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11 results on '"Toth, Reka"'

1. Three is the magic number -- distance measurement of NGC 3147 using SN 2021hpr and its siblings

Author

Barna, Barnabas, Nagy, Andrea P., Bora, Zsofia, Czavalinga, Donat R., Konyves-Toth, Reka, Szalai, Tamas, Szekely, Peter, Zsiros, Szanna, Banhidi, Dominik, Biro, Barna I., Csanyi, Istvan, Kriskovics, Levente, Pal, Andras, Szabo, Zsofia M., Szakats, Robert, Vida, Krisztian, Bodola, Zsofia, Vinko, Jozsef, Barna, Barnabas, Nagy, Andrea P., Bora, Zsofia, Czavalinga, Donat R., Konyves-Toth, Reka, Szalai, Tamas, Szekely, Peter, Zsiros, Szanna, Banhidi, Dominik, Biro, Barna I., Csanyi, Istvan, Kriskovics, Levente, Pal, Andras, Szabo, Zsofia M., Szakats, Robert, Vida, Krisztian, Bodola, Zsofia, and Vinko, Jozsef

Abstract

The nearby spiral galaxy NGC 3147 hosted three Type Ia supernovae (SNe Ia) in the past decades, which have been subjects of intense follow-up observations. Simultaneous analysis of their data provides a unique opportunity for testing the different light curve fitting methods and distance estimations. The detailed optical follow-up of SN 2021hpr allows us to revise the previous distance estimations to NGC 3147, and compare the widely used light curve fitting algorithms to each other. After the combination of the available and newly published data of SN 2021hpr, its physical properties can be also estimated with higher accuracy. We present and analyse new BVgriz and Swift photometry of SN 2021hpr to constrain its general physical properties. Together with its siblings, SNe 1997bq and 2008fv, we cross-compare the individual distance estimates of these three SNe given by the SALT code, and also check their consistency with the results from the MLCS2k2 method. The early spectral series of SN 2021hpr are also fit with the radiative spectral code TARDIS in order to verify the explosion properties and constrain the chemical distribution of the outer ejecta. After combining the distance estimates for the three SNe, the mean distance to their host galaxy, NGC 3127, is 42.5 $\pm$ 1.0 Mpc, which matches with the distance inferred by the most up-to-date LC fitters, SALT3 and BayeSN. We confirm that SN~2021hpr is a Branch-normal Type Ia SN that ejected $\sim 1.12 \pm 0.28$ M$_\odot$ from its progenitor white dwarf, and synthesized $\sim 0.44 \pm 0.14$ M$_\odot$ of radioactive $^{56}$Ni., Comment: 16 pages, 17 figures, 11 tables; accepted for publication in A&A

Published
2023
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2. SN 2010kd: Photometric and Spectroscopic Analysis of a Slow-Decaying Superluminous Supernova

Author

Kumar, Amit, Pandey, Shashi Bhushan, Konyves-Toth, Reka, Staten, Ryan, Vinko, Jozsef, Wheeler, J. Craig, Zheng, Weikang, Filippenko, Alexei V., Kehoe, Robert, Quimby, Robert, Fang, Yuan, Akerlof, Carl, Mckay, Tim A., Chatzopoulos, Emmanouil, Thomas, Benjamin P., Dhungana, Govinda, Aryan, Amar, Dastidar, Raya, Gangopadhyay, Anjasha, Gupta, Rahul, Misra, Kuntal, Kumar, Brajesh, Brahme, Nameeta, Buckley, David, Kumar, Amit, Pandey, Shashi Bhushan, Konyves-Toth, Reka, Staten, Ryan, Vinko, Jozsef, Wheeler, J. Craig, Zheng, Weikang, Filippenko, Alexei V., Kehoe, Robert, Quimby, Robert, Fang, Yuan, Akerlof, Carl, Mckay, Tim A., Chatzopoulos, Emmanouil, Thomas, Benjamin P., Dhungana, Govinda, Aryan, Amar, Dastidar, Raya, Gangopadhyay, Anjasha, Gupta, Rahul, Misra, Kuntal, Kumar, Brajesh, Brahme, Nameeta, and Buckley, David

Abstract

This paper presents data and analysis of SN 2010kd, a low-redshift ($z = 0.101$) H-deficient superluminous supernova (SLSN), based on ultraviolet/optical photometry and optical spectroscopy spanning between $-$28 and +194 days relative to $\mathit{B}$ band maximum light. The $\mathit{B}$ band light curve comparison of SN 2010kd with a subset of well-studied SLSNe I at comparable redshifts indicates that it is a slow-decaying PTF12dam like SLSN. Analytical light-curve modeling using the $\mathtt{Minim}$ code suggests that the bolometric light curve of SN 2010kd favors circumstellar matter interaction for the powering mechanism. $\mathtt{SYNAPPS}$ modeling of the early-phase spectra does not identify broad H or He lines, whereas the photospheric-phase spectra are dominated by O I, O II, C II, C IV and Si II, particularly, presence of both low and high-velocity components of O II and Si II lines. The nebular-phase spectra of SN 2010kd are dominated by O I and Ca II emission lines similar to those seen in other SLSNe I. The line velocities in SN 2010kd exhibit flatter evolution curves similar to SN 2015bn but with comparatively higher values. SN 2010kd shows a higher single-zone local thermodynamic equilibrium temperature in comparison to PTF12dam and SN 2015bn, and it has an upper O I ejected mass limit of $\sim 10~M_\odot$. The host of SN 2010kd is a dwarf galaxy with a high star-formation rate ($\sim 0.18 \pm 0.04~M_\odot$ yr$^{-1}$) and extreme emission lines., Comment: 26 pages, 16 figures, Accepted in ApJ, updated to match the accepted version

Published
2020
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3. SN 2010kd: Photometric and Spectroscopic Analysis of a Slow-Decaying Superluminous Supernova

Author

Kumar, Amit, Pandey, Shashi Bhushan, Konyves-Toth, Reka, Staten, Ryan, Vinko, Jozsef, Wheeler, J. Craig, Zheng, Weikang, Filippenko, Alexei V., Kehoe, Robert, Quimby, Robert, Fang, Yuan, Akerlof, Carl, Mckay, Tim A., Chatzopoulos, Emmanouil, Thomas, Benjamin P., Dhungana, Govinda, Aryan, Amar, Dastidar, Raya, Gangopadhyay, Anjasha, Gupta, Rahul, Misra, Kuntal, Kumar, Brajesh, Brahme, Nameeta, Buckley, David, Kumar, Amit, Pandey, Shashi Bhushan, Konyves-Toth, Reka, Staten, Ryan, Vinko, Jozsef, Wheeler, J. Craig, Zheng, Weikang, Filippenko, Alexei V., Kehoe, Robert, Quimby, Robert, Fang, Yuan, Akerlof, Carl, Mckay, Tim A., Chatzopoulos, Emmanouil, Thomas, Benjamin P., Dhungana, Govinda, Aryan, Amar, Dastidar, Raya, Gangopadhyay, Anjasha, Gupta, Rahul, Misra, Kuntal, Kumar, Brajesh, Brahme, Nameeta, and Buckley, David

Abstract

This paper presents data and analysis of SN 2010kd, a low-redshift ($z = 0.101$) H-deficient superluminous supernova (SLSN), based on ultraviolet/optical photometry and optical spectroscopy spanning between $-$28 and +194 days relative to $\mathit{B}$ band maximum light. The $\mathit{B}$ band light curve comparison of SN 2010kd with a subset of well-studied SLSNe I at comparable redshifts indicates that it is a slow-decaying PTF12dam like SLSN. Analytical light-curve modeling using the $\mathtt{Minim}$ code suggests that the bolometric light curve of SN 2010kd favors circumstellar matter interaction for the powering mechanism. $\mathtt{SYNAPPS}$ modeling of the early-phase spectra does not identify broad H or He lines, whereas the photospheric-phase spectra are dominated by O I, O II, C II, C IV and Si II, particularly, presence of both low and high-velocity components of O II and Si II lines. The nebular-phase spectra of SN 2010kd are dominated by O I and Ca II emission lines similar to those seen in other SLSNe I. The line velocities in SN 2010kd exhibit flatter evolution curves similar to SN 2015bn but with comparatively higher values. SN 2010kd shows a higher single-zone local thermodynamic equilibrium temperature in comparison to PTF12dam and SN 2015bn, and it has an upper O I ejected mass limit of $\sim 10~M_\odot$. The host of SN 2010kd is a dwarf galaxy with a high star-formation rate ($\sim 0.18 \pm 0.04~M_\odot$ yr$^{-1}$) and extreme emission lines., Comment: 26 pages, 16 figures, Accepted in ApJ, updated to match the accepted version

Published
2020
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4. Methylome-based cell-of-origin modeling (Methyl-COOM) identifies aberrant expression of immune regulatory molecules in CLL

Author

Wierzbinska, Justyna A, Toth, Reka, Ishaque, Naveed, Rippe, Karsten, Mallm, Jan-Philipp, Klett, Lara C, Mertens, Daniel, Zenz, Thorsten, Hielscher, Thomas, Seifert, Marc, Küppers, Ralf, Assenov, Yassen, Lutsik, Pavlo, Stilgenbauer, Stephan, Roessner, Philipp M, Seiffert, Martina, Byrd, John, Oakes, Christopher C, Plass, Christoph, Lipka, Daniel B; https://orcid.org/0000-0001-5081-7869, Wierzbinska, Justyna A, Toth, Reka, Ishaque, Naveed, Rippe, Karsten, Mallm, Jan-Philipp, Klett, Lara C, Mertens, Daniel, Zenz, Thorsten, Hielscher, Thomas, Seifert, Marc, Küppers, Ralf, Assenov, Yassen, Lutsik, Pavlo, Stilgenbauer, Stephan, Roessner, Philipp M, Seiffert, Martina, Byrd, John, Oakes, Christopher C, Plass, Christoph, and Lipka, Daniel B; https://orcid.org/0000-0001-5081-7869

Abstract

BACKGROUND: In cancer, normal epigenetic patterns are disturbed and contribute to gene expression changes, disease onset, and progression. The cancer epigenome is composed of the epigenetic patterns present in the tumor-initiating cell at the time of transformation, and the tumor-specific epigenetic alterations that are acquired during tumor initiation and progression. The precise dissection of these two components of the tumor epigenome will facilitate a better understanding of the biological mechanisms underlying malignant transformation. Chronic lymphocytic leukemia (CLL) originates from differentiating B cells, which undergo extensive epigenetic programming. This poses the challenge to precisely determine the epigenomic ground state of the cell-of-origin in order to identify CLL-specific epigenetic aberrations. METHODS: We developed a linear regression model, methylome-based cell-of-origin modeling (Methyl-COOM), to map the cell-of-origin for individual CLL patients based on the continuum of epigenomic changes during normal B cell differentiation. RESULTS: Methyl-COOM accurately maps the cell-of-origin of CLL and identifies CLL-specific aberrant DNA methylation events that are not confounded by physiologic epigenetic B cell programming. Furthermore, Methyl-COOM unmasks abnormal action of transcription factors, altered super-enhancer activities, and aberrant transcript expression in CLL. Among the aberrantly regulated transcripts were many genes that have previously been implicated in T cell biology. Flow cytometry analysis of these markers confirmed their aberrant expression on malignant B cells at the protein level. CONCLUSIONS: Methyl-COOM analysis of CLL identified disease-specific aberrant gene regulation. The aberrantly expressed genes identified in this study might play a role in immune-evasion in CLL and might serve as novel targets for immunotherapy approaches. In summary, we propose a novel framework for in silico modeling of reference DNA methylomes an

Published
2020

5. SN 2017cfd: A Normal Type Ia Supernova Discovered Very Young

Author

Han, Xuhui, Zheng, WeiKang, Stahl, Benjamin E., Burke, Jamison, Vinko, Jozsef, de Jaeger, Thomas, Brink, Thomas G., Cseh, Borbala, Hiramatsu, Daichi, Howell, D. Andrew, Ignacz, Bernadett, Konyves-Toth, Reka, Krezinger, Mate, McCully, Curtis, Ordasi, Andras, Pinter, Dora, Sarneczky, Krisztian, Szakats, Robert, Tang, Kevin, Vida, Krisztian, Wang, Jing, Wei, Jianyan, Wheeler, J. Craig, Xin, Liping, Filippenko, Alexei V., Han, Xuhui, Zheng, WeiKang, Stahl, Benjamin E., Burke, Jamison, Vinko, Jozsef, de Jaeger, Thomas, Brink, Thomas G., Cseh, Borbala, Hiramatsu, Daichi, Howell, D. Andrew, Ignacz, Bernadett, Konyves-Toth, Reka, Krezinger, Mate, McCully, Curtis, Ordasi, Andras, Pinter, Dora, Sarneczky, Krisztian, Szakats, Robert, Tang, Kevin, Vida, Krisztian, Wang, Jing, Wei, Jianyan, Wheeler, J. Craig, Xin, Liping, and Filippenko, Alexei V.

Abstract

The Type~Ia supernova (SN~Ia) 2017cfd in IC~0511 (redshift z = 0.01209+- 0.00016$) was discovered by the Lick Observatory Supernova Search 1.6+-0.7 d after the fitted first-light time (FFLT; 15.2 d before B-band maximum brightness). Photometric and spectroscopic follow-up observations show that SN~2017cfd is a typical, normal SN~Ia with a peak luminosity MB ~ -19.2+-0.2 mag, Delta m15(B) = 1.16 mag, and reached a B-band maximum ~16.8 d after the FFLT. We estimate there to be moderately strong host-galaxy extinction (A_V = 0.39 +- 0.03 mag) based on MLCS2k2 fitting. The spectrum reveals a Si~II lambda 6355 velocity of ~11,200 kms at peak brightness. The analysis shows that SN~2017cfd is a very typical, normal SN Ia in nearly every aspect. SN~2017cfd was discovered very young, with multiband data taken starting 2 d after the FFLT, making it a valuable complement to the currently small sample (fewer than a dozen) of SNe~Ia with color data at such early times. We find that its intrinsic early-time (B - V)0 color evolution belongs to the "blue" population rather than to the distinct "red" population. Using the photometry, we constrain the companion star radius to be < 2.5 R_sun, thus ruling out a red-giant companion., Comment: 10 pages, 7 figures, 3 tables

Published
2019
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6. SN 2017cfd: A Normal Type Ia Supernova Discovered Very Young

Author

Han, Xuhui, Zheng, WeiKang, Stahl, Benjamin E., Burke, Jamison, Vinko, Jozsef, de Jaeger, Thomas, Brink, Thomas G., Cseh, Borbala, Hiramatsu, Daichi, Howell, D. Andrew, Ignacz, Bernadett, Konyves-Toth, Reka, Krezinger, Mate, McCully, Curtis, Ordasi, Andras, Pinter, Dora, Sarneczky, Krisztian, Szakats, Robert, Tang, Kevin, Vida, Krisztian, Wang, Jing, Wei, Jianyan, Wheeler, J. Craig, Xin, Liping, Filippenko, Alexei V., Han, Xuhui, Zheng, WeiKang, Stahl, Benjamin E., Burke, Jamison, Vinko, Jozsef, de Jaeger, Thomas, Brink, Thomas G., Cseh, Borbala, Hiramatsu, Daichi, Howell, D. Andrew, Ignacz, Bernadett, Konyves-Toth, Reka, Krezinger, Mate, McCully, Curtis, Ordasi, Andras, Pinter, Dora, Sarneczky, Krisztian, Szakats, Robert, Tang, Kevin, Vida, Krisztian, Wang, Jing, Wei, Jianyan, Wheeler, J. Craig, Xin, Liping, and Filippenko, Alexei V.

Abstract

The Type~Ia supernova (SN~Ia) 2017cfd in IC~0511 (redshift z = 0.01209+- 0.00016$) was discovered by the Lick Observatory Supernova Search 1.6+-0.7 d after the fitted first-light time (FFLT; 15.2 d before B-band maximum brightness). Photometric and spectroscopic follow-up observations show that SN~2017cfd is a typical, normal SN~Ia with a peak luminosity MB ~ -19.2+-0.2 mag, Delta m15(B) = 1.16 mag, and reached a B-band maximum ~16.8 d after the FFLT. We estimate there to be moderately strong host-galaxy extinction (A_V = 0.39 +- 0.03 mag) based on MLCS2k2 fitting. The spectrum reveals a Si~II lambda 6355 velocity of ~11,200 kms at peak brightness. The analysis shows that SN~2017cfd is a very typical, normal SN Ia in nearly every aspect. SN~2017cfd was discovered very young, with multiband data taken starting 2 d after the FFLT, making it a valuable complement to the currently small sample (fewer than a dozen) of SNe~Ia with color data at such early times. We find that its intrinsic early-time (B - V)0 color evolution belongs to the "blue" population rather than to the distinct "red" population. Using the photometry, we constrain the companion star radius to be < 2.5 R_sun, thus ruling out a red-giant companion., Comment: 10 pages, 7 figures, 3 tables

Published
2019
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7. The First Post-Kepler Brightness Dips of KIC 8462852

Author

Boyajian, Tabetha. S., Alonso, Roi, Ammerman, Alex, Armstrong, David, Ramos, A. Asensio, Barkaoui, K., Beatty, Thomas G., Benkhaldoun, Z., Benni, Paul, Bentley, Rory O., Berdyugin, Andrei, Berdyugina, Svetlana, Bergeron, Serge, Bieryla, Allyson, Blain, Michaela G., Blanco, Alicia Capetillo, Bodman, Eva H. L., Boucher, Anne, Bradley, Mark, Brincat, Stephen M., Brink, Thomas G., Briol, John, Brown, David J. A., Budaj, J., Burdanov, A., Cale, B., Carbo, Miguel Aznar, Garcia, R. Castillo, Clark, Wendy J., Clayton, Geoffrey C., Clem, James L., Coker, Phillip H., Cook, Evan M., Copperwheat, Chris M., Curtis, J. L., Cutri, R. M., Cseh, B., Cynamon, C. H., Daniels, Alex J., Davenport, James R. A., Deeg, Hans J., De Lorenzo, Roberto, De Jaeger, Thomas, Desrosiers, Jean-Bruno, Dolan, John, Dowhos, D. J., Dubois, Franky, Durkee, R., Dvorak, Shawn, Easley, Lynn, Edwards, N., Ellis, Tyler G., Erdelyi, Emery, Ertel, Steve, Farfan, Rafael. G., Farihi, J., Filippenko, Alexei V., Foxell, Emma, Gandolfi, Davide, Garcia, Faustino, Giddens, F., Gillon, M., Gonzalez-Carballo, Juan-Luis, Gonzalez-Fernandez, C., Hernandez, J. I. Gonzalez, Graham, Keith A., Greene, Kenton A., Gregorio, J., Hallakoun, Na'ama, Hanyecz, Otto, Harp, G. R., Henry, Gregory W., Herrero, E., Hildbold, Caleb F., Hinzel, D., Holgado, G., Ignacz, Bernadett, Ilyin, Ilya, Ivanov, Valentin D., Jehin, E., Jermak, Helen E., Johnston, Steve, Kafka, S., Kalup, Csilla, Kardasis, Emmanuel, Kaspi, Shai, Kennedy, Grant M., Kiefer, F., Kielty, C. L., Kessler, Dennis, Kiiskinen, H., Killestein, T. L., King, Ronald A., Kollar, V., Korhonen, H., Kotnik, C., Konyves-Toth, Reka, Kriskovics, Levente, Krumm, Nathan, Krushinsky, Vadim, Kundra, E., Lachapelle, Francois-Rene, LaCourse, D., Lake, P., Lam, Kristine, Lamb, Gavin P., Lane, Dave, Lau, Marie Wingyee, Lewin, Pablo, Lintott, Chris, Lisse, Carey, Logie, Ludwig, Longeard, Nicolas, Villanueva, M. Lopez, Ludington, E. Whit, Mainzer, A., Malo, Lison, Maloney, Chris, Mann, A., Mantero, A., Marengo, Massimo, Marchant, Jon, Gonzalez, M. J. Martinez, Masiero, Joseph R., Mauerhan, Jon C., McCormac, James, McNeely, Aaron, Meng, Huan Y. A., Miller, Mike, Molnar, Lawrence A., Morales, J. C., Morris, Brett M., Muterspaugh, Matthew W., Nespral, David, Nugent, C. R., Nugent, Katherine M., Odasso, A., O'Keeffe, Derek, Oksanen, A., O'Meara, John M., Ordasi, Andras, Osborn, Hugh, Ott, John J., Parks, J. R., Perez, Diego Rodriguez, Petriew, Vance, Pickard, R., Pal, Andras, Plavchan, P., Pollacco, Don, Nunez, F. Pozo, Pozuelos, F. J., Rau, Steve, Redfield, Seth, Relles, Howard, Ribas, Ignasi, Richards, Jon, Saario, Joonas L. O., Safron, Emily J., Sallai, J. Martin, Sarneczky, Krisztian, Schaefer, Bradley E., Schumer, Clea F., Schwartzendruber, Madison, Siegel, Michael H., Siemion, Andrew P. V., Simmons, Brooke D., Simon, Joshua D., Simon-Diaz, S., Sitko, Michael L., Socas-Navarro, Hector, Sodor, A., Starkey, Donn, Steele, Iain A., Stone, Geoff, Strassmeier, Klaus G., Street, R. A., Sullivan, Tricia, Suomela, J., Swift, J. J., Szabo, Gyula M., Szabo, Robert, Szakats, Robert, Szalai, Tamas, Tanner, Angelle M., Toledo-Padron, B., Tordai, Tamas, Triaud, Amaury H. M. J., Turner, Jake D., Ulowetz, Joseph H., Urbanik, Marian, Vanaverbeke, Siegfried, Vanderburg, Andrew, Vida, Krisztian, Vietje, Brad P., Vinko, Jozsef, Von Braun, K., Waagen, Elizabeth O., Walsh, Dan, Watson, Christopher A., Weir, R. C., Wenzel, Klaus, Plaza, C. Westendorp, Williamson, Michael W., Wright, Jason T., Wyatt, M. C., Zheng, WeiKang, Zsidi, Gabriella, Boyajian, Tabetha. S., Alonso, Roi, Ammerman, Alex, Armstrong, David, Ramos, A. Asensio, Barkaoui, K., Beatty, Thomas G., Benkhaldoun, Z., Benni, Paul, Bentley, Rory O., Berdyugin, Andrei, Berdyugina, Svetlana, Bergeron, Serge, Bieryla, Allyson, Blain, Michaela G., Blanco, Alicia Capetillo, Bodman, Eva H. L., Boucher, Anne, Bradley, Mark, Brincat, Stephen M., Brink, Thomas G., Briol, John, Brown, David J. A., Budaj, J., Burdanov, A., Cale, B., Carbo, Miguel Aznar, Garcia, R. Castillo, Clark, Wendy J., Clayton, Geoffrey C., Clem, James L., Coker, Phillip H., Cook, Evan M., Copperwheat, Chris M., Curtis, J. L., Cutri, R. M., Cseh, B., Cynamon, C. H., Daniels, Alex J., Davenport, James R. A., Deeg, Hans J., De Lorenzo, Roberto, De Jaeger, Thomas, Desrosiers, Jean-Bruno, Dolan, John, Dowhos, D. J., Dubois, Franky, Durkee, R., Dvorak, Shawn, Easley, Lynn, Edwards, N., Ellis, Tyler G., Erdelyi, Emery, Ertel, Steve, Farfan, Rafael. G., Farihi, J., Filippenko, Alexei V., Foxell, Emma, Gandolfi, Davide, Garcia, Faustino, Giddens, F., Gillon, M., Gonzalez-Carballo, Juan-Luis, Gonzalez-Fernandez, C., Hernandez, J. I. Gonzalez, Graham, Keith A., Greene, Kenton A., Gregorio, J., Hallakoun, Na'ama, Hanyecz, Otto, Harp, G. R., Henry, Gregory W., Herrero, E., Hildbold, Caleb F., Hinzel, D., Holgado, G., Ignacz, Bernadett, Ilyin, Ilya, Ivanov, Valentin D., Jehin, E., Jermak, Helen E., Johnston, Steve, Kafka, S., Kalup, Csilla, Kardasis, Emmanuel, Kaspi, Shai, Kennedy, Grant M., Kiefer, F., Kielty, C. L., Kessler, Dennis, Kiiskinen, H., Killestein, T. L., King, Ronald A., Kollar, V., Korhonen, H., Kotnik, C., Konyves-Toth, Reka, Kriskovics, Levente, Krumm, Nathan, Krushinsky, Vadim, Kundra, E., Lachapelle, Francois-Rene, LaCourse, D., Lake, P., Lam, Kristine, Lamb, Gavin P., Lane, Dave, Lau, Marie Wingyee, Lewin, Pablo, Lintott, Chris, Lisse, Carey, Logie, Ludwig, Longeard, Nicolas, Villanueva, M. Lopez, Ludington, E. Whit, Mainzer, A., Malo, Lison, Maloney, Chris, Mann, A., Mantero, A., Marengo, Massimo, Marchant, Jon, Gonzalez, M. J. Martinez, Masiero, Joseph R., Mauerhan, Jon C., McCormac, James, McNeely, Aaron, Meng, Huan Y. A., Miller, Mike, Molnar, Lawrence A., Morales, J. C., Morris, Brett M., Muterspaugh, Matthew W., Nespral, David, Nugent, C. R., Nugent, Katherine M., Odasso, A., O'Keeffe, Derek, Oksanen, A., O'Meara, John M., Ordasi, Andras, Osborn, Hugh, Ott, John J., Parks, J. R., Perez, Diego Rodriguez, Petriew, Vance, Pickard, R., Pal, Andras, Plavchan, P., Pollacco, Don, Nunez, F. Pozo, Pozuelos, F. J., Rau, Steve, Redfield, Seth, Relles, Howard, Ribas, Ignasi, Richards, Jon, Saario, Joonas L. O., Safron, Emily J., Sallai, J. Martin, Sarneczky, Krisztian, Schaefer, Bradley E., Schumer, Clea F., Schwartzendruber, Madison, Siegel, Michael H., Siemion, Andrew P. V., Simmons, Brooke D., Simon, Joshua D., Simon-Diaz, S., Sitko, Michael L., Socas-Navarro, Hector, Sodor, A., Starkey, Donn, Steele, Iain A., Stone, Geoff, Strassmeier, Klaus G., Street, R. A., Sullivan, Tricia, Suomela, J., Swift, J. J., Szabo, Gyula M., Szabo, Robert, Szakats, Robert, Szalai, Tamas, Tanner, Angelle M., Toledo-Padron, B., Tordai, Tamas, Triaud, Amaury H. M. J., Turner, Jake D., Ulowetz, Joseph H., Urbanik, Marian, Vanaverbeke, Siegfried, Vanderburg, Andrew, Vida, Krisztian, Vietje, Brad P., Vinko, Jozsef, Von Braun, K., Waagen, Elizabeth O., Walsh, Dan, Watson, Christopher A., Weir, R. C., Wenzel, Klaus, Plaza, C. Westendorp, Williamson, Michael W., Wright, Jason T., Wyatt, M. C., Zheng, WeiKang, and Zsidi, Gabriella

Published
2018

8. Molecular Evolution of Early-Onset Prostate Cancer Identifies Molecular Risk Markers and Clinical Trajectories.

Author

Gerhauser, Clarissa, Gerhauser, Clarissa, Favero, Francesco, Risch, Thomas, Simon, Ronald, Feuerbach, Lars, Assenov, Yassen, Heckmann, Doreen, Sidiropoulos, Nikos, Waszak, Sebastian M, Hübschmann, Daniel, Urbanucci, Alfonso, Girma, Etsehiwot G, Kuryshev, Vladimir, Klimczak, Leszek J, Saini, Natalie, Stütz, Adrian M, Weichenhan, Dieter, Böttcher, Lisa-Marie, Toth, Reka, Hendriksen, Josephine D, Koop, Christina, Lutsik, Pavlo, Matzk, Sören, Warnatz, Hans-Jörg, Amstislavskiy, Vyacheslav, Feuerstein, Clarissa, Raeder, Benjamin, Bogatyrova, Olga, Schmitz, Eva-Maria, Hube-Magg, Claudia, Kluth, Martina, Huland, Hartwig, Graefen, Markus, Lawerenz, Chris, Henry, Gervaise H, Yamaguchi, Takafumi N, Malewska, Alicia, Meiners, Jan, Schilling, Daniela, Reisinger, Eva, Eils, Roland, Schlesner, Matthias, Strand, Douglas W, Bristow, Robert G, Boutros, Paul C, von Kalle, Christof, Gordenin, Dmitry, Sültmann, Holger, Brors, Benedikt, Sauter, Guido, Plass, Christoph, Yaspo, Marie-Laure, Korbel, Jan O, Schlomm, Thorsten, Weischenfeldt, Joachim, Gerhauser, Clarissa, Gerhauser, Clarissa, Favero, Francesco, Risch, Thomas, Simon, Ronald, Feuerbach, Lars, Assenov, Yassen, Heckmann, Doreen, Sidiropoulos, Nikos, Waszak, Sebastian M, Hübschmann, Daniel, Urbanucci, Alfonso, Girma, Etsehiwot G, Kuryshev, Vladimir, Klimczak, Leszek J, Saini, Natalie, Stütz, Adrian M, Weichenhan, Dieter, Böttcher, Lisa-Marie, Toth, Reka, Hendriksen, Josephine D, Koop, Christina, Lutsik, Pavlo, Matzk, Sören, Warnatz, Hans-Jörg, Amstislavskiy, Vyacheslav, Feuerstein, Clarissa, Raeder, Benjamin, Bogatyrova, Olga, Schmitz, Eva-Maria, Hube-Magg, Claudia, Kluth, Martina, Huland, Hartwig, Graefen, Markus, Lawerenz, Chris, Henry, Gervaise H, Yamaguchi, Takafumi N, Malewska, Alicia, Meiners, Jan, Schilling, Daniela, Reisinger, Eva, Eils, Roland, Schlesner, Matthias, Strand, Douglas W, Bristow, Robert G, Boutros, Paul C, von Kalle, Christof, Gordenin, Dmitry, Sültmann, Holger, Brors, Benedikt, Sauter, Guido, Plass, Christoph, Yaspo, Marie-Laure, Korbel, Jan O, Schlomm, Thorsten, and Weischenfeldt, Joachim

Abstract

Identifying the earliest somatic changes in prostate cancer can give important insights into tumor evolution and aids in stratifying high- from low-risk disease. We integrated whole genome, transcriptome and methylome analysis of early-onset prostate cancers (diagnosis ≤55 years). Characterization across 292 prostate cancer genomes revealed age-related genomic alterations and a clock-like enzymatic-driven mutational process contributing to the earliest mutations in prostate cancer patients. Our integrative analysis identified four molecular subgroups, including a particularly aggressive subgroup with recurrent duplications associated with increased expression of ESRP1, which we validate in 12,000 tissue microarray tumors. Finally, we combined the patterns of molecular co-occurrence and risk-based subgroup information to deconvolve the molecular and clinical trajectories of prostate cancer from single patient samples.

Published
2018

9. Molecular Evolution of Early-Onset Prostate Cancer Identifies Molecular Risk Markers and Clinical Trajectories

Author

Gerhauser, Clarissa, Favero, Francesco, Risch, Thomas, Simon, Ronald, Feuerbach, Lars, Assenov, Yassen, Heckmann, Doreen, Sidiropoulos, Nikos, Waszak, Sebastian M., Hübschmann, Daniel, Urbanucci, Alfonso, Girma, Etsehiwot G., Kuryshev, Vladimir, Klimczak, Leszek J., Saini, Natalie, Stütz, Adrian M., Weichenhan, Dieter, Böttcher, Lisa Marie, Toth, Reka, Hendriksen, Josephine D., Koop, Christina, Lutsik, Pavlo, Matzk, Sören, Warnatz, Hans Jörg, Amstislavskiy, Vyacheslav, Feuerstein, Clarissa, Raeder, Benjamin, Bogatyrova, Olga, Schmitz, Eva Maria, Hube-Magg, Claudia, Kluth, Martina, Huland, Hartwig, Graefen, Markus, Lawerenz, Chris, Henry, Gervaise H., Yamaguchi, Takafumi N., Malewska, Alicia, Meiners, Jan, Schilling, Daniela, Reisinger, Eva, Eils, Roland, Schlesner, Matthias, Strand, Douglas W., Bristow, Robert G., Boutros, Paul C., von Kalle, Christof, Gordenin, Dmitry, Sültmann, Holger, Brors, Benedikt, Sauter, Guido, Plass, Christoph, Yaspo, Marie Laure, Korbel, Jan O., Schlomm, Thorsten, Weischenfeldt, Joachim, Gerhauser, Clarissa, Favero, Francesco, Risch, Thomas, Simon, Ronald, Feuerbach, Lars, Assenov, Yassen, Heckmann, Doreen, Sidiropoulos, Nikos, Waszak, Sebastian M., Hübschmann, Daniel, Urbanucci, Alfonso, Girma, Etsehiwot G., Kuryshev, Vladimir, Klimczak, Leszek J., Saini, Natalie, Stütz, Adrian M., Weichenhan, Dieter, Böttcher, Lisa Marie, Toth, Reka, Hendriksen, Josephine D., Koop, Christina, Lutsik, Pavlo, Matzk, Sören, Warnatz, Hans Jörg, Amstislavskiy, Vyacheslav, Feuerstein, Clarissa, Raeder, Benjamin, Bogatyrova, Olga, Schmitz, Eva Maria, Hube-Magg, Claudia, Kluth, Martina, Huland, Hartwig, Graefen, Markus, Lawerenz, Chris, Henry, Gervaise H., Yamaguchi, Takafumi N., Malewska, Alicia, Meiners, Jan, Schilling, Daniela, Reisinger, Eva, Eils, Roland, Schlesner, Matthias, Strand, Douglas W., Bristow, Robert G., Boutros, Paul C., von Kalle, Christof, Gordenin, Dmitry, Sültmann, Holger, Brors, Benedikt, Sauter, Guido, Plass, Christoph, Yaspo, Marie Laure, Korbel, Jan O., Schlomm, Thorsten, and Weischenfeldt, Joachim

Abstract

Identifying the earliest somatic changes in prostate cancer can give important insights into tumor evolution and aids in stratifying high- from low-risk disease. We integrated whole genome, transcriptome and methylome analysis of early-onset prostate cancers (diagnosis ≤55 years). Characterization across 292 prostate cancer genomes revealed age-related genomic alterations and a clock-like enzymatic-driven mutational process contributing to the earliest mutations in prostate cancer patients. Our integrative analysis identified four molecular subgroups, including a particularly aggressive subgroup with recurrent duplications associated with increased expression of ESRP1, which we validate in 12,000 tissue microarray tumors. Finally, we combined the patterns of molecular co-occurrence and risk-based subgroup information to deconvolve the molecular and clinical trajectories of prostate cancer from single patient samples. Gerhauser et al. molecularly characterize prostate cancers diagnosed before 56 years old, which reveals an APOBEC-driven mutational process and identifies an aggressive subgroup with increased expression of ESRP1. They develop a framework to predict the order of somatic alterations and clinical outcome.

Published
2018

10. RAS-pathway mutation patterns define epigenetic subclasses in juvenile myelomonocytic leukemia

Author

Lipka, Daniel B; https://orcid.org/0000-0001-5081-7869, Witte, Tania; https://orcid.org/0000-0003-4287-1608, Toth, Reka, Yang, Jing, Wiesenfarth, Manuel, Nöllke, Peter; https://orcid.org/0000-0002-0281-4732, Fischer, Alexandra, Brocks, David, Gu, Zuguang, Park, Jeongbin, Strahm, Brigitte, Wlodarski, Marcin; https://orcid.org/0000-0001-6638-9643, Yoshimi, Ayami, Claus, Rainer, Lübbert, Michael, Busch, Hauke, Boerries, Melanie, Hartmann, Mark; https://orcid.org/0000-0002-4072-4658, Schönung, Maximilian; https://orcid.org/0000-0002-9778-9698, Kilik, Umut, Langstein, Jens, Wierzbinska, Justyna A; https://orcid.org/0000-0001-5536-3501, Pabst, Caroline, Garg, Swati, Catalá, Albert; https://orcid.org/0000-0003-0133-1752, De Moerloose, Barbara, Dworzak, Michael, Hasle, Henrik; https://orcid.org/0000-0003-3976-9231, Locatelli, Franco, Masetti, Riccardo; https://orcid.org/0000-0002-1264-057X, et al, Lipka, Daniel B; https://orcid.org/0000-0001-5081-7869, Witte, Tania; https://orcid.org/0000-0003-4287-1608, Toth, Reka, Yang, Jing, Wiesenfarth, Manuel, Nöllke, Peter; https://orcid.org/0000-0002-0281-4732, Fischer, Alexandra, Brocks, David, Gu, Zuguang, Park, Jeongbin, Strahm, Brigitte, Wlodarski, Marcin; https://orcid.org/0000-0001-6638-9643, Yoshimi, Ayami, Claus, Rainer, Lübbert, Michael, Busch, Hauke, Boerries, Melanie, Hartmann, Mark; https://orcid.org/0000-0002-4072-4658, Schönung, Maximilian; https://orcid.org/0000-0002-9778-9698, Kilik, Umut, Langstein, Jens, Wierzbinska, Justyna A; https://orcid.org/0000-0001-5536-3501, Pabst, Caroline, Garg, Swati, Catalá, Albert; https://orcid.org/0000-0003-0133-1752, De Moerloose, Barbara, Dworzak, Michael, Hasle, Henrik; https://orcid.org/0000-0003-3976-9231, Locatelli, Franco, Masetti, Riccardo; https://orcid.org/0000-0002-1264-057X, and et al

Abstract

Juvenile myelomonocytic leukemia (JMML) is an aggressive myeloproliferative disorder of early childhood characterized by mutations activating RAS signaling. Established clinical and genetic markers fail to fully recapitulate the clinical and biological heterogeneity of this disease. Here we report DNA methylome analysis and mutation profiling of 167 JMML samples. We identify three JMML subgroups with unique molecular and clinical characteristics. The high methylation group (HM) is characterized by somatic PTPN11 mutations and poor clinical outcome. The low methylation group is enriched for somatic NRAS and CBL mutations, as well as for Noonan patients, and has a good prognosis. The intermediate methylation group (IM) shows enrichment for monosomy 7 and somatic KRAS mutations. Hypermethylation is associated with repressed chromatin, genes regulated by RAS signaling, frequent co-occurrence of RAS pathway mutations and upregulation of DNMT1 and DNMT3B, suggesting a link between activation of the DNA methylation machinery and mutational patterns in JMML.

Published
2017

11. Metabolomics and transcriptomics identify pathway differences between visceral and subcutaneous adipose tissue in colorectal cancer patients: the ColoCare study.

Author

Liesenfeld, David B, Liesenfeld, David B, Grapov, Dmitry, Fahrmann, Johannes F, Salou, Mariam, Scherer, Dominique, Toth, Reka, Habermann, Nina, Böhm, Jürgen, Schrotz-King, Petra, Gigic, Biljana, Schneider, Martin, Ulrich, Alexis, Herpel, Esther, Schirmacher, Peter, Fiehn, Oliver, Lampe, Johanna W, Ulrich, Cornelia M, Liesenfeld, David B, Liesenfeld, David B, Grapov, Dmitry, Fahrmann, Johannes F, Salou, Mariam, Scherer, Dominique, Toth, Reka, Habermann, Nina, Böhm, Jürgen, Schrotz-King, Petra, Gigic, Biljana, Schneider, Martin, Ulrich, Alexis, Herpel, Esther, Schirmacher, Peter, Fiehn, Oliver, Lampe, Johanna W, and Ulrich, Cornelia M

Abstract

BackgroundMetabolic and transcriptomic differences between visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) compartments, particularly in the context of obesity, may play a role in colorectal carcinogenesis. We investigated the differential functions of their metabolic compositions.ObjectivesBiochemical differences between adipose tissues (VAT compared with SAT) in patients with colorectal carcinoma (CRC) were investigated by using mass spectrometry metabolomics and gene expression profiling. Metabolite compositions were compared between VAT, SAT, and serum metabolites. The relation between patients' tumor stage and metabolic profiles was assessed.DesignPresurgery blood and paired VAT and SAT samples during tumor surgery were obtained from 59 CRC patients (tumor stages I-IV) of the ColoCare cohort. Gas chromatography time-of-flight mass spectrometry and liquid chromatography quadrupole time-of-flight mass spectrometry were used to measure 1065 metabolites in adipose tissue (333 identified compounds) and 1810 metabolites in serum (467 identified compounds). Adipose tissue gene expression was measured by using Illumina's HumanHT-12 Expression BeadChips.ResultsCompared with SAT, VAT displayed elevated markers of inflammatory lipid metabolism, free arachidonic acid, phospholipases (PLA2G10), and prostaglandin synthesis-related enzymes (PTGD/PTGS2S). Plasmalogen concentrations were lower in VAT than in SAT, which was supported by lower gene expression of FAR1, the rate-limiting enzyme for ether-lipid synthesis in VAT. Serum sphingomyelin concentrations were inversely correlated (P = 0.0001) with SAT adipose triglycerides. Logistic regression identified lipids in patients' adipose tissues, which were associated with CRC tumor stage.ConclusionsAs one of the first studies, we comprehensively assessed differences in metabolic, lipidomic, and transcriptomic profiles between paired human VAT and SAT and their association with CRC tumor stage. We identified m

Published
2015

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