POSITIONS AVAILABLE / VACANTES

We have positions available for a Master/PhD student and a Postdoctoral fellow.

Send CV and a presentation letter to: agandarillaslab@gmail.com

PROYECTO INTERNACIONAL EN BUSCA DE ESTUDIANTES DE MÁSTER  DOCTORADO Y POSTDOCTORALES COMPETITIVOS Y MOTIVADOS PARA LA INVESTIGACIÓN

Enviar CV y carta de motivación a: agandarillaslab@gmail.com


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CURSO 'NUEVAS TECNOLOGIAS EN LA SALUD DE LA PIEL' -SPANISH-

El curso de verano que organizamos junto con el Profesor de la UC José Luis Arce Diego en Septiembre fue un éxito a decir de alumnos y por la calidad y diversidad de las ponencias de los profesores. También tuvo acogida en los medios de comunicación.
El énfasis del Curso estuvo en la importancia de la prevención y la concienciación antes que nada. Además se impartieron contenidos multidisciplinarios con el objetivo común de la Piel.

Aquí colgamos artículos en la prensa, fotos y el vínculo a un vídeo de TVE.
Esperamos repetir el año que viene.

Gracias a la Universidad de Cantabria-UC, a los patrocinadores:
ABBVIE FARMACÉUTICA SLU, INDUSTRIAL FARMACÉUTICA CANTABRIA (IFC)
CARL ZEISS MICROSCOPY/GRUPO TAPER, CLÍNICA SANZ, 
BETSON DICKINSON BIOCIENCIAS, FISHER SCIENTIFIC,
INNOVA INFORMÁTICA, ASOCIACIÓN ESPAÑOLA CONTRA EL CANCER (AECC)
HOSPITAL MARQUÉS DE VALDECILLA (HUMV)
AYUNTAMIENTO DE SANTANDER

Gracias al Rector de la Universidad y a la presidenta de la Asociación Contra el Cáncer (AEC) de Cantabria, por asistir a la Inauguración, y al Director Técnico de Desarrollo y Calidad del Sistema Cántabro de Salud, que participó en el acto de clausura.

Y sobre todo gracias a los alumnos del curso por su asistencia y su interés.
min.8:28: http://www.rtve.es/alacarta/videos/telecantabria/telecantabria-11-09-13/2016850/




Inauguración por el Rector, Presidenta de AEC y Directores del Curso



Directores del Curso con representantes de la Industria

La Dra Ana Freije explica la biología molecular del cáncer epitelial de piel



Tomando notas

Ponencia del Dr JR Sanz

Los Alumnos



Clausura por el Director Técnico del SCS y los Directores del Curso



NEW WORK IN JOURNAL OF DERMATOLOGICAL SCIENCE

We collaborate with Agusti Toll and Ramón Pujol of the Hospital del Mar/IMIM to investigate the mechanisms leading to agressiveness of skin carcinomas.

J Dermatol Sci. 2013 Jul 15. pii: S0923-1811(13)00245-4. doi: 10.1016/j.jdermsci.2013.07.001. [Epub ahead of print]

Epithelial to mesenchymal transition markers are associated with an increased metastatic risk in primary cutaneous squamous cell carcinomas but are attenuated in lymph node metastases.

Toll A, Masferrer E, Hernández-Ruiz ME, Ferrandiz-Pulido C, Yébenes M, Jaka A, Tuneu A, Jucglà A, Gimeno J, Baró T, Casado B, Gandarillas A, Costa I, Mojal S, Peña R, de Herreros AG, García-Patos V, Pujol RM, Hernández-Muñoz I.

Servei de Dermatologia, Hospital del Mar, Parc de Salut Mar, Barcelona, Spain; Cancer Research Program, IMIM (Institut Hospital del Mar d'Investigacions Mèdiques), Barcelona, Spain.
Abstract
BACKGROUND: Cutaneous squamous cell carcinoma (cSCC) is the second most common malignancy in humans and approximately 5% metastasize, usually to regional lymph nodes. Epithelial to mesenchymal transition (EMT) is a process involving loss of intercellular adhesion, acquisition of a mesenchymal phenotype and enhanced migratory potential; epithelial markers, such as E-cadherin, are down-regulated and mesenchymal proteins (Vimentin), increased.
OBJECTIVE: To investigate the expression of EMT markers in metastatic SCC (MSCC) and their corresponding metastases, and to correlate them with clinico-pathological factors associated with an increased risk of metastasis.
METHODS: We performed a retrospective study that included 146 cSCC samples (51 primary non-metastatic, 56 primary metastatic, 39 lymphatic metastases). Immunohistochemistry for E-cadherin, Vimentin, Snail, beta-catenin, Twist, Zeb1 and Podoplanin was performed.
RESULTS: Loss of membranous E-cadherin was observed in 77% cSCCs, with no differences between MSCC and non-MSCC. Among the transcriptional factors controlling EMT, no significant Snail1 expression was detected. Twist, Zeb1, Vimentin, beta-catenin and Podoplanin were significantly overexpressed in MSCCs. Twist ectopic expression in SCC13 cells induced Zeb1, Vimentin and Podoplanin expression and E-cadherin delocalization. These changes resulted in a scattered migration pattern in vitro. Expression of EMT markers was decreased in the metastases when compared with the corresponding primary tumors.
CONCLUSION: These results suggest that a partial EMT, characterized by the expression of Twist but without a total E-cadherin depletion, is involved in the acquisition of invasive traits by cSCC, but the process is downregulated in lymph node metastases.

KEYWORDS: Cutaneous squamous cell carcinoma, E-cadherin, Epithelial to mesenchymal transition, Metastasis, Twist, Vimentin
Copyright © 2013 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.

WE ORGANISE A MULTIDISCIPLINARY UNIVERSITY SUMMER COURSE ON THE SKIN -SPANISH-

NUEVAS TECNOLOGÍAS EN SALUD DE LA PIEL

11-13 SEPTIEMBRE, 2013
http://cursosdeverano.unican.es/Cursos/Paginas/Detalle-curso.aspx?p_id=2097

　
La piel es un problema creciente en salud pública debido a su carácter multifactorial, a su exposición al medio ambiente, y a las tendencias estéticas imperantes. El cáncer de piel es el más frecuente y ha aumentado en un 20% en las últimas décadas, especialmente en mujeres jóvenes. Sin embargo el cáncer es solo una de las muchas patologías que impactan en la calidad de vida a través de la piel, y que comprenden alteraciones inflamatorias como la psoriasis, hiperplásicas como las queratosis y las dermatitis, o degenerativas como el envejecimiento y la alopecia. Los tratamientos de estos problemas en dermatología están viviendo una evolución tecnológica importante gracias a avances en ingeniería, física y biología celular y molecular.
El curso trata la salud de la piel desde este ángulo multidisciplinar, aprovechando la diversidad de conocimiento de la UC y el Hospital de Valdecilla, y abordando temas de mucha actualidad. Se estructura de esta manera: I- Introducción a las patologías de la piel, técnicas actuales de tratamiento y diagnóstico. II- Nuevas estrategias terapéuticas emergentes desde la bioingeniería, óptica biomédica, nanotecnología, células madre y terapia génica. III- Presente y futuro del sector de la industria farmacológica, dermatológica y estética. IV- Cooperación y prevención para la salud de la piel.
El curso está dirigido a estudiantes y profesionales del ámbito público y privado de las especialidades tratadas, con el objetivo de aumentar su conocimiento y capacitación profesional en esta temática de creciente demanda social y laboral.

 

CTCFL/BORIS AND MITOSIS

Epigenetic factor CTCFL/BORIS localises to nucleoli and centrosomes of human primary epidermal keratinocytes.

BORIS accumulates in keratinocytes upon mitosis failure. It might therefore be involved in genomic instability by participating in the coordination between S phase (DNA replication, centrosome duplication) and Mitosis (DNA replication and RNA transcription arrest and chromosome condensation).

Human epidermal keratinocytes treated with an AURORA B KINASE inhibitor that blocks mitosis.
Green is centrosome marker gamma-tubulin, red is BORIS, blue is Dapi for the chromosomal DNA.
Note the abnormal metaphase figures or nuclei caused by AURB inhibition.

See also Rosa-Garrido et al, PLoS ONE 2012, 7(6): e39371. doi:10.1371/journal.pone.0039371.

INHIBITING THE KERATINOCYTE CELL CYCLE KINASES

• 48h inhibiting mitotic kinases in human skin keratinocytes irreversibly induces terminal differentiation and suppresses clonogenic potential. However,
• 48h inhibiting cell cycle entry kinase cdk2 delays differentiation and confers a higher clonogenic potential.

Further suggesting that epidermal keratinocytes need cell growth to fully differentiate.




 
Colonies of human primary keratinocytes after the treatments indicated.

Double immunofluorescence for Cyclin E (red) and the differentiation

marker involucrin (green), DNA was stained in blue by DAPI  (Upper Panels).

Note that inhibition of mitotic kinases (cdk1, Pololk) renders small, differentiated colonies,

whose cells irreversibly lose their capacity to proliferate.

Bar:100 µm. Freije et al, Oncogene, 2012, Supplementary Data.

   

EPIDERMAL STARS

We investigate the cell cycle and differentiation of skin epidermal cells. Both need to be coordinated as an orchestra to avoid neoplasic development.
In vitro, we study the links governing epidermal homeostasis that protect the skin from cancer.

Primary keratinocytes behave closely resembling the physiology of the skin.
In situ, we study skin cancer.

Our research walks on the edge between molecular developmental cues and human disease.

Primary human keratinocytes expresing a GFP form of a cell cycle regulator (GREEN) and a differentiation keratin (RED).
Skin from the Peadriatic Surgery Department of Valdecilla hospital in Santander.
Cell culture and staining by Laura Ceballos.

  

A SKIN COVER FOR 'CELL CYCLE'

A molecular switch triggers squamous differentiation and endoreplication upon cell cycle hyperactivation.






Gandarillas, Dic. 2012 -COVER- http://www.landesbioscience.com/journals/cc/



WE COVER THE CELL CYCLE

Cell Cycle journal has selected one of our images for the current December 2012 issue cover.
http://www.landesbioscience.com/journals/cc/



Deregulation of the keratinocyte cell cycle induces epidermal differentiation. Human
epidermal keratinocytes overexpressing fluorescent cyclin E (green) and the differentiation marker involucrin (red).
For more information, Gandarillas., pp. 4507–16.
See also Freije et al, 2012, http://www.nature.com/onc/journal/v31/n50/abs/onc201222a.html

 

PROYECTO EUROPEO EN ALERTA (Spanish)-

THE NEW SKIN EPIDERMAL CELL CYCLE IN CELL CYCLE -open access


Cell Cycle. 2012 Oct 31;11(24). [Epub ahead of print]
http://www.landesbioscience.com/journals/cc/article/22529/

Source http://www.ncbi.nlm.nih.gov/pubmed/23114621

The mysterious human epidermal cell cycle, or an oncogene-induced differentiation checkpoint.

Gandarillas A.

Cell Cycle, Stem Cell Fate and Cancer Laboratory; Fundación Marqués de Valdecilla-Instituto de Formación e Investigación Marqués de Valdecilla (IFIMAV); Santander, Spain; Institut National de la Santé et de la Recherche Médicale (INSERM); ADR Languedoc-Roussillon; Montpellier, France.

Abstract

  


Gandarillas, 2012, Cell Cycle

Fifteen years ago, we reported that proto-oncogene MYC promoted differentiation of human epidermal stem cells, a finding that was surprising to the MYC and the skin research communities. MYC was one of the first human oncogenes identified, and it had been strongly associated with proliferation. However, it was later shown that MYC could induce apoptosis under low survival conditions. Currently, the notion that MYC promotes epidermal differentiation is widely accepted, but the cell cycle mechanisms that elicit this function remain unresolved. We have recently reported that keratinocytes respond to cell cycle deregulation and DNA damage by triggering terminal differentiation. This mechanism might constitute a homeostatic protection face to cell cycle insults. Here, I discuss recent and not-so-recent evidence suggesting the existence of a largely unexplored oncogene-induced differentiation response (OID) analogous to oncogene-induced apoptosis (OIA) or senescence (OIS). In addition, I propose a model for the role of the cell cycle in skin homeostasis maintenance and for the dual role of MYC in differentiation.

PMID:

23114621

[PubMed - as supplied by publisher]

NEW WORK FOR PUBLICATION IN CELL CYCLE

Within this View,



The Epidermis maintains tissue structure upon hyperproliferative stimuli



- We propose a model for the coordination between cell multiplication and differentiation in human epidermis that constitutes a novel skin homeostatic mechanism against cell cycle deregulation.

- We propose a model for the dual action of the protooncogene MYC in differentiation.



Soon available online at Cell Cycle

http://www.landesbioscience.com/journals/cc/

and PubMed

http://www.ncbi.nlm.nih.gov/pubmed

 








EUROPE

On October the second, we submitted a scientific proposal to the 7FP of the European Union-HEALTH as coordinators (first stage).

·      This is the first European proposal coordinated by the FMV-IFIMAV.

·      The project links scientific centres, hospitals and Small or Medium Enterprise (SME) from 8 European countries.

·      The main objective is the translation of scientific and technological research into SME and Society.

 

http://europa.eu/index_en.htm



THE EPIGENETIC FACTOR BORIS LOCALISES TO THE NUCLEOLUS IN LIVE CELLS

Live cells expressing GREEN-fluorescent BORIS and RED-fluorescent fibrillarin,
a marker of nucleoli. From Rosa-Garrido et al, PLoS ONE, 2012.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0039371
Video formatting, María Hidalgo.

THE ROMAN PAVEMENT



In vitro cultured keratinocytes from human skin. Skin biopsy from the Marqués de Valdecilla Hospital.