T
Triparna Sen
Researcher at Memorial Sloan Kettering Cancer Center
Publications - 82
Citations - 3287
Triparna Sen is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Cancer & Cancer research. The author has an hindex of 25, co-authored 57 publications receiving 1709 citations. Previous affiliations of Triparna Sen include Washington University in St. Louis & National Cancer Research Institute.
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Abstract LB014: Targeting Stearoyl-coA desaturase (SCD) as a therapeutic strategy in STK11/KEAP1 co-mutant non-small cell lung cancer
Utsav Sen,Triparna Sen +1 more
TL;DR: Sen et al. as mentioned in this paper used CRISPR/Cas9 based genetic screening to identify stearoyl-CoA desaturase (SCD), a gene involved in ferroptosis protection, as a potential therapeutic target in the STK11/KEAP1 double mutant tumors.
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Abstract 658: AKT pathway as a therapeutic target to constrain lineage plasticity leading to histological transdifferentiation
Álvaro Quintanal-Villalonga,H Taniguchi,Yingqian Zhan,Fathema Uddin,Viola Allaj,P. Manoj,Nisargbhai S. Shah,Umesh Bhanot,Jacklynn V. Egger,Juan Jan Qiu,Elisa de Stanchina,Natasha Rekhtman,Brian Houck-Loomis,Richard Koche,Helena A. Yu,Triparna Sen,Charles M. Rudin +16 more
TL;DR: The data suggest that histological transdifferentiation is driven by epigenetic -rather than mutational- events, and indicate that transdifferentiated tumors retain molecular features of their previous LUAD state, and nominate AKT pathway as a therapeutic target to constrain lineage plasticity.
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Abstract 1370: Targeting LSD1 rescues MHC-I antigen presentation in small cell lung cancer
TL;DR: A role for LSD1 as a potent negative regulator of MHC-I-mediated antigen presentation is defined and rationale for the use of LSD1 inhibitors to augment response to immunotherapy in SCLC is provided.
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Abstract 3000: Ferroptosis evasion as a therapeutic strategy in STK11/KEAP1 co-mutant lung adenocarcinoma
Vidushi Durani,Corrin A. Wohlhieter,Álvaro Quintanal-Villalonga,Triparna Sen,P. Manoj,Charles M. Rudin +5 more
TL;DR: A potential interplay between STK11/KEAP1 function loss, ferroptosis protection, and the JAK-STAT and AKT oncogenic signaling pathways in LUAD is suggested to reveal mechanistic insight into the aggressive nature of these tumors.
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AKT inhibition as a therapeutic strategy to constrain histological transdifferentiation in EGFR-mutant lung adenocarcinoma.
Álvaro Quintanal-Villalonga,Hirokazu Taniguchi,Yingqian Zhan,Jacklynn V. Egger,Umesh Bhanot,Juan Jan Qiu,Elisa de Stanchina,Natasha Rekhtman,Brian Houck-Loomis,Richard Koche,Triparna Sen,Charles M. Rudin +11 more
TL;DR: The data supports that histological transdifferentiation from LUAD to LUSC or NE tumors is driven by epigenetic remodeling rather than by mutational events, and indicate that transdifferentiated tumors retain epigenomic features of their previous LUAD state.