Ongoing studies


Intracellular Calcium homeostasis in Pancreatic Cancer

Pancreatic ductal adenocarcinoma , the predominant form of pancreatic cáncer, is one of the leading causes of cancer related deaths in the world with a five year survival rate of 4-6%. Numerous studies have described the key role of calcium and calcium-permeable ion channels in the regulation of important tumoral processes such as: proliferation, migration and resistance to apoptosis. The main objectives of this research is to understand which calcium signalling changes occur in Pancreatic Adenocarcioma cells compared with Normal Pancreatic Ductal cells, discover the molecular basis involved in calcium signaling remodeling and study the effect of certain chemopreventive drugs in Pancreatic Adenocarcinoma cells.


Transcriptomics of calcium remodeling in colorectal cancer

Enrique Perez-Riesgo, PhD candidate

The more advance the society, the larger amount of data is generated. Thus, an interesting point of view in order to find out how the cellular mechanisms work on, or how they change in any kind of pathologies, is analyzing both data previously generated by several scientists and new data generated on one’s own. And that’s my job, my passion, torturing the data up to get as large amount of information as possible. Currently, the focus of my studies is on the association between cancer phenotype and calcium homeostasis remodeling, for what I use data from New Generation Sequencing, both obtained on our own and obtained from public repositories. This research is supported by the ASOCIACION ESPAÑOLA CONTRA EL CANCER (AECC), the Spanish association against cancer. 


Role of calcium in colorectal cancer chemoprevention

Lucía G. Gutierrez, PhD Candidate

Colorectal cancer is one of the most frequent cancer in modern societies and the most impact cancer in Spain. In spite of the fact that the early diagnosis increases the survival of the patients, another option is find out chemopreventive compounds and to understand his mechanisms of action to improve his action and to reduce the risk of appearance of recurrences.

Nowadays is known the effects of NSAIDs (Nonsteroidal Anti-inflammatory Drugs) and polyamines synthesis inhibition drugs (difluoromethylornithine, DFMO) over the reduction in the appearance of invasive adenomas but the mechanisms for which NSAIDs and DMFO carry out his action are still unknown. 

Previous studies from the lab demonstrate changes in the calcium homeostasis between normal cells and colorectal cancer cells, providing resistance to the cellular death on tumour cells. The study of the physiology of the upset cells gives us the keys to understand what it is happening in these cells and to be able to look for possible solutions to take again the normal phenotype. The main objective of the project is determinate the expression and the activity of the proteins involves in the store-operated calcium entry (SOCE) and his role in colorectal cancer chemoprevention, investigating principally the effect of DFMO over SOCE.

Our interest includes from the study in cellular lines up to culminating in studies in tissues from patients. However, our last and ambitious objective is to develop a clinical trial PACES (study of chemoprevention of colorectal cancer in patients operates to anticipate the high risk of recurrences).

So far we have achieved great advances in the comprehension of DFMO effect on the tumour cells and his capacity of partial reversion to de normal phenotype of the tumour cells using molecular technologies to genetic and protein level, physiological studies of the metabolism of the calcium and cellular death and electrophysiology studies using pach-clump technology.


Remodelling of Calcium homeostasis in aged rat hippocampal neurons

Mónica García Durillo, PhD candidate

The progressive increase in life expectancy in our society has raised the concern about age related diseases. Even though a lot discoveries have been published, further studies are required in order to have a deeper understanding regarding aging process and how age associated diseases, such as neurodegenerative diseases, work.

There is no doubt that Ca2+ signaling is dramatically important for a large number of processes in neurons such as neurotransmitter secretion, gene transcription or long-term potentiation. Recent data suggest that changes in intracellular Ca2+ homeostasis (Ca2+ remodelling) in aging neurons contributes to susceptibility to excitotoxicity and neurodegeneration. Noteworthy, understanding of Ca2+ homeostasis in aging neurons and its molecular basis may provide novel opportunities for brain neuroprotection.

Regarding this strategy, the main goal of this current PhD Thesis is to investigate the remodeling of subcellular Ca2+ homeostasis in long term cultures of rat hippocampal neurons, a model of neuronal aging in vitro.