Pathologic complete response and overall survival in breast cancer subtypes in stage III inflammatory breast cancer

Uden, Dominique J. P. van; Maaren, Marissa C. van; Bult, Peter; Strobbe, Luc J. A.; Hoeven, J. J. M. van der; Blanken-Peeters, C.F.J.M.; Siesling, Sabine; Wilt, Johannes H. W. de

doi:10.1007/s10549-019-05219-7

Cited by 40 publications

(43 citation statements)

References 32 publications

(48 reference statements)

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“…Firstly, the proportion of HER2-positive breast cancer in the IBC group was higher than the locally advanced breast cancer in non-IBC. In this study, the proportion of HER2-positive breast cancer in the IBC group (40.7%) was higher than the T4-non-IBC breast cancer group (29.8%) ( P < 0.01), which is consistent with the previous studies [ 15 , 16 ]. Thus, the IBC group was more likely to receive targeted therapy.…”

Section: Discussionsupporting

confidence: 93%

Comparison of survival in non-metastatic inflammatory and other T4 breast cancers: a SEER population-based analysis

et al. 2021

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Background Previous studies have reported poor survival rates in inflammatory breast cancer (IBC) patients than non-inflammatory local advanced breast cancer (non-IBC) patients. However, until now, the survival rate of IBC and other T4 non-IBC (T4-non-IBC) patients remains unexplored. Methods Surveillance, Epidemiology, and End Results (SEER) database was searched to identify cases with confirmed non-metastatic IBC and T4-non-IBC who had received surgery, chemotherapy, and radiotherapy between 2010 and 2015. IBC was defined as per the American Joint Committee on Cancer (AJCC) 7th edition. Breast Cancer-Specific Survival (BCSS) was estimated by plotting the Kaplan-Meier curve and compared across groups by using the log-rank test. Cox model was constructed to determine the association between IBC and BCSS after adjusting for age, race, stage of disease, tumor grade and surgery type. Results Out of a total of 1986 patients, 37.1% had IBC and mean age was 56.6 ± 12.4. After a median follow-up time of 28 months, 3-year BCSS rate for IBC and T4-non-IBC patients was 81.4 and 81.9%, respectively (log-rank p = 0.398). The 3-year BCSS rate in HR−/HER2+ cohort was higher for IBC patients than T4-non-IBC patients (89.5% vs. 80.8%; log-rank p = 0.028), and in HR−/HER2- cohort it was significantly lower for IBC patients than T4-non-IBC patients (57.4% vs. 67.5%; log-rank p = 0.010). However, it was identical between IBC and T4-non-IBC patients in both HR+/HER2- (85.0% vs. 85.3%; log-rank p = 0.567) and HR+/HER2+ (93.6% vs. 91.0%, log-rank p = 0.510) cohorts. After adjusting for potential confounding variables, we observed that IBC is a significant independent predictor for survival of HR−/HER2+ cohort (hazards ratio [HR] = 0.442; 95% CI: 0.216–0.902; P = 0.025) and HR−/HER2- cohort (HR = 1.738; 95% CI: 1.192–2.534; P = 0.004). Conclusions Patients with IBC and T4-non-IBC had a similar BCSS in the era of modern systemic treatment. In IBC patients, the HR−/HER2+ subtype is associated with a better outcome, and HR−/HER2- subtype is associated with poorer outcomes as compared to the T4-non-IBC patients.

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Section: Discussionsupporting

confidence: 93%

Comparison of survival in non-metastatic inflammatory and other T4 breast cancers: a SEER population-based analysis

et al. 2021

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“…In a retrospective study with 13,939 breast cancer patients, patients with the Luminal A subtype had the lowest pCR rate (0.3%) and the highest pCR rate was observed in HER-2 positive patients (38.7%) 27 . Most of previous studies supported that patients with HER-2 positive breast cancer who received chemotherapy combination with targeted therapy achieved the highest pCR rate, especially those treated with dual targeted therapy 8 , 27 , 28 . The total clinical response rate was 30.5% in our study and responders had a significant higher pCR rate than non-responders (50% vs 18%).…”

Section: Discussionmentioning

confidence: 94%

Early response and pathological complete remission in Breast Cancer with different molecular subtypes: a retrospective single center analysis

Jiang¹,

Wu²,

Huang³

et al. 2020

J. Cancer

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Purpose: To evaluate the association of clinical early response and pathological complete remission (pCR) in breast cancer patients with different molecular subtypes. Materials and methods: Breast cancer patients who received neoadjuvant treatment (NAT) with clinical early response assessment from October 2008 to October 2018 were retrospectively analyzed. Clinical early response was defined as tumor size decreasing ≥30% evaluated by ultrasound after two cycles of NAT. Chi-square test was used to compare the pCR rates between the responder and non-responder groups with different molecular subtypes. Multivariate logistic regression was used to identify independent factors associated with the pCR. Results: A total of 328 patients were included: 100 responders and 228 non-responders. The progesterone receptor (PR) expression was an independent factor associated with clinical early response (OR=2.39, 95%CI=1.41-4.05, P =0.001). The pCR rate of breast was 50.0% for responders and 18.0% for non-responders ( P <0.001). Regarding different molecular subtypes, responders had higher pCR rates than non-responders for patients with HER2 overexpression (OR=10.66, 95%CI=2.18-52.15, P =0.001), triple negative (OR=3.29, 95%CI=1.23-8.84, P =0.016) and Luminal (HER2-) subtypes (OR=8.58, 95%CI=3.05-24.10, P <0.001) respectively. Moreover, pCR rate can be achieved as high as 88.2% in HER2 overexpression patients with early clinical response, which was significantly higher than patients without early response (41.3%, P =0.001). Multivariate analysis showed that clinical early response was an independent factor associated with the pCR rate (OR=4.87, 95%CI=2.72-8.72, P <0.001). Conclusions: Early response was significantly associated with a higher pCR rate in breast cancer patients receiving NAT, especially for patients with HER2 overexpression subtype, which warrants further clinical evaluation.

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“…IBC patients thus exhibit lower the 5-year overall survival than other breast cancer forms. However, prognosis of IBC can be improved by trimodality treatment, namely neoadjuvant chemotherapy, surgery and radiotherapy [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Induction of heparanase via IL-10 correlates with a high infiltration of CD163+ M2-type tumor-associated macrophages in inflammatory breast carcinomas

El-Nadi

Hassan

Saleh

et al. 2020

Matrix Biology Plus

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Inflammatory breast cancer (IBC) is the most aggressive and lethal form of breast cancer, characterized by a high infiltration of tumor-associated macrophages and poor prognosis. To identify new biomarkers and to elucidate the molecular mechanisms underlying IBC pathogenesis, we investigated the expression pattern of heparanase (HPSE) and its activator cathepsin L (CTSL). First, we quantitated the HPSE and CTSL mRNA levels in a cohort of breast cancer patients after curative surgery (20 IBC and 20-non-IBC). We discovered that both HPSE and CTSL mRNA levels were significantly induced in IBC tissue vis-à-vis non-IBC patients ( p <0 .05 and p <0 .001, respectively). According to the molecular subtypes, HPSE mRNA levels were significantly higher in carcinoma tissues of triple negative (TN)-IBC as compared to TN-non-IBC ( p <0 .05). Mechanistically, we discovered that pharmacological inhibition of HPSE activity resulted in a significant reduction of invasiveness in the IBC SUM149 cell line. Moreover, siRNA-mediated HPSE knockdown significantly downregulated the expression of the metastasis-related gene MMP2 and the cancer stem cell marker CD44. We also found that IBC tumors revealed robust heparanase immune-reactivity and CD163+ M2-type tumor-associated macrophages, with a positive correlation of both markers. Moreover, the secretome of axillary tributaries blood IBC CD14+ monocytes and the cytokine IL-10 significantly upregulated HPSE mRNA and protein expression in SUM149 cells. Intriguingly, massively elevated IL-10 mRNA expression with a trend of positive correlation with HPSE mRNA expression was detected in carcinoma tissue of IBC. Our findings highlight a possible role played by CD14+ monocytes and CD163+ M2-type tumor-associated macrophages in regulating HPSE expression possibly via IL-10. Overall, we suggest that heparanase, cathepsin L and CD14+ monocytes-derived IL-10 may play an important role in the pathogenesis of IBC and their targeting could have therapeutic implications.

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Pathologic complete response and overall survival in breast cancer subtypes in stage III inflammatory breast cancer

Cited by 40 publications

References 32 publications

Comparison of survival in non-metastatic inflammatory and other T4 breast cancers: a SEER population-based analysis

Comparison of survival in non-metastatic inflammatory and other T4 breast cancers: a SEER population-based analysis

Early response and pathological complete remission in Breast Cancer with different molecular subtypes: a retrospective single center analysis

Induction of heparanase via IL-10 correlates with a high infiltration of CD163+ M2-type tumor-associated macrophages in inflammatory breast carcinomas

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