BMC Cancer 2009, 9:113 http://www.biomedcentral.com/1471-2407/9/113 dom pattern of mutations occurring in tandem at nucle- otides 146 and 152 in a number of samples from our study is quite plausible. Tandem mutation events are common in mutagen-induced mutation spectra from mutagenicity assays. Interestingly, tandem mutations have been observed at nucleotides 146 and 152 when comparing a lung cancer cell line with a matched B-lym- phoblastoid cell line [40]. Given that we suggested that mutation hotspots in our study were occurring in the OSCC tumours we can under- stand why Bandelt and Salas raised concerns about a 'switch back and forth' for mutations at 146 and 152. However, it is unknown as to whether mutations observed by us at 146 and 152 in OSCC actually occurred in the tumour or non-tumour tissue for each patient examined. Thus, it is unknown whether a switching in this sense has actually occurred. This could be confirmed by sequencing PCR products from a third tissue per case. In all probabil- ity we were wrong to conclude that the 146 and 152 muta- tions are potential biomarkers for OSCC but they may well prove to be useful biomarkers for smoking related DNA damage. In the reassessment of our data using their phylogenetic linkage approach Bandelt and Salas state that they provide a 'strong evidence of artificial recombination' and that vir- tually all the mtDNA alterations can be explained by sam- ple mixing and contamination. It is interesting that the logic applied by Bandelt and Salas means that any single somatic mutation occurring at a nucleotide that is poly- morphic between different haplotypes can simply be explained by sample mixing. In other words, by just applying the phylogenetic approach to studies involving few mtDNA mutations in such a small region of genome, you can never provide proof of contamination but just make inference. We fully respect the opinions of both authors and support their quest for accurate procedure and reporting. However, to make accusations in the liter- ature of results generated due to contamination without presenting any conclusive evidence is unwarranted and thankfully not acceptable by most journals. We question how anybody can draw such conclusions based on tiny pieces of data lacking empirical evidence and statistical support and, seemingly, a lack of understanding of muta- gen associated sequence context. Reviewers at journals should insist on reasonable use of the phylogenetic approach applied by Bandelt and Salas in addition to the rules that these authors suggest. Abbreviations mtDNA: mitochondrial DNA; rCRS: revised Cambridge Reference Sequence. Competing interests The authors declare that they have no competing interests. Authors' contributions H-JB and AS designed the study, analyzed the data, and wrote the paper. 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