MEVITEM-a phase I/II trial of vismodegib + temozolomide vs temozolomide in patients with recurrent/refractory medulloblastoma with Sonic Hedgehog pathway activation.


Journal

Neuro-oncology
ISSN: 1523-5866
Titre abrégé: Neuro Oncol
Pays: England
ID NLM: 100887420

Informations de publication

Date de publication:
02 11 2021
Historique:
pubmed: 8 4 2021
medline: 6 11 2021
entrez: 7 4 2021
Statut: ppublish

Résumé

Vismodegib specifically inhibits Sonic Hedgehog (SHH). We report results of a phase I/II evaluating vismodegib + temozolomide (TMZ) in immunohistochemically defined SHH recurrent/refractory adult medulloblastoma. TMZ-naïve patients were randomized 2:1 to receive vismodegib + TMZ (arm A) or TMZ (arm B). Patients previously treated with TMZ were enrolled in an exploratory cohort of vismodegib (arm C). If the safety run showed no excessive toxicity, a Simon's 2-stage phase II design was planned to explore the 6-month progression-free survival (PFS-6). Stage II was to proceed if arm A PFS-6 was ≥3/9 at the end of stage I. A total of 24 patients were included: arm A (10), arm B (5), and arm C (9). Safety analysis showed no excessive toxicity. At the end of stage I, the PFS-6 of arm A was 20% (2/10 patients, 95% unilateral lower confidence limit: 3.7%) and the study was prematurely terminated. The overall response rates (ORR) were 40% (95% CI, 12.2-73.8) and 20% (95% CI, 0.5-71.6) in arm A and B, respectively. In arm C, PFS-6 was 37.5% (95% CI, 8.8-75.5) and ORR was 22.2% (95% CI, 2.8-60.0). Among 11 patients with an expected sensitivity according to new generation sequencing (NGS), 3 had partial response (PR), 4 remained stable disease (SD) while out of 7 potentially resistant patients, 1 had PR and 1 SD. The addition of vismodegib to TMZ did not add toxicity but failed to improve PFS-6 in SHH recurrent/refractory medulloblastoma. Prediction of sensitivity to vismodegib needs further refinements.

Sections du résumé

BACKGROUND
Vismodegib specifically inhibits Sonic Hedgehog (SHH). We report results of a phase I/II evaluating vismodegib + temozolomide (TMZ) in immunohistochemically defined SHH recurrent/refractory adult medulloblastoma.
METHODS
TMZ-naïve patients were randomized 2:1 to receive vismodegib + TMZ (arm A) or TMZ (arm B). Patients previously treated with TMZ were enrolled in an exploratory cohort of vismodegib (arm C). If the safety run showed no excessive toxicity, a Simon's 2-stage phase II design was planned to explore the 6-month progression-free survival (PFS-6). Stage II was to proceed if arm A PFS-6 was ≥3/9 at the end of stage I.
RESULTS
A total of 24 patients were included: arm A (10), arm B (5), and arm C (9). Safety analysis showed no excessive toxicity. At the end of stage I, the PFS-6 of arm A was 20% (2/10 patients, 95% unilateral lower confidence limit: 3.7%) and the study was prematurely terminated. The overall response rates (ORR) were 40% (95% CI, 12.2-73.8) and 20% (95% CI, 0.5-71.6) in arm A and B, respectively. In arm C, PFS-6 was 37.5% (95% CI, 8.8-75.5) and ORR was 22.2% (95% CI, 2.8-60.0). Among 11 patients with an expected sensitivity according to new generation sequencing (NGS), 3 had partial response (PR), 4 remained stable disease (SD) while out of 7 potentially resistant patients, 1 had PR and 1 SD.
CONCLUSION
The addition of vismodegib to TMZ did not add toxicity but failed to improve PFS-6 in SHH recurrent/refractory medulloblastoma. Prediction of sensitivity to vismodegib needs further refinements.

Identifiants

pubmed: 33825892
pii: 6213882
doi: 10.1093/neuonc/noab087
pmc: PMC8563312
doi:

Substances chimiques

Anilides 0
Hedgehog Proteins 0
HhAntag691 0
Pyridines 0
Temozolomide YF1K15M17Y

Types de publication

Clinical Trial, Phase I Clinical Trial, Phase II Journal Article Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1949-1960

Commentaires et corrections

Type : CommentIn
Type : CommentIn
Type : CommentIn

Informations de copyright

© The Author(s) 2021. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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Auteurs

Didier Frappaz (D)

Neuro-Oncology Unit, Centre Léon Bérard, Lyon, France.

Marc Barritault (M)

Neuropathology Department, CHRU de Lyon, Lyon, France.

Laure Montané (L)

Clinical Research Platform (DRCI) of Centre Léon Bérard, Lyon, France.

Florence Laigle-Donadey (F)

Neuro-Oncology Unit, Neurology 2 Department, La pitié Salpêtrière, Paris, France.

Olivier Chinot (O)

Neuro-Oncology Unit, La Timone Marseille, Marseille, France.

Emilie Le Rhun (E)

University of Lille, U-1192, F-59000 Lille, Lille, France.
Inserm, U-1192, F-59000 Lille, Lille, France.
General and Stereotaxic Neurosurgery Service, CHU Lille, Lille, France.
Oscar Lambret Center, Lille, France.
Department of Neurology, University Hospital and University of Zurich, Zurich, Switzerland.

Alice Bonneville-Levard (A)

Neuro-Oncology Unit, Centre Léon Bérard, Lyon, France.

Andreas F Hottinger (AF)

Brain and Spine Tumor Center, Departments of Clinical Neurosciences & Oncology, CHUV Lausanne University Hospital, Lausanne, Switzerland.

David Meyronnet (D)

Neuropathology Department, CHRU de Lyon, Lyon, France.

Anne-Sophie Bidaux (AS)

Clinical Research Platform (DRCI) of Centre Léon Bérard, Lyon, France.

Gwenaële Garin (G)

Clinical Research Platform (DRCI) of Centre Léon Bérard, Lyon, France.

David Pérol (D)

Clinical Research Platform (DRCI) of Centre Léon Bérard, Lyon, France.

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