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Mutation of the tumour suppressor p33 ING1 b is rare in melanoma
Author(s) -
Stark M.,
PuigButille J.A.,
Walker G.,
Badenas C.,
Malvehy J.,
Hayward N.,
Puig S.
Publication year - 2006
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2006.07274.x
Subject(s) - melanoma , pseudogene , carcinogenesis , cancer research , mutation , biology , germline mutation , genetics , gene , microbiology and biotechnology , genome
Summary Background The p33 ING 1 b gene is involved in the p53‐dependent response to DNA damage following exposure to ultraviolet radiation, and has recently been reported to be mutated in 20% of melanoma tumours. Objectives We sought to assess the p33 ING 1 b mutation rate in our large panels of fresh melanomas and melanoma cell lines. Methods We screened 83 primary melanomas and 55 melanoma cell lines for mutations in p33 ING 1 b by single‐strand conformational polymorphism analysis and by direct sequencing. Results In contrast to previous reports, we found no somatic p33 ING 1 b mutations in our panel of melanomas. We found that some of the discrepancy between our results and previously published studies may be due to inadvertent amplification of the ING1 pseudogene ( INGX ), and/or contamination of some samples with murine Ing1 . Conclusions p33ING 1 b mutations in melanoma are rare. We have highlighted the importance of allele‐specific primer design to avoid pseudogene amplification, and also the necessity to confirm the genetic identity and species of origin of individual cell lines. Further studies are needed to clarify the possible role of p33 ING1b in melanoma tumorigenesis.