by ecancer reporter Clare Sansom

The ninth annual National Cancer Research Institute conference is the third to be held at the BT Convention Centre in Liverpool's dockland.

It began on Sunday afternoon with a welcome address from NCRI chair Harpak Kumar. He mentioned that this is the last conference before the retirement of the NCRI director, Jane Cope; asked delegates to welcome her successor, Karen Kennedy, to the conference; and highlighted some innovatory features of the meeting.

These included a focus on surgery and a continuation of last year's successful collaboration with the Royal College of Radiographers.

The post of chair of a conference scientific committee holds many hazards, but few can have been given as hard a task as Gerard Evan from the University of Cambridge. He stepped in at the last minute as a replacement for the first keynote speaker, his friend and collaborator Neal Rosen of Memorial Sloan Kettering Cancer Center in New York, who was prevented from attending by urgent family business.

Evan began by listing the properties of an ideal molecular target for cancer. This, he said, should kill tumour cells while leaving normal ones unscathed; its function should be non-redundant; and it would ideally be found in many cancers.

He highlighted the regulator Myc as a non-redundant protein in very many tumour types, but explained that completely inhibiting this protein would cause devastating toxicity to all proliferating tissues. He has shown using mouse models that genetic knockdown of Myc expression causes a dramatic, if temporary, regression of different tumours and, further, that this arises through changes to the tumour micro-environment. If – and it is still if – an antitumour drug could be developed using this principle, it might be truly generic.

Peter Sasieni of the Wolfson Institute of Preventative Medicine in London gave a fascinating lecture about cervical cancer prevention, taking the title “Cervical cancer: problem solved?”

Vaccination against the two most oncogenic human papilloma virus strains could almost eradicate the disease in the developed world by mid-century, but most women born before about 1990 will still need screening. Sasieni suggested that this was more effective in the older age groups, with more benefit gained by screening women in their sixties than their early twenties, and that testing for HPV infection could greatly increase the effectiveness of the conventional Pap smear. The question in his title may best be answered by “Yes and no”.

The third plenary, by Richard Marais of Cancer Research UK's Manchester Institute, returned to the theme of molecular mechanisms taking melanoma as an example. About 40% of melanomas have a driver mutation in the oncogene B-Raf. His group has shown that exposing skin to ultra-violet light, a known melanoma trigger, accelerates tumour development in a mouse model with this mutation. The B-Raf inhibitor vemurafenib has some success against refractory melanoma, but resistance soon develops; Marais showed that EGFR upregulation and mutations in other kinases can drive resistance to B-Raf inhibitors in tumours with this mutation.

Kumar's welcome address included one further innovation: a Twitter competition. The author of the “best” tweet sent during the conference and tagged with the hashtag #NCRI2013 will win £100 in Wisepress book vouchers. The challenge is on!