14 september 2026:

Zie ook dit artikel: https://kanker-actueel.nl/NL/ixazomib-een-proteasoomremmer-plus-subcutaan-rituximab-en-dexamethason-geeft-uitstekende-resultaten-bij-patienten-met-recidief-of-ziekteprogressie-van-ziekte-van-waldenstrom.html

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14 september 2026: Bron: . 2026 Apr 23:rs.3.rs-9405584.

AcTor, een nieuwe zogeheten mTOR-stimulator, versterkt de werking van Ixazomib bij de behandeling van Acute Myeloïde Leukemie. Het bijzondere aan deze ontdekking is dat onderzoekers uit Zweden en de VS erin zijn geslaagd AcTor, wat een molecuul is, te ontwikkelen dat een kankercel kan binnendringen en de kankercel zichzelf vernietigt door apoptose als gevolg van stressophoping. Deze aanpak is overigens alleen nog in laboratoriumstudies en muizenstudies onderzocht, maar lijkt wel heel interessant. Aldus een persbericht van de onderzoekers. 

Een citaat uit het persbericht: "Tegelijkertijd gas geven en remmen is zelden een goed idee. Toch passen onderzoekers van de Universiteit van Göteborg deze aanpak toe om leukemie te behandelen. Een nieuw medicijn dwingt kankercellen om hard te blijven werken zonder over energie te beschikken, totdat ze afsterven. De eerste studie bij muizen laat veelbelovende resultaten zien."

Nog een citaat: 

"Het molecuul, genaamd AcTor, remt een signaaleiwit dat de werking van het mTOR-eiwit beïnvloedt. mTOR fungeert als een controlecentrum dat bepaalt wanneer de cel moet groeien, zich moet opbouwen of moet rusten. De ingreep van de onderzoekers zorgt ervoor dat mTOR de volledige celactiviteit blijft stimuleren, zelfs wanneer de energieproductie in de mitochondriën wordt stilgelegd met een standaard antiproliferatief geneesmiddel. Door deze combinatie van behandelingen blijven de kankercellen het gaspedaal indrukken, terwijl tegelijkertijd de rem erop staat. Hierdoor raken de cellen op hol en sterven ze door stress.

Uit de studieresultaten blijkt dat AcTor een zeer sterk effect had op leukemie – zowel in Acute Myeloïde Leukemie-cellijnen en primaire patiëntenmonsters als in dierproeven – wanneer het werd gecombineerd met het medicijn Ixazomib. De behandeling bleef net zo effectief bij Acute Myeloïde Leukemie met een TP53-mutatie, een zeer agressieve vorm van kanker met een slechte prognose en beperkte behandelopties.
Met de nieuwe methode werden niet alleen zieke bloedcellen geëlimineerd, maar verdwenen ook leukemische stamcellen, die vaak tot ziekteprogressie en/of een recidief kunnen leiden.

"We zagen ook dat onze behandeling de afgifte van een eiwit (ADM2) op gang bracht; dit eiwit zou daarom kunnen dienen als biomarker voor de respons op de behandeling. Dit kan richting geven aan toekomstig translationeel en klinisch onderzoek," aldus een van de onderzoekers hoogleraar Leif Eriksson.

Het volledige persbericht is te lezen door op deze link te klikken: 

New method causes cancer cells to burn out

Het studierapport zoals gepubliceerd is dit:

Update in

Abstract

Background: mTORC1 activity is oncogenic. However, in the presence of chemotherapy, suppression of mTORC1 is cytoprotective. mTOR suppression requires an intact tuberous sclerosis complex (TSC), composed of TSC1, TSC2 and TBC1D7. Small molecules that activate mTOR by blocking the TSC are lacking.

Methods: We applied in silico docking and medicinal chemistry to generate AcTor, a potential first-of-its-kind TSC2 inhibitor. Because inhibition of TSC2 results in increased sensitivity to proteasome inhibitors, we combined AcTor and the proteasome inhibitor ixazomib (IXZ) in various cancer cell types.

Results: Potentiation of cytotoxic activity of IXZ by AcTor was observed across multiple acute myeloid leukemia (AML) cell lines and primary patient samples. The combination triggered a collapse of mitochondrial respiratory capacity, loss of mitochondrial membrane potential, accumulation of ROS and apoptosis. These attributes increased in drug-resistant AML. Transcriptomic profiling revealed that AcTor alone induced anabolic and oxidative phosphorylation programs, whereas AcTor/IXZ redirected the signaling towards stress-associated and pro-apoptotic transcriptional states, including a p53 pathway signature. In vivo studies revealed reduction in AML burden, depletion of blasts and of leukemic stem cells, and retention of activity upon relapse. AcTor/IXZ was equally potent in a TP53-mutated patient-derived xenograft model, exceeding the efficacy of standard-of-care.

Conclusions: As a TSC2 inhibitor, AcTor should not be used alone in cancer. When combined with proteasome inhibitors, the pharmacodynamics of AcTor shifts towards the development of a mitochondrial catastrophe in AML, which is durable, broad range, agnostic to TP53 mutations and to the acquisition of resistance to common clinical anti-AML drugs.

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Conflict of interest statement

Competing interests: A patent for AcTor has been filed. Inventors are BT, SPP, DW and LAE.

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Leukemie, AML, Acute Myeloide Leukemie, AcTor, Ixazomib, molecuul, muizenstudies, Leif Eriksson, universiteit van Göteborg, stressophoping


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