Stem cells and Cancer Laboratory

In 2001, Héctor G. Palmer obtained his PhD in Biochemistry and Molecular Biology from the Universidad Autónoma de Madrid.
While working at the Instituto de Investigaciones Biomedicas in Madrid as a Postdoctoral Fellow, he described the role of Wnt pathway, Vitamin D Receptor (VDR) and Snail transcription factors controlling human colon cancer progression.
In 2003, he was awarded a Marie Curie Intra European Fellowship,  and in 2004 he joined the Cancer Research UK (UK) as Postdoctoral Fellow under the leadership of Prof. Fiona M. Watt, where he described VDR as a novel transcriptional effector of the Wnt pathway that controls the fate of stem cells in adult epidermis. He also discovered that the central role of the Wnt signalling in tumor initiation depends on VDR function, opening a new opportunity for the use of Vitamin D based drugs to prevent cancer development.
In 2008 Héctor returned as an independent researcher and became group leader of the Stem Cells and Cancer Laboratory at VHIO. He has continued his work on the role of Wnt/beta-catenin pathway driving normal and cancer stem cell fate in epithelial tissues and its significance in tumor initiation, progression and self-renewal.

hgpalmer@vhio.net

 

PRINCIPAL INVESTIGATOR

RESEARCH LINES

The main interest of our laboratory is in understanding the molecular mechanisms that control the initiation and progression of epithelial tumors. In particular, we focus on studying how rare populations of cancer stem cells retain the ability to perpetuate tumors and how they become the drug-resistant, and studying the long-term source of their self-renewal. Colorectal cancer is a disease of high social impact and our primary focus of work. Furthermore, it is initiated from a paradigmatic tissue to study adult stem cells biology. At the molecular level, we are analyzing the role of the Wnt/beta-catenin pathway controlling the fate of normal and cancer stem cells. We are specifically interested in novel mechanism of gene transcription regulation dependent on Wnt signalling and its relevance in driving stem cell decisions: self-renewal versus differentiation. Our technical approaches include cellular and molecular biology, as well as mouse models and most importantly the analysis of live human tissue directly provided from patients with colorectal tumors. This last line of work is extremely exciting because it permits us to work directly with human cancer stem cells, which is a privileged opportunity in the field of cancer research.

SCIENTIFIC ACTIVITY

• Characterization of new molecular features of the Wnt/beta-catenin signalling pathway and their relevance in normal and cancer stem cells physiology.
• Study of the contribution of cancer stem cells to the initiation, progression and self-renewal of epithelial tumors.
• Testing the specific sensitivity of human colon cancer stem cells to anti-tumoral agents.
• Understanding the mechanisms that govern somatic stem cell physiology in tissue homeostasis and regeneration.

Stem cells (SC) have the unique capacity to self-renew and the potential to differentiate into the multiple cell lineages that are present in adult tissues, sustaining their permanent renewal and their ability to regenerate upon injury. Interestingly, many molecules and signalling pathways that control SC fate are abnormal in the initiation of cancer in the same tissues. The Wnt/beta-catenin pathway is one of these driving forces that direct stem cell fate, controlling self-renewal and selecting cell lineages throughout development and tissue homeostasis. Abnormal activation of Wnt/beta-catenin signalling leads to tumor formation, affecting the balance of SC self-renewal versus differentiation.

We study novel molecular mechanisms of the Wnt pathway that control the physiology of normal and cancer SC in epidermis and intestinal epithelium. We are developing new mouse models and analyzing isolated SC from human tumors to study the role of novel Wnt signalling mechanisms in cancer initiation and self-renewal.

PUBLICATIONS

Pendás-Franco N, García JM, Peña C, Valle N, Palmer HG, Heinäniemi M, Carlberg C, Jiménez B, Bonilla F, Muñoz A, González-Sancho JM. DICKKOPF-4 is induced by TCF/beta-catenin and upregulated in human colon cancer, promotes tumour cell invasion and angiogenesis and is repressed by 1alpha,25-dihydroxyvitamin D(3). Oncogene. 2008 Jul 24;27(32):4467-77. Epub 2008 Apr 14.
(IF: 6.440, 1 cuartil, oncology)

Palmer HG, Martínez D, Carmeliet G, Watt FM. The vitamin D receptor is required for mouse hair cycle progression but not for maintenance of the epidermal stem cell compartment.
J Invest Dermatol. 2008 Aug;128(8):2113-7.
(IF: 4.829, 1 cuartil, dermatology)

Palmer HG, Anjos-Afonso F, Carmeliet G, Takeda H, Watt FM. The vitamin D receptor is a Wnt effector that controls hair follicle differentiation and specifies tumor type in adult epidermis. PLoS ONE. 2008 Jan 23;3(1):e1483.

Ordóñez-Morán P, Larriba MJ, Palmer HG, Valero RA, Barbáchano A, Duñach M, de Herreros AG, Villalobos C, Berciano MT, Lafarga M, Muñoz A. RhoA-ROCK and p38MAPK-MSK1 mediate vitamin D effects on gene expression, phenotype, and Wnt pathway in colon cancer cells. J Cell Biol. 2008 Nov 17;183(4):697-710.
(IF: 9.598, 1 cuartil, cell biology)

Martin Hübner A, Tenbaum SP. Complete remission of palmoplantar psoriasis through Helicobacter pylori eradication: a case report. Clin Exp Dermatol. 2008 May;33(3):339-40.
(IF: 1.295, 2 cuartil, dermatology science)

 

RESEARCH PROJECTS

Funding Agency: ISCIII (FIS)
Title: “Células Madre Tumorales de Colon y la Ruta de Wnt/Beta-Catenina”
PI: Dr. H. Palmer
Duration: 2009/2011    

Funding Agency:  Fundació Olga Torres
Title: "Células Madre de Cáncer de Colon"
PI: Dr. H. Palmer
Duration: 2009-2011

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