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108 results on '"Krasny, L"'

2. Karta seismichnosti tikhookeanskogo podvizhnogo poiasa i Tikhogo Okeana (1896-1968) = The map of the seismicity of the Pacific mobile belt and the Pacific Ocean. Editor in L.I. Krasny, V.V. Fedymsky ... 1973. Ministry of Geology of the USSR = Ministerstova Geologii SSSR. Moscva 1976.

Author

Ministerstvo geologii, VSEGEI, Krasny, L. I., Fedynsky, V.V., and Soviet Union. Ministerstvo geologii.

Subjects
Geology, Physical geography
Abstract

1 color map of the Pacific Ocean in 9 sheets, each 65x76. Map was made in 1973, this is 1976 edition in Russian and English. Showing the seismic activities measured between 1896 and 1968. The map shows the seismic activity and plate tectonics of the entire Pacific region, including North and South America and the islands of Southeast Asia. Includes legend, tables, notations and graphs. Relief shown by contours and spot height. more...

Published
1976

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3. (Composite map) Karta seismichnosti tikhookeanskogo podvizhnogo poiasa i Tikhogo Okeana (1896-1968) = The map of the seismicity of the Pacific mobile belt and the Pacific Ocean. Editor in L.I. Krasny, V.V. Fedymsky ... 1973. Ministry of Geology of the USSR = Ministerstova Geologii SSSR. Moscva 1976.

Author

Ministerstvo geologii, VSEGEI, Krasny, L. I., Fedynsky, V.V., and Soviet Union. Ministerstvo geologii.

Subjects
Geology, Physical geography
Abstract

Composite of sheets 1-9, color map of the Pacific Ocean in 9 sheets, each 65x76. Map was made in 1973, this is 1976 edition in Russian and English. Showing the seismic activities measured between 1896 and 1968. The map shows the seismic activity and plate tectonics of the entire Pacific region, including North and South America and the islands of Southeast Asia. Includes legend, tables, notations and graphs. Relief shown by contours and spot height. more...

Published
1976

6. 3D Functional Genomics Screens Identify CREBBP as a Targetable Driver in Aggressive Triple-Negative Breast Cancer.

Author

Peck, B, Bland, P, Mavrommati, I, Muirhead, G, Cottom, H, Wai, PT, Maguire, SL, Barker, HE, Morrison, E, Kriplani, D, Yu, L, Gibson, A, Falgari, G, Brennan, K, Farnie, G, Buus, R, Marlow, R, Novo, D, Knight, E, Guppy, N, Kolarevic, D, Susnjar, S, Milijic, NM, Naidoo, K, Gazinska, P, Roxanis, I, Pancholi, S, Martin, L-A, Holgersen, EM, Cheang, MCU, Noor, F, Postel-Vinay, S, Quinn, G, McDade, S, Krasny, L, Huang, P, Daley, F, Wallberg, F, Choudhary, JS, Haider, S, Tutt, AN, Natrajan, R, Peck, B, Bland, P, Mavrommati, I, Muirhead, G, Cottom, H, Wai, PT, Maguire, SL, Barker, HE, Morrison, E, Kriplani, D, Yu, L, Gibson, A, Falgari, G, Brennan, K, Farnie, G, Buus, R, Marlow, R, Novo, D, Knight, E, Guppy, N, Kolarevic, D, Susnjar, S, Milijic, NM, Naidoo, K, Gazinska, P, Roxanis, I, Pancholi, S, Martin, L-A, Holgersen, EM, Cheang, MCU, Noor, F, Postel-Vinay, S, Quinn, G, McDade, S, Krasny, L, Huang, P, Daley, F, Wallberg, F, Choudhary, JS, Haider, S, Tutt, AN, and Natrajan, R more...

Abstract

Triple-negative breast cancers (TNBC) are resistant to standard-of-care chemotherapy and lack known targetable driver gene alterations. Identification of novel drivers could aid the discovery of new treatment strategies for this hard-to-treat patient population, yet studies using high-throughput and accurate models to define the functions of driver genes in TNBC to date have been limited. Here, we employed unbiased functional genomics screening of the 200 most frequently mutated genes in breast cancer, using spheroid cultures to model in vivo-like conditions, and identified the histone acetyltransferase CREBBP as a novel tumor suppressor in TNBC. CREBBP protein expression in patient tumor samples was absent in 8% of TNBCs and at a high frequency in other tumors, including squamous lung cancer, where CREBBP-inactivating mutations are common. In TNBC, CREBBP alterations were associated with higher genomic heterogeneity and poorer patient survival and resulted in upregulation and dependency on a FOXM1 proliferative program. Targeting FOXM1-driven proliferation indirectly with clinical CDK4/6 inhibitors (CDK4/6i) selectively impaired growth in spheroids, cell line xenografts, and patient-derived models from multiple tumor types with CREBBP mutations or loss of protein expression. In conclusion, we have identified CREBBP as a novel driver in aggressive TNBC and identified an associated genetic vulnerability in tumor cells with alterations in CREBBP and provide a preclinical rationale for assessing CREBBP alterations as a biomarker of CDK4/6i response in a new patient population. SIGNIFICANCE: This study demonstrates that CREBBP genomic alterations drive aggressive TNBC, lung cancer, and lymphomas and may be selectively treated with clinical CDK4/6 inhibitors. more...

Published
2021

15. Magnitnye anomalii i tektonichkie elementy severo- voctochnoi Evrazii

Author

Jorgensen, G, primary, Kisabeth, H, additional, Kisabeth, J, additional, Krasny, L, additional, Kwan, K, additional, Liu, G -D, additional, Macnab, R, additional, Morris, P, additional, Pogrebitsky, Y, additional, Qu, G -S, additional, Roest, W, additional, Verba, V, additional, Verhoef, J, additional, Wu, C -Z, additional, Xu, Z -G, additional, and Zhao, S -Q, additional more...

Published
1995
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34. Subunit interaction in cyclic AMP-dependent protein kinase of mutant lymphoma cells.

Author

Hochman, J, Bourne, H R, Coffino, P, Insel, P A, Krasny, L, and Melmon, K L

Abstract

We have previously selected and characterized mutant S49 mouse lymphoma cells that possess an adenosine 3':5'-cyclic monophosphate (cAMP)-dependent protein kinase (ATP:protein phosphotransferase, EC 2.7.1.37) with an increased apparent affinity constant (Ka) for activation by cAMP. The Ka lesion in one such mutant clone has been shown to result from a structural mutation involving the kinase holoenzyme's regulatory (R) subunit. The present report examines the interaction of R and catalytic (C) subunits of the kinases in extracts of the mutant cells and the normal "wild type" (WT) parental line. Subunit recombination experiments were performed, by using purified WT and mutant R subunits, and C subunits purified from WT cells. As compared to WT R subunits, only 1/6 as much mutant R subunit was required to reassociate with and suppress 50% of C subunit activity, at equilibrium. NaSCN activates cAMP-dependent kinase of both cell types by causing the holoenzyme to dissociate. In comparison with WT, a 2-fold higher concentration of NaSCN is required to maximally activate the kinase in mutant extracts. Both the reassociation result and the increased resistance of the mutant enzyme to a nonspecific dissociating agent strongly suggest that the mutant R subunit binds C subunit more tightly than does the WT R subunit. This interpretation raises the possibility that increased R-C subunit binding affinity in the mutant cell is responsible for the increased Ka for activation by cAMP of the mutant holoenzyme, and thus for the decreased potency of cAMP in regulating intact mutant cells. more...

Published
1977
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