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C
URRENT
O
PINION
Targeting HER2 heterogeneity in early-stage
breast cancer
Sonia Pernas
a
and Sara M. Tolaney
b
Purpose of review
HER2-positive (HER2þ) breast cancer is clinically and biologically a heterogenous disease and not all
patients benefit to the same extent from current anti-HER2 therapies.
Recent findings
Among HER2þ breast cancer, molecular intrinsic subtypes, PIK3CA mutation status, levels of HER2 gene/
protein, immune infiltration, or intratumor heterogeneity modulate HER2-treatment sensitivity. HER2-enriched
carcinomas, with high levels of HER2 and tumor-infiltrating lymphocytes (TILs) are highly sensitive to anti-
HER2 therapies, regardless of chemotherapy. Luminal A/B tumors are more estrogen receptor-dependent
than HER2-dependent, harbor higher rates of PIK3CA mutations, and are less responsive to anti-HER2
treatment. HER2 intratumoral heterogeneity that exists in approximately 10% of HER2þ disease may also
cause treatment resistance. Early changes occur during neoadjuvant anti-HER2 therapy that can predict
response. Importantly, HER2 expression is not a binary but rather a continuous variable. Overall, 34–63%
of HER2-negative breast cancers express HER2, and HER2-low tumors have become a new entity, for which
novel targeted therapies may be effective.
Summary
Although much of what is discussed currently remains investigational, it is clear that HER2þ breast cancer
is a complex disease comprising different entities. Future strategies to escalate or de-escalate treatment in
early-stage HER2þ disease should consider other biomarkers beyond HER2 and estrogen receptor status,
including intrinsic subtype, HER2 levels, and TILs; and evaluate different treatment strategies among patients
with estrogen receptor-positive/HER2þ and estrogen receptor-negative/HER2þ diseases.
Keywords
HER2, HER2-enriched, HER2-low, heterogeneity, immune-profile
INTRODUCTION
The introduction of HER2-targeting therapies to
standard treatment has dramatically improved the
prognosis for HER2-positive (HER2þ) breast cancer
patients in both the early and metastatic settings.
The discovery of the HER2 oncogene and the devel-
opment of trastuzumab, a humanized mAb that
binds to HER2 causing HER2 downregulation, were
landmarks in the treatment of this disease. Pertuzu-
mab, another mAb that binds to HER2 and prevents
HER2/HER3 formation, one of the most powerful
heterodimers that activates cell proliferation and
survival, was the second anti-HER2 agent incorpo-
rated into the treatment of early-stage HER2þ breast
cancer. In the first-line treatment of advanced dis-
ease, the combination of pertuzumab, trastuzumab,
and docetaxel resulted in an 8-year landmark overall
survival (OS) rate of 37% [1], and in the neoadjuvant
setting, the introduction of pertuzumab to standard
neoadjuvant treatment resulted in a significant
increase in pathological complete response (pCR)
rates. However, results in the adjuvant setting have
been modest. The addition of pertuzumab to tras-
tuzumab and adjuvant chemotherapy resulted in a
3-year rate of invasive disease-free survival (iDFS)
benefit only observed in node-positive patients (92
vs. 90.2%; Hazard ratio 0.81; P ¼ 0.02). This benefit
was maintained in the 6-year analysis with a 24%
decrease in iDFS and an absolute risk reduction of
a
Department of Medical Oncology, Catalan Institute of Oncology (ICO)-
H.U.Bellvitge-IDIBELL, Barcelona, Spain and
b
Department of Medical
Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA
Correspondence to Sara M. Tolaney, MD, MPH, Department of Medical
Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston,
MA 02215, USA. Tel: +1 617 632 3800;
e-mail: Sara_Tolaney@DFCI.HARVARD.EDU
Curr Opin Oncol 2020, 32:545–554
DOI:10.1097/CCO.0000000000000685
1040-8746 Copyright ß 2020 Wolters Kluwer Health, Inc. All rights reserved. www.co-oncology.com
REVIEW