Tag Archives: IKM

Cortisone does not relieve cancer pain

Blogger: Ørnulf PaulsenØrnulf-Paulsen-WEB

Ørnulf Paulsen is a PhD student at European Palliative Care Research Centre, NTNU, and Senior Consultant in palliative medicine at Telemark Hospital

Until now, clinicians have assumed that corticosteroids effectively relieve pain in cancer patients. A new study shows that this is not the case.

The results from our study have recently been published in the acknowledged Journal of Clinical Oncology.

Placebo shows same effect

Corticosteroids are widely used for the most advanced cancer patients, and pain treatment is one of the indications. The pain relieving effect, however, has never been documented in research results. Our study showed that the drug had no pain relieving effect for the cancer patients who participated in the study.

The patients received basic pain treatment with paracetamol and morphine. In the study, the patients in addition received cortisone (Medrol®, methylprednisolone) or placebo. After one week of treatment, the group receiving cortisone did not achieve better pain relief than the control group.

Corticosteroids have side effects

Cortisone is a natural hormone produced in the adrenal cortex. Synthetic cortisone is a group of drugs often called steroids or corticosteroids. The drug suppresses the body’s immune responses and has an anti-inflammatory effect. It is used in the treatment of several diseases, such as rheumatic diseases, asthma, ulcerous colitis and Crohn’s disease.

Treatment with corticosteroids causes side effects. Diabetes, skin changes, psychological changes, anxiety and muscle weakness are examples of side effects which present themselves after long term usage or high doses. Advanced cancer patients experience many symptoms, and it is of vital importance to make sure that treatment given has the desired effect and does not cause unnecessary side effects. Corticosteroids have been used in cancer treatment for decades. The drugs may have an effect in many symptoms and can increase quality of life. This might be one of the reasons for the extensive usage.

Doctor and patient

In Telemark Hospital, Cortisone no longer is used as a general pain-reliever for cancer patients. Photo: Telemark Hospital

Treatment practice needs to change

Pain is the most common symptom in cancer patients. Our study shows, however, that use of corticosteroids as a general pain-reliever is not advisable. These results point to a need for change in treatment practice. Simultaneously, the study indicates less fatigue and better appetite for patients treated with corticosteroids. Both fatigue and loss of appetite are troublesome symptoms for advanced cancer patients.

At the Hospital in Telemark, where I am a senior consultant in Palliative medicine, we have changed our practice. Corticosteroids are no longer used as a general pain-reliever, but instead used controlled, targeted and in shorter courses when we know it will have the desired effect.

Corticosteroids have previously been recommended for treatment of cancer pain in several guidelines. The European Association for Palliative Care (EAPC) is currently revising the European guidelines for pain treatment. On my recommendation, the recommendations for use of corticosteroids as pain treatment will be changed as a consequence of new research, including this study.

This study and its results will help improve everyday life for cancer patients with advanced and life limiting disease.

The research article is available online from the Journal of  Clinical Oncology: Efficacy of Methylprednisolone on Pain, Fatigue, and Appetite Loss in Patients With Advanced Cancer Using Opioids: A Randomized, Placebo-Controlled, Double-Blind Trial

The study was conducted at European Palliative Care Research Centre (PRC), NTNU, and coordinated by Telemark Hospital in Skien. In addition Department of palliative care at St. Olavs Hospital, Trondheim University Hospital as well as the cancer departments of Haraldsplass Deaconal Hospital (Bergen), Hospital of Southern Norway (Kristiansand) and Oslo University Hospital, Ullevål contributed to the study.

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Filed under Cancer, NTNUmedicine, Research

Ask a researcher: Is the 5:2 diet healthy for women?


Is the 5:2 diet healthy for women?


Answer from Catia Martins Catia Martins. Photo: Geir Mogen

5:2 diet is a type of intermittent fasting, which involves a “feed day”, where food is consumed ad libitum over a 24-hours period, alternated with a “fast day” where food intake is completely or partially restricted over 24 hours. The fasting days usually vary between 2-4 days/week.

Human studies have shown that intermittent energy restriction is as effective as isocaloric (meaning same energy content) continuous energy restriction (the conventional diet with daily energy restriction), regarding weight loss and reduction in obesity related risk factors (insulin levels, blood lipids and blood pressure).

A few studies have shown that intermittent energy restriction is associated with a lower loss of muscle mass and a lower reduction in resting metabolic rate compared with conventional diet. Some, but not all studies, show that intermittent energy restriction may increase adherence to the intervention as it would be easier to diet only some days of the week, instead of everyday, but long term studies are needed to be able to draw solid conclusions in this respect.


What about eating five days a week, and two days of fasting? (Photo: iStockPhoto).

Intermittent energy restriction seems to be safe, but mild side effects have been reported by some individuals; including fatigue, headache and lack of energy. However these are the same side effects expected with continuous energy restriction. Opposite to the general believe, intermittent energy restriction does not seem to lead to overeating (gorging) on the feed days.

The big challenge in the management of obesity is not weight loss, but the maintenance of a reduced body weight. Larger and long-term studies are needed to determine the ability of this novel diet to promote sustained weight loss in the long-term.

Overall, the available evidence from the few human trials available suggests that intermittent fasting can be used as an alternative to weight loss.

There is not enough evidence to say if 5:2 diet works differently in men compared with women

There is not enough evidence to say if 5:2 diet works differently in men compared with women. From my knowledge, no study has addressed specifically gender issues regarding intermittent fasting.

Regarding your questions if 5:2 is more or less healthy in women… well compared with what? With the conventional continuous energy restriction? 5:2 diet can, as explained, lead to a similar weight loss and improvement in risk factors as convention continuous energy restriction. A 5:2 diet can be nutritionally balanced if the diet during the 2 days of partial fasting is planned correctly so that no vitamins or minerals are deficient. One way to avoid that would be to use a vitamin and mineral supplement, another to use commercial available products which provide all the macro and micro nutrients in the right amounts (such as a very low calorie diet).

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Filed under Metabolic and Endocrine, NTNUmedicine, Spør en forsker

Taking care of knowledge

Kuiper_TrondheimAstrid Lægreid. Foto: Geir MogenBloggers: Astrid Lægreid, professor, Department of Cancer Research and Molecular Medicine and Martin Kuiper professor, Department of Biology




It is often overlooked that after you publish your research results you have not necessarily provided your new knowledge to your colleagues in the best possible way. Today’s biomedical science is very much dependent on the use of computers, to analyse and integrate the various types of data and facts that you and your fellow scientists have produced.  And whereas a computer can do many things, it has difficulty in understanding what is so easily understood by us when we read a scientific publication.

Although much research is done to improve the way computers can analyse text (the field of text mining), we excel in hiding facts and new knowledge in our publications. We use for instance words that can have multiple meanings, names that seem funny (sonic hedgehog) but do not mean anything to a computer, or we mention some facts in a context that greatly changes the meaning of a sentence (for instance by using the simple word ‘not’). We therefore need to reach out to computers and help them a bit with understanding the real knowledge that we have hidden so well in text. This is even more interesting if one wants to pursue the main goal we have set for our research at NTNU: using a systems biology approach for making new biological discoveries.

It is widely believed that a systems biology-based understanding of the human will allow great discoveries for improved health care.

a lot of papers. Photo: iStockPhotoSystems biology is based on a computer dealing with knowledge about biological systems or processes (like cell division; or regulation of the activity levels of genes). It is widely believed that a systems biology-based understanding of the human will allow great discoveries for improved health care. Systems biology has been made possible by the tremendous advancements in laboratory technologies that are now available to get massive amounts of data about the processes, cells and organs of our bodies. Once these data have been interpreted and published, system scale biomedical knowledge can be integrated into computer models in order to enable improved disease management and higher precision medicine. However, in order to succeed, we need to take proper care of this knowledge.

In our daily work we have developed various computer models of cell lines which we use in laboratory experiments, and each time we had to get the information for these models by reading many papers because only a very small amount of the information was available through databases. This made us think that it would be great of at least one part of the information for these models would be readily available for computers: information from the area of gene regulation. One small, but very important part of this is the knowledge about the system that connects the information in a particular class of proteins (transcription factors, TFs) with the particular DNA sequences in the genome in the vicinity of genes (recognition sequences, or transcription factor binding sites): This system essentially links the protein world with the DNA world and dictates which genes are active and which genes remain silent. We have recently launched a large effort in building a resource for this that covers three of the most important biological systems: human, mouse and rat (1,  2).

Of course we know that the DNA binding TFs are only a very small part of the very complex system of gene regulation, and it will take a very big group of scientists to take care of all the diverse forms of knowledge in the literature. And there we are lucky that we are not alone in realizing the importance of this. We have identified many researchers world-wide and found them willing to join us in a global consortium within the field of taking care of, or ‘curating’ gene regulation knowledge, and we are now discussing with them how we can best structure existing efforts and launch new efforts to jointly build a series of resources covering the complete domain of gene regulation in all organisms.


Systems biology is based on a computer dealing with knowledge about biological systems or processes, like cell division; or regulation of the activity levels of genes. Photo: iStockPhoto

Existing databases and knowledge sources within our consortium include amongst others the Gene Ontology databases, PAZAR, TFCat, TFactS and RegulonDB, as well as DBD- and IntAct at the European Institute of Bioinformatics (EBI).  Existing and new resources are designed in such a way that the information can be easily integrated into computer models. The consortium is named ‘Gene Regulation Consortium’ (short: GRECO), and is led by us.

Our basic objective is to extend on what we now only do for the DNA binding transcription factors from mouse, human and rat, and do it for the full field of gene regulation with many particular types of regulatory proteins, many types of regulatory RNAs, and many different structural and functional elements encoded in the DNA which allows the gene regulation system to fine-tune the activity of genes appropriate for a specific cellular function, and do it for all organisms.

The aims of GRECO are to:

  • Foster communication across the field of gene regulation
  • Assess the state of the art in annotating components and relationships important to describe gene regulation events
  • Identify common initiatives, avoid redundancy, fill knowledge gaps
  • Extend and align ontologies and controlled vocabularies
  • Promote common data exchange formats
  • Promote common curation quality guidelines
  • Attract funding to support communication and initiate new curation initiatives

We were fortunate to receive some financial support from NTNU to organize the first GRECO workshop on April 5, at the Toronto University campus, as a satellite meeting of The Seventh Conference of the International Society for Biocuration, ISB2014.  We met with partners from the UK, Switzerland, Germany, the USA, Mexico, Brazil and Saudi Arabia, presented our ideas for this initiative and laid out the foundation for a joint strategy for acquiring additional project support from international funding organisations like the National Health Institutes in the USA, the Horizon 2020 programme from the European Union, or National funding agencies like NFR.

We hope to present some of our work at the Virtual Physiological Human (VPH) Conference 2014 in Trondheim in September 2014. The VPH mission is to contribute to developing a real predictive, preventive and participatory medicine by enabling the building of stronger transdisciplinary ties between the life sciences, the mathematical sciences and engineering throughout the whole spectrum of basic, translational and applied research.


1)      Tripathi S, Christie KR, Balakrishnan R, Huntley R, Hill DP, Thommesen L, Blake JA, Kuiper M, Lægreid A. Gene Ontology Annotation of Sequence specific DNA-binding Transcription Factors: Setting the Stage for a Large Scale Curation Effort. Database  Aug 27; bat062 2013.

2)      Chawla K; Tripathi S; Thommesen L; Lægreid A; Kuiper M. TFcheckpoint: a curated compendium of specific DNA-binding RNA polymerase II transcription factors. Bioinformatics 2013 ;Volume 29.(19) p. 2519-2520.

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CEMIR seminar in Trondheim, September 4, 2014

The Centre of Molecular Inflammation Research, CEMIR, will hold the annual scientific seminar on inflammation research on September 4, 2014.

Speakers include the renowned professors

Cemir collage seminar

Clockwise from top left: Alan Aderem, Göran Hansson, Stefanie Vogel and Douglas Golenbock

The invited speakers will relate to the inflammation research area in different ways.

The seminar is open for all and you do not need to register in avance to participate.

CEMIR was established in 2013 as a Centre of Excellence appointed by the Research Council of Norway. The vision of CEMIR is to lay the foundation for identifying new therapeutic targets and developing new diagnostic tools for inflammatory diseases through an integrated 10-year programme of research and research training in molecular innate immune responses. CEMIR is hosted by the Faculty of Medicine at the Norwegian University of Science and Technology (NTNU).

Please find the full seminar program and see the titles of the talks here: CEMIR seminar 2014 programme

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How plague bacteria kill immune cells

PNAS cover

The article has the cover image for the current issue of PNAS. (May 20, 2014)

Many bacteria kill considerable numbers of host cells upon infection. However, the mechanisms behind the cell death are in many cases unclear. A recent article in PNAS by the the CEMIR-affiliated researcher professor Egil Lien,  describes how the bacteria Yersinia pestis, the causative agent of plague, kills key immune cells called macrophages by apoptosis mediated by kinase RIP1 and caspase-8 together with RIP3.

Apoptosis is often considered to be a “silent” type of cell death. However, we found that the death was accompanied by inflammatory processes via IL-18 and IL-1b generating inflammasomes and transcription factor NF-kB, also via RIP kinases and caspase-8. Importantly, mice deficient in caspase-8 and RIP3 were highly susceptible to bacterial infection, suggesting a key pathway for anti-bacterial defenses.

The article made it to the cover in the current issue of PNAS. Learn more about the image here.

Egil Lien. Foto: NTNU

Professor Egil Lien. Foto: NTNU


Wenga, D. , Marty-Roixa, R., Ganesana, S., Proulxb, M.K., Vladimera, G.I., Kaiserc, W.J., Mocarskic, E.S., Pouliota, K., Chand, F.K., Mellihere, M.A., Harrisf, P.A., Bertinf, J.,  Goughf, P. J., Shayakhmetovg, D.M., Goguenb, J.D., Fitzgeralda, K.A., Silvermana, N., Lien, E. Caspase-8 and RIP kinases regulate bacteria-induced innate immune responses and cell death. PNAS (published online).



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Filed under Infection, NTNUmedicine, Research

A new mechanism explaining the anti-inflammatory effect of HDL is revealed



Bloggers: Nathalie Niyonzima and Eivind Samstad




Atherosclerosis is a progressive disease that was once believed to be a disease of cholesterol storage. Today, it is well acknowledged that atherosclerosis is an inflammatory disease, and that cells and signalling molecules from the innate immune system shape the course of the disease in various ways. The defence of the normal artery depends on innate immune responses provided by endothelial cells. When challenged by inflammation, macrophages and other cells of the immune responses are recruited to the artery wall. The macrophage is an integral component to the pathogenesis of atherosclerosis, functioning at the intersection of inflammation and cholesterol homeostasis. Atherosclerotic plaque formation is driven by the persistence of lipid-laden macrophages in the artery wall. The mechanisms by which these cells become trapped, and thereby establishing chronic inflammation, remain unknown (Peter Libby, Nature 2011).


Atherosclerosis. Illustration: iStock

There has long been a focus on finding therapeutic methods to reduce the levels of cholesterol in the arterial wall. Studies have shown that high HDL levels are associated with reduced cardiovascular risk. This is mainly due to HDL’s ability to transport excess cholesterol in arterial macrophages to the liver for excretion (i.e., reverse cholesterol transport). Despite considerable understanding of HDL and its metabolism, therapies that aim to increase HDL levels have not been successful. Because of the heterogeneity in HDL particles, just increasing HDL levels has not been beneficial, reflecting the qualitative changes in the particles. HDL has also been shown to have other functions beyond cholesterol transport – several studies have shown that HDL is anti-inflammatory, but the mechanisms behind this are not well understood (Xuewei Zhu, Ann.Rev.Nutr 2012).

In a recent study published in the prestigious journal Nature Immunology, our research partners have taken a closer look at the anti-inflammatory effects of HDL (De Nardo, et.al, Nature 2013). They identified that HDL’s anti-inflammatory effects are mediated through the induction of ATF3. ATF3 is a key transcriptional regulator of innate immune response genes, which is induced by TLR stimulation and other stimuli, and acts as negative regulator of proinflammatory cytokines (Elisabeth S.Gold, JEM 2012).

Using mouse model and human bone marrow dendritic cells (BMDMs) treated with native HDL or reconstituted HDL prior to TLR stimuli; they showed that HDL regulates inflammation in macrophages by inhibiting transcription of proinflammatory genes such as IL-1β, IL-6 and IL-12.

In order to confirm that the anti-inflammatory effects of HDL were mediated through an inflammatory repressor, they performed microarray analysis on resting BMDMs and HDL-pretreated BMDMs subsequently stimulated with TLR ligand. ATF3 was the most induced transcription factor in the presence of HDL, and it was shown to bind to the promoters of several proinflammatory genes, thereby regulating inflammation.

They demonstrated the relevance of these findings by using Apoe-deficient mice fed a high-fat diet and injected with HDL. They observed that mice treated with HDL had lesser inflammation than the untreated ones, and that the induction of ATF3 correlated with the downregulation of proinflammatory cytokines.

Besides promoting cholesterol efflux from macrophages, HDL has been shown to protect endothelial integrity by promoting endothelial repair mechanisms. Using a model of vascular repair, they showed that the protective effects of HDL on endothelial repair are for the most part driven by ATF3.

These results provide us a link between HDL and its anti-inflammatory properties that has been a puzzle over long time. The fact that ATF3 is required for the anti-inflammatory effects of HDL shows that ATF3 is a key point for endothelial damage and inflammation. The current study has laid the foundation for understanding the regulatory mechanisms that control inflammation in atherosclerosis and other chronic inflammatory diseases.

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CEMIR recruits more researchers

Kari HålandBlogger: Kari Håland





Centre of Molecular Inflammation Research (CEMIR) keeps growing and is entering its second year with plans for increased research activity and more positions.

CEMIR was established on 1. January 2013 as part of the Research Council of Norway’s third round of Centres of Excellence (SFFs). CEMIR’s vision is to find out how sensors in the immune system initiates and regulates inflammatory responses. This new knowledge will be used in disease models to identify new therapeutic targets and diagnostic tools for inflammatory diseases.

Celleforskning. Foto: Geir Mogen

Trude Helen Flo with colleague Jane Awuh. (Photo: Geir Mogen)

This spring, CEMIR is recruiting for several research positions: 3 Post Docs, 2 PhD positions and 1 Staff Engineer. The Post Doc positions have now been announced.

“When CEMIR announced similar positions in 2013, we saw 220 applications,” says Director Terje Espevik. “This gives us a great opportunity to choose the best researchers and to find the most promising research talents.”

CEMIR moved into the new Kunnskapssenteret at Øya Campus in Trondheim in 2013. “We have excellent premises with plenty of room for our employees. The colocation of the centre gives us an excellent basis for establishing a unified milieu, and for cooperation and the exchange of ideas across the research groups,” Espevik says. “At the same time we remain close to the Department (the Department of Cancer Research and Molecular Medicine) in the neighbouring Gastrosenteret, which makes it easy to cooperate both organisationally and translationally.”

As part of becoming a centre, CEMIR has introduced several fixed meeting points bringing together the researchers at the centre. This includes weekly seminars and an article club where the aim is the share knowledge and to get feedback in terms of potential improvements or new research ideas from other colleagues at the centre. The SFF consist of research groups from various related subject fields, and there is no doubt that such close cooperation and exchange of ideas is beneficial.

“We look forward to having even more talented people that will contribute to the knowledge in our field. We constantly discover new research questions that we would like to explore further,” Espevik says.

A central question to CEMIR’s research is how inflammation can be so closely connected to many seemingly different chronic diseases. CEMIR’s research programme has a hypothesis that the key to new therapeutic targets for chronic inflammatory diseases can be found in the early stages of the inflammatory response where sensors in the innate immune system are activated.

The announced Post Docs are in the following areas:

  • Inflammation and Bone Disease. Project leader: Therese Standal, therese.standal@ntnu.no
  • Inflammation in Pregnancy. Project leader: Ann-Charlotte Iversen, ann-charlotte.iversen@ntnu.no
  • Host-pathogen Interactions in Mycobacterial Infection. Project leader: Trude Helen Flo, trude.flo@ntnu.no

Full job descriptions and more information can be found at the recruitment site Jobbnorge:

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Looking for the perfect immune response


Blogger:Trude Helen Flo, co-director CEMIRtrude_helen_flo_FotografGei

The Research Council of Norway has recently awarded grants under the funding scheme Independent Basic Research Projects – Medicine, Health Sciences and Biology (FRIMEDBIO). There is tough competition for this funding nationally, and only the best projects get through. The Faculty of Medicine, NTNU, has been awarded funding for three talented young researchers, three research projects and two post docs. You can read about all these projects on the blog over the coming weeks. Trude Helen Flo and her colleagues at CEMIR were awarded funding to their research project: New Principles of mycobacterial killing in host macrophages (MycoHosPath).

Mycobacterial infections are a global health problem. Tuberculosis (TB) is caused by a bacterium known as Mycobacterium tuberculosis (Mtb) and kills more than 1.4 million people worldwide each year. Environmental mycobacteria like Mycobacterium avium can cause disease in immunocompromised people like HIV/AIDS patients who are not on anti-retroviral treatment. Mycobacterial infections require long treatment with antibiotics and drug resistance is emerging. Thus we need new drugs and vaccines in order to reach the UN millennium goal of eradication of tuberculosis.

To discover new therapeutic targets we need to learn more about the mycobacterium and how it interacts with its human host.


Mycobacterium tuberculosis (Mtb) and kills more than 1.4 million people worldwide each year

To discover new therapeutic targets we need to learn more about the mycobacterium and how it interacts with its human host.

Some major scientific and technological advances during the last decade have contributed significantly to progress in the field: studying the genetic makeup of mycobacteria provides clues about how the bacteria may infect and survive in the host. On the other hand, studying genetic variations in humans also provides insights in to how humans may become susceptible to mycobacterial infections.

Major breakthroughs in how our first line of defense, the innate immune response, can discriminate between different pathogens and shape the following second line of defense, the adaptive immune response, was awarded the 2011 Nobel Prize in Medicine. The adaptive immune response is crucial for the development of immunological memory. Despite these major advances, we still lack a complete understanding of mycobacterial immunity.

TB incidence rates and multidrug-resistant TB cases (click to enlarge image)


The primary research goal of the MycoHosPath project is to identify new principles of mycobacterial killing during acute and chronic infection. We will approach this by studying the interplay between three cellular pathways that are central for killing and intracellular survival of mycobacteria: Phagocytosis, Inflammatory signaling and Autophagy.

Untitled-1Phagocytosis is the process by which bacteria are taken up by innate immune cells like macrophages and dendritic cells. Normally this leads to destruction, but pathogenic mycobacteria have found ways to avoid it.

Autophagy is a similar process used by cells to detect and degrade garbage in their interior, including intracellular pathogens. Understanding how mycobacteria avoid these killing mechanisms and survive within macrophages may aid in discovery of new drug targets.

Inflammatory signaling is the macrophage response to infection. Infected macrophages produce potent molecules to alarm and recruit other immune cells to help clear the infection. Some of these molecules also help the infected cell to directly kill the invading micobes. However, since pathogenic mycobacteria can live in our body for a lifetime, this does not work perfectly. If we can improve our understanding on how a perfect immune response to mycobacteria should look like we could contribute to new vaccine strategies.

The combined processes of phagocytosis, autophagy and inflammatory signaling in host macrophages, and strategies used by the mycobacterium to manipulate them to its own advantage, will influence activation of mycobacterium-specific immune cells that we need to clear the infection and create immunity to further infection.

Our research group studies several of these aspects in the bacterium, in cells isolated from healthy and HIV-infected individuals, and in mouse model systems. As part of SFF-CEMIR we have access to national and international expertise on inflammation research and advanced imaging, state-of-the-art methodologies and new labs in Kunnskapssenteret.

We have also engaged strong national and US collaborators on autophagy and mycobacterial research who will contribute in what we hope will be a successful project. We are looking forward to realizing MycoHosPath next year.

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The tumour’s microenvironment important in breast cancer development

Tonje SteigedalBlogger: Tonje Strømmen Steigedal





Our bodies constantly renew their cells. In healthy individuals this is tightly regulated so that old cells are removed at the same time as new ones are produced. Cancer arises when this regulation gets out of control due to, for example, mutations in the DNA. A tumour consisting of large numbers of cancer cells is formed.

Lungevev fra mus

Lung tissue from mice: Healthy lung cells in blue with metastasis (cancer cells) shown in brown. (Photo: TS Steigedal)

In the environment around the cancer cells there are also many other types of cells that affect how the tumour develops. These cells are called stromal cells and include fibroblasts (connective tissue cells), macrophages (inflammation cells) and endothelium cells (blood vessel cells). Cancer cells can programme the stromal cells to their advantage so that the cancer cells get even better growing conditions.

In addition to cancer cells and stromal cells, there are also many other molecular components in the tumour’s microenvironment. Examples of such proteins include growth factors that stimulate cell division and cytokines that regulate inflammation reactions. In addition there are also large scaffold proteins outside the cells ensuring structure and support to all cells. Without such framework proteins the body would just be a random heap of different types of cells. This type of scaffold is called an extracellular matrix.

Exploiting the environment

Cancer cells exploit the other cells and proteins in the tumour microenvironment to their advantage so that the tumour can grow, divide and eventually spread (metastasise) to other organs. More and more attention is now given to the mapping and understanding of the tumour microenvironment’s composition in connection with cancer development.

Much speaks for the makeup of the tumour microenvironment playing a decisive role in how tumours develop and whether they spread. And perhaps this information could say something about how the tumour will respond to treatment. We now work on characterising tumours’ microenvironment and the goal is to understand how the composition of the microenvironment affects cancer development.

We have used a mouse model of breast cancer which has been modified so that the mice develop breast cancer in a predictable manner. By analysing the tumour microenvironment’s composition in tumours from different stages of cancer, we can say something about how they change throughout the tumour development. We have used advanced methods to map the complete composition of proteins in the tumour microenvironment.


Tumour samples from modified mice models: 1) Low-grade tumour with few cancer cells (red) and very little visible ECM/collagen (blue). White areas are normal fat tissue. 2) Late-stage: invasive, aggressive tumour packed with cancer cells and lots of ECM/collagen. The tumour becomes fibrous and hard. (Photo: TS Steigedal).

New biomarkers for breast cancer?

We now see that some of these proteins also seem to appear in human breast cancer, and we wish to understand what function these proteins have. If we could understand what they mean to the cancer cells, we could perhaps use these proteins as new biomarkers for diagnosis and prognosis, and the goal is also to identify new targets for treatment and therapy of breast cancer.

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Filed under Cancer, NTNUmedicine, Research

Pictures from the CEMIR opening

Today we open our new  Centre of Excellence, CEMIR, Centre of Molecular Inflammation Research. A central topic for the centre is how inflammation can play a part in so many apparently different chronic diseases. Here are some pictures from the opening and the opening seminar.

Mange ville få med seg det spennende seminaret ifm åpningen av CEMIR.

Many wished to participate at the seminar held in connection with the opening of CEMIR.

Fornøyde forskere, fra venstre: nestleder CEMIR, Trude Helene Flo, leder for CEMIR, Terje Espevik, Insituttleder Institutt for kreftforskning og molekylær medisin Magne Børset.

Happy researchers, from the left: Co-Director at CEMIR, Trude Helene Flo, Director of CEMIR, Terje Espevik, Head of the Department of cancer research and molecular medicine, Magne Børset.

Dekan Stig Slørdahl var overlykkelig da han fant ut at begge  søknadene fra Det medisinske fakultet for Senter for Fremragende Forskning gikk gjennom.

Dean Stig Slørdahl was extremely pleased when he found out that both applications for Centres of Excellence from the Faculty of medicine were granted.


Instituttleder Magne Børset sier vi har grunn til å være stolte, og spesielt lederne ved CEMIR, for det nye senteret.

Head of Department Magne Børset says we have reasons to be proud, and especially the leaders of CEMIR, for the new CoE status.



Liv Furuberg from the Research Council of Norway.


Noen av tilbakemeldingene fra ekspertpanelet ifm tildeling av Senter for Fremragende Forskning

Some of the feedback from the panel of experts in connection with the awarding of the CoE status.

Fra presentasjonen til Forskningsrådet.

From the Research Council of Norway’s presentation.


Leder for CEMIR viser at betennelser har betydning for flere sykdommer som fedme, diabetes, alzheimer, allergier og kreft.

The Director of CEMIR shows that inflammation plays a part in several diseases such as obesity, diabetes, Alzheimer’s, allergies and cancer.

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