Treatment response and clinical outcomes of patients with triple negative invasive apocrine breast carcinoma.

C Courtnie Brown (UCLA Jonsson Comprehensive Cancer Center, Los Angeles, CA) P Paige Brown A Alexis Ann LeVee (Department of Medicine, Division of Hematology/Oncology, University of California Los Angeles, Los Angeles, CA) M Marla Lipsyc-Sharf (University of California, Los Angeles, Los Angeles, CA) A Aashini Master (UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA) R Rena Desai Callahan (UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA) M Mina S. Sedrak (UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA) K Kelly Elizabeth McCann (UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA) S Samer Alkassis (UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA) M Mediget Teshome (UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA) S Susan Ann McCloskey (University of California, Los Angeles, Los Angeles, CA) J Jennifer Baker (Department of Microbiology, Immunology and Molecular Genetics, David Geffen Scho, Los Angeles, CA) J Joanne B. Weidhaas (Department of Radiation Oncology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA) A Aditya Bardia N Nicholas Patrick McAndrew (UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA)

Abstract

e12727 Background: Invasive apocrine carcinoma (IAC) is a rare subtype of breast cancer that is classically triple negative (TN) and associated with lower grade and proliferation rates compared to ductal triple negative breast cancer. Despite these pathologic features that suggest a lack of response to cytotoxic chemotherapy, apocrine and non-apocrine breast cancers are commonly managed with similar systemic treatment approaches. We investigated the treatment courses and outcomes of patients with TN-IAC. Methods: We conducted a retrospective cohort study using electronic medical record review of patients diagnosed with early-stage IAC treated at a single academic institution to determine treatment courses and outcomes. We identified patients in which “apocrine” was used as a descriptor of pathology. Given inconsistent pathologic definitions, patients were classified into two groups. Classical apocrine (c-IAC) tumors were defined as TN disease with pathology specifically designated as “IAC” or invasive ductal carcinoma with apocrine features with low grade (grade 1–2) and Ki-67 ≤ 20%. The “Other Apocrine” group consisted of those patients with high grade disease with apocrine features, Ki-67 > 20%, and/or HER2 or hormone receptor positivity. Patients with de novo metastatic disease and those without invasive disease were excluded. Data collected included clinicopathologic characteristics and type of local/regional and systemic therapies received. Our primary outcome was recurrence free interval (RFI) defined as the absence of recurrence from the time of diagnosis to the last documented follow up date. Results: We identified 69 cases with apocrine used as a descriptor of pathology. Of those 69, we identified 18 c-IAC cases and 41 Other Apocrine cases. c-IAC patients were more likely to have chemotherapy omitted (39% vs 5%, p value of .024). In the c-IAC group there were 0 recurrences over the median follow up of 52.7 months. Among the Other Apocrine patients there were 13 recurrences over the median follow up of 104.5 months. Conclusions: Patients with TN c-IAC had no documented recurrences and were less likely to receive chemotherapy than patients with other types of apocrine-related carcinoma of the breast. Classical apocrine carcinoma of the breast represents an identifiable subtype of breast cancer which may allow for chemotherapy de-escalation. Cohort characteristics. Category c-IAC (n=18) Other Apocrine (n=41) Age (median, range) 67.5 (44-89) 62 (30-87) ER+ (>10%) (%) 0 (0) 16 (39) HER2+ (%) 0 (0) 15 (37) Elevated Ki67 ≥ 20% (%) 3 (17) 22 (54) Tumor Size in cm (median, range) 1.7 (0.8-4.1) 2.0 (0.3-11.0) Node positive (%) 3 (17) 16 (39) Receipt of chemotherapy (%) 11 (61) 39 (95) Median Follow Up (months) 52.7 (3.7-171.8) 104.5 (<0.1-292.6) Recurrence, n (%) 0 (0) 13 (32%)

Article Details

Volume / Issue Vol. 44, Issue 16_suppl
Published June 01, 2026
ISSN 0732-183X
Publisher Lippincott Williams & Wilkins

Journal Info

Journal of Clinical Oncology

Lippincott Williams & Wilkins

ISSN: 0732-183X Health Sciences

Authors (15)

C

Courtnie Brown

UCLA Jonsson Comprehensive Cancer Center, Los Angeles, CA

P

Paige Brown

A

Alexis Ann LeVee

Department of Medicine, Division of Hematology/Oncology, University of California Los Angeles, Los Angeles, CA

M

Marla Lipsyc-Sharf

University of California, Los Angeles, Los Angeles, CA

A

Aashini Master

UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA

R

Rena Desai Callahan

UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA

M

Mina S. Sedrak

UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA

K

Kelly Elizabeth McCann

UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA

S

Samer Alkassis

UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA

M

Mediget Teshome

UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA

S

Susan Ann McCloskey

University of California, Los Angeles, Los Angeles, CA

J

Jennifer Baker

Department of Microbiology, Immunology and Molecular Genetics, David Geffen Scho, Los Angeles, CA

J

Joanne B. Weidhaas

Department of Radiation Oncology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA

A

Aditya Bardia

N

Nicholas Patrick McAndrew

UCLA Health Jonsson Comprehensive Cancer Center, Los Angeles, CA