Author

Kamal N. Menghrajani

Memorial Sloan Kettering Cancer CenterORCID 0000-0002-6357-6475Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cancer Biology· 1 Genomics· 1

Signature Assays, Organisms & Methods

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Organism:human· 2 Approach:benchmark study· 1 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Assay:DNA methylation· 1 Research Focus:drug response / drug discovery· 1 Approach:experimental assay· 1

Frequent Co-Authors

Sean M. DevliniD· 2 shared Aaron James StonestromiD· 1 shared Agnes J. VialeiD· 1 shared Ahmet ZehiriD· 1 shared Aishwarya KrishnaniD· 1 shared Akifumi Takaori‐KondoiD· 1 shared Alberto Bueno Costa· 1 shared Alexandra G. SmithiD· 1 shared

Activity by Year

2020-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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2 shared papersCancer Biology

Sean M. DevlinORCID

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2 papers

Recent·Most cited

Targetable Treatment Resistance in Thyroid Cancer with Clonal Hematopoiesis

Vera Tiedje, Pablo Sánchez Vela, Julie L. Yang, Brian R. Untch, Laura Boucai, Aaron James Stonestrom, Alberto Bueno Costa, Sebastià Franch‐Expósito, Avi Srivastava, Marina Kerpelev, Jillian Greenberg, Mathew Wereski, Amanda R. Kulick, Kevin Chen, Tianyue Qin, , Ross L. Levine

This study identifies TET2-mutant clonal hematopoiesis in thyroid cancer microenvironments and shows that TGFβ signaling from these macrophages mediates resistance to BRAF/MEK inhibition, with TGFβ inhibition restoring sensitivity.

bioRxiv · Oct 10, 2024 · PreprintCancer Biology

Implications of TP53 Allelic State for Genome Stability, Clinical Presentation and Outcomes in Myelodysplastic Syndromes

Elsa Bernard, Yasuhito Nannya, Robert Paul Hasserjian, Sean M. Devlin, Heinz Tuechler, Juan Santiago Medina-Martinez, Tetsuichi Yoshizato, Yusuke Shiozawa, Ryunosuke Saiki, Luca Malcovati, Max Fine Levine, Juan E. Arango, Yangyu Zhou, Francesc Gessé Solé, Catherine A. Cargo, , Elli Papaemmanuil

The paper examines TP53 allelic states in MDS patients, finding that bi-allelic targeting is linked to worse outcomes, while mono-allelic targeting does not differ from wild-type patients.

Nature Medicine · Aug 3, 2020Peer-reviewedGenomics