CCBIO-seminar 23. april 2026 – Richard Dillon

Foreleser: 

Richard Dillon, Clinical Senior Lecturer in Cancer Genetics in the Department of Medical & Molecular Genetics, School of Basic & Medical Biosciences, at King's College London, and Consultant Haematologist at Guy’s Hospital, London, UK

Tittel:

MRD in AML — what, where, when, and does it matter?

Vert:

Professor Bjørn Tore Gjertsen

Tid og sted:

Auditorium 4, BB-bygget

23. april 2026 kl. 14.30–15.30

Påmelding er ikke nødvendig. Merk derimot at hvis du er student og trenger studiepoeng for oppmøte, må du ha meldt deg opp i Studentweb for dette emnet for gjeldende semester.

Sammendrag:

In recent years, there has been great progress in the development, technical validation, and international standardisation of techniques for the assessment of measurable residual disease (MRD) for patients with acute myeloid leukaemia (AML) achieving haematological remission. Additionally, an abundance of data from large multicentre clinical trials has confirmed that detectable MRD is associated with adverse outcomes regardless of measurement technique, timepoint, or baseline risk group.

Recent data indicate that, as well as providing powerful prognostic information, changing treatment based on MRD results can improve outcomes. One example is the selection of patients for allogeneic transplantation in first complete remission based on their early MRD response. Furthermore, multiple studies have demonstrated that patients with serially rising levels of MRD (now called MRD relapse) inevitably progress to frank haematological relapse without intervention, but this can be averted using pre-emptive therapy.

In the last few years, several independent studies have shown that NGS-based assays for ultrasensitive detection of FLT3 ITD are strongly prognostic both after intensive chemotherapy and before transplant, and provide additional information to established molecular markers such as NPM1 mutation and flow cytometry. These assays are now beginning to be deployed in routine clinical care in many countries and may highlight patients with MRD relapse who can receive pre-emptive salvage therapy with FLT3 inhibitors.

There are a number of other promising targeted approaches for patients with MRD relapse in patients without FLT3 mutation. For patients with NPM1 mutation, the combination of venetoclax with low-dose cytarabine or azacytidine appears extremely effective to “erase” MRD, either as a bridge to transplant or as definitive therapy.

There is a wide range of novel molecularly targeted therapies in development for AML, many with activity restricted to molecularly defined subgroups. Investigation of their role in the treatment of MRD relapse is likely to prove extremely fruitful.