It was a privilege to attend the IMW conference in New Delhi and I would like to thank the UKMF Executive Committee for selecting my abstract as a bursary winner. The meeting was a great success being very well organised and attended by delegates and speakers from across the globe. The conference provided me with the opportunity to listen to presentations given by leaders within the field and to also present some data that I have generated as part of my PhD studies. I had a poster presentation and was encouraged by the interest and constructive comments that I received. Some of the feedback has provided me with new ideas and avenues to explore.
Particularly relevant to my research and a highlight was the scientific session on ‘myeloma genomics and disease evolution’. This session summarised the current understanding of disease evolution, both from MGUS to myeloma and at relapse following therapeutic pressure. The accumulation of genetic aberrations and an increase in clonal complexity is the traditional view of how MGUS progresses to myeloma and a suspected cause for relapsefollowing successful treatment. There is howevergrowing evidence that not all patients follow this rule.Dr Seckinger (abstract no OP-015) outlined that many key driver mutations (e.g. NRAS, KRAS), copy number abnormalities and translocationsseen at relapseare alreadypresent at presentation and even in the premalignant stages of MGUS and asymptomatic myeloma. This concept has been suggested in other cancer types, most recently by the team of Dr Sottoriva from the Institute of Cancer Research who has provided evidence for a‘neutralevolution’ theory of cancer pathogenesisacross a variety of cancer types (Williams MJ,et al,Nature Genetics 2016, 48(3): 238-244). This has also been shown in myelomausing data generated from whole exome sequencing of 463 patients enrolled to the Myeloma XI trial. Thisdata was presented by Dr Kaiser (abs no OP-016) who showed that patients with evidence of neutral evolution may have a poorer outcomes, being less responsive to immunomodulatory therapy. In contrastDr Terragna (abs no OP-019)showedthat the emergence of new genetic aberrations lead to changesin clonal and subclonal dominance causing treatment resistance and relapse in many patients.Trying to predict what ‘signatures’ are associated with relapse in certain patient groups is likely to be vital in developing a personalised treatment approach and should be a focus of future research.