Cancer Research in Switzerland - Krebsliga Schweiz

160
Our research projects aim at understanding the role of
fatty acids, miR-21 and PTEN in the development of hepatic
precancerous lesions and HCC. Experimental approaches
using mouse genetic models fed special diets,
and proteomic analyses to identify new factors modulated
by miR-21/PTEN, are undertaken to reach this goal.
Our research should allow us to better understand the
molecular basis of liver cancer, in particular in the setting
of metabolic diseases. In addition, the pertinence of future
therapeutic interventions restoring normal miR-21
and PTEN activities in hepatocytes to prevent or treat liver
cancer should also be evaluated.
Project coordinator
Dr Michelangelo Foti
Département de physiologie cellulaire et
métabolisme
Centre médical universitaire (CMU)
Faculté de médecine
Université de Genève
1, rue Michel-Servet
CH-1211 Genève 4
Phone +41 (0)22 379 52 04
Fax +41 (0)22 379 52 60
michelangelo.foti@unige.ch
Gruber Günther | BIG 3-07: A randomised phase III
study of radiation doses and fractionation schedules
for ductal carcinoma in situ (DCIS) of the breast
(KFS 02527-02-2010)
Duration: 01.02.2010 – 01.02.2013
Patients with ductal carcinoma in situ (DCIS) (precursor
for breast cancer) are normally treated with breast-conserving
surgery and postoperative radiotherapy (RT). This
worldwide ongoing phase III trial is testing the influence
of RT duration (different fractionation) and RT dose (+/–
tumour bed boost) on local failure rates and quality of life
(QoL).
Aim of the study
Individualization of postoperative RT for patients with
DCIS after breast-conserving surgery for optimal tumour
control and less toxicity.
Methods
Patients will be randomised into 4 treatment arms: 1)
ARM A (25x whole breast RT) or 2) ARM B (16x whole
breast RT) or 3) ARM C (ARM A + 8x boost) or 4) ARM D
(ARM B + 8x boost). Clinical and biological parameters
for local failure will be evaluated. QoL will be measured.
Potential gain for the patients
Radiotherapeutic individualization and optimization of
different RT schemes in regard to local control and influence
on QoL in patients with DCIS.
Project coordinator
PD Dr. Günther Gruber
Institut für Radiotherapie
Klinik Hirslanden
Witellikerstrasse 40
CH-8032 Zürich
Phone +41 (0)44 387 25 50
Fax +41 (0)44 387 25 51
guenther.gruber@hirslanden.ch
Hegi Monika E. | Targeting the EGFR/PI3K pathway
in glioblastoma, what matters? (KFS 02670-08-2010)
Duration: 01.02.2011– 01.02.2014
Glioblastoma is the most aggressive and most common
tumour of the brain, with a median survival of only 15
months despite modern therapies. New cancer drugs specifically
target aberrantly modified or activated molecules
in the tumour cells that are thought to be essential for aggressive
growth and thus, may represent the molecular
“Achilles heel”. We are investigating the regulatory network
associated with the growth-promoting effect of the
epidermal growth factor receptor (EGFR) that is highly
amplified in 50 % of all glioblastoma.
We will combine molecular data of glioblastoma tissue
from patients treated with an inhibitor of the EGFR, with
data from experimental investigations of the EGFR network
in glioblastoma cell lines and mouse models. The
aim is to identify critical molecular “hubs” of the network
that need to be targeted for inactivation of its growthpromoting
mechanisms. The goal is to propose effective
combination therapies, adapted to the molecular makeup
of glioblastoma.
Project coordinator
Prof. Dr Monika E. Hegi
Laboratoire de biologie et génétique des tumeurs
Service de neurochirurgie
Centre hospitalier universitaire vaudois (CHUV)
(BH19-110)
Rue du Bugnon 46
CH-1011 Lausanne
Phone +41 (0)21 314 25 82/81
Fax +41 (0)21 314 25 87
monika.hegi@chuv.ch
Heim Markus Hermann | Hepatocarcinogenesis in
chronic hepatitis C (KLS 02552-02-2010)
Duration: 01.07.2010 – 01.07.2012
Hepatocellular carcinoma is usually the consequence of
chronic liver inflammation, for example chronic viral hepatitis
C. The mechanisms responsible for carcinogenesis
are not known. The aim of the study is to identify molecular
mechanisms that are involved in hepatocarcinogenesis
in chronic hepatitis C.
We study liver cells that we infect with hepatitis C virus.
We specifically investigate if important cellular processes
such as DNA repair are impaired in cells infected with hepatitis
C virus. We showed that an important phosphatase
(PP2A) is induced by hepatitis C. PP2A inhibits another
enzyme, PRMT1, which regulates histones through methylation
of arginine amino acids. Histones are proteins that
are important for the correct packaging of DNA in the nucleus.
We plan to further investigate whether the changes
induced by hepatitis C virus could be corrected by drugs
such as S-adenosyl-L-methionine (SAMe) that correct the
enzyme activity of PRMT1.
Project coordinator
Prof. Dr. Markus Hermann Heim
Klinik für Gastroenterologie und Hepatologie
Universitätsspital Basel
Petersgraben 4
CH-4031 Basel
Phone +41 (0)61 265 51 74
markus.heim@unibas.ch