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The Genetics of Pancreatic Cancer

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The Genetic Profiles of Pancreatic Cancer

Some of the most commonly used cell lines of pancreatic cancer are listed below with their profile of mutations:

Cell Line K-ras AKT2
19q
9p
LOH
p16
HD
p16
Mut
13q
LOH
BRCA2
Mut
17p
LOH
p53
Mut
MKK4
HD
MKK4
Mut
18q
LOH
DPC4
HD
DPC4
Mut
DCC
HD
 
AsPc1 12 Asp Ampl. LOH - 2 bp
del.
LOH - LOH 1 bp del. HD - LOH - 100 Thr -
BxPc3 - Poss.
Ampl.
LOH HD
LOH - LOH 220 Cys - - LOH HD   -
CAPAN1 12 Val - LOH HD
LOH 1 bp del. LOH 159 Val - 221 Stop LOH - 343 Stop -
CAPAN2 12 Val - LOH - 6 bp
ins.
- -
- - - LOH - - -
CFPAC1 12 Val -
- Meth LOH - LOH 242 Arg - - LOH HD   -
COLO 357       - Meth       -     LOH HD   -
HS766T 61 His - LOH - Splicing - -
-
rearr. - - LOH HD   -
MiaPaCa2 12 Cys - LOH HD
- - LOH 248 Trp - - LOH - - HD
Panc1 12 Asp Ampl. LOH HD
LOH - LOH 273 His - - LOH - - -
Su86.86 12 Asp Ampl. LOH HD
LOH - LOH 245 Ser - - LOH - - -

"-" refers to absence of the genetic alteration. Blank spaces refer to undetermined data points. In tumors with homozygous deletions ("HD"), the gene is not present, and mutations ("Mut") cannot be assayed. For small intragenic deletions ("del.") and insertions ("ins."), the number of basepairs ("bp") involved is given. "Splicing" refers to a splice site mutation predicted to interfere with correct splicing of the precursor RNA to form the mature mRNA. For K-ras,  p53, and DPC4, the codon and amino acid change are shown.  AsPc1 is reported to have constitutive TCF4 activity, but no mutation of beta-catenin.  Hs766T is reported to also have constitutive TCF activity along with a mutation of the beta-catenin gene, but newly purchased samples of this cell line have shown no mutation in beta-catenin.  The amplicon on 19q13 contains the AKT2 gene in three lines, but there is a report of an amplicon of 19q13 in BxPc3 that lacks AKT2 amplification . COLO 357 refers to the cell line available from ECACC.   Methylation of the p16 promoter ("Meth.") is associated with absence of RNA expression. Hs766T is reported to have a rearrangement ("rearr.") of one allele of p53, and the other allele appears to have a deletion involving exons 2 through 4, resulting in an inactive p53 gene. No alterations of the LKB1/STK11 gene are reported in these cell lines.  Additional abnormalities are known, such as the homozygous deletions of 8p22 and 18q22 in MiaPaCa2, but it is not clear that these affect any key genes for cancer development.