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Lack of TTC4 Mutations in Melanoma

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Lack of TTC4 Mutations in Melanoma View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector LETTERS TO THE EDITOR Lack of TTC4 Mutations in Melanoma To the Editor: account the corrected deduced amino acid sequence (with an extra 31 amino acids at the carboxyl terminus of the protein) A combination of karyotypic (Thompson et al, 1995; Zhang et described in Poetsch et al (2000). Using the primer pairs: al, 1999; Smedley et al, 2000) and loss of heterozygosity TTC270F: 5¢-GAA GGC AGG GCA TCA GCT CTG-3¢ and (Dracopoli et al, 1989; Walker et al, 1995) analyses have shown TTC869R: 5¢-GCT TTA GCC CTC ATT TCC AG-3¢, that the short arm of chromosome 1 is frequently deleted in TTC777F: 5¢-CTG AAA CAC TTT GCC GAG G-3¢ and melanoma and other tumor types (reviewed in Schwab et al, TTCStopR: 5¢-CAG TAT GTC CAG CTG ATT CAG-3¢, 1996). In general, multiple regions of 1p are nonrandomly we generated two overlapping polymerase chain reaction affected, with the most common abnormalities in melanoma fragments of 599 and 753 bp, respectively. affecting bands 1p36, 1p22±21, and 1p11. Thus there may be Polymerase chain reaction ampli®cation was performed in a ®nal multiple tumor suppressor genes on this chromosome arm. volume of 50 ml, containing 75 ng of DNA, 1 3 reaction buffer, Several candidates have already been tested, including p73,a 0.2 mM of deoxyribonucleoside triphosphate, 1.5 mM magnesium p53 homolog mapping to 1p36, in which no mutations have chloride, and 1.25 units of TF1 DNA Polymerase (Fisher Biotech). been detected in melanoma (Tsao et al, 1999), and only A ``touch-down'' protocol was employed, with an initial extremely rare changes in other cancers (Davis and Dowdy, denaturation at 94°C for 3 min, followed by two cycles of 94°C 2001). To date, no chromosome 1p tumor suppressor gene for 60 s, 65°C for 90 s, and 72°C for 90 s, after which the candidate associated with the development of a signi®cant annealing temperature was decreased by 2°C every two cycles to proportion of a particular cancer type has been identi®ed. 55°C, when 35 cycles were performed, followed by a ®nal Su et al (1999) isolated a candidate tumor suppressor gene on extension of 72°C for 5 min. Polymerase chain reaction products chromosome 1p31.3, a region frequently deleted in breast cancer. were puri®ed from 2% agarose gels using a QiaQuick Gel The gene, termed TTC4, is a member of a family of genes that Puri®cation Kit (Qiagen). Sequence reactions employed the contain tetratricopeptide repeat motifs. Members of this gene original primers under the following thermocycler conditions: 25 family are involved in a diverse range of intracellular activities, cycles of 96°C for 30 s, 50°C for 15 s, and 60°C for 4 min, prior to including cell cycle control, protein kinase inhibition, neuro- electrophoresis and analysis on an ABI Prism 377 DNA genesis, and tumorigenesis (reviewed in Su et al, 2000). No TTC4 sequencer. Sequences were compared with the GenBank database mutations were detected in a panel of 20 sporadic breast tumors sequence using Bionavigator EclustalW program (http://www. studied by Su et al (2000); however, the involvement of this gene in bionavigator.com) and BLASTN (http://www.ncbi.nlm.nih.gov/ melanoma development has been suggested by Poetsch et al (2000), BLAST). who analyzed a series of DNA from melanomas and precursor Although we detected two of the polymorphisms reported by lesions (35 naevi, 32 primary, and 25 metastatic tumors, and four Poetsch et al (2000), we found no other changes in the TTC4 melanoma cell lines). Whereas no TTC4 mutations were detected open reading frame. The complete cDNA ampli®ed faithfully in in the nevi, mutations causing amino acid substitutions predicted to two overlapping fragments for all samples, indicating there were affect protein function were detected in four of 32 (12.5%) primary no intragenic deletions, nor intronic mutations affecting splicing. melanomas, six of 25 (24%) metastatic melanomas, and one of four The ®nding that > 61% of cell lines analyzed carried one or (25%) cell lines. No TTC4 mutation was present in the patients' other polymorphism also provides evidence that large deletions corresponding constitutional DNA, thus indicating they occurred that remove the entire gene are uncommon. Similarly, they as somatic events. Three polymorphisms were also detected argue that promoter mutations resulting in transcriptional (T139A, C504T, and an insertion in intron 2), with frequencies silencing of one allele is unlikely to be a signi®cant mechanism of 48%, 6%, and 3%, respectively. These nucleotide changes were of TTC4 inactivation. In contrast, Poetsch et al (2000) found predicted to cause no change in the TTC4 protein product and all mutations in 11 of 61 (18%) of melanoma-derived samples three were observed in healthy controls. (fresh tumors and cell lines). Because some of our lines are Apart from CDKN2A and PTEN, no other tumour hemizygous for chromosome 1p, we cannot completely pre- suppressors have mutation frequencies as high as 25% in clude the possibility of a role for TTC4 haploinsuf®ciency in melanomas; therefore, to assess further the role of TTC4 melanoma development, nor a role for dominant-negative mutations in melanoma development, we sequenced the acting mutations present in vivo, which must be lost for complete cDNA in a panel of 40 melanoma cell lines. These propagation in culture. Both scenarios seem very unlikely, lines were established in the laboratories of Dr Peter Parsons however, given that one primary melanoma and all metastases and Dr Chris Schmidt at the Queensland Institute of Medical in the German study had lost the wild-type allele, indicating Research (Royal Brisbane Hospital, QLD, Australia); all derived that if TTC4 plays a part in melanoma development it is via from primary cutaneous melanomas or metastases thereof, and loss-of-function characteristic of classical tumor suppressors. are a subset of those described in Castellano et al (1997). Reasons for the discrepancy in TTC4 somatic mutation Primers were designed based on the published genomic frequencies between the two studies (0% vs 18%) may include sequence (GenBank accession no. AF073887), taking into our failure to detect point mutations in our study, differences in Manuscript received January 21, 2002; revised February 12, 2002; ethnicity of the two populations, and different environmental accepted for publication February 21, 2002. factors. As we reliably detected the two most common TTC4 Reprint requests to: Dr. Nick Hayward, Queensland Institute of Medical polymorphisms, it is unlikely that we missed other mutations. Research, P.O. Royal Brisbane Hospital, QLD 4029, Australia. Frequencies of these polymorphisms (T139A and C504T) were Email: [email protected] 48% and 6%, respectively, in the samples from north-eastern 0022-202X/02/$15.00 ´ Copyright # 2002 by The Society for Investigative Dermatology, Inc. 186 VOL. 119, NO. 1 JULY 2002 LETTERS TO THE EDITOR 187 Germany studied by Poetsch et al (2000), compared with 61% (49 REFERENCES of 80 chromosomes) and 5% (four of 80 chromosomes) in the Castellano M, Pollock P, Walters M, et al: CDKN2A/p16 is inactivated in most Australian samples in our study. The similarity in polymorphism melanoma cell lines. Cancer Res 57:4868±4875, 1997 frequencies indicates that there is no signi®cant difference in Davis P, Dowdy S: p73. Int J Biochem Cell Biol 33:935±939, 2001 genetic background between the two populations that may account Dracopoli NC, Harnett P, Bale SJ, Stanger BZ, Tucker MA, Housman DE, Kefford for the major difference in reported mutation frequency. It is not RF: Loss of alleles from the distal short arm of chromosome 1 occurs late in melanoma tumor progression. Proc Natl Acad Sci USA 86:4614±4618, 1989 known whether differences in environment could account for the Poetsch M, Dittberner T, Cowell JK, Woenckhaus C: TTC4, a novel candidate discrepancy; however, it is dif®cult to envisage how the major tumor suppressor gene at 1p31 is often mutated in malignant melanoma of the environmental risk factor for melanoma development (exposure to skin. Oncogene 19:5817±5820, 2000 ultraviolet radiation; Whiteman and Green, 1999) could contribute Smedley D, Sidhar S, Birdsall S, Bennett D, Herlyn M, Cooper C, Shipley J: to the difference. Unless one invokes an environmental carcinogen Characterization of chromosome 1 abnormalities in malignant melanomas. Genes Chromosom Cancer 28:121±125, 2000 other than ultraviolet radiation, it seems more likely that there Su G, Roberts T, Cowell JK: TTC4, a novel human gene containing the would be less somatic mutations detected in north-eastern tetratricopeptide repeat and mapping to the region of chromosome 1p31 that is Germany than in Australia. frequently deleted in sporadic breast cancer. Genomics 55:157±163, 1999 Overall, in stark contrast to the study of Poetsch et al (2000), Su G, Casey G, Cowell JK: Genomic structure of the human tetratricopeptide repeat- containing gene, TTC4, from chromosome region 1p31, and mutation analysis our results do not indicate a signi®cant role for TTC4 in breast cancers. Int J Mol Med 5:197±200, 2000 mutations in melanoma development. Although TTC4 initially Thompson FH, Emerson J, Olson S, et al: Cytogenetics of 158 patients with regional appeared a good candidate, the search for tumor suppressor or disseminated melanoma. Subset analysis of near-diploid and simple genes on 1p continues. karyotypes. Cancer Genet Cytogenet 83:93±104, 1995 Tsao H, Zhang X, Majewski P, Haluska F: Mutational and expression analysis of the p73 gene in melanoma cell lines. Cancer Res 59:172±174, 1999 Walker GJ, Palmer JM, Walters MK, Hayward NK: A genetic model of melanoma This work was supported by the National Health and Medical Research Council.
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