RARE DISEASE DAY 2017 – FRIEDREICH ATAXIA:RESEARCHERS AT FRATAGENE THERAPEUTICS AND UNVERSITY OF ROME “TOR VERGATA” HAVE IDENTIFIED A NEW THERAPEUTIC TARGET
Researchers at Fratagene Therapeutics, led by Dr. Alessandra Rufini, in collaboration with researchers at the Department of Biomedicine and Prevention of the University of Rome “Tor Vergata”, coordinated by Prof. Roberto Testi, have identified a new therapeutic target relevant for Friedreich ataxia (FA).
FA is a rare disease, a genetic neurodegenerative affection of children and young adults that progressively leads to disability and that still lacks an approved therapy. The discovery of a new therapeutic target, the enzyme RNF126, paves the way to the development of a new class of drugs able to restore the levels of frataxin, the protein defective in FA, therefore providing hope of cure. The results of this work have just been published in the prestigious journal Cell Reports.
Fratagene Therapeutics is a biotech company created by Prof. Roberto Testi, at the Department of Biomedicine and Prevention of the University of Rome “Tor Vergata”, with the aim of attracting the necessary resources to the development of a cure for FA. Fratagene Therapeutics is part of a long-term research endehavour in innovative drug discovery carried out by Prof. Testi group, funded by Telethon, by the Friedreich Ataxia Research Alliance USA and by two European Research Council grants (an Advanced Grant and a Proof-of-Concept grant).
Benini et a., http://www.cell.com/cell-reports/fulltext/S2211-1247(17)30149-3
“Human Connectome Project”: Personality traits linked to differences in brain structure. PROF. NICOLA TOSCHI
Our personality may be shaped by how our brain works, but in fact the shape of our brain can itself provide surprising clues about how we behave - and our risk of developing mental health disorders - suggests a study published today. According to psychologists, the extraordinary variety of human personality can be broken down into the so-called 'Big Five' personality traits, namely neuroticism (how moody a person is), extraversion (how enthusiastic a person is), openness (how open-minded a person is), agreeableness (a measure of altruism), and conscientiousness (a measure of self-control).
In a study published today in the journal Social Cognitive and Affective Neuroscience, an international team of researchers from the UK, US, and Italy have analysed a brain imaging dataset from over 500 individuals that has been made publicly available by the Human Connectome Project, a major US initiative funded by the National Institutes of Health. In particular, the researchers looked at differences in the brain cortical anatomy (the structure of the outer layer of the brain) as indexed by three measures - the thickness, area, and amount of folding in the cortex - and how these measures related to the Big Five personality traits.
"Evolution has shaped our brain anatomy in a way that maximizes its area and folding at the expense of reduced thickness of the cortex," explains Dr Luca Passamonti from the Department of Clinical Neurosciences at the University of Cambridge. "It's like stretching and folding a rubber sheet - this increases the surface area, but at the same time the sheet itself becomes thinner. We refer to this as the 'cortical stretching hypothesis'."
"Cortical stretching is a key evolutionary mechanism that enabled human brains to expand rapidly while still fitting into our skulls, which grew at a slower rate than the brain," adds Professor Antonio Terracciano from the Department of Geriatrics at the Florida State University. "Interestingly, this same process occurs as we develop and grow in the womb and throughout childhood, adolescence, and into adulthood: the thickness of the cortex tends to decrease while the area and folding increase."
In addition, as we get older, neuroticism goes down - we become better at handling emotions. At the same time, conscientiousness and agreeableness go up - we become progressively more responsible and less antagonistic.
The researchers found that high levels of neuroticism, which may predispose people to develop neuropsychiatric disorders, were associated with increased thickness as well as reduced area and folding in some regions of the cortex such as the prefrontal-temporal cortices at the front of the brain.
In contrast, openness, which is a personality trait linked with curiosity, creativity and a preference for variety and novelty, was associated with the opposite pattern, reduced thickness and an increase in area and folding in some prefrontal cortices.
"Our work supports the notion that personality is, to some degree, associated with brain maturation, a developmental process that is strongly influenced by genetic factors," says Dr Roberta Riccelli from Italy.
"Of course, we are continually shaped by our experiences and environment, but the fact that we see clear differences in brain structure which are linked with differences in personality traits suggests that there will almost certainly be an element of genetics involved," says Professor Nicola Toschi from the University 'Tor Vergata' in Rome. "This is also in keeping with the notion that differences in personality traits can be detected early on during development, for example in toddlers or infants."
The volunteers whose brains were imaged as part of the Human Connectome Project were all healthy individuals aged between 22 and 36 years with no history of neuro-psychiatric or other major medical problems. However, the relationship between differences in brain structure and personality traits in these people suggests that the differences may be even more pronounced in people who are more likely to experience neuro-psychiatric illnesses.
"Linking how brain structure is related to basic personality traits is a crucial step to improving our understanding of the link between the brain morphology and particular mood, cognitive, or behavioural disorders," adds Dr Passamonti. "We also need to have a better understanding of the relation between brain structure and function in healthy people to figure out what is different in people with neuropsychiatric disorders."
This is not the first time the researchers have found links between our brain structure and behaviour. A study published by the group last year found that the brains of teenagers with serious antisocial behaviour problems differ significantly in structure to those of their peers.
Riccelli, R et al. Surface-based morphometry reveals the neuroanatomical basis of the five-factor Model. Social Cognitive and Affective Neuroscience; 25 Jan 2016; DOI: 10.1093/scan/nsw175
The launch event for the journal Biomedicine & Prevention, which met with success, was held on December 14, 2016 at the Rome headquarters of the Italian National Research Council (Centro Nazionale delle Ricerche).
The occasion was attended by over a hundred guests hailing not only from the medical sphere but also from the fields of biology, chemistry, physics, and engineering. Many colleagues from the Department were also present.
Prof. Leonardo Palombi, Editor-in-chief of the journal and Head of the eponymous Biomedicine and Prevention Department at the University of Rome “Tor Vergata”, together with Prof. Sandro Mancinelli, who served as moderator for the event, presided over interesting addresses delivered by the Honorable Rector of the University, Prof. Giuseppe Novelli, and by the President of the Italian National Institute of Health (Istituto Superiore di Sanità), Prof. Walter Ricciardi.
These opening addresses were followed by technical presentations from the event’s overseas guest speakers:
- Prof. Felicity Astin
- Prof. Lang Tran
- Dr. Cornelius Bartels
- Dr. Graham Fraser
In closing, well-wishes and expressions of interest in participating were conveyed by:
- Società Italiana di Igiene e Medicina Preventiva
- Fondazione SIMG
- Federazione Nazionale Collegi IPASVI
- Società Italiana di Scienze Infermieristiche
- Società Italiana di Medicina del Lavoro e Igiene Industriale
- Società Italiana di Ematologia
- Società Italiana di Psichiatria
- Società Italiana di Ginecologia e Ostetricia
- Società Italiana di Mutagenesi Ambientale
- Società Italiana di Fisica Medica
- Collegio Italiano dei Professori di Anatomia Patologica
Compared with their peers, male youths with severe antisocial behavior problems appear to have significant differences in brain structure, suggesting their problem behavior stems from early life changes in brain development.
So concludes a study by an international team published in the Journal of Child Psychology and Psychiatry.
First author Graeme Fairchild, associate professor in abnormal psychology at the University of Southampton in the United Kingdom, and colleagues used magnetic resonance imaging (MRI) to examine the brain structure of teenage and young adult men diagnosed with conduct disorder.
First author Graeme Fairchild, associate professor in abnormal psychology at the University of Southampton in the United Kingdom, and colleagues used magnetic resonance imaging (MRI) to examine the brain structure of teenage and young adult men diagnosed with conduct disorder.
Conduct disorder is a cluster of persistent behavioral problems displayed in childhood and adolescence, such as aggressive and destructive behavior, stealing, and lying. In older children, it can also include staying out all night and use of weapons.
The researchers note that evidence already exists that the brains of people with serious behavior problems are different, but this tends to be simplistic and focused in limited regions, such as the amygdala - the brain's emotion center.
However, conduct disorder is a complex behavioral disorder, and one might expect the brain differences to be more complex and affect more than one brain region, they suggest.
Therefore, in their investigation, the team looked for brain regions with similar or different thicknesses as this might indicate coordinated or non-coordinated development between regions.
For the study, the researchers carried out MRI brain scans on 58 male teenagers and young adults diagnosed with conduct disorder. They also included 25 peers without such a diagnosis, as typically developing, "healthy" controls. The participants were all aged 16-21.
'Most of the brain is involved'
The researchers found that participants with childhood onset conduct disorder - sometimes referred to as "early starters" - had a strikingly higher number of cases where brain regions had the same thickness as controls.
In contrast, the participants with adolescent-onset conduct disorder - sometimes termed "late starters" - had a lower number of cases where brain regions had the same thickness compared with controls.
The researchers confirmed the findings with a separate, independent sample of 37 participants with conduct disorder and 32 healthy controls. All participants in this second sample were male, aged 13-18.
Prof. Fairchild says the differences between the youths with both forms of conduct disorder and their healthy peers "show that most of the brain is involved, but particularly the frontal and temporal regions of the brain."
He argues that the findings are "compelling evidence" that conduct disorder is a "real psychiatric disorder," and not just an exaggerated form of teenage rebellion as some experts have suggested.
The study also indicates there are important differences in the brains of people who develop conduct disorder early in childhood and those who develop it later during their teens.
However, while the findings highlight the key role the brain plays in the development of conduct disorder, they do not explain how the changes come about. For example, to what extent are they influenced by people's genes, and to what extent are they affected by the environment they are raised in?
While the study does not answer these questions, the researchers believe the findings could help to measure the effect of interventions. Using a brain map of conduct disorder it might be possible, for example, to see if interventions such as psychological therapy can reverse some of the changes noted in the study.
ROME – A group of researchers from the University of Rome “Tor Vergata” and the Fondazione Santa Lucia has identified a potential new approach to treating spinal muscular atrophy (SMA) which directly tackles the gene mutation responsible for the disease.
The study, funded by the Fondazione Telethon, was coordinated by Claudio Sette, Associate Professor at the Department of Biomedicine and Prevention, University of Rome “Tor Vergata”. The study’s findings have appeared in the scientific publication The Journal of Cell Biology.
Spinal muscular atrophy (SMA) is a neuromuscular disease characterized by the progressive death of motor neurons, the nerve cells in the spinal cord that relay motor commands to the muscles. The disease is caused by mutations in the genes called SMN1 and SMN2, which lead to the production of insufficient levels of the SMN protein that is associated with the survival of motor neurons. To date, all attempts to correct the genetic defect responsible have failed to yield the desired results.
The research group led by Claudio Sette had already in recent years identified a protein, called Sam68, involved in certain processes key to the progression of the disease. In this new study, the researchers developed animal (mouse) models of SMA in which Sam68 was eliminated. They were thus able to observe that mice lacking the Sam68 protein showed a significant improvement in the survival of motor neurons and, more generally, in the health and functionality of affected muscles. This thus paves the way for a new therapeutic approach to this as-yet incurable disease, in respect of which however very interesting prospects have emerged in recent years thanks to research. In particular, at the start of 2015 two international clinical trials got underway, in which Italian patients will also be able to participate, testing the efficacy of two different drugs in combating the disease. According to a statement issued by the University of Rome “Tor Vergata”, this undertaking has in part been made possible with the support of the Fondazione Telethon.
Spinal muscular atrophy (SMA) – Spinal muscular atrophy (SMA) is a neuromuscular disease characterized by the progressive death of motor neurons, the nerve cells in the spinal cord that control muscle movement.
It affects around 1 in every 10,000 newborn babies and is the most common genetic cause of infant death. There are three forms of the disease, of which type I is the most serious and affects about half of SMA patients. In this type, affected infants exhibit signs of the disease already from birth or within their first few months of life, manifesting as severe and progressive signs of respiratory insufficiency.
Children suffering from type II, also termed the “intermediate form”, acquire the ability to sit but not to walk unaided, and often present respiratory complications as well as other signs, such as scoliosis.
Type III is the least severe, often begins to manifest after the first few years of life, and is always accompanied by successful development of the ability to walk, although in some cases this capability may subsequently be lost.
The disease is caused by a defect in the SMN1 gene that encodes for a protein called SMN. The counterpart SMN2 gene remains functional in SMA patients, but leads to the production of insufficient levels of the SMN protein.
The mode of transmission is autosomal recessive: parents are healthy carriers of the genetic defect and have a 25% probability of transmitting the disease to each of their children. The disease is diagnosed through genetic testing. At present, there is no definitive cure, though numerous studies are underway to evaluate potential treatments. A few drugs are currently being trialed.
Tor Vergata: The MYC‐interfering polypeptide, Omomyc, impairs the carcinogenic potential of human glioblastoma stemlike cells (GSCs)
Cancer stemlike cells are key to cancer development and therapy. The MYC‐interfering polypeptide, Omomyc, impairs the carcinogenic potential of human glioblastoma stemlike cells (GSCs) and affects proper MYC genomic localization. This indicates that the gene regulatory nodes determining GSC identity are MYC dependency.
MYC deregulation is common in human cancer and has a role in sustaining the aggressive cancer stem cell populations. MYC mediates a broad transcriptional response controlling normal biological programmes, but its activity is not clearly understood. We address MYC function in cancer stem cells through the inducible expression of Omomyc—a MYC‐derived polypeptide interfering with MYC activity—taking as model the most lethal brain tumour, glioblastoma. Omomyc bridles the key cancer stemlike cell features and affects the tumour microenvironment, inhibiting angiogenesis. This occurs because Omomyc interferes with proper MYC localization and itself associates with the genome, with a preference for sites occupied by MYC. This is accompanied by selective repression of master transcription factors for glioblastoma stemlike cell identity such as OLIG2, POU3F2, SOX2, upregulation of effectors of tumour suppression and differentiation such as ID4, MIAT, PTEN, and modulation of the expression of microRNAs that target molecules implicated in glioblastoma growth and invasion such as EGFR and ZEB1. Data support a novel view of MYC as a network stabilizer that strengthens the regulatory nodes of gene expression networks controlling cell phenotype and highlight Omomyc as model molecule for targeting cancer stem cells.
Cancer stemlike cells are key to cancer development and therapy. The MYC‐interfering polypeptide, Omomyc, impairs the carcinogenic potential of human glioblastoma stemlike cells (GSCs) and affects proper MYC genomic localization. This indicates that the gene regulatory nodes determining GSC identity are MYC dependent.
Omomyc occupies DNA E‐boxes targeted by MYC network complexes, weakening the gene expression programme control nodes and facilitating phenotype changes in the presence of appropriate stimuli.
Expression of Omomyc in GSCs—in vitro and in xenografts—rebalances their transcriptome towards differentiation and tumour suppression by affecting the transcript levels of master transcription factors and key non‐coding RNAs.
Blunting MYC activity by Omomyc restrains GSC tumorigenic features—self‐renewal, proliferation, differentiation, migration and tumour vascularization—in vitro and in vivo by both cell‐autonomous and non‐cell‐autonomous mechanisms.
1) How would you introduce the background to your research to someone who is completely unfamiliar with your field?
Neurogenesis is the process underlying brain development and it is executed by the neural stem cells, which generate neurons and glial cells. The proper regulation of neurogenesis requires that neural stem cells divide to amplify the population of cells in the growing brain. However, it also requires that these cells differentiate into mature neurons upon proper stimuli. The balance between these two activities is essential to achieve the right number of neurons without depleting the neural stem cells population. Such balance is achieved through a fine regulation of cell metabolism and gene expression. One layer of such regulation involves flexible processing of precursor messenger RNAs to yield multiple proteins from each gene. Several RNA processing factors modulate these mechanisms in the developing brain. One of them, SAM68, is highly expressed in neural stem cells and it was previously implicated in the pathogenesis of neurodegenerative diseases.
2) What exact question did you set out to answer?
SAM68 expression oscillates during mouse brain development, with a peak at times of intense neurogenesis and a sharp decline after birth. This observation suggested that SAM68 might be involved in the regulation of neurogenesis. Thus, we set out to investigate its role during brain development in mouse embryos.
3) What is the most important finding of your paper?
We found that the expression levels of SAM68 dictate the fate of neural stem cells. High expression promotes their self-renewal and amplification of the stem cell pool; low expression triggers their differentiation into neurons. We also linked SAM68 function to regulation of Aldehyde Dehydrogenase 1A3 (ALDH1A3) expression, an enzyme that fuels glycolytic metabolism in stem cells. We discovered that SAM68 binds an alternative polyadenylation signal in the ALDH1A3 transcript, preventing its premature termination and insuring expression of a functional enzyme. Thus, our study identifies SAM68 as a key regulator of neural stem cell self-renewal through maintenance of high glycolytic metabolism.
4) What is the most important next step and/or future challenge that follows on from your paper?
RNA metabolism plays a major role in brain development regulation and is often altered in neurodegenerative and intellectual diseases. Our future goal is to investigate whether functional defects in SAM68 are involved in such pathologies and to develop tools to rescue the molecular defects underlying them.
2016 AIRC-FIRC GUIDO VENOSTA PRIZE AWARDED TO PROF. FRANCESCO LO COCO OF ROME’S “TOR VERGATA” UNIVERSITY
The Biennial “Guido Venosta” Prize was established in 1996 and is aimed exclusively at young Italian researchers who have particularly distinguished themselves in research towards developing new therapeutic approaches to neoplasia. The Prize is part of a push to bring recognition to a group of persons playing a key role in the battle against cancer, namely, young researchers within Italian institutes, institutions, and universities.
Prof. Francesco Lo Coco (Full Professor at the Department of Biomedicine and Prevention of the University of Rome “Tor Vergata”, and awarded the Venosta Prize for his studies on acute promyelocytic leukemia) was previously the winner in the Health Section of the 14th edition of the Sapio Award for Italian Research (Premio Sapio). Thanks also to contributions made over the last 20 years by the Italian research community, promyelocytic leukemia is now curable in over 80% of cases with a combination of chemotherapy and retinoic acid (a derivative of vitamin A).
However, the known side effects of chemotherapy (nausea and vomiting, infections, immune suppression, hair loss, and so on), though in most instances transitory, have a very negative effect on the quality of life of patients and are associated with a significant risk of mortality. The Italo-German study (conducted 75% in Italy and coordinated at Tor Vergata) clearly demonstrates the possibility of curing this form of leukemia without exposure to the serious toxic effects of chemotherapy.
The studies conducted by Prof. Lo Coco have contributed significantly to the development of innovative therapies that have enabled the achievement of a very high cure rate for a once fatal disease. His work has also concretely demonstrated the feasibility and worth of “chemotherapy-free” treatments in oncology.
News item in Le Scienze
Article in Nature
A European study conducted by the University of Leuven, Belgium and the University of Rome “Tor Vergata”, in conjunction with researchers from the VIB in Belgium and the CNCR in the Netherlands, has investigated the possibility that changes in the form of the most common inherited intellectual disability – fragile X syndrome – already take place in embryo, when neuronal cells migrate to build the cerebral cortex. The findings, published in the scientific journal Nature Neuroscience, demonstrate when and how the malfunction of a single gene causes seemingly imperceptible changes during embryonic development and the early stages of postnatal life.
The team led by Prof. Claudia Bagni of the Department of Biomedicine and Prevention at the University of Rome “Tor Vergata”, in collaboration with the University of Leuven and the University of Amsterdam, has identified a critical role played by the FMRP protein during embryonic development of the cerebral cortex. The study reveals that the absence of FMRP leads to a delay in the proper formation of the cortex, as well as showing that FMRP is responsible for the morphological transformation of neurons.
For further detail, read here
ERC awards PoC grant funding to “FAST” project headed by Prof. Roberto Testi
The European Research Council (ERC) has approved follow-up funding – in the form of a Proof of Concept (or PoC) grant – for the potential commercial development of therapeutic products devised by the “FAST” (or Friedreich’s Ataxia Seeks Therapy) project. The “FAST” project, led by Prof. Roberto Testi, director of the Laboratory of Signal Transduction at the Department of Biomedicine and Prevention of the University of Rome “Tor Vergata” and Full Professor of Immunology at the said University, was previously awarded an Advanced Grant by the ERC (under the Seventh Framework Programme [sic]) of around 1.5 million euro. Friedreich’s ataxia (FRDA) is a serious genetic disorder that affects the peripheral nervous system of children and adolescents, mainly between the ages of 5 and 15 years. Young people affected begin to present motor coordination disturbances that lead, more or less rapidly, to severe disability, often accompanied by cardiac insufficiency and reduced life expectancy. The genetic defect involves the gene tasked with the production of a protein called “frataxin”. In FRDA patients, the frataxin gene functions poorly and produces little protein, causing the death of nerve cells essential for motor coordination. Patients with FRDA make use of antioxidant drugs but as yet there is no effective specific treatment.
Testi’s research group has devised chemical molecules capable of increasing frataxin levels, or better still, of halting the degradation of frataxin. “Our approach”, explains Testi, “has been to actually think about how to make existing frataxin last longer. We have found that part of the frataxin produced is degraded even before being utilized, which is why we have focused on how to prevent this degradation and are working on transforming some of these molecules into drugs”.
The PoC grant was established to help bridge the gap between academia and industry, and to enable originators of a new treatment (as in this case) to receive funding for definitive proof of concept, so as to facilitate the protection of intellectual property and scouting for industry partners.
FMRP PROTEIN RESPONSIBLE FOR FRAGILE X SYNDROME INTELLECTUAL DISABILITY ALSO INVOLVED IN BREAST CANCER PROGRESSION
“The fragile X protein binds mRNAs involved in cancer progression and modulates metastasis formation”:
Rossella Lucá, Michele Averna, Francesca Zalfa, Manuela Vecchi, Fabrizio Bianchi, Giorgio La Fata, Franca del Nonno, Roberta Nardacci, Marco Bianchi, Paolo Nuciforo, Sebastian Munck, Paola Parrella, Rute Moura, Emanuela Signori, Robert Alston, Anna Kuchnio, Maria Giulia Farace, Vito Michele Fazio, Mauro Piacentini, Bart De Strooper, Tilmann Achsel, Giovanni Neri, Patrick Neven, D. Gareth Evans, Peter Carmeliet, Massimiliano Mazzone, and Claudia Bagni
More information on the EMBO Molecular Medicine journal is available at:
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Prof. Claudia Bagni
Department of Biomedicine and Prevention
University of Rome “Tor Vergata”
Ph. (Italy): +39 347 464 6896
Ph. (Belgium): +32 499 459 167
A research group led by Prof. Claudia Bagni of the Department of Biomedicine and Prevention at the University of Rome “Tor Vergata”, in collaboration with the VIB/University of Leuven, Belgium, has discovered the way in which the fragile X syndrome protein (FMRP) contributes to the progression of breast cancer. In accomplishing this objective, Prof. Bagni’s team also worked with various research centers and hospitals in Italy (including the IFOM-IEO Campus in Milan and the Campus Bio-Medico University of Rome) as well as abroad (both in Belgium and the United Kingdom). The researchers have demonstrated that FMRP acts as a molecular “switch” that is capable of controlling the levels of other proteins involved in different stages of the progression of breast cancer, such as the spread of cancer cells in the bloodstream and the invasion of other organs to form metastases. The study has been published online in the international scientific journal EMBO Molecular Medicine.
“Breast cancer is the most common form of cancer in women. This type of cancer can recur even many years after treatment, giving rise to metastases which spread throughout the body. We have shown that there is a close link between the levels of the FMRP protein in tumor tissue and the ability of cancer cells to spread to other organs. I hope that our discovery can pave the way for the development of new tests to predict the likelihood of metastasization in breast cancer”, stated Prof. Bagni of the University of Rome “Tor Vergata” and the VIB/University of Leuven.
The researchers found very high levels of FMRP in a large percentage of highly-invasive breast tumors (using the tissue microarray approach) and also examined the effect on cancer cells of modulation of FMRP levels, using a mouse model to study breast cancer. In this mouse model, an increase in FMRP levels in the primary tumor led to a rapid and massive spread of cancer cells in the bloodstream and to the development of metastases in the lungs. In contrast, a reduction in levels of the protein led to a decrease in the formation of metastases in the lungs. Another interesting point is that people with fragile X syndrome, who lack the FMRP protein, have a reduced risk of developing breast cancer, as well as an unusual protection against the invasiveness and aggressiveness of this and of other forms of cancer.
There have been extensive studies done on the role played by FMRP in the brain, where the absence of this protein leads to fragile X syndrome, the most common form of inherited intellectual disability in humans. However, this study explored for the first time the direct relationship that exists between FMRP levels and the progression of breast cancer.
“Previous studies indicated that patients with fragile X syndrome had a lower risk of developing cancer, but little is still known about the molecular events that give rise to this beneficial effect. We have shown that high levels of the FMRP protein in human breast tissue samples are linked to an increased risk of developing cancer and particularly to a higher risk of the spread of cancer cells to other tissues in the body”, underlined Prof. Claudia Bagni, who headed the study. “Our results suggest that FMRP can act as a master regulator of a large group of molecules involved in various stages of breast cancer progression. We hope that FMRP levels can be used in the future as an indicator of aggressiveness in breast cancer in order to predict the likelihood of metastatic spread to other organs like the lungs”.