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«The new reality of the Mediterranean: accelerating impacts of climate change”

Speaker: Samira Khodayar Pardo
Institution: Head of the Meteorology and Climatology Department of the Mediterranean Center for Environmental Studies (CEAM), Valencia, Spain, and Distinguished Researcher of Excellence (CIDEGENT-GVA)
Place: CIPF conference room

The Mediterranean basin is a hot spot for climate change warming up to 1.5 times faster than the rest of the world with the Mediterranean Sea warming three times more than the oceans (MedECC 2020). A consensus exists about the magnification of extreme phenomena in the area under climate change (IPCC 2021). In fact, several types of risks currently affect and will continue affecting the region severely, from more frequent extreme weather events such as heat waves, droughts, or floods, to increasing sea surface temperature and coastal erosion due to rising sea levels. The impacts affect the region’s ecosystems, economic activities, and, ultimately, human health. In addition, the effects also spread like “cascades” that generate multiple impacts in all socioeconomic sectors. Current change and future scenarios consistently point to significant and increasing risks during the coming decades in most impact domains such as water and energy resources, ecosystems, agriculture and food, fishery, health, and human security.

The impacts of climate change have accelerated on the Mediterranean coast of the Iberian Peninsula in the last decades. In this presentation, we will discuss this acceleration based on observations of the notorious and progressive rise in atmospheric and sea surface temperature and the generalized reduction of mean accumulated precipitation in the region. In this context, the magnification of extreme weather phenomena in the region will be described in detail focusing on the spatio-temporal evolution of terrestrial and marine heat waves, as well as extreme precipitation in the autumn period.

Thesis Title: Funciones del factor de inicio de la traducción eucariota 5A2 en el cáncer de pulmón

Author: Arantxa Martínez Férriz

PhD. Supervisors: Rosa Farràs Rivera, Dr. Ramón Serrano Salom

Summary:

El factor de iniciación eucariota 5A (eIF-5A), un factor de traducción esencial, es activado postraduccionalmente por la poliamina espermidina. Dos genes humanos codifican eIF-5A, eIF5- A1 cuya expresión es constitutiva, y eIF5-A2 que se encuentra frecuentemente sobreexpresado en tumores humanos. incluyendo el cáncer de pulmón no microcítico (CPNM). Recientemente se ha correlacionado la sobreexpresión de eIF5A2 con la transición epitelio-mesenquimal (EMT) y la metástasis. eIF-5A2 se considera una diana terapéutica muy atractiva en el cáncer dado que su expresión se asocia con cáncer, y los ratones knock-out para eIF-5A2 son viables y tienen un desarrollo normal. Sin embargo, la regulación de eIF-5A2, su activación y su papel funcional como factor de traducción en células cancerosas aún no se conoce bien. El presente trabajo de tesis doctoral tiene como objetivo caracterizar el papel patológico de eIF5A2 en el desarrollo del CPNM. Para ello, hemos estudiado el papel de eIF5A2 en la proliferación, motilidad e invasión celular. Así mismo, se ha estudiado el efecto de su inhibición farmacológica en líneas celulares de CPNM. Los resultados obtenidos sugieren la existencia de una regulación entre las isoformas eIF5A1 y eIF5A2 para compensar la expresión de ambos homólogos. Además, nuestros datos apuntan a una coordinación temporal y posicional entre las vías TGFβ1 y eIF5A2 para impulsar la traducción de proteínas necesarias para la organización del citoesqueleto y la adquisición de características de motilidad propias de células invasivas. Por tanto, eIF5A2 podría ser empleado como un biomarcador de mal pronóstico en CPNM y su inhibición farmacológica podría emplearse como una posible herramienta terapéutica en aquellos casos en los que eIF5A2 se encuentre sobreexpresado.

12:00 – 12:30 Paula Doria

12:30 – 13:00 Javier González Fernández

Speaker: Amanda Sferruzzi-Perri
Institution: Physiology, Development and Neuroscience Department, Centre for Trophoblast Research, University of Cambridge. United Kingdom.
Place: CIPF conference room

Abstract:

Speaker: Prof. Jochen Prehn
Institution: Centre for Systems Medicine Dublin, Ireland
Place: Salón de Actos Jerónimo Forteza CIPF

TITLE: Bugs, Fungi and Cells in Cells – the weird side of colorectal cancer and tumour progression

Abstract: My talk will focus on two new aspects of cancer biology and tumour progression in the setting of colorectal cancer: the role of the microbiome and the role of cell dynamics and formation of cell-in-cell structures.

Entosis is a form of non-phagocytic cell-in-cell (CIC) interaction where a living cell enters into another. Tumours show evidence of entosis, however factors controlling entosis remain to be elucidated.  I will present data showing that death receptor activation is a potent induces of entosis in colon cancer cells.  Induction of entosis and apoptosis by an activation of death receptors by ligands such as TRAIL occurred simultaneously and required the presence of caspase-8. Analysis of colorectal cancer tumours showed a significant association between expression levels of TRAIL and CICs. Notably, the presence of CICs in the invasive front regions of colorectal tumors was significantly correlated with adverse patient prognosis.

Dysbiosis of the microbiome has also been implicated in colorectal cancer (CRC) development, progression and response to therapy. Fusobacterium nucleatum (Fn), a commensal Gram-negative anaerobe from the Fusobacteriales order, is an onco-bacterium in CRC as a causal relationship between Fn prevalence and CRC pathogenesis, progression and treatment response has been reported in vivo. We showed that Fn/Fusobacteriales prevalence is associated with immune involvement (decrease in macrophages M1 and increase in macrophages M2) and activation of specific signalling programs (inflammation, DNA damage, WNT, metastasis, proliferation, cell cycle) in the host tumours, and is prognostic in particular in mesenchymal CRC tumors. We also systematically investigated alterations in the bacteriome and mycobiome of CRC patients in tumours and matched adjacent mucosa resulting in the identification of microbiome-based subtypes associated with host clinico-pathological and molecular characteristics. Tumours and adjacent mucosa samples were classified into 4 microbial subtypes, termed C1 to C4, based on the bacteriome and mycobiome composition. Microbial subtypes were associated with distinct tumour and patient phenotypes including T stage, tumour location, history of colon polyps and other malignancies, age, lymphovascular invasion and p53 status and disease-free survival.

12:00 – 12:30 Gergana Mincheva

12:30 – 13:00 Irene Soler

12:00 – 12:30 Milagros Buffa

12:30 – 13:00 María Ibáñez