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2. Automatic application of power analysis countermeasures

Author

Bayrak, AG, Regazzoni, F, Novo, D, Brisk, P, Standaert, FX, and Ienne, P

Subjects
Side-channel attacks, power analysis attacks, software countermeasures, compiler, Computer Hardware & Architecture, Computer Software, Distributed Computing, Computer Hardware
Abstract

We introduce a compiler that automatically inserts software countermeasures to protect cryptographic algorithms against power-based side-channel attacks. The compiler first estimates which instruction instances leak the most information through side-channels. This information is obtained either by dynamic analysis, evaluating an information theoretic metric over the power traces acquired during the execution of the input program, or by static analysis. As information leakage implies a loss of security, the compiler then identifies (groups of) instruction instances to protect with a software countermeasure such as random precharging or Boolean masking. As software protection incurs significant overhead in terms of cryptosystem runtime and memory usage, the compiler protects the minimum number of instruction instances to achieve a desired level of security. The compiler is evaluated on two block ciphers, AES and Clefia; our experiments demonstrate that the compiler can automatically identify and protect the most important instruction instances. To date, these software countermeasures have been inserted manually by security experts, who are not necessarily the main cryptosystem developers. Our compiler offers significant productivity gains for cryptosystem developers who wish to protect their implementations from side-channel attacks.

Published
2015

3. Fine-mapping identifies two additional breast cancer susceptibility loci at 9q31.2

Author

Ashworth, Alan, Van 'T Veer, Laura, Orr, N, Dudbridge, F, Dryden, N, Maguire, S, Novo, D, Perrakis, E, Johnson, N, Ghoussaini, M, Hopper, JL, and Southey, MC

Abstract

© The Author 2015. Published by Oxford University Press. All rights reserved.We recently identified a novel susceptibility variant, rs865686, for estrogen-receptor positive breast cancer at 9q31.2. Here, we report a fine-mapping analysis of the 9q31.2 susc

Published
2015

4. An EDA-friendly protection scheme against side-channel attacks

Author

Bayrak, AG, Velickovic, N, Regazzoni, F, Novo, D, Brisk, P, and Ienne, P

Abstract

This paper introduces a generic and automated methodology to protect hardware designs from side-channel attacks in a manner that is fully compatible with commercial standard cell design flows. The paper describes a tool that artificially adds jitter to the clocks of the sequential elements of a cryptographic unit, which increases the non-determinism of signal timing, thereby making the physical device more difficult to attack. Timing constraints are then specified to commercial EDA tools, which restore the circuit functionality and efficiency while preserving the introduced randomness. The protection scheme is applied to an AES-128 hardware implementation that is synthesized using both ASIC and FPGA design flows. © 2013 EDAA.

Published
2013

5. Selective flexibility: Breaking the rigidity of datapath merging

Author

Stojilovic, M, Novo, D, Saranovac, L, Brisk, P, and Ienne, P

Abstract

Hardware specialization is often the key to efficiency for programmable embedded systems, but comes at the expense of flexibility. This paper combines flexibility and efficiency in the design and synthesis of domain-specific datapaths. We merge all individual paths from the Data Flow Graphs (DFGs) of the target applications, leading to a minimal set of required resources; this set is organized into a column of physical operators and cloned, thus generating a domain-specific rectangular lattice. A bus-based FPGA-style interconnection network is then generated and dimensioned to meet the needs of the applications. Our results demonstrate that the lattice has good flexibility: DFGs that were not used as part of the datapath creation phase can be mapped onto it with high probability. Compared to an ASIC design of a single DFG, the speed of our domain-specific coarse-grained reconfigurable datapath is degraded by a factor up to 2x, compared to 3-4x for an FPGA; similarly, our lattice is up to 10x larger than an ASIC, compared to 20-40x for an FPGA. We estimate that our array is up to 6x larger than an ASIC accelerator, which is synthesized using datapath merging and has limited or null generality. © 2012 EDAA.

Published
2012

8. 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

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.

Published
2021

11. Treatment

Author

Goodwin, C. S., Worsley, B., Pillai, E., Willems, V., Janisch, H. D., Langmaack, H., Sanchez, P., Alcalde, M., Lancho, A., Carpintero, P., Garcia, R., Pajares, J. M., Grigoriev, P. Ya., Isakov, V. A., Iakovenko, E. P., Iakovenko, A. V., Vogt, K., Hahn, H., Rehmann, I. H., Hedding-Eckerich, M., Blessing, J., Sobala, G. M., Lynch, D. A. F., Gallacher, B., Dixon, M. F., Axon, A. T. R., Bayerdörffer, E., Mannes, G., Sommer, A., Höchter, W., Weingart, J., Hatz, R., Miehlke, S., Lehn, N., Ruckdeschel, G., Dirschedl, P., Stolte, M., Adamek, R. J., Wegener, M., Birkholz, S., Opferkuch, W., Rühl, G. H., Wedmann, B., Labenz, J., Gyenes, E., R’hl, G. H., Börsch, G., Maieron, R., Rizzi, C., Zoratti, L., Andreoli, S., Da Broi, G. L., Beltrami, C. A., Chengyl, Zhuya, Yangiong, Mou, Jiesong, Hua, Zhenhua, Zhang, Bierti, L., Bolis, E. G., Di Battista, R., de Franchis, R., McAvinchey, D. J., Laurence, M., O’Riordan, J., Fantazi, M., Khawaja, M., Bologna, E, Stroppiana, M., Peyre, S., Pulitano’, R., Sategna-Guidetti, C., Martin, E., Alarcön, T., Sanz, J. C., Jimonez, M. I., López-Brea, M., Burette, A., Glupczynski, Y., Deprez, C., Di Mario, F., Ferrana, M., Battaglia, G., Dotto, P., Vianello, F., Grasso, G. A., Fiocca, R., Villiani, L., Luinetti, O., Gianatti, A., Boldorini, R., Lazzaroni, M., Bianchi Porro, G., Trespi, E., Perego, M., Alvisi, C., Cesana, B., Solcia, E., Logan, R. P. H., Greaves, R. R., Gummett, P. A., Walker, M. M., Karim, Q. N., Duggan, A. E., Baron, J. H., Misiewicz, J. J., Lohmarm, J., Porst, L. H. H., Schönlebe, J., Riedel, H., Catalano, F., Rizzo, G., Ayoubi Khajekini, M. T., Branciforte, G., Inserra, G., Liberti, A., Suriani, R., Pallante, C., Ravizza, M., Mazzucco, D., Galliano, D., Malandrino, M., Oneglio, R., Colozza, M., Gaia, E., Sallio, F., Colozza, D., Grandis, C., Forte, G. B., Bottiglieri, M. E., Durasco, R., Grimaldi, E., Rocco, P., Xia, H. X., Daw, M. A., Sant, S., Beattie, S., Keane, C. T., O’Morain, C. A., Larsson, H., Berglund, M. L., Tessaro, P., Schiavon, R., Contini, M. G., Ton, T., Norberto, L., Cassaro, M., Rugge, M., Guido, M., Baffa, R., Gloriosa, S., Turatello, F., Naccarato, R., Collins, R., O’Moram, C., Kemmer, T. P., Dominguez-Munoz, J. E., Klingel, H., Malfertheiner, P., McCarthy, C. J., McDermott, M., Hourihane, D., O’Morain, C., Droy-Lefiax, M. T., Forestier, B., Guillomain, D., Plique, O., Brugmann, D., Mégraud, F., Lamouliatte, H., Bernard, P. H., Cayla, R., Mégraud, M., de Mascarel, A., Quintonl, A., McLaren, A., McDowell, S. R., McColm, A. A., O’Malley, C., Bagshaw, J., Bouffant, F., Marelli, P., Cellini, L., Campa, M., Dainelli, B., Soldani, G., del Tacca, M., Ferrini, G., Larcinese, G., Semperlotti, N., Molnar, Gy., Fzentmihalyi, A., Takats, A., Gero, G., Penyige, J., Mark, Gy., Martínez-Gómez, J., García-Novo, D., Acuña-Quinõs, D., Gimeno, M., Vigneri, S., Termini, R., Scialabba, A., Pisciotta, G., Gusmaroli, R., Milesi, F., Mule, P., Menegatti, M., Reale, C., Holten, J., and Vaira, D.

Published
1992
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12. Glioblastoma-derived exosomes alter extracellular matrix deposition of astrocytes to facilitate tumor cell migration

Author

Kössinger, D, Novo, D, Barnett, S, Pollard, S, Chalmers, A, and Norman, J

Subjects
ddc: 610, 610 Medical sciences, Medicine, neoplasms, nervous system diseases
Abstract

Objective: Despite multimodal treatment survival in primary glioblastoma still remains poor. One of the main difficulties treating these tumors is caused by invasion of glioblastoma cells into surrounding and distant brain tissue. The aim of this study is to determine whether glioblastoma cells can [for full text, please go to the a.m. URL], 69. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Mexikanischen und Kolumbianischen Gesellschaft für Neurochirurgie

Published
2018
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14. Fine-mapping identifies two additional breast cancer susceptibility loci at 9q31.2

Author

Orr, N., Dudbridge, F., Dryden, N., Maguire, S., Novo, D., Perrakis, E., Johnson, N., Ghoussaini, M., Hopper, J.L., Southey, M.C., Apicella, C., Stone, J., Schmidt, M.K., Broeks, A., Van't Veer, L.J., Hogervorst, F.B., Fasching, P.A., Haeberle, L., Ekici, A.B., Beckmann, M.W., Gibson, L., Aitken, Z., Warren, H., Sawyer, E., Tomlinson, I., Kerin, M.J., Miller, N., Burwinkel, B., Marme, F., Schneeweiss, A., Sohn, C., Guenel, P., Truong, T., Cordina-Duverger, E., Sanchez, M., Bojesen, S.E., Nordestgaard, B.G., Nielsen, S.F., Flyger, H., Benitez, J., Zamora, M.P., Perez, J.I.A., Menendez, P., Anton-Culver, H., Neuhausen, S.L., Brenner, H., Dieffenbach, A.K., Arndt, V., Stegmaier, C., Hamann, U., Brauch, H., Justenhoven, C., Bruning, T., Ko, Y.D., Nevanlinna, H., Aittomaki, K., Blomqvist, C., Khan, S., Bogdanova, N., Dork, T., Lindblom, A., Margolin, S., Mannermaa, A., Kataja, V., Kosma, V.M., Hartikainen, J.M., Chenevix-Trench, G., Beesley, J., Lambrechts, D., Moisse, M., Floris, G., Beuselinck, B., Chang-Claude, J., Rudolph, A., Seibold, P., Flesch-Janys, D., Radice, P., Peterlongo, P., Peissel, B., Pensotti, V., Couch, F.J., Olson, J.E., Slettedahl, S., Vachon, C., Giles, G.G., Milne, R.L., McLean, C., Haiman, C.A., Henderson, B.E., Schumacher, F., Marchand, L. le, Simard, J., Goldberg, M.S., Labreche, F., Dumont, M., Kristensen, V., Alnaes, G.G., Nord, S., Borresen-Dale, A.L., Zheng, W., Deming-Halverson, S., Shrubsole, M., Long, J.R., Winqvist, R., Pylkas, K., Jukkola-Vuorinen, A., Grip, M., Andrulis, I.L., Knight, J.A., Glendon, G., Tchatchou, S., Devilee, P., Tollenaar, R.A.E.M., Seynaeve, C.M., Asperen, C.J. van, Garcia-Closas, M., Figueroa, J., Chanock, S.J., Lissowska, J., Czene, K., Darabi, H., Eriksson, M., Klevebring, D., Hooning, M.J., Hollestelle, A., Deurzen, C.H.M. van, Kriege, M., Hall, P., Li, J.M., Liu, J.J., Humphreys, K., Cox, A., Cross, S.S., Reed, M.W.R., Pharoah, P.D.P., Dunning, A.M., Shah, M., Perkins, B.J., Jakubowska, A., Lubinski, J., Jaworska-Bieniek, K., Durda, K., Ashworth, A., Swerdlow, A., Jones, M., Schoemaker, M.J., Meindl, A., Schmutzler, R.K., Olswold, C., Slager, S., Toland, A.E., Yannoukakos, D., Muir, K., Lophatananon, A., Stewart-Brown, S., Siriwanarangsan, P., Matsuo, K., Ito, H., Iwata, H., Ishiguro, J., Wu, A.H., Tseng, C.C., Berg, D. van den, Stram, D.O., Teo, S.H., Yip, C.H., Kang, P., Ikram, M.K., Shu, X.O., Lu, W., Gao, Y.T., Cai, H., Kang, D., Choi, J.Y., Park, S.K., Noh, D.Y., Hartman, M., Miao, H., Lim, W.Y., Lee, S.C., Sangrajrang, S., Gaborieau, V., Brennan, P., McKay, J., Wu, P.E., Hou, M.F., Yu, J.C., Shen, C.Y., Blot, W., Cai, Q.Y., Signorello, L.B., Luccarini, C., Bayes, C., Ahmed, S., Maranian, M., Healey, C.S., Gonzalez-Neira, A., Pita, G., Alonso, M.R., Alvarez, N., Herrero, D., Tessier, D.C., Vincent, D., Bacot, F., Hunter, D.J., Lindstrom, S., Dennis, J., Michailidou, K., Bolla, M.K., Easton, D.F., Silva, I.D., Fletcher, O., Peto, J., GENICA Network, kConFab Investigators, Australian Ovarian Canc Study Grp, Obstetrics & Gynecology, Medical Oncology, Pathology, Ophthalmology, Cardiothoracic Surgery, and Clinical Genetics

Subjects
Asian Continental Ancestry Group, Adult, Hepatocyte Nuclear Factor 3-alpha, Risk, binding, European Continental Ancestry Group, Kruppel-Like Transcription Factors, estrogen-receptor-alpha, Breast Neoplasms, GATA3 Transcription Factor, Polymorphism, Single Nucleotide, White People, Kruppel-Like Factor 4, Asian People, SDG 3 - Good Health and Well-being, Medizinische Fakultät, common variants, expression, Humans, Genetic Predisposition to Disease, ddc:610, Genetic Association Studies, Aged, Association Studies Articles, Estrogen Receptor alpha, Chromosome Mapping, foxa1, Middle Aged, confer susceptibility, analyses reveal, Enhancer Elements, Genetic, risk locus, Genetic Loci, functional variants, genome-wide association, Female, Chromosomes, Human, Pair 9
Abstract

We recently identified a novel susceptibility variant, rs865686, for estrogen-receptor positive breast cancer at 9q31.2. Here, we report a fine-mapping analysis of the 9q31.2 susceptibility locus using 43 160 cases and 42 600 controls of European ancestry ascertained from 52 studies and a further 5795 cases and 6624 controls of Asian ancestry from nine studies. Single nucleotide polymorphism (SNP) rs676256 was most strongly associated with risk in Europeans (odds ratios [OR] = 0.90 [0.88-0.92]; P-value = 1.58 × 10(-25)). This SNP is one of a cluster of highly correlated variants, including rs865686, that spans ∼14.5 kb. We identified two additional independent association signals demarcated by SNPs rs10816625 (OR = 1.12 [1.08-1.17]; P-value = 7.89 × 10(-09)) and rs13294895 (OR = 1.09 [1.06-1.12]; P-value = 2.97 × 10(-11)). SNP rs10816625, but not rs13294895, was also associated with risk of breast cancer in Asian individuals (OR = 1.12 [1.06-1.18]; P-value = 2.77 × 10(-05)). Functional genomic annotation using data derived from breast cancer cell-line models indicates that these SNPs localise to putative enhancer elements that bind known drivers of hormone-dependent breast cancer, including ER-α, FOXA1 and GATA-3. In vitro analyses indicate that rs10816625 and rs13294895 have allele-specific effects on enhancer activity and suggest chromatin interactions with the KLF4 gene locus. These results demonstrate the power of dense genotyping in large studies to identify independent susceptibility variants. Analysis of associations using subjects with different ancestry, combined with bioinformatic and genomic characterisation, can provide strong evidence for the likely causative alleles and their functional basis. ispartof: Human Molecular Genetics vol:24 issue:10 pages:2966-84 ispartof: location:England status: published

Published
2015

15. An EDA-friendly protection scheme against side-channel attacks

Author

Bayrak, A. G., Velickovic, N., Francesco Regazzoni, Novo, D., Brisk, P., Ienne, P., and Macii, Enrico

Abstract

This paper introduces a generic and automated methodology to protect hardware designs from side-channel attacks in a manner that is fully compatible with commercial standard cell design flows. The paper describes a tool that artificially adds jitter to the clocks of the sequential elements of a cryptographic unit, which increases the non-determinism of signal timing, thereby making the physical device more difficult to attack. Timing constraints are then specified to commercial EDA tools, which restore the circuit functionality and efficiency while preserving the introduced randomness. The protection scheme is applied to an AES-128 hardware implementation that is synthesized using both ASIC and FPGA design flows. © 2013 EDAA.

Published
2013
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47. Selective flexibility: Breaking the rigidity of datapath merging

Author

Stojilović, M., Novo, D., Saranovac, L., Philip Brisk, Ienne, P., Rosenstiel, Wolfgang, and Thiele, Lothar

Subjects
010302 applied physics, 0103 physical sciences, 0202 electrical engineering, electronic engineering, information engineering, 02 engineering and technology, Hardware_ARITHMETICANDLOGICSTRUCTURES, Hardware_REGISTER-TRANSFER-LEVELIMPLEMENTATION, 01 natural sciences, 020202 computer hardware & architecture
Abstract

Hardware specialization is often the key to efficiency for programmable embedded systems, but comes at the expense of flexibility. This paper combines flexibility and efficiency in the design and synthesis of domain-specific datapaths. We merge all individual paths from the Data Flow Graphs (DFGs) of the target applications, leading to a minimal set of required resources; this set is organized into a column of physical operators and cloned, thus generating a domain-specific rectangular lattice. A bus-based FPGA-style interconnection network is then generated and dimensioned to meet the needs of the applications. Our results demonstrate that the lattice has good flexibility: DFGs that were not used as part of the datapath creation phase can be mapped onto it with high probability. Compared to an ASIC design of a single DFG, the speed of our domain-specific coarse-grained reconfigurable datapath is degraded by a factor up to 2x, compared to 3-4x for an FPGA; similarly, our lattice is up to 10x larger than an ASIC, compared to 20-40x for an FPGA. We estimate that our array is up to 6x larger than an ASIC accelerator, which is synthesized using datapath merging and has limited or null generality. © 2012 EDAA.

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