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Table 2 Putative novel drivers in ovarian cancer

From: Integrated analysis of recurrent properties of cancer genes to identify novel drivers

Ovarian carcinoma sample

Gene

Ovarian cell lines with increased proliferation

Pathway/Biological process

Reference

TCGA-04-1525

SETDB1

NA

PI3K/RAS

[95]

 

SIPA1L1

NA

Cytoskeleton organisation

[96]

TCGA-09-2051

SPTLC1

1

MYC

[97]

TCGA-10-0927

GTF3

10

RB

[98]

 

SQRDL

1

Amino acid metabolism

[99]

TCGA-13-0717

GRIT

NA

JNK/MAPK

[100]

TCGA-13-0755

ANXA2

2

Vesicle transport

[101]

 

FBLN1

1

Cell adhesion

[97]

 

FEN1

4

DNA repair

[102]

 

GSS

3

Glutathione metabolism

[103]

 

KDM5B

14

RB

[104]

 

MBNL1

3

Splicing regulation

[105]

 

PKP4

NA

WNT

[106]

 

U2SURP

NA

WNT

[97]

 

WDR61

NA

Chromatin regulation

[107]

TCGA-13-1408

F11R

0

Cell adhesion

[108]

 

PELI1

NA

PI3K/RAS

[109]

 

PTPRG

23

WNT

[110]

 

TAF12

18

Transcriptional activation

[111]

 

TIAM1

25

JNK/MAPK

[112]

TCGA-13-1506

BTBD2

NA

NF-kB (transcription)

[113]

TCGA-13-1510

RIOK3

7

Unknown

NA

TCGA-23-1024

FAM59A

NA

JNK/MAPK

[114]

 

PBX2

22

Transcriptional activation

[115]

TCGA-24-1431

ANKZF1

NA

Unknown

NA

 

ATP1B1

0

Ion transport

[116]

TCGA-24-1544

CCDC93

10

Unknown

NA

 

HDAC6

1

Chromatin regulation

[117]

TCGA-24-1546

SUGP1

7

Splicing regulation

[99]

 

VAV1

14

JNK/MAPK

[118]

TCGA-24-1567

HTATSF1

5

Splicing regulation

[119]

 

INADL

NA

Cell-cell interactions

[120]

 

KAL1

0

Cell adhesion

[121]

 

RAGEF2

25

JNK/MAPK

[122]

TCGA-25-1623

PSD3

NA

Transcriptional activation

[123]

TCGA-25-1627

KAT2B

9

WNT

[124]

 

PIK3R4

1

PI3K/RAS

[125]

 

TTF2

25

Transcriptional repression

[126]

TCGA-25-1630

APEX1

9

DNA repair

[127]

 

ATG3

NA

Autophagy

[128]

 

CAT

2

PI3K/RAS

[129]

 

DCAF6

NA

Transcriptional activation

[130]

TCGA-25-1633

SASH3

0

Antigen receptor signalling

[131]

TCGA-25-1634

GSN

5

TP53

[132]

 

MCM4

15

G1/S transition

[133]

 

RBL2

25

RB

[134]

TCGA-25-2391

RASA1

5

PI3K/RAS

[135]

TCGA-25-2393

ANO1

0

Ion transport

[131]

 

FUT1

1

Antigen synthesis

[136]

 

MCM4

15

G1/S transition

[137]

 

PRKCQ

22

PI3K/RAS

[138]

 

RB1CC1

8

RB

[121]

 

ZC3H14

NA

Translation

[139]

TCGA-36-1570

PSD3

NA

Transcriptional activation

[140]

TCGA-36-1574

NRCAM

NA

Cell adhesion

[141]

 

NSMAF

NA

NF-kB (transcription)

[142]

 

PASK

24

Translation

[143]

TCGA-36-1577

PRKD1

1

Transcriptional activation

[144]

  1. Shown are 23 ovarian carcinomas hosting 58 putative driver mutations in 56 genes. Two genes (MCM4 and PSD3) were mutated in two tumours. For 40 genes with available RNAi data [71], the number of ovarian cell lines where an increased in cell growth was observed upon gene silencing is shown. Thirteen carcinomas (57% of the total) bear mutations in pathways previously associated with ovarian cancer, and six of them (26% of the total) had alterations in transcription-related pathways. A detailed description of the effects of each mutation is shown in Additional file 2, Table S7.