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  1. Article ; Online: Modeling saltwater intrusion risk in the presence of uncertainty.

    Tran, Dat Q / Nguyen, Nguyen N T / Huynh, Minh V T / Bairagi, Subir K / Le, Kieu N / Tran, Ty V / Durand-Morat, Alvaro

    The Science of the total environment

    2023  Volume 908, Page(s) 168140

    Abstract: The Mekong Delta is one of the most productive rice-producing regions in the world, exporting approximately one-fifth of the global rice traded annually. Previous studies note that saltwater intrusion is a serious concern, and the intensity of saltwater ... ...

    Abstract The Mekong Delta is one of the most productive rice-producing regions in the world, exporting approximately one-fifth of the global rice traded annually. Previous studies note that saltwater intrusion is a serious concern, and the intensity of saltwater intrusion is primarily driven by sea level rise, land subsidence, anthropogenic sediment starvation, and upstream hydro-infrastructure developments. However, these studies often rely on scenario-based approaches instead of an integrated approach to assess the possible impacts of saltwater intrusion. Using an integrated hydrodynamic-statistical-economic model, we investigate how and the extent to which these drivers may impact the saltwater intrusion. We also examine the costs and returns of two popular saltwater intrusion control policies, i.e., hard-engineering structural and soft-land use planning. When comparing the baseline scenarios, the findings indicate that anthropogenic forces lead to a four times greater saltwater intrusion intensity than the climate change-induced sea level rise. The results further reveal a 50 % or less chance that annual saltwater-affected areas would exceed 1.93 million ha for the baseline, but the likelihood is highly likely to be 100 % with a sea level rising of 22 cm. Under the combined effects of sea-level rise, land subsidence, and riverbed incision, our model shows that the probability of annual saltwater-affected areas staying above 2.30 million ha is almost equal to one. This finding implies that a large share of the current rice-planted areas of the Delta could be wiped out of production for at least one season a year. The findings show that a combination of hard and soft policies would be a more sustainable and cost-effective strategy to lower the intensity and risks of saltwater intrusion. Therefore, there is an urgent need for better coordination of governance and investments among regions within the Delta and counties in the whole Mekong River Basin.
    Language English
    Publishing date 2023-11-02
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 121506-1
    ISSN 1879-1026 ; 0048-9697
    ISSN (online) 1879-1026
    ISSN 0048-9697
    DOI 10.1016/j.scitotenv.2023.168140
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Getting a Handle on RAS-targeted Therapies: Cysteine Directed Inhibitors.

    Huynh, Minh V / Campbell, Sharon L

    Mini reviews in medicinal chemistry

    2015  Volume 16, Issue 5, Page(s) 383–390

    Abstract: Directly inhibiting oncogenic RAS proteins has proven to be an arduous task, as after more than thirty years of intensive investigation, no clinically relevant therapies exist. Recently, two classes of selective small molecule inhibitors that target a ... ...

    Abstract Directly inhibiting oncogenic RAS proteins has proven to be an arduous task, as after more than thirty years of intensive investigation, no clinically relevant therapies exist. Recently, two classes of selective small molecule inhibitors that target a cysteine-containing RAS mutant have been developed, representing the first directed approaches to specifically inhibit an oncogenic KRAS mutant. In this mini-review, we first assess the development and targeting strategies associated with novel cysteine-directed RAS inhibitors. Next, we describe the variable oncogenic potency of the KRAS G12C mutant when compared to other KRAS G12 mutants. Lastly, we evaluate how the redox properties of KRAS G12C may play a role in differential signaling and tumorigenic potency of the oncogene, the efficacy of small molecules targeting this specific RAS mutant and further development of directed oncogenic RAS inhibitors.
    MeSH term(s) Allosteric Regulation/drug effects ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/metabolism ; Antineoplastic Agents/therapeutic use ; Cysteine/metabolism ; Guanosine Diphosphate/analogs & derivatives ; Guanosine Diphosphate/metabolism ; Guanosine Diphosphate/therapeutic use ; Humans ; Mutation ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Small Molecule Libraries/metabolism ; Small Molecule Libraries/pharmacology ; Small Molecule Libraries/therapeutic use ; ras Proteins/antagonists & inhibitors ; ras Proteins/genetics ; ras Proteins/metabolism
    Chemical Substances Antineoplastic Agents ; Small Molecule Libraries ; Guanosine Diphosphate (146-91-8) ; ras Proteins (EC 3.6.5.2) ; Cysteine (K848JZ4886)
    Language English
    Publishing date 2015-09-18
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2104081-3
    ISSN 1875-5607 ; 1389-5575
    ISSN (online) 1875-5607
    ISSN 1389-5575
    DOI 10.2174/1389557515666151001154352
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Oncogenic KRAS G12C: Kinetic and redox characterization of covalent inhibition.

    Huynh, Minh V / Parsonage, Derek / Forshaw, Tom E / Chirasani, Venkat R / Hobbs, G Aaron / Wu, Hanzhi / Lee, Jingyun / Furdui, Cristina M / Poole, Leslie B / Campbell, Sharon L

    The Journal of biological chemistry

    2022  Volume 298, Issue 8, Page(s) 102186

    Abstract: The recent development of mutant-selective inhibitors for the oncogenic ... ...

    Abstract The recent development of mutant-selective inhibitors for the oncogenic KRAS
    MeSH term(s) Kinetics ; Mutation ; Oxidation-Reduction ; Proto-Oncogene Proteins p21(ras)/genetics ; Sulfhydryl Compounds
    Chemical Substances Sulfhydryl Compounds ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2022-06-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2022.102186
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: RHOA

    Schaefer, Antje / Hodge, Richard G / Zhang, Haisheng / Hobbs, G Aaron / Dilly, Julien / Huynh, Minh V / Goodwin, Craig M / Zhang, Feifei / Diehl, J Nathaniel / Pierobon, Mariaelena / Baldelli, Elisa / Javaid, Sehrish / Guthrie, Karson / Rashid, Naim U / Petricoin, Emanuel F / Cox, Adrienne D / Hahn, William C / Aguirre, Andrew J / Bass, Adam J /
    Der, Channing J

    Science signaling

    2023  Volume 16, Issue 816, Page(s) eadg5289

    Abstract: Cancer-associated mutations in the guanosine triphosphatase (GTPase) RHOA are found at different locations from the mutational hotspots in the structurally and biochemically related RAS. ... ...

    Abstract Cancer-associated mutations in the guanosine triphosphatase (GTPase) RHOA are found at different locations from the mutational hotspots in the structurally and biochemically related RAS. Tyr
    MeSH term(s) Animals ; Humans ; Mice ; Actins ; Guanosine Triphosphate ; p21-Activated Kinases ; Proto-Oncogene Proteins p21(ras) ; Receptor, IGF Type 1 ; rhoA GTP-Binding Protein/genetics ; Signal Transduction ; Stomach Neoplasms/genetics
    Chemical Substances Actins ; Guanosine Triphosphate (86-01-1) ; IGF1R protein, human ; p21-Activated Kinases (EC 2.7.11.1) ; PAK1 protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Receptor, IGF Type 1 (EC 2.7.10.1) ; rhoA GTP-Binding Protein (EC 3.6.5.2) ; RHOA protein, human (124671-05-2) ; RhoA protein, mouse (EC 3.6.5.2)
    Language English
    Publishing date 2023-12-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.adg5289
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Functional and biological heterogeneity of KRAS

    Huynh, Minh V / Hobbs, G Aaron / Schaefer, Antje / Pierobon, Mariaelena / Carey, Leiah M / Diehl, J Nathaniel / DeLiberty, Jonathan M / Thurman, Ryan D / Cooke, Adelaide R / Goodwin, Craig M / Cook, Joshua H / Lin, Lin / Waters, Andrew M / Rashid, Naim U / Petricoin, Emanuel F / Campbell, Sharon L / Haigis, Kevin M / Simeone, Diane M / Lyssiotis, Costas A /
    Cox, Adrienne D / Der, Channing J

    Science signaling

    2022  Volume 15, Issue 746, Page(s) eabn2694

    Abstract: Missense mutations at the three hotspots in the guanosine triphosphatase (GTPase) RAS- ... ...

    Abstract Missense mutations at the three hotspots in the guanosine triphosphatase (GTPase) RAS-Gly
    MeSH term(s) Actins ; Carcinoma, Pancreatic Ductal/genetics ; GTP Phosphohydrolases/genetics ; Humans ; Mutation ; Pancreatic Neoplasms/genetics ; Proto-Oncogene Proteins p21(ras)/genetics ; Pancreatic Neoplasms
    Chemical Substances Actins ; KRAS protein, human ; GTP Phosphohydrolases (EC 3.6.1.-) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2022-08-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.abn2694
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Mutation-specific RAS oncogenicity explains NRAS codon 61 selection in melanoma.

    Burd, Christin E / Liu, Wenjin / Huynh, Minh V / Waqas, Meriam A / Gillahan, James E / Clark, Kelly S / Fu, Kailing / Martin, Brit L / Jeck, William R / Souroullas, George P / Darr, David B / Zedek, Daniel C / Miley, Michael J / Baguley, Bruce C / Campbell, Sharon L / Sharpless, Norman E

    Cancer discovery

    2014  Volume 4, Issue 12, Page(s) 1418–1429

    Abstract: Unlabelled: NRAS mutation at codons 12, 13, or 61 is associated with transformation; yet, in melanoma, such alterations are nearly exclusive to codon 61. Here, we compared the melanoma susceptibility of an NrasQ61R knock-in allele to similarly designed ... ...

    Abstract Unlabelled: NRAS mutation at codons 12, 13, or 61 is associated with transformation; yet, in melanoma, such alterations are nearly exclusive to codon 61. Here, we compared the melanoma susceptibility of an NrasQ61R knock-in allele to similarly designed KrasG12D and NrasG12D alleles. With concomitant p16INK4a inactivation, KrasG12D or NrasQ61R expression efficiently promoted melanoma in vivo, whereas NrasG12D did not. In addition, NrasQ61R mutation potently cooperated with Lkb1/Stk11 loss to induce highly metastatic disease. Functional comparisons of NrasQ61R and NrasG12D revealed little difference in the ability of these proteins to engage PI3K or RAF. Instead, NrasQ61R showed enhanced nucleotide binding, decreased intrinsic GTPase activity, and increased stability when compared with NrasG12D. This work identifies a faithful model of human NRAS-mutant melanoma, and suggests that the increased melanomagenecity of NrasQ61R over NrasG12D is due to heightened abundance of the active, GTP-bound form rather than differences in the engagement of downstream effector pathways.
    Significance: This work explains the curious predominance in human melanoma of mutations of codon 61 of NRAS over other oncogenic NRAS mutations. Using conditional "knock-in" mouse models, we show that physiologic expression of NRASQ61R, but not NRASG12D, drives melanoma formation.
    MeSH term(s) AMP-Activated Protein Kinase Kinases ; Alleles ; Animals ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Codon ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Gene Deletion ; Gene Order ; Genes, ras ; Genetic Loci ; Genotype ; Guanosine Triphosphate/metabolism ; Humans ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/mortality ; Melanoma/pathology ; Mice ; Mitogen-Activated Protein Kinases/metabolism ; Mutation ; Neoplasm Metastasis ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Binding ; Protein Serine-Threonine Kinases/genetics ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins B-raf/metabolism ; Tumor Burden
    Chemical Substances Codon ; Oncogene Proteins, Fusion ; Guanosine Triphosphate (86-01-1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; STK11 protein, human (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; AMP-Activated Protein Kinase Kinases (EC 2.7.11.3)
    Language English
    Publishing date 2014-09-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-14-0729
    Database MEDical Literature Analysis and Retrieval System OnLINE

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