Hwajin Lee
@hwajin2k
Currently at UPPThera, Cheif Operating Officer; Seoul National University, Adjunct PI Formerly at Celltrion, Inc. Ph.D in Cellular and Molecular Medicine, JHSOM
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Feature Selection and Dimension Reduction for Single Cell RNA-Seq based on a Multinomial Model biorxiv.org/content/10.110…
Personal News: Today marked a new beginning, and a beginning’s end. I am grateful for the support I received at @IcahnMountSinai where I started my career as an independent researcher. I am looking forward to my new role at @C2iGenomics, an innovative liquid biopsy company.
Exciting to see @KirstenKubler (now faculty at BIH @berlinnovation & @ChariteBerlin) present this recent collaborative work b/t @getz_lab and Dr. Rinath Jeselsohn on tamoxifen-associated #UterineCancer at #SABCS21! Check out the press release in her 🧵 to learn more!!
It was an honor to present our work on tamoxifen-associated #UterineCancer in #BreastCancer patients at #SABCS21. Our findings introduce a new concept that drugs can substitute for the mutant-driven activation of signaling pathways.
Important study about #IMiD neosubstrate SAR with design implications for molecular glue & CRBN-targeted #PROTACs (incl. dual MoA PROTACs like KT-413, NX-2127). Of note, comprising ARV-110's magic fluorine IMiD warhead. biorxiv.org/content/10.110… @biorxivpreprint @ChoudharyLab
Kristen Baltgalvis @VividionRx @BayerPharma sharing first data for a so far untouched E3 ligase highjacked with covalent binders for bifunctional degrader applications. Further of note: cell type variability of PROTACs & E3 fractional engagement data @Undruggable #TPD21
Impressive data shared by Ryan Potts @Amgen about how they QUALITY check previously unused E3 ligases for #PROTAC applications. Clearly showing how many more ligase are still out there to be highjacked for degrading disease causing proteins. @Undruggable #TPD21
Our recent work combining in vivo CRISPR screens, E3 ligase protein degradation, and cancer immunology. Congratulations to Xiaoqing, @ShengqingGu @ctokheim and Binbin, and collaborator @maverybrown !
Now online! In vivo CRISPR screens identify the E3 ligase Cop1 as a modulator of macrophage infiltration and cancer immunotherapy target dlvr.it/S8SFlX
cell.com
In vivo CRISPR screens identify the E3 ligase Cop1 as a modulator of macrophage infiltration and...
Large-scale in vivo CRISPR screens reveal that Cop1 knockout in cancer cells stabilizes C/ebpδ protein, suppressing macrophage infiltration and enhancing anti-tumor immunity.
science.sciencemag.org/content/373/65… gastrojournal.org/article/S0016-… The two articles (one from myself and Dr.Shivdasani's group) both point towards the gastric cell-of-origin for Barrett's Metaplasia and Esophageal Adenocarcinoma. Hope more breakthrough works on cancer cell-of-origin would come up!
gastrojournal.org
Hybrid Stomach-Intestinal Chromatin States Underlie Human Barrett’s Metaplasia
Tissue metaplasia is uncommon in adults because established cis-element programs resist rewiring. In Barrett’s esophagus, the distal esophageal mucosa acquires a predominantly intestinal character,...
Our editorial on the excellent MSK paper by Ceyhan-Birsoy et al. is out academic.oup.com/jnci/advance-a…
academic.oup.com
Li-Fraumeni Syndrome in the Cancer Genomics Era
A syndrome is a medical condition characterized by 1 or more symptoms or signs that occur together in a person more frequently than expected by chance. His
That @ArvinasInc ER-degrading #PROTAC ARV-471 is lenalidomide-based was one surprise. The bigger surprise is that they separated the imide epimers to provide a diastereomerically pure degrader. This question has been around for some time, but I never saw it done before. #AACR21
Circulating tumor DNA is readily detectable among Ghanaian breast cancer patients supporting non-invasive cancer genomic studies in Africa medrxiv.org/content/10.110…
Nice works from the Sanger institute. These data, along with other pre-existing datasets, would boost researches on revealing how the somatic mutation landscape is formed during the course of normal aging and cancer progression.
Awesome two papers from Sanger on mutations in non cancerous tissues.
🔴Review about the major mutation biases that operate across the cancer genome and the molecular mechanisms that cause them. By @BenLehner @CRGenomica and @FranSupek @IRBBarcelona ➡️bit.ly/CRG_MutationsH…
"Scales and mechanisms of somatic mutation rate variation across the human genome" a Perspective in @repair_DNA, by yours truly and @BenLehner authors.elsevier.com/a/1ZnYA5aisDG3… in Cutting-edge Perspectives in Genomic Maintenance VI
A (brief) tweetorial (@CharlesSwanton request) for our latest work - Epigenetic evolution and lineage histories of chronic lymphocytic leukaemia nature.com/articles/s4158…
Analyzing these types of data would also reveal how the environmental agents intertwine with the chromatin landscape or other factors associated with the mutation accumulation patterns for normal tissues and cells. cell.com/cell/fulltext/…
Great work with really nice presentation!
Thanks #AACR2019 for the opportunity to present our #PanCancer #Study of #Cancer #CellOfOrigin. It is a privilege of working with @rosa2003, Will Foulkes, @PolakPaz and @gaddyg. In case you missed my talk, the whole story can be found here: biorxiv.org/content/10.110… @broadinstitute
Apparently this would be more of a underrated issue for some of the minorities. Hope much more genomics data from Asian and other races would come out and get attentions by scientific and medical communities.
Increasing diversity in all forms of scientific research important!! Genetic research has a white bias, and it may be hurting everyone's health - PBS NewsHour apple.news/A7c3FYK7OQ_Kv5…
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