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The RAS superfamily and related pathways in health and disease

Life and Matter Sciences International Symposium Thursday and Friday, May, 16th and 17th, 2019 Santander

General information

Venue: Palacio de La Magdalena. Avenida de la Magdalena s/n. 39005. Santander. Cantabria.

Simultaneous interpretation will be available. Free registration


Organized by:

Fundación Ramón Areces

In cooperation with:

Genetracer Biotech, Santander Ciudad, The Company of Biologist, Universidad de Cantabria, Merck, Air Liquide, Biogen, Ciberonc, CSIC, Fisher Scientific, Palex, Proquinorte, Sarstedt y VWR.


Luis Miguel Lozano Instituto de Biomedicina y Biotecnología de Cantabria. Universidad de Cantabria. CSIC. SODERCAN.



Piero Crespo Instituto de Biomedicina y Biotecnología de Cantabria (IBBTEC) CSIC-University of Cantabria.  

Mariano Barbacid Consejo Científico Fundación Ramón Areces. Centro Nacional de Investigaciones Científicas (CNIO).

Xosé R. Bustelo Centro de Investigación del Cáncer, CSIC-University of Salamanca. 

Eugenio Santos Centro de Investigación del Cáncer, CSIC-University of Salamanca. 

Silvestre Vicent Centro de Investigación Médica Aplicada (CIMA). University of Navarra. 

  • Description
  • Programme

RAS subfamily constitute the gene family most frequently mutated in human cancer: 22%, 8.2% and 3.7% for KRAS, NRAS and HRAS respectively. To these figures must be added those cases in which mutational activation is detected in downstream effectors. Overall, the proportion of human neoplasias harboring oncogenic mutations in RASinduced pathway constituents exceeds 50%. This fraction, significant as is, somewhat undervalues those referring to specific tumors: 99% of pancreatic carcinomas show KRAS mutational activation; 80% of melanomas harbor mutations in RAS-related pathways; while in thyroid cancer this figure reaches 75% of the cases. In addition, a wealth of gain- and loss-of-function genetic approaches using animal and cellular models mechanistically links RAS-induced pathways to cancer initiation, promotion and progression. It is therefore hardly surprising that these biochemical pathways rank among the most scrutinized in search of targets for oncological therapeutic intervention.

The members of the RAS superfamily behave as ''molecular switches'' that fluctuate between inactive and active states, two conformations that depend on the binding of either GDP or GTP, respectively. Based on structural and functional criteria, this superfamily can be subdivided in several groups, including the RAS, RAP and RHO/RAC families. In the active, GTP-bound state, these GTPases bind to a large collection of effector molecules that, in turn, lead to the stimulation of signaling cascades that promote general cellular responses such as cytoskeletal changes, cell cycle progression and cell proliferation and survival, among many others.

The plasticity of RAS superfamily members in terms of subcellular localization, regulation, binding to effectors, and crosstalk with other cellular pathways has put them in a central regulatory point for a quite large number of cellular processes. Unfortunately, the toll that we have to pay for such important functions in vivo is the development of diseases when these routes become dysfunctional. Indeed, activating mutations of RAS or of components of its effector pathways are common in human cancers, with special incidence in some of the most aggressive tumors for which there are no efficacious treatments. Tumor types frequently harboring RAS oncogenes include pancreatic ductal adenocarcinoma (PDAC) one of the deadliest human cancer; non-small cell lung carcinoma, a tumor type for which the five year survival is less than 10%; and metastatic melanoma, with a survival rate of about 5%, among others.

Not surprisingly, for more than two decades, this has led to a colossal, comprehensive and multidimensional scrutiny of RAS-mediated signaling pathways. In order to understand how these signals impinge on the different biological processes involved in carcinogenesis, with the aim of finding molecular targets for the potential development of therapeutic agents whereby aberrant RAS signals, and, subsequently, tumor progression, could be inhibited.

With the perspective provided by more than thirty years of progress in the field, we are now in an excellent position to review the state-of-the-art of some of these developments, the challenges that have arisen during preclinical and clinical stages and how novel venues of research on the RAS field make conceivable new strategies towards the development of antitumor agents, alternative or complementary, to those currently in use and, for the first time in the history of biomedicine, the design of new therapies based on the specific blockage of molecular targets of RAS superfamilydependent routes. Some of these new therapeutic approaches have been already moved from the bench to the bedside.

In this context, this meeting aims at providing a format for the exchange of ideas and information, to discuss the latest research findings and methodological advances in the RAS-mediated signaling pathways, and to foster interactions amongst groups that investigate these signal transduction pathways at the structural, biochemical, signaling, physiological and/or pathological level. Special topics of attention will be those related to the systems biology of these routes, the analysis of their mechanism of regulation and action, the information derived from animal models, their role in human carcinogenesis, and the new therapeutic avenues that are being developed to manipulate their function.

From other perspective, this meeting will constitute a continuation of the Fundación Ramón Areces-sponsored meeting "Antitumoral targets upstream and downstream of RAS GTPases" held in the same venue in 2012 and remembered in the field as a highly successful gathering.

There will be no poster sessions, but a few slots for short talks will be available to present outstanding data. If you wish to be considered for one of these, please send a 200-250 abstract to: crespop@unican.es

Thursday, 16th

8:30 h.


9:00 h.

Opening ceremony

Mariano Barbacid 
Scientific Council Fundación Ramón Areces. Centro Nacional de Investigaciones Oncológicas (CNIO). Madrid, España

9:20 h.

Inaugural lecture

Targeting KRAS directly

Frank McCormick 
Helen Diller Family Comprehensive Cancer Center, University of California. San Francisco, EEUU.

Session 1: A system biology view of RAS signaling



10:20 h.

 Chair: Channing Der


Computational analysis of RAS signalling networks

Walter Kolch
Systems Biology Ireland; University College Dublin. Irlanda.

11:00 h.

Novel synthetic vulnerabilities in the RAS pathway in lung cancer

Alejandro Sweet-Cordero
Helen Diller Family Comprehensive Cancer Center. University of California San Francisco, EEUU.

11:40 h.


Session 2: New regulatory aspects in RAS signaling



12:10 h.

 Chair: Channing Der


Defective cellular phenotypes associated to Sos1/2 deficiency

Eugenio Santos
Centro de Investigación del Cáncer; Universidad de Salamanca, España.

12:50 h.

Isoform and codon-specific RAS biology

Ian A. Prior
Department of Cellular and Molecular Physiology; University of Liverpool, Reino Unido.

13:30 h.

Phosphorylation regulates oncogenic KRAS activity in colorectal cancer cells

Neus Agell
Departamento de Ciencias Biomédicas; Universidad de Barcelona, España.

14:10 h.


15:30 h.

Sponsor's Talk: Clinical impact and predictive biomarkers in cancer research of RAS/RAF/MAPK pathway

Juan Pablo Fusco
Genetracer Biotech. España.

Session 3: Signaling convergence with other pathways



15:45 h.

 Chair: Manuela Baccarini


Identification of R-RAS2 as a new and potent oncogenic driver

Xosé R. Bustelo
Centro de Investigación del Cáncer; Universidad de Salamanca, España.

16:25 h.

Short talk: PDEdelta inhibitors spring back- new compound design principles for a surrogate K-Ras target

Daniel Abankwa
University of Luxenbourg. Luxemburgo. 

16:40 h.

The role of the Rac activator Tiam1 in small cell lung cancer

Angeliki Malliri
Paterson Institute for Cancer Research; University of Manchester, Reino Unido.

17:20 h.

Short talk: RIT1 oncoproteins escape LZTR1-mediated proteolysis

Pau Castel   
University of California. San Francisco, EE.UU.

17:35 h.

Dysfunctions of RAS and RAS-like Proteins association with Developmental Disorders

Mohammad Reza Ahmadian  
Institute of Biochemistry and Molecular Biology II; Heinrich Heine University Düsseldorf, Alemania.

Friday, 17th

Session 4: RAS dinamics in tumors



09:30 h.

 Chair: Hans Bos


Transcriptional and post-transcriptional mechanisms in KRAS-driven tumorigenesis

Silvestre Vicent
Centro de Investigación Médica Aplicada (CIMA); Universidad de Navarra, España.

10:10 h.

Metabolic dependencies of mutant KRAS lung tumors

Carla Martins
Hutchison/MRC Research Centre; University of Cambridge, Reino Unido.

10:50 h.

Oncogenic RAS-dependent Determinants of Tumor Fitness

Dafna Bar-Sagi
NYU Langone Health; Nueva York, EEUU.

11:30 h.


Session 5: New therapeutical strategies



12:00 h.

 Chair: Dafna Bar-Sagi


The use of KRAS mutant tumor organoids to identify drug combinations for treatment

Johannes L. Bos
Oncode Institute; Center for Molecular Medicine; University Medical Center Utrecht, Países Bajos.

12:40 h.

Short talk: Individual KRAS mutations confer unique signaling profiles and sensitivities to targeted agents in colorectal cancer

Jonathan Chernoff
Fox Chase Cancer Center. Filadelfia. EE.UU.

12:55 h.

Drugging ‘undruggable’ RAS: will MYC do the trick?

Channing Der
School of Medicine; University of North Carolina at Chapel Hill, EEUU.

13:35 h.

Understanding novel features of KRAS biology to discover new therapeutic vulnerabilities

Chiara Ambrogio
Dana Farber Cancer Institute; Harvard University Boston, EEUU.

14:15 h.

Short talk: KRAS-specific inhibition using a DARPin binding to a site in the allosteric lobe

Nicolas Beri
Oxford University. Oxford. UK.

14:30 h.


15:30 h.

Short Talk: Quantitative vs qualitative MAPK signalling in lung adenocarcinoma

David Santamaria
European Institute of Chemistry and Biology (IECB). France.

Session 6: RAS downstream signaling



15:45 h.

 Chair: Angeliki Malliri


c-RAF, the master regulator of KRAS oncogenic signaling

Mariano Barbacid
Scientific Council Fundación Ramón Areces. Centro Nacional de Investigaciones Oncológicas (CNIO). Madrid, España.

16:25 h.

Moonlight jobs & regulatory feedbacks: division of labor in the ERK pathway

Manuela Baccarini
Max F. Perutz laboratories Viena, Austria.

17:05 h.

It takes more than two phosphates to turn-on ERK

Piero Crespo
Instituto de Biomedicina y Biotecnología de Cantabria; Santander, España.

17:45 h.

Short talk: Role of Raf in colorectal carcinogenesis 3D cultures

Coralie Dorard
Max F Perutz laboratories. Viena. Austria.

18:00 h.

Closing lecture: Oncogenic RAS control of the tumour immune microenvironment

Julian Downward 
Francis Crick Institute, Londres, Reino Unido.

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