BJMO - volume 13, issue 1, february 2019
A. Hébrant PhD, Ir , A. Jouret-Mourin MD, PhD, G. Froyen PhD, J. Van der Meulen PhD, M. De Man MD, R. Salgado MD, PhD, M. van den Eynde , N. D’Haene MD, PhD, G. Martens MD, PhD, E. van Cutsem , H.A. Poirel MD, PhD, S. Tejpar MD, PhD, J.L. van Laethem MD, PhD, K. Geboes MD, PhD, P. Pauwels MD, PhD, F. Dedeurwaerdere MD, B. Maes MD, PhD, J. De Grève MD, PhD, J. Vanhuysse , P. Peeters MD, L. Vanacker MD, M. Gomez-Galdon , M. Chintinne MD, PhD, A. Hendlisz MD, PhD, G. de Hertogh , X. Sagaert MD, PhD, M. Peeters MD, PhD, P. Vannuffel , P. Lefesvre MD, PhD, J. Vermeij , M. Simoens , T. Van den Mooter MD, N. van Damme , M. Van den Bulcke PhD
The Belgian Commission of Personalized Medicine has been created to advise the federal government on all matters related to personalised medicine in oncology, including the reimbursement of molecular tests. Here, we propose the Belgian strategy for molecular testing in the digestive tumours within a scientific-based framework. For each tested biomarker, a clinical test level is attached, which is key to establish the relevance of the test and to define the reimbursement. For each digestive tumour type, the different molecular tests are represented as decision trees with its test utility, test level and a brief technical test description.
(BELG J MED ONCOL 2019;13(1):4–10)
Read moreBJMO - 2017, issue 3, february 2017
R.B. Shahi MSc, B. Caljon , S. De Brakeleer PhD, L. Decoster MD, PhD, C. Fontaine MD, L. Vanacker MD, M. Vanhoeij , I. Pauwels , M-L. Bonduelle , S. Van Dooren PhD, D. Croes , E. Teugels PhD, J. De Grève MD, PhD
BJMO - volume 10, issue 7, november 2016
J. De Grève MD, PhD, L. Decoster MD, PhD, R.B. Shahi MSc, C. Fontaine MD, L. Vanacker MD, I. Pauwels , E. Denayer MD, PhD, S. De Brakeleer PhD, E. Teugels PhD
Inhibition of Poly (ADP-ribose) polymerase 1 has relatively recently entered the clinic. The ground-breaking drug both scientifically and clinically was olaparib, but several other PARP inhibitors are in development. This treatment is the first to therapeutically exploit mutant recessive cancer genes. In this review we discuss the discovery of this treatment, the preclinical and clinical studies, as well as some future perspectives.
(BELG J MED ONCOL 2016;10(7):263–275)
Read moreBJMO - volume 9, issue 1, february 2015
L. Vanacker MD, D. Smeets PhD, A. Hoorens MD, PhD, E. Teugels PhD, R. Algaba MD, M.F. Dehou MD, A. De Becker MD, D. Lambrechts PhD, J. De Grève MD, PhD
We present the case of a 30-year-old male patient with a high grade neuroendocrine carcinoma and an adenocarcinoma developed in a tubulovillous adenoma of the colon, with diffuse liver metastasis. He underwent a right hemicolectomy and received four courses of postoperative chemotherapy with cisplatin and etoposide, followed by high dose chemotherapy with autologous stem cell support. After this treatment there was a complete biochemical and radiological remission. Now, 48 months after diagnosis the patient is alive and in unmaintained complete remission. The occurrence of a high grade neuroendocrine carcinoma in a low grade colon adenocarcinoma without any intermediate phenotypes was intriguing. Comparative exome sequencing of DNA from the malignant components revealed six somatic changes in cancer consensus genes. In both tumours, we detected mutations in APC and KRAS, as well as in BCL9 and FOXP1. Only in the neuroendocrine carcinoma component did we find a mutation in SMARCA4. All mutations were absent in germ-line DNA. The finding of several identical somatic mutations in both components in the subsequent exome sequencing supports a clonal relationship between the neuroendocrine carcinoma and the synchronous adenocarcinoma. We suggest that a mutation in SMARCA4A may be responsible for the abrupt transition to the aggressive neuroendocrine phenotype.
(BELG J MED ONCOL 2015;9(1):31–34)
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