@MingLiLabi
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Member, Memorial Sloan Kettering Cancer Center Views expressed are not affiliated with my employer.
New York, NY
Joined July 2011
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Glad to share our review article from talented @LiangliangJi and coauthors @NatRevImmunol on the fascinating topic of monocytes and macrophages in cancer. Understanding their contextual roles across primary and metastatic tumors shall guild their therapeutic targeting.
High rate ATP production accounts for the Warburg Effect, perhaps in support of energy-demanding processes such as PI3K signaling in effector T cells
Excited to share our new paper led by @mattabolite in collaboration with Saharon Rosset showing that the Warburg Effect is the result of faster ATP production by glycolysis than respiration. A 🧵... 1/n pnas.org/doi/10.1073/pnas.24…
Congrats to Andrea @SchietingerLab for the very well deserved @CancerResearch Frederick W. Alt Award! Brilliant science for cancer cure!!
Ming Li retweeted
Now online! Dynamic allostery drives autocrine and paracrine TGF-β signaling dlvr.it/TDJlBm
Glad to share our review article @AnnualReviews on tissue-resident innate and adaptive lymphocytes in cancer. Defining their identities and sensing mechanisms shall guide targeting such prewired and priming-dependent defense responses for cancer therapies. doi.org/10.1146/annurev-immu…
Ming Li retweeted
28 cancers are now treatable with immunotherapy, thanks to the work of the Cancer Research Institute. Explore our Impact Report, and discover how CRI is transforming the lives of cancer patients on a global scale: bit.ly/3u0MMLe #CancerResearch #Immunotherapy
Thanks to @MSKCancerCenter for covering it!
MSK's Dr. Ming Li (@MingLiLab) discusses how his lab is working to harness the power of the immune system against #cancer — including a new paper just out in @ImmunityCP. bit.ly/3G7H7Wt
Reprogram tumor-associated macrophages to outcompete endothelial progenitor cells and suppress tumor neoangiogenesis. Excited to share our new study @ImmunityCP by brilliant @miahdo1 , Wei Shi, and @CancerResearch fellow @LiangliangJi and collaborators!
Growing bigger had a survival advantage for non-minimal cells and not growing bigger had a survival advantage for minimal cells.
A mind-blowing paper has come out today in @Nature
In 2016, JC Venter Institute scientists trimmed a bacterial genome to its barest minimum required for life to synthesize what they called a "minimal genome" (science.org/doi/10.1126/scie…).
Today, a group of scientists from Indiana University reports how that minimal genome evolved over 2000 generations in comparison to the non-minimal genome.
The authors found that even when you reduce a bacterial genome to its absolute minimum where every nucleotide matters, the genome undergoes mutational events generation after generation as much as the non-minimal genome. One simply cannot stop the evolution.
Just over 300 days of evolution (equivalent to 40,000 years in humans) the minimal cell has gained everything it lacked in fitness on day one in comparison to the non-minimal cell.
When comparing the evolved traits between the minimal and non-minimal cells, the scientists found something striking. The evolutionary process increased the cell size of non-minimal cells but not that of the minimal cell. But that is not the striking part.
The scientists were able to identify the key mutation that resulted in cell size evolution. And it turned out that the mutation that helped the non-minimal cells to grow bigger is the same that helped the minimal cells to stay smaller. Growing bigger had a survival advantage for non-minimal cells and not growing bigger had a survival advantage for minimal cells. So, the mutation had a context-dependent effect. This just demonstrates that the evolutionary effects on traits have no absolute direction. All that matter is what is beneficial for the organism's survival.
The conclusion of the paper is metaphorically a quote from the Jurassic Park movie:
“Listen, if there’s one thing the history of evolution has taught us is that life will not be contained. Life breaks free. It expands to new territories, and it crashes through barriers painfully, maybe even dangerously, but . . . life finds a way". (scienmag.com/artificial-cell…)
nature.com/articles/s41586-0…
Ming Li retweeted
Excited to introduce scKINETICS, an algorithm for joint inference of gene regulatory mechanism and cellular velocity, co-developed by the amazing duo of @CassBurdziak and @juuuulianaar
academic.oup.com/bioinformat…
Reprogram tumor-associated macrophages to outmatch cancer cell competition. Excited to share our new study @Nature by brilliant @CancerResearch fellow @XianZhang2016 and collaborators! rdcu.be/dfA6f
Ming Li retweeted
Our lab's latest paper on peripheral tolerance mechanisms in skin is out now in @Nature. Congrats to @martinadamo for leading this and thanks to collaborators from @KrishnaswamyLab and @yalederm.
nature.com/articles/s41586-0…
Celebrating cancer immunology and immunotherapy discoveries supported by #CancerResearch (70 years and going strong) and other agencies to create a world #Immune2Cancer
Ming Li retweeted
Check out this perspective on nutrient acquisition and metabolism control of macrophage responses in tumor, a collaboration between @XianZhang2016 @LiangliangJi & @MingLiLab @ImmunityCP #ASCO23 hubs.li/Q01RP-dM0
Glad to share a perspective on nutrient acquisition and metabolism control of macrophage responses in tumor @ImmunityCP with @CancerResearch fellows @XianZhang2016 @LiangliangJi authors.elsevier.com/a/1gOy2…
Glad to share a holistic immuno-oncology perspective through the lens of #TGFb @NatRevImmunol with implication for preclinical model choice for drug testing rdcu.be/cZJ5r
Ming Li retweeted
Online now: Tumor-associated macrophages expressing the transcription factor IRF8 promote T cell exhaustion in cancer dlvr.it/SbhR0m
Ming Li retweeted
New in @ImmunityCP: a team led by the @MingLiLab at MSK reports a unique function for tumor-associated macrophages (TAMs) in dampening tumor immunity — an immune regulation mechanism they're optimistic might be targeted with #immunotherapy in the future. cell.com/immunity/fulltext/S…
Tumor-associated macrophages present cancer cell antigen and drive cytotoxic T cell exhaustion. Check out our story from brilliant Briana Nixon, @dkuo @arihakimi and collaborators authors.elsevier.com/a/1fzsa…