Skip to main content

Table 3 Candidate stem cell-specific genes for each cancer type

From: Cancerouspdomains: comprehensive analysis of cancer type-specific recurrent somatic mutations in proteins and domains

Cancer Type(Percentage)

Genes(Percentage)

ACC (56.5)

HDAC2 (5.4), ERCC2 (20.7), GARS (38.0), PRR34 (8.7)

BLCA (30.3)

CHEK2 (6.1), ERCC2 (9.7),KMT2C (20.9)

BRCA (8.2)

KMT2C (6.9), PILRB (0.8), HLA_DRB5 (0.7)

CHOL (33.3)

CHEK2 (8.3),KMT2C (25),GIMAP8 (2.8)

COAD (1.5)

HLA_DPA1 (1.5),

ESCA (9.3)

NREP (2.2),BRINP1 (7.7)

GBM (4.4)

CHEK2 (1.8),TSHZ2 (2.5)

HNSC (20.4)

CHEK2 (3.8), LIN28B (1.5), BRINP1 (3.1), KMT2C (12.0), NPR3 (2.7)

KICH.21.2)

DIMT1 (1.5),KMT2C (13.6),HLA_DRB5 (7.6), HLA_DQA1 (3)

LIHC (5)

HTR7 (5)

KIRC (11.1)

DNMT3B (3.1), CHEK2 (2.2), RRAS2 (1.8), NREP (0.7), TNFSF10 (1.3), FYB (2.9),

SMARCC2 (3.1), RCSD1 (2), HLA_DRB5 (1.8)

KIRP (7.1)

CHEK2 (5.9), DPH3(1.2)

LGG (9.3)

CHEK2(3.9),HDAC2(1.7),ZBTB20(4.6)

LUAD (42.0)

SPDL1 (1.8), CHEK2 (7.2), TRPC4 (7.2), CDH6 (7.2), GIMAP1 (2.2), KMT2C (17.8), PILRB (2.2), TSHZ2 (6.8), NPR3 (4.6), FYB (5.5)

OV (2.6)

BOD1 (0.9), HAS2 (1.7)

PAAD (57.3)

CHEK2 (17.0), BBS9 (9.4), GARS (5.8), SLC24A1 (9.4), KMT2C (17), SMARCC2 (13.5), NPR3 (8.8), AFTPH (13.5)

PCPG (14.3)

CHEK2 (5.1), NUSAP1 (4.0), KMT2C (5.1),

HLA_DRB5(1.1)

PRAD (8.9)

CHEK2(3.5),KMT2C(5.4)

SARC (4.3)

ZNF788 (2.8), BRINP1 (2.0)

SKCM (37.3)

GDF3 (8.0), CCDC90B (4.0), CDH6 (10.7), KMT2C (16.0), GIMAP5 (6.7) ,GIMAP7 (6.7),GIMAP1 (6.7),GIMAP8 (12)

STAD (32.3)

CHEK2 (5.4), SOHLH2 (4.4), BRINP1 (5.9), KMT2C (16.5), TSHZ2(7.2),ZBTB20(9)

TGCT (2.8)

C10orf128 (2.1), HLA_DRB5 (2.1), HLA_DQA1 (1.4)

THCA (4.8)

CHEK2 (1.4), GDF3 (0.8), RIOK2 (0.8), HLA_DRB5 (1.7)

THYM (5.7)

CHEK2 (5.7)

UCEC (9.7)

ATP11C (9.7)

UCS(15.8)

CHEK2(7),KMT2C(10.)

UVM(13.8)

CHEK2(7.5),NUSAP1(5),HLA_DRB5(5)

Pan Cancer(24.3)

CHEK2 (4.1), SOHLH2 (1), BRINP1 (2.2), TRPC4 (2.4), CDH6 (2.1), KMT2C (10.6), PILRB (0.8)

,HLA_DRB5 (1.1), TSHZ2 (2.6), NPR3 (1.7),GIMAP1 (0.9), GIMAP8(1.7),ZBTB20(2.1)