Min K. Tsai

464 total citations
11 papers, 221 citations indexed

About

Min K. Tsai is a scholar working on Molecular Biology, Health Information Management and Cancer Research. According to data from OpenAlex, Min K. Tsai has authored 11 papers receiving a total of 221 indexed citations (citations by other indexed papers that have themselves been cited), including 9 papers in Molecular Biology, 3 papers in Health Information Management and 3 papers in Cancer Research. Recurrent topics in Min K. Tsai's work include Electronic Health Records Systems (3 papers), Cancer Genomics and Diagnostics (3 papers) and RNA modifications and cancer (2 papers). Min K. Tsai is often cited by papers focused on Electronic Health Records Systems (3 papers), Cancer Genomics and Diagnostics (3 papers) and RNA modifications and cancer (2 papers). Min K. Tsai collaborates with scholars based in United States, Germany and China. Min K. Tsai's co-authors include Monte M. Winslow, Rui Tang, Christopher W. Murray, Jennifer J. Brady, Pauline Chu, Laura Andrejka, Ian P. Winters, Christian A. Kunder, Chuan Li and K. Rosanna and has published in prestigious journals such as Nature Communications, The Journal of Experimental Medicine and Nature Cell Biology.

In The Last Decade

Min K. Tsai

9 papers receiving 217 citations

Peers

Min K. Tsai

MB

ONCOL

CR

IMMUN

PRM

Justin H. Gundelach United States

Alexandra Kuzyk Canada

Rui‐Zhao Dong China

Jorge Vaz Pinto Neto Brazil

Bahman Zarandi Iran

Yuting Qian China

Zahraa Rahal United States

Courtney L. Andersen United States

Fanjun Cheng China

Justin H. Gundelach United States

Min K. Tsai

108 ×0.8

MB

65 ×1.2

ONCOL

33 ×0.7

CR

23 ×0.6

IMMUN

18 ×0.6

PRM

Citations per year, relative to Min K. Tsai Min K. Tsai (= 1×) peers Justin H. Gundelach

Countries citing papers authored by Min K. Tsai

Since Specialization

Citations

This map shows the geographic impact of Min K. Tsai'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 Min K. Tsai with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Min K. Tsai more than expected).

Fields of papers citing papers by Min K. Tsai

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Min K. Tsai. 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 Min K. Tsai. The network helps show where Min K. Tsai may publish in the future.

Co-authorship network of co-authors of Min K. Tsai

This figure shows the co-authorship network connecting the top 25 collaborators of Min K. Tsai. A scholar is included among the top collaborators of Min K. Tsai 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 Min K. Tsai. Min K. Tsai is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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11 of 11 papers shown

1.

Shuldiner, Emily G., Kálmán Somogyi, Christopher W. Murray, et al.. (2025). EML4−ALK Variant-Specific Genetic Interactions Shape Lung Tumorigenesis. Cancer Discovery. 16(1). 46–65.

2.

Shuldiner, Emily G., Saswati Karmakar, Min K. Tsai, et al.. (2025). Aging represses oncogenic KRAS-driven lung tumorigenesis and alters tumor suppression. Nature Aging. 5(11). 2263–2278.

3.

Gonzalez, Michael, Daniel Lu, Maryam Yousefi, et al.. (2023). Phagocytosis increases an oxidative metabolic and immune suppressive signature in tumor macrophages. The Journal of Experimental Medicine. 220(6). 34 indexed citations

4.

Tang, Rui, Emily G. Shuldiner, Marcus R. Kelly, et al.. (2023). Multiplexed screens identify RAS paralogues HRAS and NRAS as suppressors of KRAS-driven lung cancer growth. Nature Cell Biology. 25(1). 159–169. 16 indexed citations

5.

Murray, Christopher W., Jennifer J. Brady, Hongchen Cai, et al.. (2022). LKB1 drives stasis and C/EBP-mediated reprogramming to an alveolar type II fate in lung cancer. Nature Communications. 13(1). 1090–1090. 12 indexed citations

6.

Pierce, Sarah E., Jeffrey M. Granja, M. Ryan Corces, et al.. (2021). LKB1 inactivation modulates chromatin accessibility to drive metastatic progression. Nature Cell Biology. 23(8). 915–924. 34 indexed citations

7.

Tang, Rui, Ian L. Linde, Nicholas J. Kramer, et al.. (2020). A versatile system to record cell-cell interactions. eLife. 9. 32 indexed citations

8.

Murray, Christopher W., Jennifer J. Brady, Min K. Tsai, et al.. (2019). An LKB1–SIK Axis Suppresses Lung Tumor Growth and Controls Differentiation. Cancer Discovery. 9(11). 1590–1605. 62 indexed citations

9.

Godin, Paul, Beth Woods, Min K. Tsai, et al.. (2003). A new instrument for medical decision support and education: the Stanford Health Information Network for Education. 81. 11–11. 5 indexed citations

10.

Godin, Paul J., et al.. (1999). New paradigms for medical decision support and education: the Stanford Health Information Network for Education.. PubMed. 20(2). 1–14. 13 indexed citations

11.

Tsai, Min K., et al.. (1997). The Stanford Health Information Network for Education: integrated information for decision making and learning.. PubMed. 505–8. 13 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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