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5 results on '"Carrasco-Alfonso, Marlene"'

1. CARTITUDE-2: Efficacy and safety of ciltacabtagene autoleucel (cilta-cel), a BCMA-directed CAR T-cell therapy, in patients with progressive multiple myeloma (MM) after one to three prior lines of therapy.

Author

Agha, Mounzer E., Cohen, Adam D., Madduri, Deepu, Cohen, Yael C., Delforge, Michel, Hillengass, Jens, Goldschmidt, Hartmut, Weisel, Katja, Raab, Marc-Steffen, Scheid, Christof, Schecter, Jordan Mark, De Braganca, Kevin C., Varsos, Helen, Wang, Liwei, Vogel, Martin, Carrasco-Alfonso, Marlene, Akram, Muhammad, Wu, Xiaoling, Nesheiwat, Tonia, Einsele, Hermann, Agha, Mounzer E., Cohen, Adam D., Madduri, Deepu, Cohen, Yael C., Delforge, Michel, Hillengass, Jens, Goldschmidt, Hartmut, Weisel, Katja, Raab, Marc-Steffen, Scheid, Christof, Schecter, Jordan Mark, De Braganca, Kevin C., Varsos, Helen, Wang, Liwei, Vogel, Martin, Carrasco-Alfonso, Marlene, Akram, Muhammad, Wu, Xiaoling, Nesheiwat, Tonia, and Einsele, Hermann

Published
2021

2. CARTITUDE-2: Efficacy and safety of ciltacabtagene autoleucel (cilta-cel), a BCMA-directed CAR T-cell therapy, in patients with progressive multiple myeloma (MM) after one to three prior lines of therapy.

Author

Agha, Mounzer E., Cohen, Adam D., Madduri, Deepu, Cohen, Yael C., Delforge, Michel, Hillengass, Jens, Goldschmidt, Hartmut, Weisel, Katja, Raab, Marc-Steffen, Scheid, Christof, Schecter, Jordan Mark, De Braganca, Kevin C., Varsos, Helen, Wang, Liwei, Vogel, Martin, Carrasco-Alfonso, Marlene, Akram, Muhammad, Wu, Xiaoling, Nesheiwat, Tonia, Einsele, Hermann, Agha, Mounzer E., Cohen, Adam D., Madduri, Deepu, Cohen, Yael C., Delforge, Michel, Hillengass, Jens, Goldschmidt, Hartmut, Weisel, Katja, Raab, Marc-Steffen, Scheid, Christof, Schecter, Jordan Mark, De Braganca, Kevin C., Varsos, Helen, Wang, Liwei, Vogel, Martin, Carrasco-Alfonso, Marlene, Akram, Muhammad, Wu, Xiaoling, Nesheiwat, Tonia, and Einsele, Hermann

Published
2021

3. Genetic and epigenetic fine mapping of causal autoimmune disease variants.

Author

Farh, Kyle Kai-How, Farh, Kyle Kai-How, Marson, Alexander, Zhu, Jiang, Kleinewietfeld, Markus, Housley, William J, Beik, Samantha, Shoresh, Noam, Whitton, Holly, Ryan, Russell JH, Shishkin, Alexander A, Hatan, Meital, Carrasco-Alfonso, Marlene J, Mayer, Dita, Luckey, C John, Patsopoulos, Nikolaos A, De Jager, Philip L, Kuchroo, Vijay K, Epstein, Charles B, Daly, Mark J, Hafler, David A, Bernstein, Bradley E, Farh, Kyle Kai-How, Farh, Kyle Kai-How, Marson, Alexander, Zhu, Jiang, Kleinewietfeld, Markus, Housley, William J, Beik, Samantha, Shoresh, Noam, Whitton, Holly, Ryan, Russell JH, Shishkin, Alexander A, Hatan, Meital, Carrasco-Alfonso, Marlene J, Mayer, Dita, Luckey, C John, Patsopoulos, Nikolaos A, De Jager, Philip L, Kuchroo, Vijay K, Epstein, Charles B, Daly, Mark J, Hafler, David A, and Bernstein, Bradley E

Abstract

Genome-wide association studies have identified loci underlying human diseases, but the causal nucleotide changes and mechanisms remain largely unknown. Here we developed a fine-mapping algorithm to identify candidate causal variants for 21 autoimmune diseases from genotyping data. We integrated these predictions with transcription and cis-regulatory element annotations, derived by mapping RNA and chromatin in primary immune cells, including resting and stimulated CD4(+) T-cell subsets, regulatory T cells, CD8(+) T cells, B cells, and monocytes. We find that ∼90% of causal variants are non-coding, with ∼60% mapping to immune-cell enhancers, many of which gain histone acetylation and transcribe enhancer-associated RNA upon immune stimulation. Causal variants tend to occur near binding sites for master regulators of immune differentiation and stimulus-dependent gene activation, but only 10-20% directly alter recognizable transcription factor binding motifs. Rather, most non-coding risk variants, including those that alter gene expression, affect non-canonical sequence determinants not well-explained by current gene regulatory models.

Published
2015

4. Genetic and epigenetic fine mapping of causal autoimmune disease variants.

Author

Farh, Kyle Kai-How, Farh, Kyle Kai-How, Marson, Alexander, Zhu, Jiang, Kleinewietfeld, Markus, Housley, William J, Beik, Samantha, Shoresh, Noam, Whitton, Holly, Ryan, Russell JH, Shishkin, Alexander A, Hatan, Meital, Carrasco-Alfonso, Marlene J, Mayer, Dita, Luckey, C John, Patsopoulos, Nikolaos A, De Jager, Philip L, Kuchroo, Vijay K, Epstein, Charles B, Daly, Mark J, Hafler, David A, Bernstein, Bradley E, Farh, Kyle Kai-How, Farh, Kyle Kai-How, Marson, Alexander, Zhu, Jiang, Kleinewietfeld, Markus, Housley, William J, Beik, Samantha, Shoresh, Noam, Whitton, Holly, Ryan, Russell JH, Shishkin, Alexander A, Hatan, Meital, Carrasco-Alfonso, Marlene J, Mayer, Dita, Luckey, C John, Patsopoulos, Nikolaos A, De Jager, Philip L, Kuchroo, Vijay K, Epstein, Charles B, Daly, Mark J, Hafler, David A, and Bernstein, Bradley E

Abstract

Genome-wide association studies have identified loci underlying human diseases, but the causal nucleotide changes and mechanisms remain largely unknown. Here we developed a fine-mapping algorithm to identify candidate causal variants for 21 autoimmune diseases from genotyping data. We integrated these predictions with transcription and cis-regulatory element annotations, derived by mapping RNA and chromatin in primary immune cells, including resting and stimulated CD4(+) T-cell subsets, regulatory T cells, CD8(+) T cells, B cells, and monocytes. We find that ∼90% of causal variants are non-coding, with ∼60% mapping to immune-cell enhancers, many of which gain histone acetylation and transcribe enhancer-associated RNA upon immune stimulation. Causal variants tend to occur near binding sites for master regulators of immune differentiation and stimulus-dependent gene activation, but only 10-20% directly alter recognizable transcription factor binding motifs. Rather, most non-coding risk variants, including those that alter gene expression, affect non-canonical sequence determinants not well-explained by current gene regulatory models.

Published
2015

5. Genetic and epigenetic fine mapping of causal autoimmune disease variants.

Author

Farh, Kyle Kai-How, Farh, Kyle Kai-How, Marson, Alexander, Zhu, Jiang, Kleinewietfeld, Markus, Housley, William J, Beik, Samantha, Shoresh, Noam, Whitton, Holly, Ryan, Russell JH, Shishkin, Alexander A, Hatan, Meital, Carrasco-Alfonso, Marlene J, Mayer, Dita, Luckey, C John, Patsopoulos, Nikolaos A, De Jager, Philip L, Kuchroo, Vijay K, Epstein, Charles B, Daly, Mark J, Hafler, David A, Bernstein, Bradley E, Farh, Kyle Kai-How, Farh, Kyle Kai-How, Marson, Alexander, Zhu, Jiang, Kleinewietfeld, Markus, Housley, William J, Beik, Samantha, Shoresh, Noam, Whitton, Holly, Ryan, Russell JH, Shishkin, Alexander A, Hatan, Meital, Carrasco-Alfonso, Marlene J, Mayer, Dita, Luckey, C John, Patsopoulos, Nikolaos A, De Jager, Philip L, Kuchroo, Vijay K, Epstein, Charles B, Daly, Mark J, Hafler, David A, and Bernstein, Bradley E

Abstract

Genome-wide association studies have identified loci underlying human diseases, but the causal nucleotide changes and mechanisms remain largely unknown. Here we developed a fine-mapping algorithm to identify candidate causal variants for 21 autoimmune diseases from genotyping data. We integrated these predictions with transcription and cis-regulatory element annotations, derived by mapping RNA and chromatin in primary immune cells, including resting and stimulated CD4(+) T-cell subsets, regulatory T cells, CD8(+) T cells, B cells, and monocytes. We find that ∼90% of causal variants are non-coding, with ∼60% mapping to immune-cell enhancers, many of which gain histone acetylation and transcribe enhancer-associated RNA upon immune stimulation. Causal variants tend to occur near binding sites for master regulators of immune differentiation and stimulus-dependent gene activation, but only 10-20% directly alter recognizable transcription factor binding motifs. Rather, most non-coding risk variants, including those that alter gene expression, affect non-canonical sequence determinants not well-explained by current gene regulatory models.

Published
2015

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