Results about: cancer

Recent years have seen a paradigm shift in our understanding of gene activity and regulation. It is now clear that processing of primary transcripts as well as translational control open a myriad of opportunities for gene regulation, which are extensively used in virtually every human gene.

<p>Angel R Nebreda</p>

The Signalling and Cell Cycle Laboratory focuses on studying the basic mechanisms of cell regulation, especially regarding how external signals are interpreted by cells to modulate cell proliferation, differentiation and survival. Our research centers on two main subjects:

<p>Stracker</p>

The recognition of many types of DNA lesions activates the cellular DNA damage response (DDR). The DDR orchestrates the appropriate cellular programs to maintain genome integrity after genotoxic stress.

A high resolution description of the structure and dynamics of proteins is a very useful tool to study the properties and the function of these important biomacromolecules and, most importantly, to understand how changes in sequence or environment can lead to disease.

<p>Luders</p>

Candidates with a strong interest in the microtubule cytoskeleton who would like to join our group should e-mail a cover letter with CV including contact information for references to jens.ludersirbbarcelona.org.

Our research focuses on three angles of peptide and protein chemistry: the design, synthesis and structure of bioactive molecules. From a structural perspective, we apply modern NMR techniques to study complex molecular recognition processes.

TLK protein inhibition activates the innate immune system

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.

Mutations in cancer genomes: foggy with a chance of thunderstorms

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.