Metaplastic Breast Carcinoma: Experience of a Tertiary Cancer Center in the Middle East

Abstract

Background: Metaplastic breast cancer (MetBC) represents a therapeutic challenge. We evaluated the impact of clinicopathological characteristics and treatment modalities on outcomes among MetBC patients treated at our center. Methods: Women with stage I-III MetBC were reviewed from our database from 2005-2018. Kaplan-Meier method was used to calculate locoregional-failure-free survival (LRFFS), overall-survival (OS) and distant-metastases-free survival (DMFS). We assessed associations with survival outcomes by log-rank tests. Multivariate Cox proportional-hazards models were used to identify independent predictors of LRFFS, OS and DMFS. Results: 81 patients were eligible for the study. Median age at diagnosis was 48 years. 90.1% had G-III tumors, 64.2% were pathologically node negative and lympho-vascular invasion (LVI) was absent in 72.8%. 67.8% were triple negative, and 7.4% were HER2-neu positive. Most (66.7%) patients underwent mastectomy. Free margins were achieved in the entire cohort, however, 17.3% had close margin (<2 mm). Almost all patients received chemotherapy. 75.3% received radiotherapy, 23.5% received hormonal therapy and 6.2% received Trastuzumab. With a median follow-up of 54 months, 18.5% developed loco-regional recurrence and 34.6% relapsed distally. Five-year OS was 66.0%. On multivariate analysis: adjuvant radiotherapy correlated with better OS ( P < .0001), and tumor size >5 cm, nodal involvement and LVI correlated with worse OS, ( P = .019, P = .021, P = .028, respectively). There were no survival differences with respect to age, triple negativity, and morphologic subtype. Conclusion: We report the largest single institutional series on MetBC in the Middle East region. MetBC confers worse survival outcomes, and more aggressive local and systemic treatment strategies should be investigated.

Clinicopathologic Features of Metaplastic Breast Carcinoma: Experience From a Tertiary Cancer Center of North India

“…In our series, 14 patients (50%) experienced locally advanced disease T3/T4 disease and two patients (7.1%) were metastatic at presentation. Even though the lymphatic spread is less common, the reported incidence of nodal spread varies from around 27-64% [9,13] [14,15]. The aforementioned observation is significantly higher when compared to our study (10.3%).…”

“…Axillary nodal involvement was recognized in eight patients (32%) in our study. LVI was present in five patients (17.9%), which is lower than that chronicled by Rakha et al (21%) and Erjan et al (27.2%) [ 14 , 15 ]. The prevalence of DCIS in MBC is less compared to IBC NST, which is associated with 80% DCIS.…”

“…The prevalence of DCIS in MBC is less compared to IBC NST, which is associated with 80% DCIS. Rakha et al documented the DCIS component in 42% of their cohort while Erjan et al registered this finding in 39.5% of cases [ 14 , 15 ]. The aforementioned observation is significantly higher when compared to our study (10.3%).…”

“…Erjan et al reported that in 33 of the 81 MBC patients (~ 40%) who received NACT, 14 patients (42.4%) had disease progression, and only two patients (6%) achieved a pathological complete response[15]. In our series, 14 patients (50%) received NACT, out of which five patients (35.7%) harbored stable disease, another five (35.7%) manifested disease progression, four (28.6%) illustrated partial response, and none evinced complete response.…”

Nanomaterial-assisted CRISPR gene-engineering – A hallmark for triple-negative breast cancer therapeutics advancement

“…However, 30% of BC deaths occur because of TNBC destructive pathology and metastasis [ 10 , 11 ]. It has the most rapid and aggressive metastasis, and progression compared to other forms of BC [ 3 ], and generally occurs in premenopausal women, who hardly survive longer than two years [ 12 , 13 ]. Additionally, TNBC has been conveyed to be more usual in either germline-based (20–25%), or somatic (5–10%) deficit in BRCA DNA repair associated ( BRCA ) gene [ 14 ], which shelters TP53 mutation that deactivates p53 protein [ 3 ].…”