Evidence map›Paper›PMID 42597706›Full record

ArticleImmuno-oncology technology2026

Germline

J Kay, M A Harris, L E Lara Gonzalez, C T van Geelen, K A Clarke, B Virassamy, F Caramia, J-M Pang, M M R O'Malley, M L Hun and 6 more

Abstract read
In one paragraph

Article in Immuno-oncology technology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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

16 authors.

J KayDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
M A HarrisDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
L E Lara GonzalezDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
C T van GeelenDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
K A ClarkeDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
B VirassamyDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
F CaramiaDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
J-M PangDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
M M R O'MalleyDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
M L HunDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
R SalgadoDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
H ThorneDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
J VisvaderDivision of Cancer Biology and Stem Cells, The Walter and Eliza Hall Institute of Medical Research, Victoria, Australia.
P J NeesonDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
P K DarcyDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.
S LoiDepartment of Research, The Peter MacCallum Cancer Centre, Melbourne, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Germline Patients and methods: We collected peripheral blood mononuclear cells (PBMCs) from healthy donors and treatment-naïve patients diagnosed with early-stage breast cancer with or without a gBRCA1 PV. T cells derived from PBMC were activated Results: Patients with gBRCA1 PV had significantly reduced circulating T cell counts compared with WT individuals. BRCA1 protein was highly expressed in healthy donor activated T cells, but significantly reduced expression was observed in gBRCA1 patients compared with WT. Activated T cells from gBRCA1 carriers displayed a distinct transcriptional profile with significantly impaired proliferation and decreased effector molecule production. TCR sequencing of TILs extracted from TNBC tumours from gBRCA1 carriers revealed significantly more hyperexpanded T cell clones than in WT patients, with hyperexpansion correlating with increased tumour mutation burden ( Conclusions: Circulating T cells from gBRCA1 carriers exhibit intrinsic T cell dysfunction. This phenotype may be clinically relevant in the context of antitumour immunity, cancer development, progression and response to immunotherapy treatment.

Indexed as

BRCA1breast cancerimmunityT cell dysfunctionT cell receptortumour-infiltrating lymphocyte

Identifiers

PMID42597706
PMCPMC13470316

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.