Cell lines database

p53 database

p53 mutations in cell lines

The hanbook of p53 mutation in cell lines

Cell lines with a controversial p53 status

The NCI 60 panel

Bladder cancer cell lines

Brain cancer cell lines

Breast cancer cell lines

Cervical carcinoma

Colorectal cancer cell lines

Esophageal cancer cell lines

Gastric cancer cell lines

Head and Neck cancer cell lines

Leukemia / Lymphoma cell lines

NSCLC cancer cell lines

Ovarian cancer cell lines

Pancreatic cancer cell lines

Sarcoma cell lines

SCLC cancer cell lines

Melanoma cell lines

Hepatocellular carcinoma

References

THE NCI-60 PANEL

Cell lines with an inconclusive p53 status are shown in red.

more information can be found here: Berglind et al., in press: download the manuscript

Cell line
ATCC number
DNA
Protein
ref
consensus
comment
LYMPHOMA LEUKEMIA
CCRF-CEM CCL-119   R248Q 1018
R175H+R248Q
Two mutations in separate alleles
c.524G>A, c.743G>A R175H+R248Q 3
c.524G>A, c.743G>A R175H+R248Q 2249
HL-60 CCL-240   R248L 1018
p53 null
 
null p.M1_*394del 3000
null p.M1_*394del 2249
K-562 CCL-243 c.406_407insC p.Q136fs*13 269
p.Q136fs*13
p53 RNA and protein are undetectable in this cell line
c.406_407insC p.Q136fs*13 2249
MOLT-4 CRL-1582 wt   3
Inconclusive
The status of MOLT-4 is highly heterogeneous in the literature. The report of a wt status could be due to the fact that only exons 5 to 8 (residues 126-306) were screened in several publications
wt   1018
c.331C>G L111V 2242
c.743G>A R248Q 27
c.916C>T R306X 2249
RPMI-8226 CCL-155   R285L 1018
E285K
This mutant is temperature-sensitive
c.853G>A E285K 2249
c.853G>A E285K 98
SR CRL-2262 wt   1018
wt
 
wt   2249
NSCLC
A549 CCL-185 wt   1018
wt
 
wt   16
wt   2249
EKVX   del187-224 (exon 6)   1018
Inconclusive
Possible splicing defect. See below for more information
c.609_610GG>TT p.V203_E204>V 2249
HOP-62     Ins 212-225 1018
See below for more explanation
c.673-2A>G  (splice junction) p.? 2249
HOP-92     p.R175L 1018
R175L
 
c.524G>T p.R175L 2249
NCI-H226 CRL-5826   P309A 1018
Inconclusive
 
c.473G>T R158L 92
  wt 2249
NCI-H23 CRL-5800 c.738G>C R246I 17
R246I
 
  R246I 1018
c.738G>C R246I 2249
NCI-H322M   c.743G>T R248L 92
R248L
 
  R248L 1018
c.743G>T R248L 2249
NCI-H460 HTB-177 wt   1018
wt
 
wt   2249
NCI-H522 CRL-5810   191delG 1018
p.P191fs*57
 
c.572_572delC p.P191fs*57 2249
c.572_572delC p.P191fs*58 92
COLON
COLO-205 CCL-222   G266E 1018
Inconclusive
 
c.308_333>TA p.Y103_L111>L 492
c.308_333>TA 103del27 2249
HCC-2998     R213X 1018
R213X
 
c.637C>T R213X 2249
HCT-116 CCL-247 wt   1018
wt
 
wt   2249
HCT-15 CCL-225 c.722C>T, c.1101-2A>C  (splice junction) p.S241F, p.? 2249
Inconclusive
 
  P153A 1018
c.722C>T S241F 2251
HT-29 HTB-38 c.818G>A R273H 492
R273H
 
c.818G>A R273H 2249
KM12     H179R 1018
Inconclusive
 
c.215delG p.R72fs*51 2249
SW620 CCL-227 c.818G>A, c.925C>T R273H, P309S 9
R273H + P309S
SW480 and SW620 are derived from the same individual with a similar p53 alteration. The P309S mutation is not always reported
  R273H 1018
c.818G>A, c.925C>T R273H, P309S 2249
CENTRAL NERVOUS SYSTEN
SF268   c.818G>A R273H 664
R273H
 
  R273H 1018
c.818G>A R273H 2249
SF295     p.R248Q 1018
R248Q
 
c.743G>A p.R248Q 2249
SF539   wt   1018
Inconclusive
 
c.1024delC p.R342fs*3 2249
SNB75     E258K 1018
E258K
 
c.772G>A E258K 2249
U251/SNB19   c.818G>A R273H 632
R273H
 
  R273H 1018
c.818G>A R273H 2249
MELANOMA
LOXIMV1   wt   1018
wt
 
wt   2249
Malme-3M HTB-64 wt   1018
wt
 
wt   2249
M14     G266E 1018
G266E
 
c.797G>A G266E 2249
SK-MEL-2 HTB-68   G245S 1018
G245S
 
c.733G>A G245S 2249
SK-MEL-28 HTB-72 c.434_435TG>GT L145R 2249
L145R
 
c.434T>G L145R 1570
  C145V 1018
SK-MEL-5 HTB-70 wt   1018
wt
 
wt   2249
UACC-257   wt   1018
wt
 
wt   2249
UACC-62   wt   1018
wt
 
    2249
MDA-MB-435     G266E 1018
G266E
This cell line was originally reported as a breast carcinoma cell line but recent SNP analysis indicates that it is similar to the M14 melanoma cell line
c.797G>A G266E 2029
c.797G>A G266E 2249
MDA-N     G266E 1018
G266E
This cell line was originally reported as a breast carcinoma cell line but recent SNP analysis indicates that it is similar to the M14 melanoma cell line.  It is a derivative of MDA-MB-435 tranfected with a plasmid expressing erbB2
OVARY
IGROV1   wt   1018
Inconclusive
 
wt   606
c.377A>G Y126C 2249
OVCAR-3 HTB-161 c.743G>A R248Q 144
R248Q
 
  R248Q 1018
c.743G>A R248Q 2249
OVCAR-4   wt   1018
Inconclusive
 
c.388C>G L130V 2249
OVCAR-5     ins224 1018
Inconclusive
 
wt   2249
OVCAR-8   c.376-1G>A   2249
Splicing defect
See below for more explanation
  del 126-132 1018
NCI/ADR-RES   c.376-1G>A   2249
Splicing defect
Originally named MCF-7/AdrR cells,  later re-designated NCI/ADR-RES.  Was recently found to be identical to OVCAR-8
  del 126-132 1018
  126del21 983
SK-OV-3 HTB-77   H179R 1018
Inconclusive
p53 RNA and protein are undetectable in this cell line: see below for more explanation
c.267delC p.S90fs*33 2249
RENAL
786-0 CRL-1932   P278A 1018
Inconclusive
 
c.832C>G, c.560-2A>G  (splice junction) p.P278A, p.? 2249
A498 HTB-44 wt   1018
wt
 
wt   2249
ACHN CRL-1611 wt   1018
wt
 
wt   2249
CAKI-1 HTB-46 wt   1018
wt
 
wt   2249
RXF393     R175H 1018
R175H
 
c.524G>A R175H 2249
SN12C     E336X 1018
E336X
 
c.1006G>T E336X 2249
TK10     L264R 1018
L264R
 
c.791T>G L264R 2249
U031   wt   1018
wt
 
wt   2249
PROSTATE
DU-145 HTB-81   P223L 1018
P223L + V274F
See below for more explanation
c.820G>T V274F 2249
c.668C>T + c.820G>T P223L + V274F 3001
c.668C>T + c.820G>T P223L + V274F 59
PC-3 CRL-1435 c.414delC p.K139fs*31 2249
p53 RNA and protein are undetectable in this cell line
 
  138del 1018
c.414delC 138del 59
BREAST
BT-549 HTB-122 c.747G>C R249S 24
R249S
 
  R249S 1018
c.747G>C R249S 2249
Hs 578T HTB-126 c.469G>T V157F 76
V157F
 
c.469G>T V157F 2249
  D157E 1018
MCF7 HTB-22 wt   1018
wt
 
wt   249
MDA-MB-231 HTB-26 c.839G>A R280K 24
R280K
 
  R280K 1018
T47D HTB-133 c.580C>T L194F 9
L194F
 
c.580C>T L194F 1018

In EKVX, the deletion of codon 187 to 224 detected on RNA-based analysis (ref 1018) corresponds exactly to the deletion of the entire exon 6, a strong argument for a splicing defect. Genomic analysis did not reveal a splicing defect but a tandem mutation at codons 203 and 204 in exon 6 (ref 2049). If the two cell lines analysed were really EKVX, this result suggests that a mutation at either codon 203 and/or 204 could affect p53 gene splicing

In OVCAR-8, the 126-132 deletion detected by the RNA-based assay (ref 1018) concerns the first six residues of exon 5. Genomic analysis (ref 2049) described a mutation in the acceptor site of exon 5 and a splicing defect leading to a shift of the normal donor site of exon 5 that skips 18 nucleotides (6 aa residues) in exon 5. Examination of the DNA sequence at codon 132 reveals an AG dinucleotide sequence preceded by a pyrimidine tract similar to those found in the splice donor sequence. The same situation is observed for NCI/ADR- RES that has been recently shown to be an ovarian carcinoma cell line originating from the same patient as OVCAR-8.

In HOP-62, RNA-based analysis (ref 1018) detected an insertion between codon 212-225 but no information about the insertion sequence was available. Codon 225 is at the boundary of exon 6 and intron 6 suggesting a splicing defect, as analysis at the genomic level (ref 2049) confirms the presence of a splice mutation in the acceptor signal of exon 6

In the majority of publications, the p53 status of the SK-OV-3 cell line is stated as “p53 null”. In fact, close examination of the original manuscript shows that the p53 gene in SK-OV-3 is not deleted and did not sustain any gross rearrangement but neither p53 RNA or protein are found. In these publications, no p53 mutations were found but the recent analysis performed at the Sanger Institute detected a deletion of a single nucleotide at position 267 (codon 90) (Ikediobi et al., 2006). It is therefore possible that nonsense-mediated mRNA decay (NMD) eliminates p53 aberrant mRNA. NMD has been observed in the human leukaemia cell line K562 where p53 is also inactivated via a 1 base pair insertion at nucleotide 136

 

 
 
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