Inflammatory breast cancer: New factors contribute to disease etiology: A review

Mohamed, Mona Mostafa; Al-Raawi, Diaa; Sabet, Salwa; El-Shinawi, Mohamed

doi:10.1016/j.jare.2013.06.004

Cited by 46 publications

(54 citation statements)

References 130 publications

(158 reference statements)

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“…Inflammatory breast cancer (IBC) is usually distinguished from non-IBC by specific morphologic, phenotypic, biologic properties, and a poorer outcome (41). We found higher baseline tumor glucidic metabolism (SUV1 max ) in IBC than in non-IBC.…”

Section: Biologic Biomarkers Of Tumor Responsementioning

confidence: 74%

Identification of Biomarkers Including 18FDG-PET/CT for Early Prediction of Response to Neoadjuvant Chemotherapy in Triple-Negative Breast Cancer

Humbert

Riedinger

Charon-Barra

et al. 2015

Clinical Cancer Research

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Purpose: To investigate the value of the metabolic tumor response assessed with 18 F-fluorodeoxyglucose positron emission tomography (FDG-PET), compared with clinicobiologic markers to predict pathologic complete response (pCR) to neoadjuvant chemotherapy (NAC) in women with triple-negative breast cancer (TNBC).Experimental Design: Fifty consecutive women with TNBC and an indication for NAC were prospectively included. Different pretreatment clinical, biologic, and pathologic biomarkers, including SBR grade, the Ki-67 proliferation index, androgen receptor expression, EGF receptor (EGFR), and cytokeratin 5/6 staining, were assessed. Tumor glucose metabolism at baseline and its change after the first cycle of NAC (DSUV max ) were assessed using FDG-PET.Results: The pCR rate was 42%. High Ki-67 proliferation index (P ¼ 0.016), negative EGFR status (P ¼ 0.042), and high DSUV max (P ¼ 0.002) were significantly associated with pCR. In multivariate logistic regression, both negative EGFR status (OR, 6.4; P ¼ 0.043) and high DSUV max (OR, 7.1; P ¼ 0.014) were independent predictors of pCR. Using a threshold at À50%, tumor DSUV max predicted pCR with a negative, a positive predictive value, and an accuracy of 79%, 70%, and 75%, respectively. Combining a low DSUV max and positive EGFR status could predict non-pCR with an accuracy of 92%.Conclusions: It is important to define the chemosensitivity of TNBC to NAC early. Combining EGFR status and the metabolic response assessed with FDG-PET can help the physician to early predict the probability of achieving pCR or not. Given these results, the interest of response-guided tailoring of the chemotherapy might be tested in multicenter trials.

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Section: Biologic Biomarkers Of Tumor Responsementioning

confidence: 74%

Identification of Biomarkers Including 18FDG-PET/CT for Early Prediction of Response to Neoadjuvant Chemotherapy in Triple-Negative Breast Cancer

Humbert

Riedinger

Charon-Barra

et al. 2015

Clinical Cancer Research

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“…IBC patients with CTCs in the peripheral blood had abnormalities in adaptive immunity that may impact tumor cell dissemination (72). IBC carcinoma tissues exhibit marked monocytes/ macrophages infiltrates localized around tumor emboli (73). This influx of macrophages within the IBC tumor microenvironment correlated with increase in the number of positive lymph node metastasis and expression of cathepsins and MMPs.…”

Section: Sclc and Ctcsmentioning

confidence: 99%

Circulating tumor cell interactions with macrophages: implications for biology and treatment

Hamilton¹,

Rath²

2017

Transl. Lung Cancer Res.

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CTCs. SCLC has an unfavorable prognosis due to rapid dissemination and early chemoresistant relapses. SCLC CTCs recruit macrophages and elicit secretion of various cytokines and the six CTC lines expresschitinase-3-like-1 (CHI3L1), vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP9) in abundance. CHI3L1 is cytokine/growth factor expressed in inflammation and cancer and found to be correlated to metastasis and a dismal prognosis. In conclusion, SCLC CTCs have acquired the essential means for aggressiveness and invasion in a tumor microenvironment specifically shaped by macrophages and inflammation.

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“…Inflammatory breast cancer (IBC) is the most aggressive and lethal form of primary breast cancer (1,2). IBC is a clinically and pathologically unique subtype of breast cancer that accounts for up to 5% of breast cancer.…”

Section: Introductionmentioning

confidence: 99%

“…The inflammatory skin response results from dermal lymphatic invasion, a hallmark of IBC, whereby lymphovascular spaces are occupied by tumor emboli (2). The presence of multiple dermal and stromal tumor emboli is distinguishing pathologic characteristics of IBC (2).…”

Section: Introductionmentioning

confidence: 99%

“…The contradictory nature of the immune data highlights the necessity of elucidating the relationship among the immune response, IBC tumorigenesis, and subsequent treatments. IBC immunotherapies are currently under investigation in the preclinical setting (2). Given the active IBC immune component and the recent clinical benefit of immune checkpoint inhibitors in cancer treatment (7), IBCs may represent a clinically unique breast cancer population that may benefit from immunomodulating agents.…”

Section: Introductionmentioning

confidence: 99%

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Genomic and Immunological Tumor Profiling Identifies Targetable Pathways and Extensive CD8+/PDL1+ Immune Infiltration in Inflammatory Breast Cancer Tumors

Hamm

Moran

Rao

et al. 2016

Molecular Cancer Therapeutics

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Inflammatory breast cancer (IBC) is a rare and aggressive form of breast cancer that remains poorly understood at the molecular level. Comprehensive tumor profiling was performed to understand clinically actionable alterations in IBC. Targeted next-generation sequencing (NGS) and IHC were performed to identify activated pathways in IBC tumor tissues. siRNA studies examined the impact of IBC genomic variants in cellular models. IBC tumor tissues were further characterized for immune infiltration and immune checkpoint expression by IHC. Genomic analysis identified recurrent alterations in core biologic pathways, including activating and targetable variants in HER/PI3K/mTOR signaling. High rates of activating HER3 point mutations were discovered in IBC tumors. Cell line studies confirmed a role for mutant HER3 in IBC cell proliferation. Immunologic analysis revealed a subset of IBC tumors associated with high CD8infiltration. Immune infiltration positively correlated with an NGS-based estimate of neoantigen exposure derived from the somatic mutation rate and mutant allele frequency, iScore. Additionally, DNA mismatch repair alterations, which may contribute to higher iScores, occurred at greater frequency in tumors with higher immune infiltration. Our study identifies genomic alterations that mechanistically contribute to oncogenic signaling in IBC and provides a genetic basis for the selection of clinically relevant targeted and combination therapeutic strategies. Furthermore, an NGS-based estimate of neoantigen exposure developed in this study (iScore) may be a useful biomarker to predict immune infiltration in IBC and other cancers. The iScore may be associated with greater levels of response to immunotherapies, such as PD-L1/PD-1-targeted therapies.

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Inflammatory breast cancer: New factors contribute to disease etiology: A review

Cited by 46 publications

References 130 publications

Identification of Biomarkers Including 18FDG-PET/CT for Early Prediction of Response to Neoadjuvant Chemotherapy in Triple-Negative Breast Cancer

Identification of Biomarkers Including 18FDG-PET/CT for Early Prediction of Response to Neoadjuvant Chemotherapy in Triple-Negative Breast Cancer

Circulating tumor cell interactions with macrophages: implications for biology and treatment

Genomic and Immunological Tumor Profiling Identifies Targetable Pathways and Extensive CD8+/PDL1+ Immune Infiltration in Inflammatory Breast Cancer Tumors

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