Biological and clinical features of triple negative Invasive Lobular Carcinomas of the breast. Clinical outcome and actionable molecular alterations.

Androgen receptor ERBB2 gene mutations HER2/PI3K/AKT pathway Luminal androgen receptor subtype Triple negative invasive lobular carcinoma

Journal

Breast (Edinburgh, Scotland)
ISSN: 1532-3080
Titre abrégé: Breast
Pays: Netherlands
ID NLM: 9213011

Informations de publication

Date de publication:
Oct 2021
Historique:
received: 06 03 2021
revised: 05 06 2021
accepted: 23 06 2021
pubmed: 5 7 2021
medline: 16 10 2021
entrez: 4 7 2021
Statut: ppublish

Résumé

We report here for the first time, a comprehensive characterization of biological and clinical features of early-stage triple negative Invasive Lobular Carcinomas(TN-ILCs) METHODS: We analyzed all consecutive patients with early-stage TN-ILC operated at two reference cancer-centers between 1994 and 2012. Primary objective was to assess the invasive disease-free survival(iDFS). Co-primary objective was to assess biological features of TN-ILCs, including molecular intrinsic subtypes based on PAM-50 assay, expression of androgen receptor (AR) and mutational status of ERBB2-gene. Additionally, DNA mutational status of an independent cohort of 45 TN-ILCs from three databases were analyzed, to confirm mutations in ERBB2-gene and to identify other recurrently mutated genes. Among 4152 ILCs, 74(1.8%) were TN and were analyzed. The iDFS at 5 and 10 years of FUP were 50.4%(95%CI,38.0-61.6) and 37.2%(95%CI,25.5-48.8), respectively. The molecular subtype was defined through PAM50-classifier for 31 out of 74 TN-ILCs: 48% were Luminal-A(15/31), 3% luminal-B(1/31), 32% HER2-enriched (10/31), and only 16% basal-like(5/31). Luminal tumors expressed AR more frequently than non-luminal tumors (AR≥1% in 94% of luminal tumors versus 53% in non-luminal tumors; p-value = 0.001). 20% of TN-ILCs analyzed(7/35), harbored a pathogenetic and actionable mutation in the ERBB2-gene. Analysis of the independent cohort of 45 TN-ILCs from three different databases, confirmed similar percentage of pathogenetic and actionable mutations in ERBB2-gene(20%; 9/45). Among the top 10 molecular pathways significantly enriched for recurrently mutated genes in TN-ILCs(FDR<0.05), there were ErbB-signaling and DNA-damage-response pathways. TN-ILCs are rare tumors with poor prognosis. Their specific biological features require newly defined targeted therapeutic strategies.

Sections du résumé

BACKGROUND BACKGROUND
We report here for the first time, a comprehensive characterization of biological and clinical features of early-stage triple negative Invasive Lobular Carcinomas(TN-ILCs) METHODS: We analyzed all consecutive patients with early-stage TN-ILC operated at two reference cancer-centers between 1994 and 2012. Primary objective was to assess the invasive disease-free survival(iDFS). Co-primary objective was to assess biological features of TN-ILCs, including molecular intrinsic subtypes based on PAM-50 assay, expression of androgen receptor (AR) and mutational status of ERBB2-gene. Additionally, DNA mutational status of an independent cohort of 45 TN-ILCs from three databases were analyzed, to confirm mutations in ERBB2-gene and to identify other recurrently mutated genes.
RESULTS RESULTS
Among 4152 ILCs, 74(1.8%) were TN and were analyzed. The iDFS at 5 and 10 years of FUP were 50.4%(95%CI,38.0-61.6) and 37.2%(95%CI,25.5-48.8), respectively. The molecular subtype was defined through PAM50-classifier for 31 out of 74 TN-ILCs: 48% were Luminal-A(15/31), 3% luminal-B(1/31), 32% HER2-enriched (10/31), and only 16% basal-like(5/31). Luminal tumors expressed AR more frequently than non-luminal tumors (AR≥1% in 94% of luminal tumors versus 53% in non-luminal tumors; p-value = 0.001). 20% of TN-ILCs analyzed(7/35), harbored a pathogenetic and actionable mutation in the ERBB2-gene. Analysis of the independent cohort of 45 TN-ILCs from three different databases, confirmed similar percentage of pathogenetic and actionable mutations in ERBB2-gene(20%; 9/45). Among the top 10 molecular pathways significantly enriched for recurrently mutated genes in TN-ILCs(FDR<0.05), there were ErbB-signaling and DNA-damage-response pathways.
CONCLUSIONS CONCLUSIONS
TN-ILCs are rare tumors with poor prognosis. Their specific biological features require newly defined targeted therapeutic strategies.

Identifiants

pubmed: 34217971
pii: S0960-9776(21)00407-0
doi: 10.1016/j.breast.2021.06.011
pmc: PMC8261657
pii:
doi:

Substances chimiques

Biomarkers, Tumor 0
Receptor, ErbB-2 EC 2.7.10.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

94-101

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.

Auteurs

Fabio Conforti (F)

Division of Medical Oncology for Melanoma & Sarcoma, IEO, European Institute of Oncology IRCCS, Milan, Italy. Electronic address: fabio.conforti@ieo.it.

Laura Pala (L)

Division of Medical Oncology for Melanoma & Sarcoma, IEO, European Institute of Oncology IRCCS, Milan, Italy.

Eleonora Pagan (E)

Department of Statistics and Quantitative Methods, University of Milan-Bicocca, Milan, Italy.

Elena Guerini Rocco (EG)

Division of Pathology, IEO, European Institute of Oncology, IRCCS, Milano, Department of Oncology and Hemato-Oncology, University of Milan, Milan, Italy.

Vincenzo Bagnardi (V)

Department of Statistics and Quantitative Methods, University of Milan-Bicocca, Milan, Italy.

Emilia Montagna (E)

Division of Medical Senology, IEO, European Institute of Oncology IRCCS, Milan, Italy.

Giulia Peruzzotti (G)

Division of Data Management, IEO, European Institute of Oncology IRCCS, Milan, Italy.

Tommaso De Pas (T)

Division of Medical Oncology for Melanoma & Sarcoma, IEO, European Institute of Oncology IRCCS, Milan, Italy.

Caterina Fumagalli (C)

Division of Pathology, IEO, European Institute of Oncology, IRCCS, Milano, Italy.

Silvana Pileggi (S)

Department of Oncology, Mario Negri Institute for Pharmacological Research, IRCCS, Italy.

Chiara Pesenti (C)

Department of Oncology, Mario Negri Institute for Pharmacological Research, IRCCS, Italy.

Sergio Marchini (S)

Department of Oncology, Mario Negri Institute for Pharmacological Research, IRCCS, Italy.

Giovanni Corso (G)

Division of Senology, European Institute of Oncology, IRCCS, Milan, Italy.

Caterina Marchio' (C)

Department of Medical Sciences, University of Torino, Turin, Italy; Unit of Pathology, Candiolo Cancer Institute - FPO, IRCCS, Candiolo, TO, Italy.

Anna Sapino (A)

Department of Medical Sciences, University of Torino, Turin, Italy; Unit of Pathology, Candiolo Cancer Institute - FPO, IRCCS, Candiolo, TO, Italy.

Rossella Graffeo (R)

High Risk Clinic, Oncological Genetics Service, Oncology Institute of Southern Switzerland, Ospedale Italiano, Lugano, Switzerland.

Laetitia Collet (L)

Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium.

Philippe Aftimos (P)

Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium.

Christos Sotiriou (C)

Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium.

Martine Piccart (M)

Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium.

Richard D Gelber (RD)

Department of Data Sciences, Dana-Farber Cancer Institute, Harvard Medical School, Harvard T.H. Chan School of Public Health, Frontier Science & Technology Research Foundation, Boston, USA.

Giuseppe Viale (G)

Department of Pathology, IEO, European Institute of Oncology IRCCS & State University of Milan, Milan, Italy.

Marco Colleoni (M)

Division of Medical Senology, IEO, European Institute of Oncology IRCCS, Milan, Italy.

Aron Goldhirsch (A)

MultiMedica San Giuseppe Hospital, Milan, Italy.

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Classifications MeSH