Thanks to CPTAC!

I am so inspired by the words: “The launch of this dataset supports the Biden-Harris Administration’s Cancer Moonshot℠ goal of accelerating cancer research by improved sharing of data.”

Wen-Wei Liang et al. (wustl.edu) 這一篇,提及 HNSC tumor cell 致癌過程中有一個” immunosuppression switch”,文章中說是STAT5A。第二個重點,proteogenomic analysis把kinase又了連回來,好比FGFR2, EGFR 治療靶點有了更強的依據。第三點,Graphic abstract清楚劃出 hypomethylation 導致 FGFR2 濃度上升; hypermethylation 導致 STAT5A 濃度下降。

08/23 今天讀完總論這一篇:真是妙極、絕極! 原來一直以來使用TCGA檢體還需考慮缺血 (因會導致MAP signaling爆衝問題)。

  • The first challenge: isoform issues. Remember to
    • (1) Using the same versions of genome assembly and gene annotation for the processing of data from all omics platforms and all cancer types. (2) Reporting gene-level quantification when isoform level analysis is unrealistic. (3) applying a consistent and transparent rule for representative isoform selection when representative isoform selection is needed but the data are isoform agnostic, e.g., phosphosite localization annotation.
  • A second challenge: embracing the full proteogenomic landscape as the molecular characterization of cells and tissues becomes more complete.
  • Finally, PTMs. Both experimental and computational approaches are being developed to improve PTM peptide identification, which will help alleviate the missing value problem in PTM proteomics.
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