Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Jan 11;13:256. doi: 10.1038/s41467-021-27731-5

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 3 — a Summary of TCGA data showing the most common chromosomal deletions (blue) and amplifications (red) in human lung adenocarcinoma (LUAD) tumor samples. Chromosome arm 8p contains the human GATA4 gene. Chromosome 8 is highlighted. b CD8 T cell-associated transcripts are decreased in GATA4-deleted tumors in lung adenocarcinoma. c Analysis of the abundance of tumor-infiltrating lymphocytes (TILs) in TCGA tumor samples of various subtypes. Tumor samples were corrected for tumor purity before calling copy number alterations. TCGA RNA-seq data were used to calculate the association between GATA4 copy number and the abundance of TIL subtypes in each tumor type. Color indicates the FDR of the correlation between GATA4 copy number and the abundance of TIL subtypes. Darker colors indicate higher significance. Abbreviations are breast adenocarcinoma (BRCA; n = 256 GATA4 loss, n = 460 no GATA4 loss), lung adenocarcinoma (LUAD; n = 120 GATA4 loss, n = 319 no GATA4 loss), melanoma (SKCM; n = 20 GATA4 loss, n = 82 no GATA4 loss), colorectal adenocarcinoma (COAD; n = 97 GATA4 loss, n = 167 no GATA4 loss), bladder adenocarcinoma (BLCA; n = 138 GATA4 loss, n = 262 no GATA4 loss), prostate adenocarcinoma (PRAD; n = 147 GATA4 loss, n = 266 no GATA4 loss), liver hepatocellular carcinoma (LIHC; n = 216 GATA4 loss, n = 149 no GATA4 loss), lung squamous cell carcinoma (LUSC; n = 124 GATA4 loss, n = 229 no GATA4 loss), and head and neck squamous cell carcinoma (HNSC; n = 148 GATA4 loss, n = 363 no GATA4 loss). d Analysis of the association of loss of GATA4/8p with TIL subtypes in samples with or without the co-associated CNA + 8q in colorectal adenocarcinoma. e Extended CNA profile normalization analysis across tissue types with respect to TIL subtype abundance associations. Here we normalized tumor cohorts for all GATA4//8p-correlated and anticorrelated CNAs in each subtype, beyond just the +8q co-association. Abbreviations are breast adenocarcinoma (BRCA; n = 127 GATA4 loss, n = 313 no GATA4 loss), lung adenocarcinoma (LUAD; n = 63 GATA4 loss, n = 277 no GATA4 loss), uterine corpus endometrial carcinoma (UCEC; n = 19 GATA4 loss, n = 92 no GATA4 loss), colorectal adenocarcinoma (COAD; n = 47 GATA4 loss, n = 131 no GATA4 loss), bladder adenocarcinoma (BLCA; n = 68 GATA4 loss, n = 202 no GATA4 loss), liver hepatocellular carcinoma (LIHC; n = 148 GATA4 loss, n = 114 no GATA4 loss), lung squamous cell carcinoma (LUSC; n = 60 GATA4 loss, n = 200 no GATA4 loss), and head and neck squamous cell carcinoma (HNSC; n = 73 GATA4 loss, n = 323 no GATA4 loss). f GATA4 copy number loss is co-associated with TP53 loss (mutation or deletion) in most tumor types. P-values are calculated using hypergeometric tests.