·Leukemia
DOI 10.1038/s41375-019-0473-1
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Fig. 1 WES analysis for 20 PTCL, NOS cases. a The number of coding mutations (top), frequency of mutational signature (middle), and a heatmap showing the distribution of mutations in TET2 , RHOA , IDH2 , TP53 , and CDKN2A alterations, TFH markers, sample source, and molecular subtype are depicted. All panels are aligned, with the vertical tracks representing 20 PTCL, NOS cases. b Two mutational signatures identi fi ed by pmsignature algorithm in PTCL, NOS. Signature 1 was predominated by age-related C > T transitions at CpG dinucleotides, while signature 2 (of unknown etiology) consisted of C
Fig. 1 WES analysis for 20 PTCL, NOS cases. a The number of coding mutations (top), frequency of mutational signature (middle), and a heatmap showing the distribution of mutations in TET2 , RHOA , IDH2 , TP53 , and CDKN2A alterations, TFH markers, sample source, and molecular subtype are depicted. All panels are aligned, with the vertical tracks representing 20 PTCL, NOS cases. b Two mutational signatures identi fi ed by pmsignature algorithm in PTCL, NOS. Signature 1 was predominated by age-related C > T transitions at CpG dinucleotides, while signature 2 (of unknown etiology) consisted of CCC-BY · From the PDF
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Fig. 3 Commonly affected functional pathways in PTCL, NOS. Driver alterations, including mutations, CNAs, and SVs, are summarized according to their functionalities. Frequencies of mutations (left) and CNAs/SVs (right) are expressed as the percentage of altered cases in 133 PTCL, NOS cases. Major determinants of the molecular
Fig. 3 Commonly affected functional pathways in PTCL, NOS. Driver alterations, including mutations, CNAs, and SVs, are summarized according to their functionalities. Frequencies of mutations (left) and CNAs/SVs (right) are expressed as the percentage of altered cases in 133 PTCL, NOS cases. Major determinants of the molecularCC-BY · From the PDF
Image 4
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CC-BY · From the PDF
Fig. 6 Clinical and genetic differences among three molecular subtypes of PTCL, NOS. a Comparison of tumor cell fraction among three molecular subtypes of PTCL, NOS. Fisher ' s exact test. b Kaplan -Meier survival curves of overall survival of 46 PTCL, NOS cases strati fi ed by molecular subtype. The prognostic impact on survival was evaluated by log-rank test. c Comparison of frequencies of somatic alterations among the entire cohort ( n = 133) and each molecular subtype ( n = 50, 42, and
Fig. 6 Clinical and genetic differences among three molecular subtypes of PTCL, NOS. a Comparison of tumor cell fraction among three molecular subtypes of PTCL, NOS. Fisher ' s exact test. b Kaplan -Meier survival curves of overall survival of 46 PTCL, NOS cases strati fi ed by molecular subtype. The prognostic impact on survival was evaluated by log-rank test. c Comparison of frequencies of somatic alterations among the entire cohort ( n = 133) and each molecular subtype ( n = 50, 42, andCC-BY · From the PDF
Fig. 7 Genetic alterations in molecules associated with immune evasion and transcriptional regulation. a Positions and types of somatic mutations encoded in HLA-A (NM_002116), PDCD1 (NM_005018), IRF2BP2 (NM_001077397), and YTHDF2 (NM_001173128) detected in 133 PTCL, NOS cases. IRF2BP2 mutations observed in 81 ATL cases are also shown. b Validation of CRISPR/Cas9-mediated targeting of IRF2BP2 gene by amplicon sequencing. Representative sequencing data for mock- (left) and sgIRF2BP2-1- (right) transfected samples were visualized with IGV. c Relative expression of IRF2BP2 mRNA in Jurkat cells transfected with the indicated sgRNA vectors ( n = 4). Expression values were normalized to the mock-transfected
Fig. 7 Genetic alterations in molecules associated with immune evasion and transcriptional regulation. a Positions and types of somatic mutations encoded in HLA-A (NM_002116), PDCD1 (NM_005018), IRF2BP2 (NM_001077397), and YTHDF2 (NM_001173128) detected in 133 PTCL, NOS cases. IRF2BP2 mutations observed in 81 ATL cases are also shown. b Validation of CRISPR/Cas9-mediated targeting of IRF2BP2 gene by amplicon sequencing. Representative sequencing data for mock- (left) and sgIRF2BP2-1- (right) transfected samples were visualized with IGV. c Relative expression of IRF2BP2 mRNA in Jurkat cells transfected with the indicated sgRNA vectors ( n = 4). Expression values were normalized to the mock-transfectedCC-BY · From the PDF

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Metadata

Authors
Watatani, Y., Sato, Y., Miyoshi, H., Sakamoto, K., Nishida, K., Gion, Y., Nagata, Y., Shiraishi, Y., Chiba, K., Tanaka, H., Zhao, L., Ochi, Y., Takeuchi, Y., Takeda, J., Ueno, H., Kogure, Y., Shiozawa, Y., Kakiuchi, N., Yoshizato, T., Nakagawa, M. M., Nanya, Y., Yoshida, K., Makishima, H., Sanada, M., Sakata-Yanagimoto, M., Chiba, S., Matsuoka, R., Noguchi, M., Hiramoto, N., Ishikawa, T., Kitagawa, J., Nakamura, N., Tsurumi, H., Miyazaki, T., Kito, Y., Miyano, S., Shimoda, K., Takeuchi, K., Ohshima, K., Yoshino, T., Ogawa, S., & Kataoka, K.
ORCID
Venue
Leukemia
Publisher
Springer Science and Business Media LLC
Published
2019-05-15
Volume
33
Issue
12
Pages
2867-2883
ISSN
  • 0887-6924
  • 1476-5551
DOI
10.1038/s41375-019-0473-1
Cited by
195
References
3
Language
en
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CoChat. (2026). Citation check: Molecular heterogeneity in peripheral T-cell lymphoma, not otherwise specified revealed by comprehensive genetic profiling. https://app.cochat.ai/papers/10.1038/s41375-019-0473-1
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Watatani, Y., Sato, Y., Miyoshi, H., Sakamoto, K., Nishida, K., Gion, Y., Nagata, Y., Shiraishi, Y., Chiba, K., Tanaka, H., Zhao, L., Ochi, Y., Takeuchi, Y., Takeda, J., Ueno, H., Kogure, Y., Shiozawa, Y., Kakiuchi, N., Yoshizato, T., . . . Kataoka, K. (2019). Molecular heterogeneity in peripheral T-cell lymphoma, not otherwise specified revealed by comprehensive genetic profiling. Leukemia. https://doi.org/10.1038/s41375-019-0473-1