Management of brain metastases in breast cancer: a review of current practices and emerging treatments

Mills, Matthew; Figura, Nicholas; Arrington, John A.; Yu, Hsiang-Hsuan Michael; Etame, Arnold B.; Vogelbaum, Michael A.; Soliman, Hatem; Czerniecki, Brian J.; Forsyth, Peter; Han, Hyo S.; Ahmed, Kamran A.

doi:10.1007/s10549-020-05552-2

Cited by 59 publications

(47 citation statements)

References 144 publications

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“…23,24 Metastasis is also an important risk factor for cancer recurrence after clinical surgery, chemotherapy, or radiotherapy. 25,26 Because of high recurrence and high metastasis, HCC is one of the malignant tumors with the highest mortality rate. The identification of mechanism in HCC metastasis is in a need for HCC treatment and prognosis.…”

Section: Discussionmentioning

confidence: 99%

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

Zhang¹,

Tian²,

Bei³

et al. 2020

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Background: Our recent study identified that human chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing family member 2 (CMTM2) was deregulated in hepatocellular carcinoma (HCC) tissues and posed as a potential tumor suppressor. However, the mechanism of CMTM2 in HCC occurrence and development has not been well elaborated. Materials and Methods: The expression of CMTM2 was knocked-down by RNA interruption in Huh-7 and SMMC7721 cells. Cell proliferation ability was detected by CCK8 test and colony formation assay. The cell invasion and migration were measured by wound healing and Transwell assay. Results: We found that the cell proliferation was significantly increased by interruption of CMTM2 expression, both in Huh-7 and SMMC7721 cells. Moreover, down-regulated CMTM2 could promote the invasion and migration ability of HCC cells through inducing the epithelial-mesenchymal transition (EMT) process. We further discovered that both the expression of CMTM2 and the EMT-associated marker E-cadherin were decreased in the same thirty cases of HCC tissues compared with the corresponding adjacent non-tumor tissues. Pearson correlation test showed that there was a significantly positive correlation between CMTM2 and E-cadherin in HCC tissues (P<0.05). Conclusion: Based on the results of cell model and HCC tissues, our study suggests that down-regulated CMTM2 promotes HCC metastasis through inducing the EMT process.

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Section: Discussionmentioning

confidence: 99%

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

Zhang¹,

Tian²,

Bei³

et al. 2020

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“…40 The loss of BBB integrity due to neuroinflammation, upregulation of proteolytic enzymes, and direct destruction by TNBC cells may promote metastatic invasion. 41 The partial destruction of the BBB leads to increased invasion of tumor cells and related molecules, thereby potentially promoting tumor cell brain colonization. When tumor cells enter the brain, they mainly gather at the branching points of cerebral vessels and further exude and invade.…”

Section: Tnbc Cellsmentioning

confidence: 99%

Understanding Patterns of Brain Metastasis in Triple-Negative Breast Cancer and Exploring Potential Therapeutic Targets

et al. 2021

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Triple-negative breast cancer (TNBC) is a highly malignant subtype of breast cancer. High invasiveness and heterogeneity, as well as a lack of drug targets, are the main factors leading to poor prognosis. Brain metastasis (BM) is a serious event threatening the life of breast cancer patients, especially those with TNBC. Compared with that for hormone receptor-positive and HER2-positive breast cancers, TNBC-derived BM (TNBCBM) occurs earlier and more frequently, and has a worse prognosis. There is no standard treatment for BM to date, and one is urgently required. In this review, we discuss the current knowledge regarding the developmental patterns of TNBCBM, focusing on the key events in BM formation. Specifically, we consider (i) the nature and function of TNBC cells; (ii) how TNBC cells cross the blood-brain barrier and form a fenestrated, more permeable bloodtumor barrier; (iii) the biological characteristics of TNBCBM; and (iv) the infiltration and colonization of the central nervous system (CNS) by TNBC cells, including the establishment of premetastatic niches, immunosurveillance escape, and metabolic adaptations. We also discuss putative therapeutic targets and precision therapy with the greatest potential to treat TNBCBM, and summarize the relevant completed and ongoing clinical trials. These findings may provide new insights into the prevention and treatment of BM in TNBC patients.

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“…Breast cancer brain metastases (BCBM) have become an increasingly common diagnosis in advanced breast cancer [1]. Triple negative and HER2+ breast cancers have been identified as risk factors for the development of brain metastases [2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Capecitabine and stereotactic radiation in the management of breast cancer brain metastases

et al. 2021

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Background Little is known about the safety and efficacy of concurrent capecitabine and stereotactic radiotherapy in the setting of breast cancer brain metastases (BCBM). Methods Twenty-three patients with BCBM underwent 31 stereotactic sessions to 90 lesions from 2005 to 2019 with receipt of capecitabine. The Kaplan-Meier method was used to calculate overall survival (OS), local control (LC), and distant intracranial control (DIC) from the date of stereotactic radiation. Imaging was independently reviewed by a neuro-radiologist. Results Median follow-up from stereotactic radiation was 9.2 months. Receptor types of patients treated included triple negative (n = 7), hormone receptor (HR)+/HER2- (n = 7), HR+/HER2+ (n = 6), and HR−/HER2+ (n = 3). Fourteen patients had stage IV disease prior to BCBM diagnosis. The median number of brain metastases treated per patient was 3 (1 to 12). The median dose of stereotactic radiosurgery (SRS) was 21 Gy (range: 15–24 Gy) treated in a single fraction and for lesions treated with fractionated stereotactic radiation therapy (FSRT) 25 Gy (24–30 Gy) in a median of 5 fractions (range: 3–5). Of the 31 stereotactic sessions, 71% occurred within 1 month of capecitabine. No increased toxicity was noted in our series with no cases of radionecrosis. The 1-year OS, LC, and DIC were 46, 88, and 30%, respectively. Conclusions In our single institution experience, we demonstrate stereotactic radiation and capecitabine to be a safe treatment for patients with BCBM with adequate LC. Further study is needed to determine the potential synergy between stereotactic radiation and capecitabine in the management of BCBM.

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Management of brain metastases in breast cancer: a review of current practices and emerging treatments

Cited by 59 publications

References 144 publications

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

<p>Down-Regulated CMTM2 Promotes Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma</p>

Understanding Patterns of Brain Metastasis in Triple-Negative Breast Cancer and Exploring Potential Therapeutic Targets

Capecitabine and stereotactic radiation in the management of breast cancer brain metastases

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