Evidence map›Paper›PMID 42105598›Full record

Trial reportESMO open2026

Efficacy of olaparib in advanced cancers with somatic or germline mutations in BAP1, BARD1, BRIP1 and PALB2.

S Joris, H Denys, J Collignon, M Rasschaert, D T de Roodenbeke, F P Duhoux, J L Canon, S Tejpar, J Mebis, L Decoster and 2 more

Abstract readClinical Trial, Phase II
PubMed Full text at PMC Publisher
In one paragraph

Trial report in ESMO open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

S JorisDepartment of Medical Oncology, UZ Brussel, Brussel, Belgium. Electronic address: Sofie.Joris@uzbrussel.be.
H DenysDepartment of Medical Oncology, University Hospital Ghent, Ghent, Belgium.
J CollignonDepartment of Medical Oncology, CHU Sart Tilman, Liège, Belgium.
M RasschaertDepartment of Medical Oncology, UZA, Antwerpen, Belgium.
D T de RoodenbekeDepartment of Medical Oncology, Institut Jules Bordet-Université libre de Bruxelles, Brussel, Belgium.
F P DuhouxDepartment of Medical Oncology, Cliniques universitaires Saint-Luc, Brussel, Belgium.
J L CanonDepartment of Medical Oncology, GHdC, Charlerloi, Belgium.
S TejparDepartment of Medical Oncology, UZ Leuven, Leuven, Belgium.
J MebisDepartment of Medical Oncology, Jessa Ziekenhuizen, Hasselt, Belgium.
L DecosterDepartment of Medical Oncology, UZ Brussel, Brussel, Belgium.
P AftimosDepartment of Medical Oncology, Institut Jules Bordet-Université libre de Bruxelles, Brussel, Belgium.
J De GrèveDepartment of Medical Oncology, UZ Brussel, Brussel, Belgium; Department of Medical Genetics, UZ Brussel, Brussels, Belgium.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOlaparib is registered for use in ovarian, breast, pancreatic and prostate cancers with a BRCA1/2 mutation and/or mutations in other homologous recombination deficiency (HRD) genes. HRD gene mutations are also found in other cancer types, and these cancers may also benefit from olaparib therapy. We aimed to evaluate the efficacy of olaparib in advanced cancers harboring a (likely) pathogenic germline or somatic mutation in a gene involved in homologous recombination (HR). PATIENTS AND

methodsThis investigator-initiated, open-label, basket phase II trial evaluates the efficacy of olaparib in patients with advanced tumors harboring HR gene mutations following progression on standard-of-care therapies. Cohorts were stratified based on the presence of either somatic or germline mutations in the same HR-related gene. Although results from the completed cohorts have been previously published, this report presents a case series focusing on cohorts with rare gene alterations.

resultsIn patients who harbor a tumor mutation in ARID1A, ATR, ATRX, BLM, CDK12, CHEK1, DDR2, ERCC4, FANCE, GEN1, MRE11A, NBN, POLE, RAD21, RAD50, RAD51C, RAD51D, RAD52 and SLX4, no responses were observed. In the BAP1, BARD1, BRIP1 and PALB2 cohorts, objective responses were detected.

conclusionOlaparib demonstrated meaningful clinical activity across different cancer types with somatic or germline mutations in BAP1, BARD1, BRIP1 and PALB2.

Indexed as

NeoplasmsPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsAdultAgedDNA-Binding ProteinsFanconi Anemia Complementation Group N ProteinFanconi Anemia Complementation Group ProteinsFemaleGerm-Line MutationHumansMaleMiddle AgedRNA HelicasesTumor Suppressor ProteinsBAP1 protein, humanBARD1 protein, humanBRIP1 protein, humanDNA-Binding ProteinsFanconi Anemia Complementation Group N ProteinFanconi Anemia Complementation Group ProteinsolaparibPALB2 protein, humanPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsRNA HelicasesTumor Suppressor ProteinsUbiquitin-Protein LigasesUbiquitin ThiolesteraseBAP1BARD1BRIP1olaparibPALB2

Identifiers

PMID42105598
PMCPMC13187586

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.