Indoleamine 2, 3-dioxygenase (IDO) inhibition for cancer therapy

BJMO - volume 11, issue 9, february 2017

L. Brochez MD, PhD, I. Chevolet MD, PhD, A. Meireson , V. Kruse MD, PhD

Indoleamine 2,3-dioxygenase (IDO, also referred to as IDO1) has been demonstrated to be a normal endogenous mechanism of acquired peripheral immune tolerance in vivo. This manuscript reviews the currently available data on the role of IDO in cancer and the current results obtained with IDO inhibition in clinical trials in humans. Preliminary results with IDO inhibitors, usually combined with other anti-cancer drugs, seem encouraging. Further studies are needed to clarify the conditions in which IDO inhibitors can be of value as an anti-cancer strategy. In addition, further research should address whether the expression of IDO in tissue or blood can be a marker to select patients who can benefit most from IDO inhibition.

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Treatment of metastatic melanoma: an update on the Belgian situation

BJMO - volume 10, issue 6, september 2016

V. Kruse MD, PhD, I. Chevolet MD, PhD, K. De Wolf MD, P. Ost MD, PhD, L. Brochez MD, PhD


The therapeutic landscape for the treatment of metastatic melanoma has been changing dramatically over the last years. Given the availability of several promising drugs, choosing the best sequence for the individual patient has become a challenge. Immunotherapy by means of checkpoint-inhibitors, such as the anti-CTLA4-antibody ipilimumab and the anti-PD1-antibodies nivolumab and pembrolizumab, has demonstrated unprecedented long-term survival rates. When prescribing an immunotherapeutic agent, the clinician should be aware that the patient is at risk of developing an immune-related adverse event, especially when anti-CTLA4 and anti-PD1 are administered together. A promising future strategy to increase response rates of the checkpoint-inhibitors is combining them with radiotherapy. Hereby an abscopal effect is induced, reducing both irradiated and non-irradiated tumour lesions. Another therapeutic strategy is based on the presence of a BRAF mutation among approximately 40–50% of melanoma patients. For those patients, combined therapy with a BRAF inhibitor and a MEK inhibitor is valued to be a convincing regimen, especially in case of a high disease burden, elevated LDH and a performance status of 1–2. In contrast, T-VEC is a valuable therapeutic option for patients with limited disease.

(BELG J MED ONCOL 2016;10(6):215–222)

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