Dept. of Experimental Oncology
European Institute of Oncology (IEO)
Via Ripamonti, 435
20141 Milan Italy
Research in our group aims at understanding the
biological and molecular pathways by which Myc regulates
cell proliferation and oncogenesis. In particular, we
are interested in the links between Myc and cell cycle
control, focusing on the function of cyclin-dependent
kinases (CDKs), their regulatory subunits (cyclins)
and their inhibitors (CKIs). We are also exploring the
molecular mechanisms by which Myc regulates gene expression,
with special emphasis on the co-factors that are recruited
by Myc to target promoters in live cells. We are addressing
how Myc and these co-factors modify chromatin, and how
these modifications participate in transcriptional control.
Finally, we are identifying the genes that are directly
bound by Myc in the genome of human cells.
Professor, Department of Molecular Biology
Lewis Thomas Laboratory
Princeton, NJ 08544-1014
We are interested in understanding the basic mechanisms
of oncogenic transformation, in particular the function
of the Myc and E2F transcription factor families which
are misregulated or overexpressed in a large fraction
of human cancers. The oncogenic activity of these transcription
factors depends on protein domains associated with transcriptional
activation, which provides an avenue to study both cancer
biology and the mechanisms of gene regulation. Our recent
experimental approach has been based on the observation
that dominant interfering alleles of the Myc protein
form protein complexes with nuclear factors that are
essential for Myc and E2F function. The novel factors
uncovered in these studies have proven to be components
of highly conserved chromatin modifying complexes that
function in many other gene regulatory pathways. Studies
of these complexes and their role in oncogenic transformation
are a primary focus of my current research. We are also
interested in defining the functional components of
the Myc oncogenic pathway.
Institute for Clinical Molecular Biology und Tumour
D-81377 Munich, Germany
Phone: 089/ 7099-512
Fax: 089/ 7099-500
Expression of the c-myc gene is essential for proliferation
of mammalian cells. A large number of growth factors activates
c-myc expression by different signaling pathways. In lymphoma
development c-myc is often activated by chromosomal translocation
to one of the immunoglobulin gene (Ig) loci. Other tumors
often show amplification or rearrangement of the c-myc
locus. Constitutive expression of c-myc in animal models
induce various forms
of cancer. Aim of our research is to understand the cellular
function of c-myc and its dysfunction and dysregulation
in tumor development.
The c-myc gene encodes a nuclear protein (Myc) with typical
features of a transcription factor. A large number of
"Myc-regulated" or "Myc target" genes
has been described. The functional and genetic analysis
of these target genes will be a major issue of our laboratory
within the next years.
Institute of Molecular Biology and Tumor Research
Phillipps-University of Marburg
D-35033 Marburg, Germany
Our group works on the function of human myc genes.
We try to understand how mutations of these genes contribute
to the genesis of human tumors.
N. Eisenman, Ph.D.
Member, Fred Hutchinson Cancer Research Center
Member, National Academy of Sciences
Our lab studies the "Max Network"- this includes
Myc, Max and other Max interacting proteins including
Mad, Mnt and Mga. We are interested in the mechanisms
underlying transcriptional activation and repression
by these proteins and the nature of the specific genes
whose expression they regulate. We also employ genetic
strategies in mice and flies to understand the biological
functions of Max network proteins. more...
Dean W. Felsher, M.D., Ph.D.
Stanford University School of Medicine
Palo Alto, CA
My laboratory studies how oncogenes, such as MYC, initiate and
susatain tumorigenesis. We have developed novel model systems
whereby we can conditionally activate oncogenes in normal human and
mouse cells in tissue culture on in transgenic mice to address three
questions: How does oncogene activation initiate the process of
tumorigenesis? How does oncogene inactivation induce tumor
regression? How do tumors escape the requirement of partiuular
oncogenes to sustain their neoplastic properties?
Molecular Oncology Group
Max-Planck-Institute of Biochemistry
Am Klopferspitz 18 A
We are interested in all aspects of c-MYC biology, its
role in cancer and its use as a therapeutic target.
In order to identify new c-MYC target-genes we have
employed SAGE (serial analysis of gene expression) and
microarray analysis. Recently, we described the SAGE-based
identification of more than 400 genes, which are differentially
regulated after ectopic c-MYC expression in primary
human cells (Menssen and Hermeking, 2002). After verification
using microarray analysis and real-time PCR, some of
the c-MYC-induced genes were further characterized using
chromatin immuno-precipitation assays to detect the
presence of c-MYC at the promoters of these genes (e.g.
Cdk4, Cyclin B1, Prohibitin). We are currently analysing
some of these genes to determine their relevance for
c-MYC-induced phenotypes, as shown in case of the gene
encoding cyclin-dependent kinase 4 (Cdk4) (Hermeking
et al., 2000).
Molecular Biology of Cancer Group
Dpto. de Biología Molecular, Facultad de Medicina
39011 Santander, Spain
Research in our lab aims to the study of the roles of
c-Myc and Mads proteins in leukemia cell growth, apoptosis
and differentiation, focusing in myeloid leukemia as
our predominant model system. In particular we are interested
a) The functional cross-talk between Myc and p53 in
the apoptosis and transactivation activities, and the
mechanisms underlying the Myc-mediated interference
of p53 functions in this model; b) The interference
between Myc and the cyclin-dependent kinases inhibitors
p21 and p27 at the transcriptional and post-translational
levels and its effects on myeloid cell differentiation
elicited by these inhibitors; c) The cross-talk between
Myc and Ras in the proliferation of chronic myeloid
leukemia cells and the activation of downstream targets
of Ras pathways; and d) Myc and Mad expression in human
chronic myeloid leukemia and the effects on the action
of drugs used in this disease.
Division of Cellular and Molecular Biology
Ontario Cancer Institute, PMH
610 University Ave., Toronto, ON
Canada M5G 2M9
Regulation and Function of the Myc Oncogene:
We have focussed on identifying Myc-repressed genes
as recent evidence suggests Myc repression is tightly
linked to transformation. We have shown that Myc can
negatively regulate specific target. To identify additional
Myc-induced and repressed gene targets we are conducting
a gene CHIP approach. To identify the key function and
the critical regions of the Myc protein which are critical
for Myc transformation activity we are conducting a
detailed structure/function study of the Myc protein.
This work is coupled with our recent endeavors to identify
Myc-binding proteins critical for Myc function using
a novel two-hybrid approach, called the repressed transactivator
Finally, for a myc-activated cell to develop into a
tumour, Myc-triggered apoptosis must be controlled and
we are delineating the mechanism of Myc-induced death.
In addition, to identify genetic events which can inhibit
Myc-induced apoptosis and thereby cooperate with Myc
in the transformation process, we are using a retroviral
cDNA expression system to functionally clone cDNAs whose
product can abrogate apoptosis in a manner similar to
bcl-2. By this approach we have been able to identify
novel genes as well as known genes whose function in
apoptosis regulation had not yet been realized. Thus
we have a focused research program directed at understanding
Myc regulation and function in tumour initiation and
Prochownik, M.D. Ph.D.
Division of Hematology/Oncology
Childrens Hospital of Pittsburgh
Rangos Research Center, Room 6120
3460 Fifth Avenue
Pittsburgh, PA 15213
Our current research interests are largely aimed at identifying
and characterizing target genes modulated by members of
the MYC family, at determining how these genes mediate
the known phenotypes of the MYC proteins, and at identifying
the pathways through which the products of these target
genes mediate their MYC-like phenotypes.
We are also interested in studying how different MYC target
genes are differentially regulated by other members of
the MYC family (for example c-MYC vs. L-MYC) and to what
extent the expression of these target genes is tissue-specific.
Finally, we are interested in identifying novel proteins
that interact with modify the transcriptional activity
of MYC proteins.
M. Sedivy, Ph.D.
Professor of Medical Science
Department of Molecular Biology, Cell Biology and Biochemistry
Division of Biology and Medicine
Providence, RI 02912
We are primarily interest in the physiological function
of c-Myc in normal cells, and the mechanisms by which
it modulates cell growth and proliferation. Our approach
has been primarily a genetical one, involving the engineering
of knockout cell lines, and further derivatives expressing
conditional c-myc alleles. We are currently engaged in
the construction c-myc knockouts in human cells. Our expression
profiling studies have helped to reveal the amazing number
and variety of c-Myc target genes. A significant challenge
for the future will be to integrate this wealth of information
into a meaningful biological framework of Myc function.
Andrei Thomas-Tikhonenko, Ph.D.
Assistant Professor of Pathology
Department of Pathobiology
University of Pennsylvania
We investigate neoplastic transformation by the Myc oncoprotein. One area of our research is the negative regulation by Myc of various members of the thrombospondin-1 superfamily which suppress both cell proliferation and recruitment of vascular endothelial cells in solid tumors. In parallel, we are studying hematopoietic malignancies induced via transduction of p53-null bone marrow precursors with Myc-encoding retroviruses. Myc-regulated proteins appear to contribute to cell proliferation, survival, and differentiation, and some of them represent potential therapeutic targets.
Van Dang, M.D., Ph.D.
Department of Medicine and
The Johns Hopkins Kimmel Cancer Center
Johns Hopkins University
Ross Building, Room 1025
720 Rutland Avenue
Baltimore, MD 21205
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