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Disease-specific mutations in mature lymphoid neoplasms: recent advances.

Sakata-Yanagimoto M, Enami T, Yokoyama Y, Chiba S - Cancer Sci. (2014)

Bottom Line: Detecting these mutations is highly valuable in diagnosing MLN subtypes.Defining these mutations also sheds light on the molecular pathogenesis of MLN, furthering development of molecular targeting therapies.In this review, we focus on the disease-specific gene mutations in MLN discovered by recent massive sequencing technologies.

View Article: PubMed Central - PubMed

Affiliation: Department of Hematology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Department of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan; Department of Hematology, University of Tsukuba Hospital, Tsukuba, Japan.

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Disease-specific mutations in T-cell large granular lymphocytic leukemia and natural killer (NK)/T-cell lymphoma. Both JAK and signal transducer and activator of transcription (STAT) are mediators of diverse cytokine signaling. After binding of the cytokine to the receptor, JAK proteins are activated, followed by phosphorylation (P) of STATs. Activated STATs are dimerized and enter the nucleus to initiate target gene transcription. Both JAK3 mutation in NK/T-cell lymphoma and STAT3 mutation in T-cell large granular leukemia enhance the JAK/STAT signaling pathway.
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fig03: Disease-specific mutations in T-cell large granular lymphocytic leukemia and natural killer (NK)/T-cell lymphoma. Both JAK and signal transducer and activator of transcription (STAT) are mediators of diverse cytokine signaling. After binding of the cytokine to the receptor, JAK proteins are activated, followed by phosphorylation (P) of STATs. Activated STATs are dimerized and enter the nucleus to initiate target gene transcription. Both JAK3 mutation in NK/T-cell lymphoma and STAT3 mutation in T-cell large granular leukemia enhance the JAK/STAT signaling pathway.

Mentions: In this review, we describe newly identified mutations associated with MLN that occur frequently (>20%) in and substantially specific to disease subtypes (Table1, Figs3). We also address how to use information relevant to gene mutations for diagnostic applications as well as future therapeutic applications.


Disease-specific mutations in mature lymphoid neoplasms: recent advances.

Sakata-Yanagimoto M, Enami T, Yokoyama Y, Chiba S - Cancer Sci. (2014)

Disease-specific mutations in T-cell large granular lymphocytic leukemia and natural killer (NK)/T-cell lymphoma. Both JAK and signal transducer and activator of transcription (STAT) are mediators of diverse cytokine signaling. After binding of the cytokine to the receptor, JAK proteins are activated, followed by phosphorylation (P) of STATs. Activated STATs are dimerized and enter the nucleus to initiate target gene transcription. Both JAK3 mutation in NK/T-cell lymphoma and STAT3 mutation in T-cell large granular leukemia enhance the JAK/STAT signaling pathway.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317900&req=5

fig03: Disease-specific mutations in T-cell large granular lymphocytic leukemia and natural killer (NK)/T-cell lymphoma. Both JAK and signal transducer and activator of transcription (STAT) are mediators of diverse cytokine signaling. After binding of the cytokine to the receptor, JAK proteins are activated, followed by phosphorylation (P) of STATs. Activated STATs are dimerized and enter the nucleus to initiate target gene transcription. Both JAK3 mutation in NK/T-cell lymphoma and STAT3 mutation in T-cell large granular leukemia enhance the JAK/STAT signaling pathway.
Mentions: In this review, we describe newly identified mutations associated with MLN that occur frequently (>20%) in and substantially specific to disease subtypes (Table1, Figs3). We also address how to use information relevant to gene mutations for diagnostic applications as well as future therapeutic applications.

Bottom Line: Detecting these mutations is highly valuable in diagnosing MLN subtypes.Defining these mutations also sheds light on the molecular pathogenesis of MLN, furthering development of molecular targeting therapies.In this review, we focus on the disease-specific gene mutations in MLN discovered by recent massive sequencing technologies.

View Article: PubMed Central - PubMed

Affiliation: Department of Hematology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; Department of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan; Department of Hematology, University of Tsukuba Hospital, Tsukuba, Japan.

Show MeSH
Related in: MedlinePlus