4.8 Article

Decoupling genetics, lineages, and microenvironment in IDH-mutant gliomas by single-cell RNA-seq

期刊

SCIENCE
卷 355, 期 6332, 页码 -

出版社

AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aai8478

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资金

  1. Smith Family Foundation
  2. V Foundation for Cancer Research
  3. Merkin Institute Fellows at the Bead Institute
  4. American Cancer Society
  5. NIH-NCI brain cancer SPORE [P50CA165962]
  6. Broad Institute Broadnext10 program
  7. National Brain Turner Society
  8. Rachel Molly Markoff Foundation
  9. NIH [NS065743]
  10. American Brain. Tumor Association and Neurosurgery Research and Education Foundation
  11. Human Frontier Science Program fellowship
  12. Rothschild fellowship
  13. Placide Nicod Foundation
  14. EMBO long-term fellowship
  15. Burroughs-Wellcome Fund CAMS
  16. K12 Paul Calabresi Career Award for Clinical Oncology Training Program in Nervous System Tumors [K12CA090354]
  17. Hughes Medical Institute
  18. Klarman Family Foundation
  19. STARR cancer consortium
  20. NCI [1U24CA180922, R33CA202820]
  21. Koch Institute Support from NCI [P30-CA14051]
  22. Ludwig Center
  23. Me Broad Institute
  24. Burroughs-Wellcome Fund CAMS [BPIF 1007616.02]
  25. California Institute of Regenerative Medicine [RB4-06093, RN3-06510]
  26. Virginia and D. K. Ludwig Fund for Cancer Research
  27. MGH Department of Pathology
  28. [1S10RR023440-01A1]

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Tumor subclasses differ according to the genotypes and phenotypes of malignant cells as well as the composition of the tumor microenvironment (TME). We dissected these influences in isocitrate dehydrogenase (IDH)-mutant gliomas by combining 14,226 single-cell RNA sequencing (RNA-seq) profiles from 16 patient samples with bulk RNA-seq profiles from 165 patient samples. Differences in bulk profiles between IDH-mutant astrocytoma and oligodendroglioma can be primarily explained by distinct TME and signature genetic events, whereas both tumor types share similar developmental hierarchies and lineages of glial differentiation. As tumor grade increases, we find enhanced proliferation of malignant cells, larger pools of undifferentiated glioma cells, and an increase in macrophage over microglia expression programs in TME. Our work provides a unifying model for IDH-mutant gliomas and a general framework for dissecting the differences among human tumor subclasses.

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