Eugene Lifshits

7.8k total citations · 1 hit paper
13 papers, 2.6k citations indexed

About

Eugene Lifshits is a scholar working on Molecular Biology, Oncology and Pulmonary and Respiratory Medicine. According to data from OpenAlex, Eugene Lifshits has authored 13 papers receiving a total of 2.6k indexed citations (citations by other indexed papers that have themselves been cited), including 12 papers in Molecular Biology, 9 papers in Oncology and 8 papers in Pulmonary and Respiratory Medicine. Recurrent topics in Eugene Lifshits's work include Lung Cancer Treatments and Mutations (8 papers), PI3K/AKT/mTOR signaling in cancer (6 papers) and HER2/EGFR in Cancer Research (4 papers). Eugene Lifshits is often cited by papers focused on Lung Cancer Treatments and Mutations (8 papers), PI3K/AKT/mTOR signaling in cancer (6 papers) and HER2/EGFR in Cancer Research (4 papers). Eugene Lifshits collaborates with scholars based in United States, Norway and Switzerland. Eugene Lifshits's co-authors include Jeffrey A. Engelman, Pasi A. Jänne, John V. Heymach, Kreshnik Zejnullahu, George N. Naumov, Kwok‐Kin Wong, Cyril H. Benes, Hiromichi Ebi, Lewis C. Cantley and Ryohei Katayama and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Journal of Clinical Investigation and Cancer Research.

In The Last Decade

Eugene Lifshits

13 papers receiving 2.6k citations

Hit Papers

PF00299804, an Irreversible Pan-ERBB Inhibitor, Is Effect... 2007 2026 2013 2019 2007 100 200 300 400 500
What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

  1. PF00299804, an Irreversible Pan-ERBB Inhibitor, Is Effective in Lung Cancer Models with EGFR and ERBB2 Mutations that Are Resistant to Gefitinib
    2007 598 citations Jeffrey A. Engelman, Kreshnik Zejnullahu et al. Cancer Research profile →

Peers

Eugene Lifshits
Anthony M. D’Amelio United States
Dalia Ercan United States
Shinji Takeuchi Japan
Roberta Minari Italy
Rosa Caputo Italy
C. Martin Curtis United States
Jane Kendrew United Kingdom
Maria E. Arango United States
Andreas Zoephel Austria
Santiago Viteri Spain
Anthony M. D’Amelio United States
Eugene Lifshits
Citations per year, relative to Eugene Lifshits Eugene Lifshits (= 1×) peers Anthony M. D’Amelio

Countries citing papers authored by Eugene Lifshits

Since Specialization
Citations

This map shows the geographic impact of Eugene Lifshits's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Eugene Lifshits with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Eugene Lifshits more than expected).

Fields of papers citing papers by Eugene Lifshits

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Eugene Lifshits. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Eugene Lifshits. The network helps show where Eugene Lifshits may publish in the future.

Co-authorship network of co-authors of Eugene Lifshits

This figure shows the co-authorship network connecting the top 25 collaborators of Eugene Lifshits. A scholar is included among the top collaborators of Eugene Lifshits based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Eugene Lifshits. Eugene Lifshits is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

13 of 13 papers shown
1.
Rogers, Michael S., Katherine B. Novak, David Zurakowski, et al.. (2014). Spontaneous Reversion of the Angiogenic Phenotype to a Nonangiogenic and Dormant State in Human Tumors. Molecular Cancer Research. 12(5). 754–764. 11 indexed citations
2.
Hata, Aaron N., Alan T. Yeo, Anthony C. Faber, et al.. (2014). Failure to Induce Apoptosis via BCL-2 Family Proteins Underlies Lack of Efficacy of Combined MEK and PI3K Inhibitors for KRAS-Mutant Lung Cancers. Cancer Research. 74(11). 3146–3156. 60 indexed citations
3.
Corcoran, Ryan B., Katherine A. Cheng, Aaron N. Hata, et al.. (2013). Abstract PR09: Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS-mutant cancer models. Molecular Cancer Therapeutics. 12(5_Supplement). PR09–PR09. 1 indexed citations
4.
Qi, Jie, Michele McTigue, Andrew M. Rogers, et al.. (2011). Multiple Mutations and Bypass Mechanisms Can Contribute to Development of Acquired Resistance to MET Inhibitors. Cancer Research. 71(3). 1081–1091. 168 indexed citations
5.
Ebi, Hiromichi, Ryan B. Corcoran, Anurag Singh, et al.. (2011). Receptor tyrosine kinases exert dominant control over PI3K signaling in human KRAS mutant colorectal cancers. Journal of Clinical Investigation. 121(11). 4311–4321. 153 indexed citations
6.
Katayama, Ryohei, Tahsin M. Khan, Cyril H. Benes, et al.. (2011). Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK. Proceedings of the National Academy of Sciences. 108(18). 7535–7540. 425 indexed citations
7.
Ercan, Dalia, Kreshnik Zejnullahu, Kimio Yonesaka, et al.. (2010). Amplification of EGFR T790M causes resistance to an irreversible EGFR inhibitor. Oncogene. 29(16). 2346–2356. 181 indexed citations
8.
Naumov, George N., Monique B. Nilsson, Tina Cascone, et al.. (2009). Combined Vascular Endothelial Growth Factor Receptor and Epidermal Growth Factor Receptor (EGFR) Blockade Inhibits Tumor Growth in Xenograft Models of EGFR Inhibitor Resistance. Clinical Cancer Research. 15(10). 3484–3494. 279 indexed citations
9.
Faber, Anthony C., Danan Li, Young-Chul Song, et al.. (2009). Differential induction of apoptosis in HER2 and EGFR addicted cancers following PI3K inhibition. Proceedings of the National Academy of Sciences. 106(46). 19503–19508. 247 indexed citations
10.
Amin, Dhara N., Diane R. Bielenberg, Eugene Lifshits, John V. Heymach, & Michael Klagsbrun. (2008). Targeting EGFR activity in blood vessels is sufficient to inhibit tumor growth and is accompanied by an increase in VEGFR-2 dependence in tumor endothelial cells. Microvascular Research. 76(1). 15–22. 47 indexed citations
11.
Yuan, Tina L., Hak Soo Choi, Aya Matsui, et al.. (2008). Class 1A PI3K regulates vessel integrity during development and tumorigenesis. Proceedings of the National Academy of Sciences. 105(28). 9739–9744. 74 indexed citations
12.
Engelman, Jeffrey A., Kreshnik Zejnullahu, Eugene Lifshits, et al.. (2007). PF00299804, an Irreversible Pan-ERBB Inhibitor, Is Effective in Lung Cancer Models with EGFR and ERBB2 Mutations that Are Resistant to Gefitinib. Cancer Research. 67(24). 11924–11932. 598 indexed citations breakdown →
13.
Engelman, J. A., Toru Mukohara, Kreshnik Zejnullahu, et al.. (2006). Allelic dilution obscures detection of a biologically significant resistance mutation in EGFR-amplified lung cancer. Journal of Clinical Investigation. 116(10). 2695–2706. 374 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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