Aaron N. Hata - Concepedia

Author

Aaron N. Hata

Massachusetts General Hospital ORCID

Also Known As

A Hata, A N Hata, A. HATA, A. Hata, A.N. Hata, Aaron Hata, Aaron N Hata, Aaron N. Hata, Aaron N Hata, Aaron N. Hata

500

Publications

14.3K

Citations

H-Index

Concepts

All Affiliations

Massachusetts General Hospital Harvard University Dana-Farber Cancer Institute Broad Institute Center for Cancer Research

About

Aaron N. Hata is an author at Massachusetts General Hospital specializing in medicine, cell biology, and tumor biology.

Top Concepts

#	Concept	H-Index	Publications	Citations
1	Medicine	19	23	3.5K
2	Health Sciences	3	3	345
3	Natural Sciences	2	2	76
4	Engineering	1	1	12
5	Biochemistry	1	1	67

Aaron N. Hata

Publications

11.5K

Citations

H-Index

Page 1

	Year	Citations
<i>EGFR</i> Mutations and <i>ALK</i> Rearrangements Are Associated with Low Response Rates to PD-1 Pathway Blockade in Non–Small Cell Lung Cancer: A Retrospective Analysis Justin F. Gainor, Alice T. Shaw, Lecia V. Sequist, Clinical Cancer Research	2016	1.2K
Tumor cells can follow distinct evolutionary paths to become resistant to epidermal growth factor receptor inhibition Aaron N. Hata, Matthew J. Niederst, Hannah L. Archibald, Nature Medicine Tumor BiologyDevelopmental BiologyDistinct Evolutionary PathsMedicineTumor Cells	2016	968
A single-cell and single-nucleus RNA-Seq toolbox for fresh and frozen human tumors Michal Slyper, Caroline Porter, Orr Ashenberg, Nature Medicine	2020	751
Clinical Acquired Resistance to KRASG12C Inhibition through a Novel KRAS Switch-II Pocket Mutation and Polyclonal Alterations Converging on RAS–MAPK Reactivation Noritaka Tanaka, Chendi Li, Meagan B. Ryan, Cancer Discovery	2021	475
Cycling cancer persister cells arise from lineages with distinct programs Yaara Oren, Michael Tsabar, Michael S. Cuoco, Nature Tumor BiologyLineage PlasticityCell DivisionTumor HeterogeneityCancer Persister Cells	2021	472
Heterogeneity Underlies the Emergence of <i>EGFR</i> T790 Wild-Type Clones Following Treatment of T790M-Positive Cancers with a Third-Generation EGFR Inhibitor Zofia Piotrowska, Matthew J. Niederst, Chris Karlovich, Cancer Discovery	2015	453
Landscape of Acquired Resistance to Osimertinib in <i>EGFR</i> -Mutant NSCLC and Clinical Validation of Combined EGFR and RET Inhibition with Osimertinib and BLU-667 for Acquired <i>RET</i> Fusion Zofia Piotrowska, Hideko Isozaki, Jochen K. Lennerz, Cancer Discovery	2018	434
Synthetic Lethal Interaction of Combined BCL-XL and MEK Inhibition Promotes Tumor Regressions in KRAS Mutant Cancer Models Ryan B. Corcoran, Katherine A. Cheng, Aaron N. Hata, Cancer Cell Tumor BiologyRadiation OncologyMedicineSynthetic Lethal InteractionImmune Checkpoint Inhibitor	2012	378
Impact of <i>EML4-ALK</i> Variant on Resistance Mechanisms and Clinical Outcomes in <i>ALK</i>-Positive Lung Cancer Viola W. Zhu, Satoshi Yoda, Beow Y. Yeap, Journal of Clinical Oncology Lymphoid NeoplasiaAlk-positive NsclcMedicineImmunologyPathology	2018	313
Sequential ALK Inhibitors Can Select for Lorlatinib-Resistant Compound <i>ALK</i> Mutations in ALK-Positive Lung Cancer Satoshi Yoda, Michael S. Lawrence, Benjamin J. Burke, Cancer Discovery	2018	298

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