Highlights of the 22nd EACR meeting and tackling glioblastoma

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Published: 16 Jul 2012
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Dr Joan Seoane – Vall d’Hebron Institute of Oncology, Spain

Dr Joan Seoane talks to ecancer at EACR 22 in Barcelona about the highlights of the meeting and the need for advancement in treating glioblastoma.


Dr Seoane notes that all of the highlights at this year’s EACR meeting centered on tailored medicine and biomarkers to develop better treatment; with focus also given to translational research and getting information from the laboratory to the clinic quicker.


The meeting also alerted researchers and doctors to the importance to cancer stem cells and the metabolic impact of cancer and how this can be targeted.


In addition, Dr Seoane pays particular attention to glioblastoma and the need to work through collaborations to correct the insufficient treatment methods for this disease.

22nd European Association for Cancer Research, 7-10 July 2012, Barcelona, Spain


Highlights of the 22nd EACR meeting and tackling glioblastoma


Dr Joan Seoane – Vall d’Hebron Institute of Oncology, Spain



Dr Seoane, we’re here at the EACR in Barcelona and you are part of the local organising committee. Can you give us some highlights of this meeting, this very exciting meeting?


This meeting has a lot of highlights, several of them. All of them are around one very important concept and it’s tailored medicine – trying to find biomarkers that will help us develop better treatments. Also it’s about the translational research – how we have to integrate the molecular mechanisms that we are finding in tumours with clinical research in order to transfer all the information that we are getting from the molecular mechanisms quickly to the clinical research and also to the patient to improve his treatments. This has to be very fast and the only way to get this done is to get together basic and clinical researchers doing this translational research. So this is the overall concept of the meeting. We had very nice talks about how genomics are important in order to characterise tumours, how there is this intra-tumoural heterogeneity in terms of mutations in different sub-clones of a particular tumour which is something that is complicating the research in cancer but we have to deal with this complex characteristic of tumours. We have also seen how not only there is intra-tumoural heterogeneity in terms of genomics but also in epigenomics and in states of differentiation the cancer stem cells. Also we will hear about metabolic impact of cancer and the cancer cells and how metabolism can also be a therapeutic target. So we are touching many different things – angiogenesis, metastasis and others, but all have the same concept and it’s tailored medicine, we need biomarkers, we need new targets and new drugs, getting together biomarkers with drugs and also in the context of translational research.


In your specific field you work on glioblastomas, is this also the case?


It’s very important in this case. Glioblastoma is one of the most aggressive tumours and the only way to tackle glioblastoma is to do it multidisciplinarily with different components all together trying to improve the treatment and also trying to find biomarkers and better treatments. The treatments that we have already, we have right now, are not efficient enough and so we need to get new treatments, we need to understand the heterogeneity of glioblastoma. So there has been this recent important meeting funded by the Stelios Foundation that kindly wanted to induce this meeting to get together, the top researchers in glioblastoma. There also we were discussing about how to find new biomarkers for new treatments and how to understand the complexity of glioblastoma.


So is there any hope? Because, as you say, glioblastoma…


There are hopes, there are hopes. We have some clinical trials with some responses, now the question is how to find the characteristics that predict the response and this is the challenge right now.


So even glioblastoma is very heterogenic?


Yes, glioblastoma is very heterogeneous among tumours, among patients but also we think the tumour. This is very clear. So we know right now that what we call glioblastoma in fact we can subdivide it into four different subtypes based on the molecular characteristics – neural, proneural, mesenchymal and classic but also we know that within the tumour mass there are different cells with different characteristics. We have what we call glioma initiating cells, cells that are very poorly differentiated that have characteristics of stem cells and these cells are responsible for the re-initiation of tumours and also for the resistance to treatment. So we need to understand the biology of these cells in order to find new therapeutic targets against these cells and also the non-cancerous stem cells combined.


It’s also quite a rare tumour, are there enough patients to do…?


It’s not so rare and what I have to say is that this is the most aggressive tumour so we really need to get to do something because right now the overall survival, the median overall survival is fourteen months, so it’s something that we really need to study to get better treatments. Also, the other thing that is very interesting is that through the study of the molecular mechanisms of glioblastoma we are understanding other tumour types because there are some mechanisms that are also present in other tumour types and what we are studying, for example, in glioma initiating cells and cancer initiating cells of glioma, we can also translate it to other tumour types and this is very important. So what we have, for example, I am in Vall d’Hebron in the Vall d’Hebron Hospital and the Vall d’Hebron Institute of Oncology, and in order to understand the mechanisms of glioma what we do is we try to study the glioma, glioblastoma, as close as possible to the patient and to do that. So we generate models, mouse models, that reproduce the tumour of a patient in the mouse. So we get samples from the neurosurgeons, we get very fast samples, we have viable cells, we get these cells, we inoculate them in the brain of the immune compromised mice, these cells generate tumours. Those tumours have the same mutations as the patient, the same characteristics. Now we can study the biology of those tumours and, most importantly, we can study how these tumours are more responsive to one treatment or to another. And that information is not only important to understand which are the biomarkers that will predict response, but this information can go to the patient in order to advise the patient to get to a particular clinical trial.


So we’ll follow you and let’s hope that something good comes out.


We are hoping and we are really optimistic in this sense.


Thank you.


Thank you.