Y. Tamimi et al., HOMOZYGOUS DELETIONS OF P16(INK4) OCCUR FREQUENTLY IN BILHARZIASIS-ASSOCIATED BLADDER-CANCER, International journal of cancer, 68(2), 1996, pp. 183-187
We have studied p16(INK4) mutation (by PCR-SSCP) and deletion (by Sout
hern blotting and/or multiplex PCR) in a series of 47 bilharziasis-ass
ociated tumors from Egypt and compared the results with those obtained
on a series of 17 established bladder cell lines and non-bilharziasis
-associated bladder cancers from the Netherlands. In the cell lines we
found 9 homozygous deletions and 1 mutation (59% of p16(INK4) alterat
ions in cell lines), whereas in cases from the Netherlands deletions w
ere found in 4 of 22 samples. No mutations were detected in the 46 sam
ples screened. Interestingly, in bilharziasis-associated bladder cance
r, deletions were present in 23 samples and mutations in a further 2 E
ases (53% of p16(INK4) alteration in bilharziasis-associated bladder c
ancer). No correlation was found between p16(INK4) alteration and hist
opathological data. Likewise, the same frequency of alteration was fou
nd in tumors with different differentiation patterns (squamous, transi
tional or adenocarcinoma). Three conclusions can be drawn from our fin
dings: (i) p16(INK4) alterations are more frequent in cell lines than
in primary tumors; (ii) in primary bladder tumors (bilharziasis-associ
ated or not), p16(INK4) deletions are much more frequent than p16(INK4
) mutations; (iii) p16(INK4) alterations are more frequent in bilharzi
asis-associated bladder tumors than in other bladder tumors. This high
frequency of deletion is not related to a specific histological type
but to the specific etiology of these tumors. (C) 1996 Wiley-Liss, Inc
.