Garry P. Nolan, Rachford and Carlota A. Harris Endowed Professor at Stanford University, shared a post on X:
“Metastasis is the infiltrator. It is the means by which cancers start in one part of the body and suddenly end up elsewhere, spreading destruction, and by simple statistics, enabling the genomic diversity that promotes drug resistance for the cancer.
How does this happen?
Well, it appears part of the problem starts, at least for head and neck cancer, with tumor cells initiating organizational changes in the lymph node wherein cancer has established itself, and initiated pro-cancer environments both locally and at a distance. Myeloid cells and cancer-associated fibroblasts are somehow instructed by distant cancer to “open the door” for seeding of the originating cancer, which then further enables spread to nearby locales.
In layman’s terms… they prepare the ground elsewhere for their own defense. Cancer uses your own immune system against you. Congratulations to MH in my lab and to the many others from the collaborative University of Heidelberg and Mainz German Cancer Network who worked this out. The work offers new avenues of attack against such cancers by targeting cell-cell interactions beyond the current therapeutic framework. It also means we might be able to see, in non-metastatic lymph nodes, niche rearrangements that indicate cancer is nearby. It is now an open-source article online and in press at Cancer Cell.”
Title: Lymph node colonization induces tissue remodeling via immunosuppressive fibroblast-myeloid cell niches supporting metastatic tolerance
Authors: Maximilian Haist, Marc-A. Baertsch, Nathan E. Reticker-Flynn, Guolan Lu, Tim N. Kempchen, Pauline Chu, Gustavo Vazquez, Han Chen, John B. Sunwoo, Weiruo Zhang, Eyiwunmi Laseinde, Bonny Adami, Stefanie Zimmer, Justus Kaufman, Quynh Thu Le, Andrew J. Gentles, Christina S. Kong, Sylvia K. Plevritis, Yury Goltsev, John W. Hickey, Garry P. Nolan
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