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THE NEWSLETTER OF THE INTERNATIONAL
LUDWIG INSTITUTE FOR CANCER RESEARCH
Dr. Hugh Butt
August 2008
Remembering Dr. Hugh Butt, Former Chair
of the Scientific Advisory Committee
The LICR community will remember Hugh R.
Butt, MD, with respect and gratitude for the
commitment and sound judgment with which
he participated in launching the Institute, and
for his expertise in guiding its scientific activities
for more than fifteen years. Dr. Butt died
on August 16, at the age of ninety-eight.
Dr. Butt was personally selected by LICR
Founder Daniel K. Ludwig to direct the scientific
establishment, staffing and programs
of the developing LICR. He also defined the
character and set the course for the Institute’s
global activities as Chairman of the Scientific
Advisory Committee from 1971 to 1987. “The
Ludwig Institute for Cancer Research has now
emerged as the largest international academic
institute focused on cancer in the world,”
says Dr. Lloyd Old (LICR Chairman). “Hugh
Butt’s critical role in launching the Institute
stands as his enduring legacy to mankind’s
battle against this disease.”
Remembering Dr. Hugh Butt, Former Chair of the Scientific Advisory
Committee...............................................................................................1
Dr. Vilma Martins Elected President of the Brazilian Society for Cell
Biology.....................................................................................................3
Research Profile: Aristidis Moustakas, PhD, LICR Uppsala Branch...........4
LICR Endorses the World Cancer Declaration...........................................7
Research Highlights.................................................................................8
In Brief.....................................................................................................9
Selected Manuscrips................................................................................10
Dr. Anthony Burgess (Founding Director,
LICR Melbourne Branch) remembers Dr. Butt
as someone who was uncompromising in his
dedication to establishing a top quality research
institute. “His strength of character,
honesty and leadership was both inspirational
and defining,” he says. “I have never met anyone
more determined to ensure that only excellence
was good enough. [….] His work for
the LICR will be remembered for many years
to come.”
Dr. Butt was lauded internationally for his
accomplishments in medicine; including the
discovery that vitamin K stopped bleeding in
patients with jaundice, previously a fatal condition.
He published his vitamin K study in
1938, while still a medical resident. The findings
changed the practice of hepatology, the
branch of medicine that incorporates the study
and management of disorders of the liver, gallbladder,
biliary tree and pancreas.
A native of Virginia, USA, Dr. Butt graduated
from the University of Virginia Medical School
in 1934, after which entered the Mayo Graduate
School. He subsequently held appointments
at the Mayo Clinic for more than fifty
years: as Chairman of the Division of Gastroenterology
and Internal Medicine, as Professor
of Medicine at the Mayo Graduate School of
Medicine, and on the Board of Governors and
Board of Trustees. (Continued on p2)

(Continued from p1) In the early 1960s, he
served as President of the two most prestigious
medical societies in his field: the American
Gastroenterological Association and the
American Association for the Study of Liver
Diseases. In the early 1970s, he began his appointment
with the LICR and as President of
the American College of Physicians (ACP). He
was named a fellow in the Royal College of
Physicians (London, UK) in 1971. In 1973, he
received a mastership from the ACP, an elite
achievement award which at that time had
been awarded to fewer than 100 physicians.
Known for his forthrightness and humor,
Dr. Butt developed lifelong friendships with
many patients, one of whom was Mr. Steven
Fiterman. To him and his parents, Shirley and
Miles Fiterman, Dr. Butt was more than just a
physician: “He had the ability to affect an entire
family, to accept them as one of theirs. He
was loved by our entire family.” In 1990, the
Fitermans established, through the American
Gastroenterological Association, the Hugh R.
Butt Award for Distinguished Achievement in
Hepatology and Nutrition, which each year is
awarded to an eminent clinician.
Post-retirement, Dr. Butt devoted more time
to his longtime interest in art. He was a selftaught
metal sculptor and used farm implements,
old tools, wire and other metals to create
whimsical figures. Dr. Butt’s sculptures
were featured in three solo exhibitions at the
Rochester Art Center (Rochester, USA), most
recently in 2006, and have been exhibited in
several galleries across the country. One of his
sculptures—representing a DNA molecule—
is displayed prominently in LICR’s New York
Office.
Dr. Butt and his late wife, Mary Dempwolf,
had four children: Lucy Butsch, Selby Beeler,
the late Charles Butt, and Frances Cohn. He
also had seven grandchildren and twelve great
grandchildren.
Hugh R. Butt, “A Little Boy from
Galaxy Four” (1996). Steel and
hardware. Courtesy of Lloyd J. Old.
LICRNewsLink
“Hugh’s uncompromising commitment to
excellence, his inherent dissatisfaction with
the status quo, and his insistence on a closer
integration between laboratory and clinical
research, gave rise to principles that still
guide the Institute today. Hugh’s uncanny
eye for spotting talent and leadership potential
in young scientists, as evidenced by
the outstanding achievements of the Founding
Directors selected to lead the Institute’s
Branches, are testimony to Hugh’s continuing
impact on the Institute’s activities.”
Lloyd J. Old, MD,
LICR Chairman
“(Hugh Butt) was one of the key architects
of LICR as we know it today. We will not
forget him in Lausanne, where his frequent
visits in the early days of the Branch were
always productive and stimulating.”
H. Robson MacDonald, PhD
Director, LICR Lausanne Branch
”We are saddened by the news and will always
remember Dr. Butt’s crucial contribution
to the Ludwig Institute.”
Thierry Boon, PhD
Founding Director, LICR Brussels Branch
August 2008 2

Dr. Vilma Martins
Dr. Vilma Martins Elected President
of the Brazilian Society for Cell Biology
We are very pleased to announce that Dr.
Vilma Martins (Associate Member, LICR São
Paulo Branch) has been elected President of
the Brazilian Society for Cell Biology (SBBC).
The SBBC is committed to improving the
quality of cell biology research in Brazil and
to strengthen its relevance, in both a national
and an international context.
The election of Dr. Martins was announced on
July 29, during the general assembly of the
SBBC in São Paulo. “This position is an honor
for me and an enormous responsibility,” Dr.
Martins comments. “Many Brazilian scientists
are counting on the President and the Directory
Members to do whatever we can to improve
their conditions to do research in Brazil.”
Dr. Martins earned her PhD in Biochemistry
and Molecular Biology from the University
of São Paulo. She has headed the Cellular
and Molecular Biology Group at the LICR
São Paulo Branch since 2002, and was earlier
this year appointed Associate Member. Her
research is focused on the protein PrPC, the
cellular equivalent of the prion protein that
causes a number of neurodegenerative diseases
such as Creutzfeldt-Jakob disease and mad
cow disease. Dr. Martins and her colleagues
have demonstrated that PrPC is important for
several fundamental processes in the developing
and adult nervous system, including cell
survival and differentiation. Their findings
also indicate that PrPC loss-of-function plays a
role in the pathogenesis of prion diseases. The
group is now working together with the Brazilian
Ministry of Health to set up screens for
molecular markers of prion diseases in human
populations. Dr. Martins holds an esteemed
five-year International Research Scholars award
from the Howard Hughes Medical Institute
(HHMI) and has received additional fellowships
from the São Paulo State Foundation for
the Advancement of Science (FAPESP).
LICRNewsLink
Officially founded in 1990, the SBBC was first
conceived during a meeting held in 1978 on
the initiative of LICR alumnus Dr. Luis Carlos
Uchoa Junqueira, who was one of the first
Members of the São Paulo Branch. Since its
foundation, the society has provided an interactive
forum for discussion and sharing of
knowledge in the cell biology field, and participates
in the training of investigators and
building of human resources. Through its affiliation
with national science organizations—
the Federation of Experimental Biology Societies
(FeSBE) and the Brazilian Society for
the Progress of Science (SBPC)—the SBBC
encourages its members to be engaged in scientific
policy issues and to help form public
opinion on questions that call for scientific
knowledge, such as the use of embryonic stem
cells and laboratory animals in biomedical research.
The SBBC also interacts with the International
Federation of Cell Biology (IFCB),
the American Society of Cell Biology (ASCB)
and the Ibero-American Federation of Cell Biology
(IAFCB).
August 2008 3

Dr. Aristidis
Moustakas
Research Profile:
Aristidis Moustakas, PhD, LICR Uppsala Branch
Dr. Aristidis (Aris) Moustakas was born in
Greece and earned his PhD in Genetics at the
University of Minnesota, USA. In the early
1990s, he joined the laboratory of Dr. Harvey
Lodish at the Whitehead Institute for
Biomedical Research in Massachusetts, USA,
first as a postdoctoral fellow and later as a Research
Associate. There, he began to investigate
transforming growth factor beta (TGFb),
a cell-to-cell signaling protein that regulates
a wide spectrum of cellular processes and the
function of which is perturbed in many types
of cancer.
Dr. Moustakas moved to Sweden in 1998 and
joined the LICR Uppsala Branch as an Assistant
Member. A year later, he established the
TGFb Signaling Group with a team of six scientists.
The group expanded considerably during
2007 and now includes twelve members
(the group leader, four post-doctoral fellows,
six PhD students, and a senior technician) of
eight different nationalities. Their research
covers various aspects of TGFb signaling, from
signal transduction to cancer biology.
Smad Regulation and Function
TGFb regulates cellular processes such as cell
growth, differentiation, and tumorigenesis
via a group of proteins known as ‘Smads’. The
Smads transmit signals from type I and type II
TGFb receptors on the cell surface into the cell
nucleus, where they regulate gene expression.
Previous work by the team has clarified how
some Smads shuttle in and out of the nucleus
in response to changes in TGFb signaling. The
investigators are now turning their attention
to the activity of Smads inside the nucleus.
Smads can modify the expression of hundreds
of genes by cooperating with different DNAbound
factors, some of which act by modifying
the structure of chromatin (the substance of
chromosomes). “We study novel mechanisms
that regulate the activity of Smad proteins in
LICRNewsLink
the nucleus by focusing on nuclear proteins
that interact with the Smads and regulate the
function of chromatin,” Dr. Moustakas says.
The protein CTCF, which organizes chromatin
into functional domains, is of particular
interest to his team since it appears to have a
role in the TGFb pathway and since its sibling
protein, BORIS, is deregulated in many types
of cancer.
The TGFb- Smad pathway. Type I and type II receptors
bind to TGFb and activate the intracellular proteins
Smad2 and Smad3. Upon binding to Smad4, these proteins
translocate to the cell nucleus and regulate gene expression
together with other transcription factors. Courtesy of R.
Bergström.
“We also concentrate on factors that determine
how long time Smads stay in the nucleus,” Dr.
Moustakas explains. “Such factors include proteins
that regulate the addition of ubiquitin to
Smads.” The team provided some of the first
reports demonstrating that Smad proteins are
modified by the attachment of chains of the
small regulatory protein ubiquitin and subsequently
degraded. It appears that this mechanism
is disrupted in some tumors, with Smad
signaling being lost as a result.
Of the eight Smad proteins, the team pays particular
attention to Smad4 since it is encoded
by a known tumor suppressor gene. Inherited
August 2008 4

mutations in this gene are found in children
with Juvenile Polyposis Syndrome (JPS), a
benign intestinal polyp that can become malignant
in older age. The team is examining
potential links between Smad4 and another
signaling protein, LKB1. Mutations in the
LKB1 gene cause the Peutz-Jeghers Syndrome,
a polyp that resembles those observed in JPS.
Dissecting the Genetic Network Downstream
of TGFb
TGFb signaling has a complex impact on
tumorigenesis. The pathway suppresses the
growth of early-stage tumors by inhibiting
cell growth or by prompting cells to undergo
apoptosis (cell death), but nevertheless drives
tumorigenesis in late-stage tumors. It is not
clear what determines a cell’s response to
TGFb at the molecular level.
Dr. Moustakas and his colleagues are investigating
the function and regulation of various
TGFb-responsive genes by combining functional
experiments with global gene expression
analysis in a model system using breast
epithelial cells. This approach has allowed
them to decipher key steps in the genetic program
that mediates tumor suppression, or tumor
progression, in response to TGFb. For instance,
they recently described how signaling
via the TGFb and Notch pathways regulates
the expression of the tumor suppressor gene
p21 during cell cycle arrest. Another TGFbinduced
gene, HMGA2, has been linked to a
genetic network that promotes tumor invasiveness
and metastasis.
To expand on their gene expression analysis,
the investigators are now locating the activity
of TGFb-induced transcription factors across
the genome using chromatin immunoprecipitation
(ChIP) and high-throughput sequencing
technologies. They also employ a bioinformatics
approach to predict the most sensitive
regulatory steps in the TGFb pathway, which
LICRNewsLink
is ongoing in collaboration with the European
Biology Consortium (ENFIN).
EMT: a Mechanism of Metastasis?
About four years ago, Dr. Moustakas and his
colleagues set out to explore whether TGFbsignals
trigger metastasis during tumor progression.
They are paying particular attention
to epithelial-mesenchymal transition (EMT),
a process that switches the differentiation of
epithelial cells to a mesenchymal state during
development and is characterized by increased
cell motility and invasiveness. It appears that
TGFb signaling induces EMT in carcinomas
(advanced epithelial tumors), thereby conferring
upon cancer cells the capabilities required
for metastasis. “We want to demonstrate that
the EMT process contributes directly to the
maintenance of cells that carry tumor-initiating
and metastasis-initiating capacities,” Dr.
Moustakas says.
Epithelial cells undergo EMT in response to TGFb. The
photomicrographs show human keratinocytes responding to
TGFb1 over a course of 72 hours. The adherens junction
protein E-cadherin (red) is lost during EMT; the extracellular
matrix protein fibronectin (green) accumulates in the cytoplasm
and is also secreted in the matrix of the mesenchymal
cells; nuclei are stained blue to demarcate individual cells.
Courtesy of M. Vanlandewijck
August 2008 5

Under the auspices of the LICR Clinical Discovery
Program, the team has initiated a highthroughput
screen for chemical compounds
that inhibit EMT. Dr. Moustakas hopes to
carry this project to the development of drugs
that control cancer by preventing metastasis.
“We maintain strong confidence that the
screen will be rewarding and will bring us also
close to the world of cancer therapy,” he says,
“but this remains to be seen in the near future.”
Suggested Reading
1. Kowanetz, M., Lönn, P., Vanlandewijck, M., Kowanetz,
K., Heldin, C.-H., and Moustakas, A. (2007)
TGFb induces SIK to negatively regulate type I receptor kinase
signaling. J. Cell Biol. In press.
2. Gal, A., Sjöblom, T., Fedorova, L., Imreh, S., Beug,
H., and Moustakas, A. (2007) Sustained TGFb exposure
suppresses Smad and non-Smad signalling in mammary epithelial
cells, leading to EMT and inhibition of growth arrest
and apoptosis. Oncogene 27, 1218-1230.
3. Niimi, H., Pardali, K., Vanlandewijck, M., Heldin,
C.-H., and Moustakas, A. (2007) Notch signaling is necessary
for epithelial growth arrest by TGF-b. J. Cell. Biol.
176, 695-707.
4. Thuault, S., Valcourt, U., Manfioletti, G., Heldin,
C.-H., and Moustakas A. (2006) Transforming growth
factor-b employs HMGA2, a nuclear factor associated with
tumor progression, to elicit epithelial-mesenchymal transition.
J. Cell. Biol. 174, 175-183.
5. Kurisaki, A., Kurisaki, K., Kowanetz, M., Sugino,
H., Yoneda, Y., Heldin, C.-H., and Moustakas, A.
(2006) Nuclear export of Smad3 is mediated by exportin 4
and the Ran GTPase. Mol. Cell. Biol. 26, 1318-1332.
LICRNewsLink
August 2008 6

LICR Endorses the
World Cancer Declaration
LICR has endorsed the World Cancer Declaration
2008, a call to action by the International
Union against Cancer (UICC) to combat the
growing cancer epidemic. The World Health
Organization (WHO) estimates that global
mortality caused by cancer will rise drastically
over the coming decades, with a majority of
cancer deaths occurring in low and middle income
countries. Addressed to governments and
other health policy makers, the World Cancer
Declaration outlines specific actions that the
global cancer community should take to reduce
the burden of cancer by 2020.
The UICC is dedicated to building global control
of cancer through efforts such as public
knowledge transfer, tobacco control, capacity
building and supportive care. LICR, being
committed to improving cancer control
through integrated laboratory and clinical discovery,
does not participate in these activities
itself, but contributes through its UICC membership.
LICR has been a member of UICC
since 1984.
The World Cancer Declaration 2008 was adopted
by the UICC World Cancer Congress
during its general assembly in Geneva, Switzerland,
on August 27. It articulates a consensus
between diverse parties that have an interest
in lightening the threat posed by cancer:
governments, foundations, non-governmental
and governmental organizations, the private
sector, academia, and civil society. Priority actions
are advocated on several fronts, such as
health policy, cancer prevention and early detection,
cancer treatment, and research. The
declaration builds on the first World Cancer
Declaration, in 2006, and the Charter of Paris,
which was the first global effort to mobilize the
global cancer community to address the growing
cancer crisis.
To learn more about UICC’s call to action,
download the World Cancer Declaration 2008
from the UICC web page: www.uicc.org.
LICRNewsLink
August 2008 7

Research Highlights
MHC Mobility Modulation
Governs Antigen Recognition
by CTLs
The vigilance of the adaptive immune system
depends on how effectively cytolytic T lymphocytes
(CTLs) can track down and destroy
pathogen-infected or oncogenic cells. As CTLs
make transient contacts with adjacent cells,
their T cell receptors (TCRs) scan for distinct
antigen-derived peptides bound to MHC-I receptors
that can be expressed on the target cell
surface. According to a recent study conducted
by LICR Lausanne Branch investigators, a previously
unknown feature of MHC-I receptor
dynamics accounts for the capacity of CTLs to
rapidly identify their targets. The team found
that MHC I-peptide complexes become immobile
in newly-formed immunological synapses
(contact sites) between target cells and CTLs,
greatly increasing the sensitivity of antigen
recognition. The diffusional trapping of MHC
I-peptide complexes is caused by their association
with the intracellular adhesion molecule
ICAM-1, which plays a central role in the formation
of the synapse. The team is currently
investigating whether defects in these mechanisms
might account for the poor recognition
of some tumor cells by CTLs.
Segura JM, Guillaume P, Mark S, Dojcinovic D, Johannsen
A, Bosshard G, Angelov G, Legler DF, Vogel H, Luescher
IF. Increased mobility of MHC I - peptide complexes decreases the
sensitivity of antigen recognition. J Biol Chem. 2008 Aug 29;
283(35): 24254-63 [PMID: 18579518]
A typical contact site between a CTL and its target visualized by white-light transmission
microscopy (A) or single-molecule microscopy of fluorescently labeled peptide-MHC I complex
(B). Single complexes are recognized as diffraction-limited spots distributed all along the
synapse.
LICRNewsLink
A Gene Expression Signature
Predictive of Clinical Outcome
in Melanoma Patients
The outlook for patients who have been diagnosed
with Stage III melanoma—melanoma
that has spread to the lymph nodes—is generally
poor, with most patients progressing rapidly
to Stage IV and succumbing to their disease
within five years. However, up to 30% of
patients with Stage III melanoma will survive
past the five year mark. Without a means to distinguish
between these patient subtypes, some
patients may unnecessarily undergo aggressive,
often toxic, treatments. In order to predict clinical
outcomes of Stage III melanoma patients,
investigators at the LICR Melbourne Center
described a gene expression signature that distinguishes
those who have poor survival from
those who do not. By global DNA microarray
analysis, the investigators identified twentyone
genes that were differentially expressed in
the lymph nodes of patients with rapidly versus
slowly progressing disease. A score derived
from the gene expression data was applied prospectively
to analyze an independent patient
group. The gene expression signature correctly
predicted the clinical outcome of nine out of ten
patients, and studies in larger patients groups
are now underway. If the results are confirmed,
the signature could serve as a routine prognostic
indicator and hopefully facilitate the development
of melanoma therapies that are tailored
to individual patients.
John T, Black MA, Toro TT, Leader D, Gedye CA, Davis
ID, Guilford PJ, Cebon JS. Predicting Clinical Outcome
through Molecular Profiling in Stage III Melanoma.
Clin Cancer Res. 2008 Aug 15;14(16):5173-80 [PMID:
18698035]
August 2008 8

In Brief
Dr. Bing Ren Awarded USD
1.73 Million for Stem Cell
Research
Congratulations to Dr. Bing Ren (Associate
Member, LICR San Diego Branch), who received
a $1.73 million New Faculty II Award
by the state’s stem cell agency, the California
Institute of Regenerative Medicine (CIRM).
Dr. Ren was one of 23 young scientists and
physician-researchers to receive part of a $59
million boost to stem cell research in California.
The announcement of this prestigious
award brings the total amount of CIRM funding
received by the LICR San Diego Branch
to $2,473,053. This amount includes a Disease
Team Planning Award in June 2008 to
Dr. Webster Cavenee, Director of the LICR
San Diego Branch, seed funding previously
granted to Dr. Ren, and a facility grant. The
5-year CIRM grant will support Dr. Ren’s research
into molecular factors that regulate the
gene activity that ultimately determines the
fate of embryonic stem cells. These studies
are expected to shed light on the mechanisms
that control pluripotency—the cells’ ability to
differentiate into many different cell types—
and contribute to the understanding of how
to manipulate human embryonic stem cells for
regenerative medicine.
LICRNewsLink
Dr. Jonathan Cebon Awarded
USD 1 million from the
Melanoma Research Alliance
The Melanoma Research Alliance (MRA), a new
public charity based in Washington D.C., USA,
recently awarded 8 million USD in grants to individual
scientist and research teams to support
innovative melanoma research worldwide. An
international team headed by Dr. Jonathan Cebon
(LICR Melbourne Center) received one of
six Team Science Awards of 1 million USD. The
award will be used to explore immune targeting
of melanoma stem cells. The team also includes
Drs. Otavia Caballero (LICR New York Branch),
Winston Hide (LICR Affiliate, South African National
Bioinformatics Institute, South Africa), and
Michael Berridge (Malaghan Institute for Medical
Research, New Zealand). In addition, Dr. Jedd
Wolchok (Associate Director, Ludwig Center for
Cancer Immunotherapy) received a 200,000 USD
Established Investigator Award to support his
studies of immune responses induced by CTLA-4
targeting therapies in melanoma patients.
Dr. Richard Simpson Receives
the 2008 HUPO Distinguished
Service Award
The international Human Proteome Organization
(HUPO) has awarded its 2008 Distinguished
Service Award to Dr. Richard Simpson,
head of the Melbourne Branch’s Joint Proteomics
Research Laboratory. The award is presented each
year in recognition of distinguished scientific
achievements in the field of proteomic science.
Dr. Simpson received the award on August 20,
during the HUPO 7th Annual World Congress
in Amsterdam, Netherlands, for “indispensible
contributions in his service to HUPO since the
inauguration of HUPO in 2000.” The organization
added that Dr. Simpson has demonstrated
extraordinary commitment to the education and
training of scientists in proteomic sciences.
August 2008 9

Selected Manuscripts
Arthritis & Rheumatism
From the laboratory of Drs. Pedro Romero and
Daniel Speiser (Lausanne Branch):
Jandus C, Bioley G, Rivals JP, Dudler J, Speiser D,
Romero P. Increased numbers of circulating polyfunctional
Th17 memory cells in patients with seronegative spondylarthritides.
Arthritis Rheum. 2008 Aug;58(8):2307-17
[PMID: 18668556]
BMC Medical Genomics
From the laboratory of Dr. Luisa Villa (Director,
São Paulo Branch):
Termini L, Boccardo E, Esteves GH, Hirata R Jr, Martins
WK, Colo AE, Neves EJ, Villa LL, Reis LF. Characterization
of global transcription profile of normal and HPV-immortalized
keratinocytes and their response to TNF treatment. BMC
Med Genomics. 2008 Jun 27;1:29 [PMID: 18588690]
Journal of Medical Virology
From the laboratory of Dr. Luisa Villa (Director,
São Paulo Branch):
Junes-Gill K, Sichero L, Maciag PC, Mello W, Noronha
V, Villa LL. Human papillomavirus type 16 variants in cervical
cancer from an admixtured population in Brazil. J Med
Virol. 2008 Sep;80(9):1639-45 [PMID: 18649325]
Journal of Nuclear Medicine
From the laboratory of Dr. Andrew Scott (Director,
Melbourne Center):
Scott AM, Gunawardana DH, Kelley B, Stuckey JG,
Byrne AJ, Ramshaw JE, Fulham MJ. PET Changes Management
and Improves Prognostic Stratification in Patients
with Recurrent Colorectal Cancer: Results of a Multicenter
Prospective Study. J Nucl Med. 2008 Aug 14. Epub ahead
of print [PMID: 18703607]
Nano Letters
From the laboratories of Drs. Andrew Clayton
and Edouard Nice (Melbourne Branch):
Lees EE, Gunzburg MJ, Nguyen TL, Howlett GJ,
Rothacker J, Nice EC, Clayton AH, Mulvaney P. Experimental
Determination of Quantum Dot Size Distributions, Ligand
Packing Densities, and Bioconjugation Using Analytical
Ultracentrifugation. Nano Lett. 2008 Jul 30 [PMID:
18665653]
LICRNewsLink
Proceedings of the National Academy of Sciences
USA
From the laboratory of Dr. Donald Cleveland
(San Diego Branch):
Ilieva HS, Yamanaka K, Malkmus S, Kakinohana O,
Yaksh T, Marsala M, Cleveland DW. Mutant dynein (Loa)
triggers proprioceptive axon loss that extends survival only in
the SOD1 ALS model with highest motor neuron death. Proc
Natl Acad Sci U S A. 2008 Aug 21. Epub ahead of print
[PMID: 18719118]
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August 2008 10