ARID1A KD
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2
8
BAP1 KO
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8
CDH1 KO
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3
9
KEAP1 KO
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3
8
STK11 KO
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8
NF1 KO
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3
9
NF2 KO
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3
7
PBRM1 KO
stringlengths
3
9
PTEN KO
stringlengths
3
8
RB1 KO
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3
8
TP53 KO
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VHL KO
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TP53BP1 KO
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8
PHB
TMEM209
USP14
SMCHD1
TSC2
LLGL1
NARG2
TULP2
ARID1A
HNRNPDL
KLHL15
SLC20A1
SPPL3
MRTO4
FH
MAX
SGTA
GTPBP1
EIF2AK3
HELQ
MAPKAP1
SMARCB1
ENO3
LIN7C
DGUOK
MID1IP1
RNF7
UGP2
RAB25
CCDC71L
HOXC9
C20orf173
HNRNPH2
PRDX1
CSK
RBBP7
UNC13D
MYL6
APEX1
MSL1
PAPOLA
CCDC65
PIK3CA
LZTS1
ECHDC2
DYRK2
AHR
CA11
FLT3LG
CAB39
FBXL4
NGLY1
IK
KDM5C
NR0B2
GRIN3B
BCLAF1
CTSK
ACOT9
PDIA3
COX6B2
ATP5J
CNBP
C1orf122
KBTBD6
GEMIN6
MARCH2
CAPRIN1
MAPK14
GTPBP2
SYT12
RUSC1
PARD6B
SMARCA4
P4HA1
B4GALT7
SLC39A13
CHP1
CCDC174
GYS1
C16orf96
DYRK1A
MPV17
PTRF
VPS18
NDUFS3
ELL2
ACD
CNKSR2
RB1CC1
ATP1A1
TOPBP1
SDHD
VPS37A
VGLL3
JTB
SUZ12
C1orf27
ENTPD8
ZC3H7A
STAC2
NSMF
ADRA1A
SLC35D1
C16orf72
SUCO
HSPB7
G6PC
DHX35
JTB
TGOLN2
SYVN1
MVB12A
GAK
IGF2BP1
WIPF1
MGA
C19orf40
LIPT2
TNFRSF12A
STAC2
ARID2
G6PC
UBE2K
CHTF18
CNOT4
VGLL3
TADA1
DIAPH2
SLC7A5
USP8
NDUFAF4
C1orf228
PXN
SLC30A9
MARK2
KCNA3
DDX19A
SON
MED13
KIAA0907
MMP23B
MAGEB18
WDR73
C16orf72
CHD4
MED9
PRKRA
CA4
PSPC1
FANCD2
PARD6B
UNC13D
OPRD1
SLC4A1AP
FHOD1
ZMAT5
LIPT1
TMEM79
MED13
FBXO41
BFAR
AGO4
UMPS
TMCO6
PIN1
WRAP53
ITLN2
FMO1
ATP6V1C1
EXT1
MAGOH
FAM69A
BTK
PSMC3IP
ARID2
GART
PIGH
COMMD5
STX18
FAM110C
MED4
PTGDS
BCOR
ITGB7
FKRP
PDSS1
SYNGR3
PRDX1
C10orf105
SERPINB6
RIN1
RPRD1B
FASTKD5
MAPKAP1
NUBP2
FDX1
HNRNPA3
PIN1
ATG9A
CDK10
AK2
BRIP1
KDELR1
SIRT7
BPTF
BMPR1A
IGSF3
PHF5A
TMEM261
TMEM204
CANT1
C12orf44
CCDC144A
ALS2CL
FANCL
STAMBP
FRS2
TYMS
ZNF638
NPEPPS
OR2C1
ATIC
PPP2R3C
GPRC5A
BIRC6
PRDX1
SUPT20H
SNX17
USP1
SAP130
null
AAR2
SAPCD2
DDX19A
DHODH
RMI2
SHBG
DNTTIP1
PRKRA
MCM9
UBE2T
RPRD1B
ELMO2
null
PROM2
MORF4L1
MAPK8IP3
RRAS2
SLC18A3
USH1G
PDS5A
USH1G
PPP2R3C
BPTF
USPL1
RPS6KB1
null
GTPBP2
ACTR5
ATP6V1E1
DMPK
DDX19A
EZH1
NDUFB6
ATG9A
USP48
NUP160
NDUFC1
TADA1
null
C6orf136
BIRC5
ESCO2
PMVK
DDI2
HSD11B1L
FBXW11
C16orf72
ASB6
TYMS
TYMS
PPP2R3C
null
EIF4E2
TYRO3
NUP160
GATAD2A
FANCD2
ATP6V0A2
C8orf76
SHBG
PMVK
FANCA
RAD54L
CCAR1
null
MPV17
POLQ
BPTF
CREBBP
UIMC1
MEF2BNB
BAG6
HADHB
DDX19A
SDHB
NFU1
STAT6
null
RASL10A
MCM9
IGFALS
BZW1
C2CD4D
TMCO6
BRD9
COPG1
PTTG1
NDUFC1
FAM106A
DDX19A
null
DHX35
LRCH2
CHMP6
COQ2
GPR61
RRAS2
PSMF1
SRSF6
BZW1
FANCF
null
CTBP2
null
SHARPIN
RNF20
BUB1
TFAP4
UBE2T
TBKBP1
PPP2R3C
KAT5
FANCD2
SFR1
null
COQ2
null
SDHD
RMI2
null
PIGM
TUSC2
ELMO2
OTP
TMEM261
NCSTN
YPEL5
null
EBNA1BP2
null
CAPRIN1
KIAA2013
null
SLC35B2
FANCC
BRPF1
MCM9
NDUFB6
PCNP
null
null
TAF5L
null
GAK
USP1
null
MEIOB
BUB1
PALM
BRCC3
FBXW11
MPRIP
null
null
ANKRD52
null
CAB39
IKBKG
null
USPL1
FANCF
SLC38A10
CSNK1A1
CNKSR2
JMJD8
null
null
UMPS
null
PRKRA
FANCD2
null
SDHB
null
COQ2
SOX18
DCTN1
BRIP1
null
null
GART
null
WDR7
NOL8
null
STUB1
null
MRRF
FBXO42
USP48
UBE2T
null
null
null
null
ATG9A
TSEN34
null
null
null
CTBP2
IKBKG
MOGS
USPL1
null
null
null
null
CNOT4
UBE2T
null
null
null
UIMC1
RPRD1B
PMVK
HECTD1
null
null
null
null
C12orf44
USPL1
null
null
null
BPTF
MTFMT
EBNA1BP2
TYMS
null
null
null
null
BIRC6
ALX3
null
null
null
TUSC2
DNASE1
WRAP53
FANCA
null
null
null
null
PDS5A
TYMS
null
null
null
NUMA1
KPNA4
UIMC1
FANCF
null
null
null
null
C1orf228
CHMP6
null
null
null
COA3
BRIP1
KIAA1524
null
null
null
null
null
OTUB1
SLC25A33
null
null
null
null
UBE2T
RPRD1B
null
null
null
null
null
PDIA3
null
null
null
null
null
TYMS
BRIP1
null
null
null
null
null
SPOCD1
null
null
null
null
null
SDHB
TOR4A
null
null
null
null
null
DHODH
null
null
null
null
null
FANCA
UBE2T
null
null
null
null
null
FBXW11
null
null
null
null
null
FANCF
TYMS
null
null
null
null
null
GAL
null
null
null
null
null
SLC25A33
NDUFC1
null
null
null
null
null
FBXO42
null
null
null
null
null
FAM106A
FAM106A
null
null
null
null
null
PPP2R3C
null
null
null
null
null
CAMSAP1
STUB1
null
null
null
null
null
MCM9
null
null
null
null
null
YPEL5
null
null
null
null
null
null
UBE2H
null
null
null
null
null
null
null
null
null
null
null
null
PSMF1
null
null
null
null
null
null
null
null
null
null
null
null
PHPT1
null
null
null
null
null
null
null
null
null
null
null
null
TRA2B
null
null
null
null
null
null
null
null
null
null
null
null
MXRA8
null
null
null
null
null
null
null
null
null
null
null
null
IL3
null
null
null
null
null
null
null
null
null
null
null
null
GTSE1
null
null
null
null
null
null
null
null
null
null
null
null
FANCG
null
null
null
null
null
null
null
null
null
null
null
null
C17orf53
null
null
null
null
null
null
null
null
null
null
null
null
MSMB
null
null
null
null
null
null
null
null
null
null
null
null
UMPS
null
null
null
null
null
null
null
null
null
null
null
null
MTFMT
null
null
null
null
null
null
null
null
null
null
null
null
KIAA1524
null
null
null
null
null
null
null
null
null
null
null
null
RPRD1B
null
null
null
null
null
null
null
null
null
null
null
null
TPSG1
null
null
null
null
null
null
null
null
null
null
null
null
KPNA4
null
null
null
null
null
null
null
null
null
null
null
null
BRIP1
null
null
null
null
null
null
null
null
null
null
null
null
TOR4A
null
null
null
null
null
null
null
null
null
null
null
null
IGFALS
null
null
null
null
null
null
null
null
null
null
null
null
SDHB
null
null
null
null
null
null
null
null
null
null
null
null
FANCA
null
null
null
null
null
null
null
null
null
null
null
null
RAD54L
null
null
null
null
null
null
null
null
null
null
null
null
SLC25A33
null
null
null
null
null
null
null
null
null
null
null
null
RHBDF1
null

Dataset Card for PMC_35559673_table_s datasets

Dataset Details

Dataset Description

This dataset contains the results of genome-wide CRISPR screens using isogenic knockout cells to uncover vulnerabilities in tumor suppressor-deficient cancer cells. The data were originally published by Feng et al., Sci. Adv. 8, eabm6638 (2022), and are available via PubMed Central (PMC). The supplementary tables included in this dataset provide detailed data on raw counts, essentiality calls, Bayes factors, and synthetic lethality (SL) hits. The dataset supports research into genetic dependencies and potential therapeutic targets.

  • Curated by: Feng et al., Sci. Adv. 8, eabm6638 (2022)
  • Funded by: Likely supported by institutions affiliated with the authors.
  • Shared by: Feng et al.
  • Language(s): Not applicable (biomedical dataset).
  • License: CC BY 4.0

Dataset Sources

Dataset Structure

This dataset consists of seven tables (S1-S7), each representing a different aspect of the CRISPR screen results:

  1. Table S1: Raw counts for all CRISPR screens in this study.

    • File Mapping: sciadv.abm6638_table_s1.xlsx
  2. Table S2: Binary essentiality calls matrix.

    • File Mapping: sciadv.abm6638_table_s2.xlsx
  3. Table S3: Quantile-normalized Bayes factor (QBF) matrix.

    • File Mapping: sciadv.abm6638_table_s3.xlsx
  4. Table S5: Total SL hits identified for each TSG KO screen.

    • File Mapping: sciadv.abm6638_table_s5.xlsx
  5. Table S6: Shared SL hits across each TSG KO screen.

    • File Mapping: sciadv.abm6638_table_s6.xlsx
  6. Table S7: Unique SL hits for each TSG KO screen.

    • File Mapping: sciadv.abm6638_table_s7.xlsx

Dataset Creation

Curation Rationale

This dataset was curated to facilitate research into the vulnerabilities of cancer cells deficient in tumor suppressor genes. The binary essentiality calls, synthetic lethality (SL) hits, and other data allow researchers to explore genetic interactions that could serve as potential therapeutic targets. The methodology behind the CRISPR screens and SL hit identification was detailed by Feng et al. in their 2022 study.

Data Collection and Processing

Data were collected from genome-wide CRISPR screens performed on isogenic knockout cells. The data were processed to produce raw counts, binary essentiality calls, and genetic interaction matrices, including shared and unique synthetic lethal hits.

Relevant references describing the data processing and methods can be found in the following sources:

  • Evaluation and design of genome-wide CRISPR/SpCas9 knockout screens (PMID: 28655737)
  • High-resolution CRISPR screens reveal fitness genes and genotype-specific cancer liabilities (PMID: 26627737)
  • Identifying chemogenetic interactions from CRISPR screens with drugZ (PMID: 31439014)

Who are the source data producers?

The data were produced by Feng et al., as part of their research published in Science Advances. The researchers were affiliated with academic institutions engaged in cancer genomics and CRISPR screening methodologies.

Annotations

Annotation Process

Annotations were primarily focused on identifying shared and unique synthetic lethality hits across tumor suppressor knockout screens. Automated processing tools like CRISPR analysis pipelines were employed for initial hit identification, followed by manual validation based on genetic interactions.

Who are the annotators?

The original authors, including experts in CRISPR screening and cancer genomics, performed the annotations. No third-party annotations were added.

Bias, Risks, and Limitations

The dataset is limited to specific cancer cell lines and tumor suppressor gene knockouts. As a result, the findings may not be generalizable across all cancer types. Users should exercise caution when interpreting results outside the experimental context.

Recommendations

Users should consult the references provided to better understand the experimental design and limitations. The dataset is best suited for research applications in cancer genomics, genetic interactions, and therapeutic target discovery.

Citation

BibTeX:

@article{
  doi:10.1126/sciadv.abm6638,
  author = {Xu Feng  and Mengfan Tang  and Merve Dede  and Dan Su  and Guangsheng Pei  and Dadi Jiang  and Chao Wang  and Zhen Chen  and Mi Li  and Litong Nie  and Yun Xiong  and Siting Li  and Jeong-Min Park  and Huimin Zhang  and Min Huang  and Klaudia Szymonowicz  and Zhongming Zhao  and Traver Hart  and Junjie Chen },
  title = {Genome-wide CRISPR screens using isogenic cells reveal vulnerabilities conferred by loss of tumor suppressors},
  journal = {Science Advances},
  volume = {8},
  number = {19},
  pages = {eabm6638},
  year = {2022},
  doi = {10.1126/sciadv.abm6638},
  URL = {https://www.science.org/doi/abs/10.1126/sciadv.abm6638},
  eprint = {https://www.science.org/doi/pdf/10.1126/sciadv.abm6638},
  abstract = {Exploiting cancer vulnerabilities is critical for the discovery of anticancer drugs. However, tumor suppressors cannot be directly targeted because of their loss of function. To uncover specific vulnerabilities for cells with deficiency in any given tumor suppressor(s), we performed genome-scale CRISPR loss-of-function screens using a panel of isogenic knockout cells we generated for 12 common tumor suppressors. Here, we provide a comprehensive and comparative dataset for genetic interactions between the whole-genome protein-coding genes and a panel of tumor suppressor genes, which allows us to uncover known and new high-confidence synthetic lethal interactions. Mining this dataset, we uncover essential paralog gene pairs, which could be a common mechanism for interpreting synthetic lethality. Moreover, we propose that some tumor suppressors could be targeted to suppress proliferation of cells with deficiency in other tumor suppressors. This dataset provides valuable information that can be further exploited for targeted cancer therapy. Whole-genome CRISPR screens uncover synthetic lethal interactions for tumor suppressors.}
}

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