Triple-negative breast cancer: treatment challenges and solutions

Collignon, Joëlle; Lousberg, Laurence; Schroeder, Hélène; Jérusalem, Guy

doi:10.2147/bctt.s69488

Cited by 193 publications

(117 citation statements)

References 99 publications

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“…The standard therapy for this molecular type of cancer includes agents such as taxanes, anthracyclines and cyclophosphamide [42] and is similar to other HER2- breast cancers [43]. Other therapeutic strategies include the use of poly ADP ribose polymerase inhibitors (PARP inhibitors), EGFR inhibitors, Src family kinase inhibitors and antiandrogens [43].…”

Section: Is Triple-negative Breast Cancer Diagnosis a Death Sentence?mentioning

confidence: 99%

Triple negative breast cancer: the kiss of death

et al. 2017

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One of the most controversial women malignancies, triple negative breast cancers (TNBCs) are critically overviewed here, being focused on data useful in clinical practice or to improve the therapy and patients survival. TNBCs “choose” young women and its “kiss” is, unfortunately deadly in most cases. Currently, few sparse data are available in literature concerning the origins of TNBC. Vasculogenic mimicry detected in TNBCs, seems to be determined by a population of CD133+ cells and may be stimulated by different pharmacological agents such sunitinib. Despite the fact that TNBCs do not usually metastasize through the lymphatic pathways, TNBCs may be characterized by lymphatic invasion and by an increased lymphatic microvascular density. If TNBCs treatment depends on the molecular profile of the tumor, the same statement may be postulated for TNBCs metastasis. Whether metastases have a similar phenotype as the primary tumor remains an enigma. Therefore, the question: ‘Could TNBC be subject to a standardized, unanimously accepted therapeutic strategy or is it strictly subclass-dependent?’ remains to be further investigated.

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Section: Is Triple-negative Breast Cancer Diagnosis a Death Sentence?mentioning

confidence: 99%

Triple negative breast cancer: the kiss of death

et al. 2017

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“…Patients with TNBC have poor prognosis due to the lack of effective therapeutic options (2,3). TNBC represents about 10% of all breast cancer cases and about 35% of TNBC patients suffer metastasis within years of diagnosis (4).…”

Section: Introductionmentioning

confidence: 99%

Vitamin D compounds inhibit cancer stem-like cells and induce differentiation in triple negative breast cancer

Shan

Wahler

Lee

et al. 2017

The Journal of Steroid Biochemistry and Molecular Biology

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Triple-negative breast cancer is one of the least responsive breast cancer subtypes to available targeted therapies due to the absence of hormonal receptors, aggressive phenotypes, and the high rate of relapse. Early breast cancer prevention may therefore play an important role in delaying the progression of triple-negative breast cancer. Cancer stem cells are a subset of cancer cells that are thought to be responsible for tumor progression, treatment resistance, and metastasis. We have previously shown that vitamin D compounds, including a Gemini vitamin D analog BXL0124, suppress progression of ductal carcinoma in situ in vivo and inhibit cancer stem-like cells in MCF10DCIS mammosphere cultures. In the present study, the effects of vitamin D compounds in regulating breast cancer stem-like cells and differentiation in triple-negative breast cancer were assessed. Mammosphere cultures, which enriches for breast cancer cells with stem-like properties, were used to assess the effects of 1α,25(OH)2D3 and BXL0124 on cancer stem cell markers in the triple-negative breast cancer cell line, SUM159. Vitamin D compounds significantly reduced the mammosphere forming efficiency in primary, secondary and tertiary passages of mammospheres compared to control groups. Key markers of cancer stem-like phenotype and pluripotency were analyzed in mammospheres treated with 1α,25(OH)2D3 and BXL0124. As a result, OCT4, CD44 and LAMA5 levels were decreased. The vitamin D compounds also down-regulated the Notch signaling molecules, Notch1, Notch2, Notch3, JAG1, JAG2, HES1 and NFκB, which are involved in breast cancer stem cell maintenance. In addition, the vitamin D compounds up-regulated myoepithelial differentiating markers, cytokeratin 14 and smooth muscle actin, and down-regulated the luminal marker, cytokeratin 18. Cytokeratin 5, a biomarker associated with basal-like breast cancer, was found to be significantly down-regulated by the vitamin D compounds. These results suggest that vitamin D compounds may serve as potential preventive agents to inhibit triple negative breast cancer by regulating cancer stem cells and differentiation.

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“…Indeed, highly aggressive triple-negative breast cancer (TNBC), characterized by the absence of ER, progesterone receptor (PR) or HER2, is much more prevalent in AA women [4]. TNBC suffers from lack of targeted therapy and chemotherapy remains the only option for disease management [5–7]. Doxorubicin (adriamycin), a conventional anthracycline, has been an important mainstay in the treatment of BC [8].…”

Section: Introductionmentioning

confidence: 99%

Resistin potentiates chemoresistance and stemness of breast cancer cells: Implications for racially disparate therapeutic outcomes

et al. 2017

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Breast cancer (BC) continues to be the most frequently diagnosed cancer in American women, which disproportionately affects women of African-American (AA) descent. Previously, we reported greater serum levels of resistin in AA BC patients relative to Caucasian-American (CA) patients, and established its role in growth and aggressiveness of breast tumor cells. Here we have investigated the role of resistin in BC-chemoresistance. MDA-MB-231 and MDA-MB-468 BC cells of CA and AA origin, respectively, were incubated with resistin prior to doxorubicin treatment. Our data suggest that resistin conferred chemoresistance to both BC cell lines; however, the effect on AA cells was more profound. Furthermore, the resistin-induced doxorubicin-resistance was shown to occur due to suppression of apoptosis. Resistin treatment also affected the stemness of BC cells, as suggested by reduced cell surface expression of CD24, induced expression of CD44 and ALDH1, and increased capability of cells to form mammospheres. Mechanistic studies revealed that resistin-induced chemoresistance, apoptosis and stemness of BC cells were mediated through STAT3 activation. Taken together, our findings provide novel insight into the role of resistin in BC biology, and strengthen its role in racially disparate clinical outcomes.

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Triple-negative breast cancer: treatment challenges and solutions

Cited by 193 publications

References 99 publications

Triple negative breast cancer: the kiss of death

Triple negative breast cancer: the kiss of death

Vitamin D compounds inhibit cancer stem-like cells and induce differentiation in triple negative breast cancer

Resistin potentiates chemoresistance and stemness of breast cancer cells: Implications for racially disparate therapeutic outcomes

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