TY  - JOUR
AB  - Metabolomics is a rapidly evolving and a promising research field with the expectation to improve diagnosis, therapeutic treatment prediction, and prognosis of particular diseases. Among all techniques used to assess the metabolome in biological systems, mass spectrometry imaging is the method of choice to qualitatively and quantitatively analyze metabolite distribution in tissues with a high spatial resolution, thus providing molecular data in relation to cancer histopathology. The technique is ideally suited to study tissues molecular content and is able to provide molecular biomarkers or specific mass signatures which can be used in classification or the prognostic evaluation of tumors. Recently, it was shown that FFPE tissue samples are also suitable for metabolic analyses. This progress in methodology allows access to a highly valuable resource of tissues believed to widen and strengthen metabolic discovery-driven studies.
AU  - Buck, A.
AU  - Aichler, M.
AU  - Huber, K.
AU  - Walch, A.K.
C1  - 50291
C2  - 42146
CY  - San Diego
SP  - 117-132
TI  - In situ metabolomics in cancer by mass spectrometry imaging.
JO  - Adv. Cancer Res.
VL  - 134
PB  - Elsevier Academic Press Inc
PY  - 2017
SN  - 0065-230x
ER  - 

TY  - JOUR
AB  - Deregulation of c-myc expression through chromosomal translocation is essential in the pathogenesis of Burkitt's lymphoma (BL). A characteristic feature of BL cells, compared to Epstein-Barr Virus (EBV)-immortalized B cells, is their lack of immunogenicity. To study the contribution of EBV genes and of the c-MYC protein to this phenotype, we have generated a conditional B cell system in which the viral proliferation program and expression of c-myc can be regulated independently of each other. In cells proliferating due to exogenous c-myc overexpression, the cell surface phenotype, the pattern of proliferation in single cell suspension, and the immunological characteristics of BL cells could be completely recapitulated. Yet, it had remained open whether nonimmunogenicity is the default phenotype when EBNA2 and LMP1 are switched off, or whether c-MYC actively contributes to immunosuppression. We provide evidence also for the latter by showing that c-MYC down-regulates genes of the NF-kappaB and interferon pathway in a dose-dependent fashion. c-MYC acts at at least two different levels, the level of interferon induction as well as at the level of action of type I and type II interferons on their respective target promoters. c-MYC does not block the interferon pathway completely, it shifts the balance and increases the threshold of interferon induction and action.
AU  - Schlee, M.
AU  - Schuhmacher, M.
AU  - Hölzel, M.
AU  - Laux, G.
AU  - Bornkamm, G.W.
C1  - 6212
C2  - 28291
SP  - 167-188
TI  - c-MYC impairs immunogenicity of human B cells.
JO  - Adv. Cancer Res.
VL  - 97
PB  - Elsevier
PY  - 2007
SN  - 0065-230x
ER  - 

TY  - JOUR
AU  - Stürzl, M.
AU  - Zietz, Ch.*
AU  - Monini, P.*
AU  - Ensoli, B.*
C1  - 21705
C2  - 19897
SP  - 125-159
TI  - Human Herpesvirus-8 and Kaposi's Sarcoma : Relationship with the Multistep Concept of Tumorgenesis.
JO  - Adv. Cancer Res.
PY  - 2001
SN  - 0065-230x
ER  -