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PEBC Report - Programa de Epigenética y Biología del Cáncer

PEBC Report - Programa de Epigenética y Biología del Cáncer

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Dr Montse Sanchez-Cespe<strong>de</strong>s<br />

Genes and Cancer Group<br />

Montse Sanchez-Cespe<strong>de</strong>s was born in Badalona<br />

(Barcelona) in 1968. She graduated in Biology and specialized<br />

in Genetics and Molecular Biology from the Universitat<br />

<strong>de</strong> Barcelona and carried out her Ph.D. work at the<br />

Molecular Biology of Cancer Laboratory, the Hospital<br />

”Germans Trias i Pujol” in Badalona. From 1997 to 2001 she<br />

was a Postdoctoral Fellow at the Johns Hopkins University<br />

School of Medicine (Baltimore-USA). She focused on the<br />

i<strong>de</strong>ntification of novel genetic and molecular alterations in<br />

cancer. More specifically she looked for recurrent chromosomal<br />

abnormalities in lung tumours and genetically<br />

analysed candidate tumour suppressor genes in these<br />

regions. From October 2001 to 2004 she lead the lung cancer<br />

biological research at the CNIO and from 2004 to<br />

September 2008 she was the Group Lea<strong>de</strong>r of the Lung<br />

Cancer Group at the same institution.<br />

She is member of international scientific societies and<br />

reviewer for many journals and funding agencies. Her list of<br />

over 60 original publications and reviews in international and<br />

peer-reviewed journals of prestige serves as a testament of<br />

the experience she has already accumulated in the field of<br />

cancer research. Her current research is <strong>de</strong>voted to the<br />

i<strong>de</strong>ntification of genes that are genetically altered in tumors<br />

and to the functional analysis of their implication in cancer<br />

<strong>de</strong>velopment.<br />

The complete genetic characterization of tumours is important<br />

not only to un<strong>de</strong>rstand tumour biology, but also to the<br />

<strong>de</strong>velopment of new drugs and to the selection of patients<br />

that may benefit of a given targeted cancer therapy. The<br />

promise of using proteins enco<strong>de</strong>d by mutant cancer genes<br />

as molecular targets for the <strong>de</strong>velopment of novel therapies<br />

drives en<strong>de</strong>avours to i<strong>de</strong>ntify novel mutated cancer genes as<br />

well as to create catalogues of somatic mutations in cancer.<br />

Our current projects in the laboratory are focused in the following<br />

directions:<br />

i) to i<strong>de</strong>ntify novel genes altered in cancer;<br />

ii) to un<strong>de</strong>rstand their contribution to cancer <strong>de</strong>velopment<br />

and<br />

iii) to investigate correlations with clinical and pathological<br />

characteristics.<br />

Genome-wi<strong>de</strong> screenings allow the i<strong>de</strong>ntification of the<br />

chromosomal regions that are frequently <strong>de</strong>leted in cancer<br />

and that may contain tumor suppressor genes. In lung cancer,<br />

one of the most frequently <strong>de</strong>leted chromosomal arms<br />

Postdoctoral researchers: Eva Pros,<br />

Salvador Rodriguez-Nieto<br />

PhD Stu<strong>de</strong>nts: Ester Bonastre, Sandra Castillo,<br />

Rossana G Restani, Octavio Romero<br />

Technician: Albert Coll<br />

is 19p. During the past years we unveiled that LKB1, the<br />

Peutz-Jeghers syndrome (PJS) gene, was also<br />

mutated/inactivated in lung cancer. This exciting observation<br />

led us to <strong>de</strong>vote intense efforts to fully un<strong>de</strong>rstand how<br />

LKB1 inactivation contributes to carcinogenesis. To date we<br />

have provi<strong>de</strong>d important data on the mutational profile of<br />

LKB1 in lung cancer and on its association with various<br />

molecular and clinic-pathological characteristics. We also<br />

provi<strong>de</strong>d further insights in the relationship between LKB1<br />

alterations in lung cancer and impaired AMPK activity and<br />

mTOR inhibition upon energetic stress. BRG1 is another<br />

gene that allocates on chromosome 19p and enco<strong>de</strong>s and<br />

35

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