TY  - JOUR
AB  - Despite the approval of several molecular therapies in the last years, breast cancer-associated death ranks as the second highest in women. This is due to metastatic disease, which represents a challenge for treatment. A better understanding of the molecular mechanisms of metastasis is, therefore, of paramount importance. In this review we summarize the role of micro RNAs (miRs) involved in metastasis of breast cancer. We present an overview on metastasis-promoting, -suppressing and context-dependent miRs with both activities. We have categorized the corresponding miRs according to their target classes, interaction with stromal cells or exosomes. The pathways affected by individual miRs are outlined in regard to in vitro properties, activity in metastasis-related in vivo models and clinical significance. Current approaches that may be suitable for therapeutic inhibition or restauration of miR activity are outlined. Finally, we discuss the delivery bottlenecks which present as a major challenge in nucleic acid (miR)-based therapies.
AU  - Weidle, U.H.*
AU  - Dickopf, S.*
AU  - Hintermair, C.
AU  - Kollmorgen, G.*
AU  - Birzele, F.*
AU  - Brinkmann, U.*
C1  - 52598
C2  - 44158
SP  - 17-39
TI  - The role of micro RNAs in breast cancer metastasis: Preclinical Validation and potential therapeutic targets.
JO  - Cancer Genomics Proteomics
VL  - 15
IS  - 1
PY  - 2018
SN  - 1109-6535
ER  - 

TY  - JOUR
AB  - Synthetic lethality is based on the incompatibility of cell survival with the loss of function of two or more genes, not with loss of function of a single gene. If targets of synthetic lethality are deregulated or mutated in cancer cells, the strategy of synthetic lethality can result in significant increase of therapeutic efficacy and a favourable therapeutic window. In this review, we discuss synthetic lethality based on deficient DNA repair mechanisms, activating mutations of RAS, loss of function mutations of the tumor suppressor genes p53, Rb and von Hippel-Lindau, and disruption of interactive protein kinase networks in the context of development of new anticancer agents.
AU  - Weidle, U.H.*
AU  - Maisel, D.*
AU  - Eick, D.
C1  - 6587
C2  - 28948
SP  - 159-171
TI  - Synthetic lethality-based targets for discovery of new cancer therapeutics.
JO  - Cancer Genomics Proteomics
VL  - 8
IS  - 4
PB  - International Institute of Anticancer Research
PY  - 2011
SN  - 1109-6535
ER  - 

TY  - JOUR
AU  - Hofmann, T.*
AU  - Schmitt, B.*
AU  - Mack, B.*
AU  - Lang, S.*
AU  - Gires, O.
AU  - Zeidler, R.*
C1  - 2887
C2  - 22031
SP  - 167-176
TI  - New target genes for tumor-derived soluble factors in primary monocytes.
JO  - Cancer Genomics Proteomics
VL  - 1
PY  - 2004
SN  - 1109-6535
ER  - 

TY  - JOUR
AU  - Münz, M.
AU  - Hofmann, T.*
AU  - Gänge, M.*
AU  - Junghanns, K.T.*
AU  - Zeidler, R.*
AU  - Gires, O.
C1  - 2886
C2  - 22030
SP  - 241-248
TI  - The carcinoma-associated antigen EpCam induces glyxolase 1 resulting in enhanced methylglyoxal turnover.
JO  - Cancer Genomics Proteomics
VL  - 1
PY  - 2004
SN  - 1109-6535
ER  -