Research News

<p>Cell plasticity: different and reversible identities (Cian J. Lynch, IRB Barcelona)</p>
28 Sep 2020

Researchers at IRB Barcelona’s Cellular Plasticity and Disease Laboratory propose a more efficient way to limit cell plasticity without causing cell damage.

The new method sheds light on processes in which cell plasticity is important, such as cancer and immunology.

The study has been published in the journal Nature Cell Biology and has been supported by ”la Caixa” Foundation.

22 Sep 2020

Researchers from the Structural Bioinformatics and Network Biology Laboratory at IRB Barcelona develop a system to predict tumour response to different treatments.

Called Targeted Cancer Therapy for You (TCT4U), this system has allowed them  to identify a set of complex biomarkers that are available to the medical-scientific community.

The work has been published in the journal Genome Medicine.

14 Aug 2020

Analysis of the genomes of 28,000 tumours from 66 types of cancer has led to the identification of 568 cancer driver genes

Performed by the Biomedical Genomics Lab at IRB Barcelona, the study has allowed a major update of the Integrative OncoGenomics (IntOGen) platform, aimed at identifying mutational cancer driver genes.

Published in Nature Reviews Cancer, the results provide the most complete snapshot of the compendium of cancer driver genes to date.

12 Aug 2020

The system that regulates cellular calcium levels duplicated, generating two non-equivalent systems, some one billion years ago before fungi and animals diverged evolutionarily.

The fungal models currently used for the study of mitochondrial calcium regulation are not adequate, as the system they possess is not equivalent to that of animals. Chytrids, a divergent group of fungi, would be the only fungi that possess a system similar to ours.

The study by IRB Barcelona's Comparative Genomics Laboratory has been published in the journal Nature Communications.

 

<p>Cancer cells with TLK inhibition show replication intermediates (green) at chromosome ends (red) - (IRB Barcelona)</p>
5 Aug 2020

These proteins are a potential therapeutic target for enhancing the effect of some cancer treatments.

Inhibition of TLK proteins triggers the Alternative Lengthening of Telomeres pathway, a common process in some of the most aggressive types of cancer, such as glioblastoma.

The study, performed by the Genomic Instability and Cancer Laboratory at IRB Barcelona, has been published in the journal Cell Reports.

<p>The discovered type of diffuse hypermutation is called "mutation fog". (Dave Hoefler, Unsplash)</p>
4 Aug 2020

The mechanism unveiled triggers a mutation fog, causing hundreds of mutations in each tumor, which spread through the genome of lung, head-and-neck and breast cancers.

Researchers from the Genome Data Science Lab have identified the antiviral APOBEC3A enzyme as the major cause of this new type of hypermutation.

Published in Nature Genetics, the study shows how the mutation fog process generates many oncogenic “cancer driver” mutations, thus accelerating tumour development.

2 Jul 2020

Of the 614 cell lines studied, 7% closely corresponded to a different type of cancer than that thought to give rise to the cell line.

The Genome Data Science Laboratory at IRB Barcelona has drawn up a reference list of 366 cell lines in which the genetic pattern corresponds to the type of tumour that they intend to model.

The work shows that studies using the cell lines on this reference list have a greater discovery rate, and has been published in the journal Science Advances.

 

<p>After APP cleavage at the neuronal membrane, Aβ protein self-assembles into 4 or 8 copies adopting an arrangement allowing passage of water and ions (in red) and thus disrupting ion cell homeostasis © Benjamin Bardiaux.</p>
26 Jun 2020

Researchers led by Natàlia Carulla find that specific amyloid-beta (Aβ) protein ensembles have the capacity to disrupt the membrane of neurons, causing their death.

The results have been published in the journal Nature communications.

<p>DNA lesions. Credit: Petra Korlevic</p>
25 Jun 2020

DNA damage caused by chemical mutagens is not repaired immediately and can create more genetic diversity in tumours, as lesions pass on unrepaired over several rounds of cell division.

A study by the Liver Cancer Evolution Consortium explores the evolution of tumours after chemical damage, offering interesting insights into how mutational processes work.

The work has been published in the journal Nature.

 

2 Jun 2020

A role of colibactin-producing E. coli in carcinogenesis.