2013
DOI: 10.1016/j.canlet.2012.04.023
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Breast cancer stem cells: Obstacles to therapy

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Cited by 64 publications
(74 citation statements)
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“…90 These are the breast cancer stem cells (BCSCs) which are often characterized based on their ability to initiate tumors in immunocompromised or syngeneic mice, self-renewal capacity as measured by tumor formation in secondary mice and also the ability to differentiate into the non-self-renewing cells, which constitute the tumor bulk. 91 BCSCs are commonly identified using the characteristic CD44 + /CD24 -/low marker profile or Aldefluor assays.…”
Section: Micrornas and Breast Cancer Stem Cellsmentioning
confidence: 99%
“…90 These are the breast cancer stem cells (BCSCs) which are often characterized based on their ability to initiate tumors in immunocompromised or syngeneic mice, self-renewal capacity as measured by tumor formation in secondary mice and also the ability to differentiate into the non-self-renewing cells, which constitute the tumor bulk. 91 BCSCs are commonly identified using the characteristic CD44 + /CD24 -/low marker profile or Aldefluor assays.…”
Section: Micrornas and Breast Cancer Stem Cellsmentioning
confidence: 99%
“…DLGAP5 has been proposed to be a target of the neurogenic locus notch homolog protein 3 signaling pathway (59), which is associated with embryogenesis and breast cancer tumorigenesis (60). DLAGP5 is reportedly a member of the cervical cancer interaction network (61), and has been revealed to be overexpressed in ovarian carcinoma compared with in normal ovarian epithelium (59).…”
Section: Cancer Typementioning
confidence: 99%
“…Overactivation of the Notch pathway has been implicated particularly in breast CSCs, possibly by influencing the EMT and contributing to the invasiveness of the CSCs. [26] One group investigated the effects of the bioactive compound psoralidin on Notch signaling in a breast cancer model. The plant-derived drug inhibited Notch signaling in both bulk tumor and CSCs, resulting in decreased mammosphere formation, upregulation of pro-apoptotic proteins, and inhibition of CSC proliferation.…”
Section: Regulating Csc Signaling Pathwaysmentioning
confidence: 99%