Evidence map›Paper›PMID 38118367›Full record

ArticleESMO open2024

Anthracycline-related cardiotoxicity in patients with breast cancer harboring mutational signature of homologous recombination deficiency (HRD).

L Incorvaia, G Badalamenti, G Novo, S Gori, L Cortesi, C Brando, S Cinieri, G Curigliano, G R Ricciardi, A Toss and 11 more

Open access · goldAbstract readMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Article in ESMO open, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 26% of its field
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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
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

21 authors at 10 institutions in 3 countries.

L IncorvaiaDepartment of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo.
G BadalamentiDepartment of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo.
G NovoDivision of Cardiology, University Hospital Paolo Giaccone, Palermo; Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE) "G. D'Alessandro", University of Palermo, Palermo.
S GoriOncology Department, IRCCS Sacro Cuore Don Calabria Hospital, Negrar di Valpolicella.
L CortesiDepartment of Oncology and Hematology, Azienda Ospedaliero-Universitaria di Modena, Modena.
C BrandoDepartment of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo.
S CinieriComplex Medical Oncology Unit, ASL Brindisi Senatore Antonio Perrino Hospital, Brindisi.
G CuriglianoDivision of Early Drug Development for Innovative Therapy, European Institute of Oncology, IRCCS, Milan; Department of Oncology and Hemato-Oncology, University of Milan, Milan.
G R RicciardiMedical Oncology Unit, A.O. Papardo & Department of Human Pathology, University of Messina, Messina.
A TossDepartment of Oncology and Hematology, Azienda Ospedaliero-Universitaria di Modena, Modena.
R ChiariMedical Oncology, Ospedali Riuniti Padova Sud, Monselice.
R BerardiMedical Oncology, AOU Ospedali Riuniti Umberto I-GM Lancisi-G Salesi, Polytechnic University of the Marche Region, Ancona.
Z BallatoreMedical Oncology, AOU Ospedali Riuniti Umberto I-GM Lancisi-G Salesi, Polytechnic University of the Marche Region, Ancona.
M BonoDepartment of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo.
T D Bazan RussoDepartment of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo.
V GristinaDepartment of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo.
A GalvanoDepartment of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo.
G DamerinoDivision of Cardiology, University Hospital Paolo Giaccone, Palermo.
L BlasiMedical Oncology Unit, ARNAS Civico, Palermo.
V BazanDepartment of Biomedicine, Neuroscience and Advanced Diagnostics (Bind), Section of Medical Oncology, University of Palermo, Palermo, Italy.
A RussoDepartment of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo. Electronic address: antonio.russo@usa.net.
University of Palermo · ARAzienda Ospedaliero-Universitaria di Modena · ITOspedali Riuniti Umberto I · ITAzienda Ospedaliero Universitaria Ospedali Riuniti · ITDepartment of Health · ESOspedale A. Perrino · ITOspedale Sacro Cuore Don Calabria · ITUniversity of Messina · ITUniversity of Milan · ITUniversity of Palermo · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe BRCA proteins play a key role in the homologous recombination (HR) pathway. Beyond BRCA1/2, other genes are involved in the HR repair (HRR). Due to the prominent role in the cellular repair process, pathogenic or likely pathogenic variants (PV/LPVs) in HRR genes may cause inadequate DNA damage repair in cardiomyocytes. PATIENTS AND

methodsThis was a multicenter, hospital-based, retrospective cohort study to investigate the heart toxicity from anthracycline-containing regimens (ACRs) in the adjuvant setting of breast cancer (BC) patients carrying germline BRCA PV/LPVs and no-BRCA HRR pathway genes. The left ventricular ejection fraction (LVEF) was assessed using cardiac ultrasound before starting ACR therapy and at subsequent time points according to clinical indications.

resultsFive hundred and three BC patients were included in the study. We predefined three groups: (i) BRCA cohort; (ii) no-BRCA cohort; (iii) variant of uncertain significance (VUS)/wild-type (WT) cohort. When baseline (T0) and post-ACR (T1) LVEFs between the three cohorts were compared, pre-treatment LVEF values were not different (BRCA1/2 versus HRR-no-BRCA versus VUS/WT cohort). Notably, during monitoring (T1, median 3.4 months), patients carrying BRCA or HRR no-BRCA germline pathogenic or likely pathogenic variants showed a statistically significant reduction of LVEF compared to baseline (T0). To assess the relevance of HRR on the results, we included the analysis of the subgroup of 20 BC patients carrying PV/LPVs in other genes not involved in HRR, such as mismatch repair genes (MUTYH, PMS2, MSH6). Unlike HRR genes, no significant differences in T0-T1 were found in this subgroup of patients.

conclusionOur data suggest that deleterious variants in HRR genes, leading to impaired HR, could increase the sensitivity of cardiomyocytes to ACR in early BC patients. In this subgroup of patients, other measurements, such as the global longitudinal strain, and a more in-depth assessment of risk factors may be proposed in the future to optimize cardiovascular risk management and improve long-term survival.

Indexed as

Breast NeoplasmsAnthracyclinesBRCA1 ProteinBRCA2 ProteinCardiotoxicityFemaleHomologous RecombinationHumansRetrospective StudiesStroke VolumeVentricular Function, LeftAnthracyclinesBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humananthracyclineBRCAbreast cancercardiotoxicityhomologous recombination deficiency

Identifiers

PMID38118367
PMCPMC10837774
OpenAlexW4389933521

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LicenceCC BY-NC-ND
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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.