The Min Lu Research Group

Shanghai Institute of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine
State Key Laboratory of Omics and Disease (formerly State Key Laboratory of Medical Genomics)

The Min Lu Research Group

Shanghai Institute of Hematology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine
State Key Laboratory of Omics and Disease (formerly State Key Laboratory of Medical Genomics)

Min Lu

Researcher, Doctoral supervisor

Ten representative Awards/Fund

2024  NSFC, Distinguished Young Scholars, CN

2021  NSFC, Key Program, CN

2017  MOST, Youth Principal Investigator, CN

2016  NSFC, Excellent Young Scientist Program, CN

2015  NSFC, Program for Overseas High-Level Experts Introduction, CN

2019  Royal Society of Medicine, Newton Advanced Fellowship, UK

2015  Oxford University, Athena SWAN Bronze Award, UK

2015  Parliamentary and Scientific Committee, Set for Britain, UK

2014  Oxford University, Recognition Scheme, UK

2007  Harvard University, Research Assistant Scholarship, US

Experience

2015 –            Ruijin Hospital, Shanghai Jiao Tong University School of Medicine (Professor)

2009 – 2015   Ludwig Cancer Research Oxford Branch, Oxford University (Postdoc.)

2007 – 2008   Beth Israel Deaconess Medical Center, Harvard Medical School (Co-cultured Ph.D.)

1999 – 2007   Biochemistry Institute, College of Life Science, Zhejiang University (Bachelor, Co-cultured Ph.D.)

Summary of research

There are about 10 million new cancer incidences per year that are caused by mutation and inactivation of tumor suppressor p53. Thus, a drug that can restore tumor-suppressive function to mutant p53 has tremendous clinical values, yet being one of the largest scientific challenges in medicine: 1) p53 is the most studied protein (gene) in the history; 2) at least 71 groups have reported identification of mutant p53 rescue compounds; 3) these rescue compounds have hatched over 23 clinical trials and a few Nasdaq-listed pharmaceutical companies. Yet, the most (if not all) of these rescue compounds are validated to be ineffective in rescuing mutant p53.

Min Lu has been working with p53 for about two decades. He is the obtainer of the mutant p53 rescue compounds:

1) revealed novel mechanisms underlying how p53 lose tumor-suppressive function (Cell 2014, Cancer Cell 2013, Nat Rev Mol Cell Biol 2016);

2) on Dec 24, 2020, he obtained an effective mutant p53 rescue compound ATO and revealed its structural mechanism (Cancer Cell 2021);

3) using ATO, he achieved first-in-human mutant p53 reactivation in human body (Sci Transl Med 2023);

4) on Feb 22, 2024, among the accessible generic mutant p53 rescue compounds, ATO (and its analogues) is recognized as the only effective one (Cancer Cell, 2024);

5) thus, he established the framework of pharmacological protein-function restoration (Cancer Discov 2024);

6) thus, he proposed the norm for p53-rescue clinical trials (Nat Rev Cancer 2025).

In the clinics, there are about 85 oncoprotein-targeted small molecule (namely the small molecule that can bind oncoprotein and inhibit its function), yet there is no tumor suppressor-targeted small molecule (namely the small molecule that can bind tumor suppressor and restore its function). ATO is the first effective tumor suppressor-reactivating small molecule, potentially opening the research field of tumor suppressor-targeted drug.