BJMO - 12, issue 3, february 2018
B. De Laere , M. Mayrhofer , T. Whitington , P-J. Van Dam , P. Van Oyen , C. Ghysel , J. Ampe , P. Ost MD, PhD, W. Demey MD, L. Hoekx MD, D. Schrijvers MD, PhD, B. Brouwers MD, PhD, W. Lybaert MD, E. Everaert , P. Van Kerckhove , D. De Maeseneer MD, M. Strijbos MD, PhD, A. Bols MD, PhD, K. Fransis , N. Beije , I. De Kruijff , S. Oeyen , A. Rutten MD, V. Van Dam , A. Brouwer , D. Goossens , L. Heyrman , G. Van Den Eynden MD, PhD, J. Vandebroek , J. Del-Favero , S. Sleijfer , A. Uhlen , J. Yachnin , S. Van Laere PhD, H. Grönberg , J. Lindberg , L. Dirix MD, PhD
BJMO - volume 11, issue 2, march 2017
A. Hébrant PhD, G. Froyen PhD, B. Maes MD, PhD, R. Salgado MD, PhD, M. Le Mercier PhD, N. D’Haene MD, PhD, S. De Keersmaecker PhD, K. Claes PhD, J. Van der Meulen PhD, P. Aftimos MD, J. Van Houdt PhD, K. Cuppens MD, K. Vanneste PhD, E. Dequeker PhD, S. Van Dooren PhD, J. Van Huysse MD, F. Nollet PhD, S. Van Laere PhD, B. Denys MD, V. Ghislain , C. Van Campenhout PhD, M. Van den Bulcke PhD
Targeted next generation sequencing is a complex procedure including the ‘wet bench’ and ‘dry bench’ parts. Both parts are composed of many steps for which optimal assay conditions and settings must be determined.
The aim of these guidelines is to provide generic, platform independent, recommendations for targeted next generation sequencing tests to detect acquired somatic mutations in DNA, in (haemato)-oncology that are complementary to the ISO 15189 norm (medical laboratories) in order to:
(BELG J MED ONCOL 2017;11(2):56–67)
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B. De Laere , P. Van Oyen , C. Ghysel , P. Ost MD, PhD, W. Demey MD, L. Hoekx MD, D. Schrijvers MD, PhD, B. Brouwers MD, PhD, W. Lybaert MD, E. Everaert , J. Ampe , P. Van Kerckhove , D. De Maeseneer MD, M. Strijbos MD, PhD, A. Bols MD, PhD, K. Fransis , S. Oeyen , V. Van Dam , A. Brouwer , G. Van Den Eynden MD, PhD, A. Rutten MD, J. Vandebroek , S. Van Laere PhD, L. Dirix MD, PhD
BJMO - 2017, issue 3, february 2017
P-J. Van Dam , B. Galjart , P. De Paepe MD, PhD, T. Feryn , V. Duwel , L. Dirix MD, PhD, P. Vermeulen , S. Van Laere PhD
BJMO - 2017, issue 3, february 2017
A. Brouwer , P-J. Van Dam , E. Sluydts , M. Peeters MD, PhD, P. Vermeulen , S. Van Laere PhD, L. Dirix MD, PhD
BJMO - volume 6, issue 6, december 2012
M. Marsan , P. Neven MD, PhD, P. Vermeulen , L. Dirix MD, PhD, S. Van Laere PhD
TGF-β is a major regulator and driver of many biological processes, but its main function is inhibition of cell cycle progression and apoptosis, thus establishing a tumour-protective effect in early stages of malignant transformation. However, mutational alterations can occur at different levels of the TGF-β signaling cascade. These mutations, combined with the significant influence of the tumour microenvironment on this cascade, can cause a functional shift of TGF-β from being a tumour suppressor to becoming a tumour promoter in more advanced cancers. In most tumours this will ultimately contribute to the formation of metastatic laesions. In the clinical setting of breast cancer, TGF-β plays a significant role in the acquisition of endocrine resistance. Thus, therapeutic intervention of TGF-β signaling might deliver significant benefits in the treatment of cancer. (BELG J MED ONCOL 2012;6:188–193)
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