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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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Related in: MedlinePlus

Disease-specific mutations in angioimmunoblastic T-cell lymphoma and its related cancers. Ras homolog gene family, member A (RHOA) acts as a molecular switch, cycling between a GDP-bound inactive state and a GTP-bound active state. RHOA is activated by specific guanine-exchange factors (GEFs) and inactivated by GTPase-activating proteins (GAPs). The G17V RHOA mutant in angioimmunoblastic T-cell lymphoma impairs binding capacity for GTP/GDP and inhibits activation of WT RHOA by sequestering the upstream activator GEFs.
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fig02: Disease-specific mutations in angioimmunoblastic T-cell lymphoma and its related cancers. Ras homolog gene family, member A (RHOA) acts as a molecular switch, cycling between a GDP-bound inactive state and a GTP-bound active state. RHOA is activated by specific guanine-exchange factors (GEFs) and inactivated by GTPase-activating proteins (GAPs). The G17V RHOA mutant in angioimmunoblastic T-cell lymphoma impairs binding capacity for GTP/GDP and inhibits activation of WT RHOA by sequestering the upstream activator GEFs.

Mentions: Functioning as a molecular switch, RHOA cycles between a GTP-bound active state and a GDP-bound inactive state.34 The G17V RHOA mutant functions as a dominant-negative to inhibit conversion of wild-type RHOA protein to an active state (Fig.2).31–33 Molecular mechanisms underlying the association of the G17V RHOA mutant with T-lymphomagenesis remain to be elucidated.


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 angioimmunoblastic T-cell lymphoma and its related cancers. Ras homolog gene family, member A (RHOA) acts as a molecular switch, cycling between a GDP-bound inactive state and a GTP-bound active state. RHOA is activated by specific guanine-exchange factors (GEFs) and inactivated by GTPase-activating proteins (GAPs). The G17V RHOA mutant in angioimmunoblastic T-cell lymphoma impairs binding capacity for GTP/GDP and inhibits activation of WT RHOA by sequestering the upstream activator GEFs.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig02: Disease-specific mutations in angioimmunoblastic T-cell lymphoma and its related cancers. Ras homolog gene family, member A (RHOA) acts as a molecular switch, cycling between a GDP-bound inactive state and a GTP-bound active state. RHOA is activated by specific guanine-exchange factors (GEFs) and inactivated by GTPase-activating proteins (GAPs). The G17V RHOA mutant in angioimmunoblastic T-cell lymphoma impairs binding capacity for GTP/GDP and inhibits activation of WT RHOA by sequestering the upstream activator GEFs.
Mentions: Functioning as a molecular switch, RHOA cycles between a GTP-bound active state and a GDP-bound inactive state.34 The G17V RHOA mutant functions as a dominant-negative to inhibit conversion of wild-type RHOA protein to an active state (Fig.2).31–33 Molecular mechanisms underlying the association of the G17V RHOA mutant with T-lymphomagenesis remain to be elucidated.

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