Abstract
One of the possible mechanisms contributing to the intrinsic resistance of cancer stem cells (CSCs) to conventional therapies is the inefficiency of activating the apoptotic machinery. In a recent study by Lang and colleagues, the engineered constitutively active pro-apoptotic protein BikDD, which works by inhibiting multiple Bcl-2 family members, was tested in various preclinical breast cancer models. Delivered to cells via an innovative cancer cell-specific gene-therapy approach, BikDD showed potent activity against CSCs and synergized with lapatinib and paclitaxel treatment. This novel and promising therapy warrants further translation to the clinic.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Apoptosis / drug effects*
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Apoptosis Regulatory Proteins / metabolism
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Apoptosis Regulatory Proteins / pharmacology*
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Apoptosis Regulatory Proteins / therapeutic use
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Breast Neoplasms / drug therapy*
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Breast Neoplasms / metabolism
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Breast Neoplasms / pathology
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CD24 Antigen / drug effects
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Female
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Humans
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Hyaluronan Receptors / drug effects
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Lapatinib
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Membrane Proteins / pharmacology*
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Membrane Proteins / therapeutic use
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Mice
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Mice, Inbred NOD
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Mice, SCID
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Mitochondrial Proteins
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Neoplastic Stem Cells / drug effects*
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Neoplastic Stem Cells / metabolism
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Paclitaxel / therapeutic use
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Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors*
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Quinazolines / therapeutic use
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RNA Interference
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RNA, Small Interfering
Substances
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Apoptosis Regulatory Proteins
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BIK protein, human
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CD24 Antigen
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Hyaluronan Receptors
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Membrane Proteins
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Mitochondrial Proteins
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Proto-Oncogene Proteins c-bcl-2
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Quinazolines
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RNA, Small Interfering
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Lapatinib
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Paclitaxel