Current and future diagnostic and treatment strategies for patients with invasive lobular breast cancer.


Journal

Annals of oncology : official journal of the European Society for Medical Oncology
ISSN: 1569-8041
Titre abrégé: Ann Oncol
Pays: England
ID NLM: 9007735

Informations de publication

Date de publication:
08 2022
Historique:
received: 08 03 2022
revised: 06 05 2022
accepted: 17 05 2022
pubmed: 24 5 2022
medline: 4 8 2022
entrez: 23 5 2022
Statut: ppublish

Résumé

Invasive lobular breast cancer (ILC) is the second most common type of breast cancer after invasive breast cancer of no special type (NST), representing up to 15% of all breast cancers. Latest data on ILC are presented, focusing on diagnosis, molecular make-up according to the European Society for Medical Oncology Scale for Clinical Actionability of molecular Targets (ESCAT) guidelines, treatment in the early and metastatic setting and ILC-focused clinical trials. At the imaging level, magnetic resonance imaging-based and novel positron emission tomography/computed tomography-based techniques can overcome the limitations of currently used imaging techniques for diagnosing ILC. At the pathology level, E-cadherin immunohistochemistry could help improving inter-pathologist agreement. The majority of patients with ILC do not seem to benefit as much from (neo-)adjuvant chemotherapy as patients with NST, although chemotherapy might be required in a subset of high-risk patients. No differences in treatment efficacy are seen for anti-human epidermal growth factor receptor 2 (HER2) therapies in the adjuvant setting and cyclin-dependent kinases 4 and 6 inhibitors in the metastatic setting. The clinical utility of the commercially available prognostic gene expression-based tests is unclear for patients with ILC. Several ESCAT alterations differ in frequency between ILC and NST. Germline BRCA1 and PALB2 alterations are less frequent in patients with ILC, while germline CDH1 (gene coding for E-cadherin) alterations are more frequent in patients with ILC. Somatic HER2 mutations are more frequent in ILC, especially in metastases (15% ILC versus 5% NST). A high tumour mutational burden, relevant for immune checkpoint inhibition, is more frequent in ILC metastases (16%) than in NST metastases (5%). Tumours with somatic inactivating CDH1 mutations may be vulnerable for treatment with ROS1 inhibitors, a concept currently investigated in early and metastatic ILC. ILC is a unique malignancy based on its pathological and biological features leading to differences in diagnosis as well as in treatment response, resistance and targets as compared to NST.

Sections du résumé

BACKGROUND
Invasive lobular breast cancer (ILC) is the second most common type of breast cancer after invasive breast cancer of no special type (NST), representing up to 15% of all breast cancers.
DESIGN
Latest data on ILC are presented, focusing on diagnosis, molecular make-up according to the European Society for Medical Oncology Scale for Clinical Actionability of molecular Targets (ESCAT) guidelines, treatment in the early and metastatic setting and ILC-focused clinical trials.
RESULTS
At the imaging level, magnetic resonance imaging-based and novel positron emission tomography/computed tomography-based techniques can overcome the limitations of currently used imaging techniques for diagnosing ILC. At the pathology level, E-cadherin immunohistochemistry could help improving inter-pathologist agreement. The majority of patients with ILC do not seem to benefit as much from (neo-)adjuvant chemotherapy as patients with NST, although chemotherapy might be required in a subset of high-risk patients. No differences in treatment efficacy are seen for anti-human epidermal growth factor receptor 2 (HER2) therapies in the adjuvant setting and cyclin-dependent kinases 4 and 6 inhibitors in the metastatic setting. The clinical utility of the commercially available prognostic gene expression-based tests is unclear for patients with ILC. Several ESCAT alterations differ in frequency between ILC and NST. Germline BRCA1 and PALB2 alterations are less frequent in patients with ILC, while germline CDH1 (gene coding for E-cadherin) alterations are more frequent in patients with ILC. Somatic HER2 mutations are more frequent in ILC, especially in metastases (15% ILC versus 5% NST). A high tumour mutational burden, relevant for immune checkpoint inhibition, is more frequent in ILC metastases (16%) than in NST metastases (5%). Tumours with somatic inactivating CDH1 mutations may be vulnerable for treatment with ROS1 inhibitors, a concept currently investigated in early and metastatic ILC.
CONCLUSION
ILC is a unique malignancy based on its pathological and biological features leading to differences in diagnosis as well as in treatment response, resistance and targets as compared to NST.

Identifiants

pubmed: 35605746
pii: S0923-7534(22)01167-X
doi: 10.1016/j.annonc.2022.05.006
pii:
doi:

Substances chimiques

Cadherins 0
Proto-Oncogene Proteins 0

Types de publication

Journal Article Review Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

769-785

Commentaires et corrections

Type : ErratumIn

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Disclosure The authors have declared no conflicts of interest.

Auteurs

K Van Baelen (K)

Laboratory for Translational Breast Cancer Research (LTBCR), Department of Oncology, KU Leuven, Leuven, Belgium; Departments of Gynaecology and Obstetrics, UZ Leuven, Leuven, Belgium.

T Geukens (T)

Laboratory for Translational Breast Cancer Research (LTBCR), Department of Oncology, KU Leuven, Leuven, Belgium; General Medical Oncology, UZ Leuven, Leuven, Belgium.

M Maetens (M)

Laboratory for Translational Breast Cancer Research (LTBCR), Department of Oncology, KU Leuven, Leuven, Belgium.

V Tjan-Heijnen (V)

Medical Oncology Department, Maastricht University Medical Center (MUMC), School of GROW, Maastricht, The Netherlands.

C J Lord (CJ)

The CRUK Gene Function Laboratory and Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, UK.

S Linn (S)

Department of Pathology, University Medical Center Utrecht, Utrecht, The Netherlands; Departments of Medical Oncology, Amsterdam, The Netherlands; Molecular Pathology, Netherlands Cancer Institute, Amsterdam, The Netherlands.

F-C Bidard (FC)

Department of Medical Oncology, Institut Curie, UVSQ/Paris-Saclav University, Paris, France.

F Richard (F)

Laboratory for Translational Breast Cancer Research (LTBCR), Department of Oncology, KU Leuven, Leuven, Belgium.

W W Yang (WW)

The CRUK Gene Function Laboratory and Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, UK.

R E Steele (RE)

The CRUK Gene Function Laboratory and Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, UK.

S J Pettitt (SJ)

The CRUK Gene Function Laboratory and Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, UK.

C Van Ongeval (C)

Departments of Radiology, UZ Leuven, Leuven, Belgium.

M De Schepper (M)

Laboratory for Translational Breast Cancer Research (LTBCR), Department of Oncology, KU Leuven, Leuven, Belgium; Pathology, UZ Leuven, Leuven, Belgium.

E Isnaldi (E)

Laboratory for Translational Breast Cancer Research (LTBCR), Department of Oncology, KU Leuven, Leuven, Belgium.

I Nevelsteen (I)

Surgical Oncology, UZ Leuven, Leuven, Belgium.

A Smeets (A)

Surgical Oncology, UZ Leuven, Leuven, Belgium.

K Punie (K)

General Medical Oncology, UZ Leuven, Leuven, Belgium.

L Voorwerk (L)

Departments of Medical Oncology, The Netherlands Cancer Institute, Amsterdam, The Netherlands; Tumour Biology and Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.

H Wildiers (H)

General Medical Oncology, UZ Leuven, Leuven, Belgium.

G Floris (G)

Pathology, UZ Leuven, Leuven, Belgium.

A Vincent-Salomon (A)

Department of Pathology, Institut Curie, Paris, France.

P W B Derksen (PWB)

Department of Pathology, University Medical Center Utrecht, Utrecht, The Netherlands.

P Neven (P)

Departments of Gynaecology and Obstetrics, UZ Leuven, Leuven, Belgium.

E Senkus (E)

Department of Oncology and Radiotherapy, Medical University of Gdańsk, Gdańsk, Poland.

E Sawyer (E)

School of Cancer and Pharmaceutical Sciences, Faculty of Life Sciences and Medicine, Guy's Cancer Centre, King's College London, London, UK.

M Kok (M)

Departments of Medical Oncology, The Netherlands Cancer Institute, Amsterdam, The Netherlands; Tumour Biology and Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.

C Desmedt (C)

Laboratory for Translational Breast Cancer Research (LTBCR), Department of Oncology, KU Leuven, Leuven, Belgium. Electronic address: christine.desmedt@kuleuven.be.

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Classifications MeSH