Winter 2011 Call, List of Available Laboratories for this call*

The available positions are 9 subdivided as follow:

Campus IFOM-IEO

B. Amati: 2 [Marie Curie or National Fellowship] . [position details] . [ web page ]
F. Ciccarelli: 1 [Marie Curie Fellowship] . [position details] . [ web page ]
F. d'Adda: 1 [Marie Curie Fellowship] . [position details] . [ web page ]
M. Foiani: 1 [Marie Curie Fellowship] . [position details] . [ web page ]
S. Minucci: 1 [Marie Curie Fellowship] . [position details] . [ web page ]
P.G. Pelicci: 1 [Marie Curie or National Fellowship] . [position details] . [ web page]
G. Scita: 1 [Marie Curie Fellowship] . [position details] . [ web page]
G. Testa: 1 [Marie Curie or National Fellowship] . [position details] . [ web page]
T. Vaccari: 1 [Marie Curie Fellowship] . [position details] . [ web page]

*Please note that the available positions may be subject to changes during the application period

Campus IFOM-IEO

B. Amati . [ web page ]
2 positions [Both Marie Curie or National fellowships are available for this position]
The c-myc proto-oncogene is frequently over-expressed and is a general driving force in cancer. The c-myc encoded protein (Myc) is a transcription factor that binds thousands of genomic loci in either normal or transformed cells. However, the identity of the Myc-target genes that influence tumor development, as well as the mechanisms through which Myc deregulates these genes, remain elusive questions in the field. The postdocs joining the lab will integrate an integrated effort in our group aimed at addressing these questions. Our strategy consists in the application of next-generation DNA sequencing technology to create a multi-layered set of genome-wide profiles that will globally address Myc function. We will analyze both cultured mouse cells and developing tumors in vivo in a transgenic model of Myc-induced lymphoma. The profiles to be determined include: (i.) quantitative mapping of the RNA transcriptome (coding, non-coding and small RNAs); (ii.) protein-DNA interaction maps, generated by chromatin immunoprecipitation (ChIP-seq); (iii.) epigenome (histone modifications and DNA methylation) also by ChIP-seq; (iv.) long-range DNA interactions (looping) and 3D-folding of the genome. Finally, we will ask which genes are the targets of mutations and/or epigenetic silencing in Myc-induced lymphoma, and will use high-throughput functional genomics to determine which of the above genes (whether deregulated by Myc or mutated in tumors) are critical to suppress or promote lymphomagenesis. Altogether, our data will provide an unprecedented level of insight into Myc function and into the early stages of tumor progression.

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F. Ciccarelli . [ web page ]
1 position [Marie Curie mobility fellowship is available for this position]
A post-doctoral position is available in the group of evolutionary genomics of cancer to work on detection of cancer-associated mutations. The project will concern the re-sequencing of the whole exome in several cancer patients using next generation sequencing technologies. Independence in computer programming is required, proficiency in statistics is advantageous.
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M. Foiani . [ web page ]
1 position [Only Marie Curie mobility fellowship is available for this position]
See Foiani's web page for a general introduction to his research projects.
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F. d'Adda . [ web page ]
1 position [Only Marie Curie mobility fellowship is available for this position]
A Postdoctoral position is available to study a novel class of non-coding RNA species regulating the DNA damage response in mammals. The candidate will have a strong background in non-coding RNA biogenesis and processing and will be able to quickly capitalize on our novel results on this subject and to complement our skills.
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S. Minucci . [ web page ]
1 position [Only Marie Curie mobility fellowship is available for this position]
A post-doctoral position is available to study chromatin alterations in cancer. Emphasis is on: 1) epigenomic profiling of cancer stem cells; 2) unraveling the role of chromatin modifying complexes in leukemogenesis; 3) studying the link between chromatin, DNA damage response and autophagy; 4) development of novel technological approaches to the epigenome. Previous experience in: a) chromatin high-throughput profiling, b) autophagy,
or c) animal models of cancer are of particular interest.
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P. G. Pelicci . [ web page ]
1 position [Both Marie Curie or National fellowships are available for this position]
See Pelicci's web page for a general introduction to his research projects.
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G. Scita . [ web page ]
1 position [Only Marie Curie mobility fellowship is available for this position]
Project details:Molecular characterization of the network of proteins linking actin and membrane dynamics.
One still elusive aspect of the regulation of migratory and invasive protrusion is the mechanism that enables the force generating system of the actin polymerization machinery to be connected to the plasma membrane during the extension of polarized migratory protrusions. Within this context, we have characterized in vitro and in vivo the role of Eps8 as actin capping and bundling protein. One major interactor of Eps8 is the I-BAR-containing, membrane deforming protein IRSp53 (Disanza et al., 2006; Hertzog et al.; Menna et al., 2009), which represent an important effector linking Cdc42-pathways to membrane shape and dynamics with actin regulatory proteins, including, in addition to Eps8, also VASP family proteins. The mechanisms of action and functional role of Eps8 and IRSp53-based complexes remains largely to be established. To address these issues we plan to: 1) use in vitro reconstitution experiments of IRSp53-based complexes in conjunction with liposome and actin polymerization based assays; 2) characterize the phenotype of IRSp53 null mice and exploit cells derived from null mice to address the role of this protein in cell protrusions; 3) the knowledge of the mechanisms of regulation of this network will be further utilized to explore the mechanisms whereby elevated expression of Eps8 confers migratory and invasive advantages to a subset of tumor cells of oral squamous cell carcinoma, colon and pancreatic carcinoma.
The candidates will be embedded in a group that addresses relevant biological questions using a plethora of approaches such as histology, omics, and mouse model as well as cell-free, in vitro assays with purified protein, biological assays of cell migration in 2 and 3 dimension. Candidates should hold a Ph.D. in biological sciences, chemistry or similar background. Candidates with experience in molecular and cell biology, protein or lipid biochemistry, or with animal models (for the phenotypic characterization of IRSp53 null mice) and imaging based-screening are preferred.
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G. Testa . [ web page ]
1 position [Both Marie Curie or National fellowships are available for this position]
Project details:Epigenetic circuits in neurogenesis and gliomagenesis: functional in vivo dissection and bioinformatics analysis.
We use mice and mouse embryonic stem cells as model systems to study the physiology of neural differentiation and its aberrations during gliomagenesis. We are seeking a highly motivated postdoctoral candidate, with solid expertise in one or both of two following areas:
1) the bioinformatic analysis of global expression and chromatin profiles, in order to define the genomic programs controlled by key epigenetic regulators in physiologically meaningful stages of neurogenesis and gliomagenesis.
2) neurobiology or tumor biology, in order characterize the function of histone methyltransferases and demethylases using innovative mouse models that were recently established in the lab.
Depending on the specific background, the candidate must hold an MD or PhD in Molecular Biology, Genetics, Engineering, Informatics or Biochemistry.
We are looking for a creative scientist who wishes to join an interactive team at the cutting egde of research in histone methylation and mouse genetics.
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T. Vaccari . [ web page ]
1 position [Only Marie Curie mobility fellowship is available for this position]
Project details:Post-doc position available working on endocytic control of tumor suppression.
The lab focus on the signaling pathways that are controlled by endocytosis with particular attention on Notch signaling. In particular, we are now interested in elucidating the endocytic mechanisms that prevent ectopic signaling in Drosophila tumor models and in mammalian cells. We are looking for motivated scientists with independent critical thinking and a strong background in genetics, molecular and cellular biology.
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