RHOA mutation in follicular T-cell lymphoma: Clinicopathological analysis of 16 cases.


Journal

Pathology international
ISSN: 1440-1827
Titre abrégé: Pathol Int
Pays: Australia
ID NLM: 9431380

Informations de publication

Date de publication:
Sep 2020
Historique:
received: 24 03 2020
revised: 04 06 2020
accepted: 16 06 2020
pubmed: 11 7 2020
medline: 23 6 2021
entrez: 11 7 2020
Statut: ppublish

Résumé

Follicular T-cell lymphoma (FTCL) is considered to originate from follicular helper T-cell (Tfh) cells. Angioimmunoblastic T-cell lymphoma (AITL) and peripheral T-cell lymphomas with the Tfh phenotype, derived from Tfh cells, often harbor RHOA G17V mutation. We investigated whether RHOA mutations affect the clinicopathological features of FTCL. We performed deep sequencing and Sanger sequencing for RHOA exon 2 in 16 cases of FTCL. Nine cases showed RHOA mutations, including eight with c.G50T, p.Gly17Val and one with c.G50A, p.Gly17Glu, c.A52G, p.Lys18Glu, c.T102C, p.Tyr34Tyr and c.G145T, p.Asp49Tyr. Compared to the RHOA mutation-negative group, the RHOA mutation-positive group had a higher tendency for B-immunoblasts (P = 0.06), the AITL component (P = 0.09), and higher positive rate for CD10 (P = 0.09) and BCL6 (P = 0.09), and a significantly higher positive rate for CXCL13 (P = 0.04). Although not statistically significant, the RHOA mutation-positive group showed higher values for almost all characteristic AITL features. There was no significant difference in overall survival between RHOA mutation-positive and -negative groups. The RHOA mutation may play an important role in clinicopathological characteristics and lymphomagenesis of FTCL. A more detailed investigation is needed to highlight the importance of RHOA mutations in FTCL.

Identifiants

pubmed: 32648273
doi: 10.1111/pin.12981
doi:

Substances chimiques

Biomarkers, Tumor 0
RHOA protein, human 124671-05-2
rhoA GTP-Binding Protein EC 3.6.5.2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

653-660

Informations de copyright

© 2020 Japanese Society of Pathology and John Wiley & Sons Australia, Ltd.

Références

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Auteurs

Hiroaki Miyoshi (H)

Department of Pathology, School of Medicine, Kurume University, Fukuoka, Japan.

Mamiko Sakata-Yanagimoto (M)

Department of Hematology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.

Joji Shimono (J)

Department of Pathology, School of Medicine, Kurume University, Fukuoka, Japan.

Noriaki Yoshida (N)

Department of Pathology, School of Medicine, Kurume University, Fukuoka, Japan.

Keiichiro Hattori (K)

Department of Hematology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.

Fumiko Arakawa (F)

Department of Pathology, School of Medicine, Kurume University, Fukuoka, Japan.

Eriko Yanagida (E)

Department of Pathology, School of Medicine, Kurume University, Fukuoka, Japan.

Mai Takeuchi (M)

Department of Pathology, School of Medicine, Kurume University, Fukuoka, Japan.

Kyohei Yamada (K)

Department of Pathology, School of Medicine, Kurume University, Fukuoka, Japan.

Takaharu Suzuki (T)

Department of Pathology, School of Medicine, Kurume University, Fukuoka, Japan.

Mayuko Moritsubo (M)

Department of Pathology, School of Medicine, Kurume University, Fukuoka, Japan.

Takuya Furuta (T)

Department of Pathology, School of Medicine, Kurume University, Fukuoka, Japan.

Shigeru Chiba (S)

Department of Hematology, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.

Koichi Ohshima (K)

Department of Pathology, School of Medicine, Kurume University, Fukuoka, Japan.

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